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Saturday, 22 July
23:01
Weekend reads: Stanford president to resign; untrustworthy clinical trials; cruel and fake animal experiments Retraction Watch
Would you consider a donation to support Weekend Reads, and our daily work?
The week at Retraction Watch featured:
- Journal to retract papers that cost its impact factor and spot in leading index
- Econ study retracted after researchers find undocumented alterations in the code
- Journal asks scientist to step down from editorial board after sleuths comments linked him to paper mill
- Journal editors resign, strike in dispute with Wiley over business model that maximises profit
- Florida university fires criminology professor blemished by retractions
- Sage retracting three dozen articles for compromised peer review
Our list of retracted or withdrawn COVID-19 papers is up to...
20:00
Giving Caregivers a Platform: Sam, Husband of Karyn Marie Mad In America
For many caregivers who assist their loved ones, the journey involves navigating the medical system and its many challenges. This time, the journey takes a different course, avoiding the usual psychiatric treatment model entirely as a husband helps his wife through her experiences with alters (usually classified as Dissociative Identity Disorder, or DID). Together, attachment theory and his own supportive approach have proved instrumental in helping her on her ongoing path to healing.
Sam Ruck (his pen name) has been part of the Mad in America community for a few years, providing supportive material for others caring for loved ones living with DID. The story of Sam and his wife, Karyn Marie, thrive on the tenets of love, commitment and healing, each of equal footing. Sam has also written a bookhes looking for a publisherabout his transformation as a good healing companion to his wife.
Married for 35 years, they come from a devout Evangelical faith that has evolved over time. While they attended different churches in the sam...
10:00
Regenerative Medicine and the Cell Danger Response Articles
In the first part of this series, I introduced the concept of the Cell Danger Response (CDR), an ancient defensive mechanism cells enter in response to environmental stressors. The CDR is orchestrated by the mitochondria, which switch from a metabolic type that produces energy that sustains the cell to a metabolic state focused on defending the cell (thereby making the cell much more resistant to otherwise lethal injuries).
Once the CDR is activated, the cell enters a partially dormant state (as many cellular functions depend upon the regular activity of the mitochondria) and signals other cells in its vicinity to also enter the CDR.
Ideally, the CDR should proceed through three phases (with the third, CDR3 being where the cell reintegrates with the body) and then terminate. Unfortunately, it often fails to do so, leaving the cells in a chronically impaired state where they are disconnected from the body.
Although the protective role of the CDR has a vital role in sustaining life, in the modern age, people frequently are exposed to a volume of stressors that significantly exceeds what the CDR originally evolved to handle. This results in a chronically activated CDR, which in turn gives rise to a wide range of chronic and complex illnesses.
The medical field (particularly those practicing integrative medicine) has become more and more open to the idea mitochondrial dysfunction is the root cause of many illnesses.
The CDR provides important context to that paradigm, as it illustrates mitochondrial dysfunction is not something that just happens and needs to be treated with supplementation; instead, it often needs to be viewed as an adaptive response, and to treat the mitochondrial dysfunction, the CDR itself must be the focus of treatment.
My focus was drawn back to the CDR after I realized that the most effective treatments I had found for spike protein injuries (e.g., within minutes, they created a dramatic shift in the wellbeing of the patient in some cases restoring functionality which had been lost for months) worked by either repairing the zeta potential of the body or treating the danger response. In turn, Ive come to believe these are two primary issues in patients with spike protein injuries (e.g., from the vaccines).
Unfortunately, while the CDR provides an excellent framework for understanding complex illnesses, the available tools for treating the CDR are still quite limited and require a comprehensive understanding of the CDR to use correctly. Fortunately, another field, regenerative medicine, regularly works with dormant cells and has found a variety of ways to reactivate them.
Surgery and Regenerative Medicine
Often, we run into the problem that a part of the body doesnt work right (to the point it significantly impacts someones...
How Your Future Is Being Decided for You Articles
In the featured video, Ivor Cummins interviews professor Richard Werner, author of Princes of the Yen Japan's Central Bankers and the Transformation of the Economy1 on The Fat Emperor Podcast. Werner has a Ph.D., in economics from Oxford University. He was a visiting scholar with the bank of Japan back in the 1990s.
In 1995, he created a monetary policy known as quantitative easing, which is intended to help banks get out of financial crises more rapidly and avoid long-term recession.
More recently, Werner created a community interest company called Local First, which provides communities with the know-how to set up local community banks. In this interview, he breaks down how the world works from a central banking standpoint, how ordinary people are affected by these policies, what we can expect from central bank digital currencies (CBDCs) and more.
How Central Bankers Rule the World
In his book, Princes of the Yen, Werner describes how theres a small group of insiders inside the central bank, running the whole show. While they direct the medias attention to interest rates, thats a bit of a decoy. Theyre not focused on the price of money but rather the quantity of money, measured in terms of quantity of credit creation.
This tiny core group of insiders are selected in their early 30s when they join the Bank of Japan and told that they will become governor of the bank in 30 years time. These are referred to as the princes. They control the boom-and-bust cycles in Japan, through their control of the quantity of credit.
Similar factions exist in other central banks as well, Werner says, and these central bankers are not accountable for their actions. They use this power to engineer events that serve their own purposes (typically connected to increasing their own power).
In 2003, Werner warned that the European Central Bank (ECB) was a monster that would create bank credit-driven asset bubbles and property bubbles, followed by banking crises and recessions, which is precisely what happened.
The Central Bank Plan to Monopolize Global Finance
Werner points out that while central banks are promoting CBDCs as digital currency, weve had digital currency for decades, so theres nothing new about the digital aspect of this currency. Cash paper banknotes and coins are but a small part about 3% in most countries of the total money supply. The rest is digital.
Today, central banks are the only ones authorized to issue banknotes, but regular banks create 97% of the money...
A Critical Look at 'The China Study' and Other Food Plans Articles
Editor's Note: This article is a reprint. It was originally published July 8, 2018.
Denise Minger is perhaps most noted for her comprehensive rebuttal of "The China Study" some eight years ago. She's heavily vested in the vegan versus omnivore battle, having cycled through vegetarianism and raw veganism, finally coming full circle to being an omnivore.
Minger took to vegetarianism when she was just 7 years old. "I was eating steak one night at dinner and almost choked on it. I developed some kind of phobia surrounding things with meat textures and went vegetarian overnight," she explains.
Raw Veganism Took a Toll on Health
However, during the 10 years she remained a vegetarian, she began developing food allergies, including wheat and dairy allergies. "By the time I was a teenager, I was really health-conscious," she says. "I had to get into that whole scene just to stay healthy."
At age 15, she discovered the raw vegan movement and got on the 80/10/10 diet, promoted by Dr. Douglas Graham. The diet is based on the hypothesis that we should eat what other primates eat, particularly frugivorous chimpanzees and bonobos.
"I was reading about it online at the age of 15 without having any background in human biology, physiology or anthropology I fell into this trap of logic, that humans are the only animals that cook our food. We're the only animals that eat this species-inappropriate diet, [so] I went raw vegan overnight," she says. "For one year straight, [I ate] nothing but fruits, vegetables and some nuts all uncooked.
I did great for the first month, as most people do when they stop eating crappy foods. After that, I started losing weight and muscle. My hair was falling out. My energy levels were fluctuating like crazy.
I was in high school at the time, taking the Scholastic Assessment Test (SAT). My brain fog got so bad at one point that when I was taking the SAT, I would read the question and by the time I got to the end I couldn't remember what the first part said
The kicker for me, because I've always taken great care of my teeth, was at the end of this period of raw veganism I had 16 cavities in my mouth, after a lifetime of what had previously been perfect dental health It was actually the dental health issue that really turned my mind around At that point, I had to let go of the vegan philosophy. I had to start questioning things
That's when I came across things like the Weston A. Price Foundation, which [details] what humans have been eating that has supported health in the past. I...
08:44
Freemasons are Collecting DNA and Biometric Data of Children for Tracking Purposes Medical Kidnap
What is CHiP? The Masonic Child Identification Programs Used to Track Your Child
by Patrick Webb
Leading Report
Excerpts:
According to Wikipedia, North American Masonic lodges have created the Masonic Child Identification Programs (CHIP) as a charitable endeavor to help locate and identify missing children. The Grand Lodge provides financial assistance for CHIP programs, which are run by volunteers from lower-level lodges and are manned by law enforcement and dentistry professionals.
The CHIP programs give parents the option to free-of-charge assemble an identification kit for their child. The kit includes a tooth impression card, a DNA sample, a VHS video, computer disk, or DVD of the child, a fingerprint card, and a physical description of the child. In the event that a kid is reported missing, the kits goal is to give the general public and law authorities access to vital information. The National Center for Missing and Exploited Children has praised the initiative.
In addition to a video recording the childs appearance and voice, the VHS tape or DVD contains information specific to the childs age group that can help locate kids who might be missing for causes other than abduction.
State and local law enforcement organizations have used the Masonic Child ID Program as their example for creating this service. Masonic CHIP differs from other programs in that municipal and police enforcement organizations often enter all information they get, including fingerprints, into a database.
Read the full article here.
Comment on this article at HealthImpactNews.com.
...
08:43
Freemasons are Collecting DNA and Biometric Data of Children for Tracking Purposes Vaccine Impact
What is CHiP? The Masonic Child Identification Programs Used to Track Your Child
by Patrick Webb
Leading Report
Excerpts:
According to Wikipedia, North American Masonic lodges have created the Masonic Child Identification Programs (CHIP) as a charitable endeavor to help locate and identify missing children. The Grand Lodge provides financial assistance for CHIP programs, which are run by volunteers from lower-level lodges and are manned by law enforcement and dentistry professionals.
The CHIP programs give parents the option to free-of-charge assemble an identification kit for their child. The kit includes a tooth impression card, a DNA sample, a VHS video, computer disk, or DVD of the child, a fingerprint card, and a physical description of the child. In the event that a kid is reported missing, the kits goal is to give the general public and law authorities access to vital information. The National Center for Missing and Exploited Children has praised the initiative.
In addition to a video recording the childs appearance and voice, the VHS tape or DVD contains information specific to the childs age group that can help locate kids who might be missing for causes other than abduction.
State and local law enforcement organizations have used the Masonic Child ID Program as their example for creating this service. Masonic CHIP differs from other programs in that municipal and police enforcement organizations often enter all information they get, including fingerprints, into a database.
Read the full article here.
Comment on this article at HealthImpactNews.com.
...
08:35
Freemasons are Collecting DNA and Biometric Data of Children for Tracking Purposes Health Impact News
What is CHiP? The Masonic Child Identification Programs Used to Track Your Child
by Patrick Webb
Leading Report
Excerpts:
According to Wikipedia, North American Masonic lodges have created the Masonic Child Identification Programs (CHIP) as a charitable endeavor to help locate and identify missing children. The Grand Lodge provides financial assistance for CHIP programs, which are run by volunteers from lower-level lodges and are manned by law enforcement and dentistry professionals.
The CHIP programs give parents the option to free-of-charge assemble an identification kit for their child. The kit includes a tooth impression card, a DNA sample, a VHS video, computer disk, or DVD of the child, a fingerprint card, and a physical description of the child. In the event that a kid is reported missing, the kits goal is to give the general public and law authorities access to vital information. The National Center for Missing and Exploited Children has praised the initiative.
In addition to a video recording the childs appearance and voice, the VHS tape or DVD contains information specific to the childs age group that can help locate kids who might be missing for causes other than abduction.
State and local law enforcement organizations have used the Masonic Child ID Program as their example for creating this service. Masonic CHIP differs from other programs in that municipal and police enforcement organizations often enter all information they get, including fingerprints, into a database.
Read the...
08:35
Peeping Tom Neighbors? New Doorbell Camera Links to Social Media Accounts and Uses Facial Recognition Medical Kidnap
by Brian Shilhavy
Editor, Health Impact News
Gullible and ignorant Americans are putting more and more of their private lives online often in exchange for the promise of more security.
Big Tech and law enforcement agencies want to thank those of you participating in their plans to create a complete police state where they can track every aspect of your lives through smart devices and homes, as you voluntarily surrender all the data of your personal lives to them.
When the next pandemic or other national emergency false flag event happens, it will be much easier to lock down the public, especially in the cities, as you give them direct livestream access to your homes and neighborhoods.
Irvinei is the latest startup technology company to enter the home doorbell camera market, and their technology goes a step further than current doorbell camera systems, as it allows one to link their social media accounts to the doorbell camera system, and it also uses facial recognition so it can identify almost anyone who comes to ones door, whether they consent to be recorded by the doorbell camera system or not.
A doorbell company wants to enable its buyers to identify visitors against images from social networks such as Facebook and Instagram.
Irvinei announced its doorbell promising a device with integrated fingerprint biometrics and facial recognition access control, an 8-megapixel camera and AI-powered edge lighting.
According to the firm, the product will launch soon on Kickstarter.
In a video, Irvinei suggests homeowners connect their social media accounts to its system in order to match visitors faces. The company has provided few details of its facial recognition software. (Source.)
As their video explains, they not only want the doorbell camera owner to load all their social media accounts to their system, th...
08:35
Peeping Tom Neighbors? New Doorbell Camera Links to Social Media Accounts and Uses Facial Recognition Vaccine Impact
by Brian Shilhavy
Editor, Health Impact News
Gullible and ignorant Americans are putting more and more of their private lives online often in exchange for the promise of more security.
Big Tech and law enforcement agencies want to thank those of you participating in their plans to create a complete police state where they can track every aspect of your lives through smart devices and homes, as you voluntarily surrender all the data of your personal lives to them.
When the next pandemic or other national emergency false flag event happens, it will be much easier to lock down the public, especially in the cities, as you give them direct livestream access to your homes and neighborhoods.
Irvinei is the latest startup technology company to enter the home doorbell camera market, and their technology goes a step further than current doorbell camera systems, as it allows one to link their social media accounts to the doorbell camera system, and it also uses facial recognition so it can identify almost anyone who comes to ones door, whether they consent to be recorded by the doorbell camera system or not.
A doorbell company wants to enable its buyers to identify visitors against images from social networks such as Facebook and Instagram.
Irvinei announced its doorbell promising a device with integrated fingerprint biometrics and facial recognition access control, an 8-megapixel camera and AI-powered edge lighting.
According to the firm, the product will launch soon on Kickstarter.
In a video, Irvinei suggests homeowners connect their social media accounts to its system in order to match visitors faces. The company has provided few details of its facial recognition software. (Source.)
As their video explains, they not only want the doorbell camera owner to load all their social media accounts to their system, th...
08:16
Peeping Tom Neighbors? New Doorbell Camera Links to Social Media Accounts and Uses Facial Recognition Health Impact News
by Brian Shilhavy
Editor, Health Impact News
Gullible and ignorant Americans are putting more and more of their private lives online often in exchange for the promise of more security.
Big Tech and law enforcement agencies want to thank those of you participating in their plans to create a complete police state where they can track every aspect of your lives through smart devices and homes, as you voluntarily surrender all the data of your personal lives to them.
When the next pandemic or other national emergency false flag event happens, it will be much easier to lock down the public, especially in the cities, as you give them direct livestream access to your homes and neighborhoods.
Irvinei is the latest startup technology company to enter the home doorbell camera market, and their technology goes a step further than current doorbell camera systems, as it allows one to link their social media accounts to the doorbell camera system, and it also uses facial recognition so it can identify almost anyone who comes to ones door, whether they consent to be recorded by the doorbell camera system or not.
A doorbell company wants to enable its buyers to identify visitors against images from social networks such as Facebook and Instagram.
Irvinei announced its doorbell promising a device with integrated fingerprint biometrics and facial recognition access control, an 8-megapixel camera and AI-powered edge lighting.
According to the firm, the product will launch soon on Kickstarter.
In a video, Irvinei suggests homeowners connect their social media accounts to its system in order to match visitors faces. The company has provided few details of its facial recognition software. (Source.)
07:29
Preparation, characterization, and evaluation of the antitumor effect of kaempferol nanosuspensions. GreenMedInfo
PMID: Drug Deliv Transl Res. 2023 May 6. Epub 2023 May 6. PMID: 37149557 Abstract Title: Preparation, characterization, and evaluation of the antitumor effect of kaempferol nanosuspensions. Abstract: Kaempferol (KAE) is a naturally occurring flavonoid compound with antitumor activity. However, the low aqueous solubility, poor chemical stability, and suboptimal bioavailability greatly restrict its clinical application in cancer therapy. To address the aforementioned limitations and augment the antitumor efficacy of KAE, we developed a kaempferol nanosuspensions (KAE-NSps) utilizing D--tocopherol polyethylene glycol 1000 succinate (TPGS) as a stabilizing agent, screened the optimal preparation process, and conducted a comprehensive investigation of their fundamental properties as well as the antitumor effects in the study. The findings indicated that the particle size was 186.62.6 nm of the TPGS-KAE-NSps optimized, the shape of which was fusiform under the transmission electron microscope. The 2% (w/v) glucose was used as the cryoprotectant for TPGS-KAE-NSps, whose drug loading content was 70.312.11%, and the solubility was prominently improved compared to KAE. The stability and biocompatibility of TPGS-KAE-NSps were favorable and had a certain sustained release effect. Moreover, TPGS-KAE-NSps clearly seen to be taken in the cytoplasm exhibited a stronger cytotoxicity and suppression of cell migration, along with increased intracellular ROS production and higher apoptosis rates compared to KAE in vitro cell experiments. In addition, TPGS-KAE-NSps had a longer duration of action in mice, significantly improved bioavailability, and showed a stronger inhibition of tumor growth (the tumor inhibition rate of high dose intravenous injection group was 68.91.46%) than KAE with no obvious toxicity in 4T1 tumor-bearing mice. Overall, TPGS-KAE-NSps prepared notably improved the defect and the antitumor effects of KAE, making it a promising nanodrug delivery system for KAE with potential applications as a clinical antitumor drug.
07:28
The role of flavonoids in the regulation of epithelial-mesenchymal transition in cancer. GreenMedInfo
PMID: Med Res Rev. 2023 May 5. Epub 2023 May 5. PMID: 37147865 Abstract Title: The role of flavonoids in the regulation of epithelial-mesenchymal transition in cancer: A review on targeting signaling pathways and metastasis. Abstract: One of the hallmarks of cancer is metastasis, a process that entails the spread of cancer cells to distant regions in the body, culminating in tumor formation in secondary organs. Importantly, the proinflammatory environment surrounding cancer cells further contributes to cancer cell transformation and extracellular matrix destruction. During metastasis, front-rear polarity and emergence of migratory and invasive features are manifestations of epithelial-mesenchymal transition (EMT). A variety of transcription factors (TFs) are implicated in the execution of EMT, the most prominent belonging to the Snail Family Transcriptional Repressor (SNAI) and Zinc Finger E-Box Binding Homeobox (ZEB) families of TFs. These TFs are regulated by interaction with specific microRNAs (miRNAs), as miR34 and miR200. Among the several secondary metabolites produced in plants, flavonoids constitute a major group of bioactive molecules, with several described effects including antioxidant, antiinflammatory, antidiabetic, antiobesogenic, and anticancer effects. This review scrutinizes the modulatory role of flavonoids on the activity of SNAI/ZEB TFs and on their regulatory miRNAs, miR-34, and miR-200. The modulatory role of flavonoids can attenuate mesenchymal features and stimulate epithelial features, thereby inhibiting and reversing EMT. Moreover, this modulation is concomitant with the attenuation of signaling pathways involved in diverse processes as cell proliferation, cell growth, cell cycle progression, apoptosis inhibition, morphogenesis, cell fate, cell migration, cell polarity, and wound healing. The antimetastatic potential of these versatile compounds is emerging and represents an opportunity for the synthesis of more specific and potent agents.
07:26
High polyphenol intake may help individuals to reduce systemic inflammation. GreenMedInfo
PMID: J Health Popul Nutr. 2023 May 5 ;42(1):39. Epub 2023 May 5. PMID: 37147659 Abstract Title: Inflammatory biomarkers in overweight and obese Iranian women are associated with polyphenol intake. Abstract: BACKGROUND: The evidence shows that obesity is associated with chronic inflammation in obese subjects. Polyphenols are a complex group of plant secondary metabolites that may play a role in reducing the risk of obesity and obesity-related diseases. Given the scarcity of evidence on the association between inflammatory markers and dietary polyphenols intake in overweight/obese Iranian women, the current study aims to investigate this link.METHOD: The present cross-sectional study was conducted on 391 overweight and obese Iranian women aged 18-48 years (body mass index (BMI)25 kg/m). A 147-item food frequency questionnaire (FFQ) was used to assess dietary intake, as well as anthropometric indices including weight, height, waist circumference (WC), and hip circumference (HC) and biochemistry parameters including triglyceride (TG), total cholesterol (Chole), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), serum glutamic pyruvic transaminase (SGPT), serum glutamic-oxaloacetic transaminase (SGOT), galactin-3 (Gal-3), monocyte chemoattractant protein-1 (MCP-1), transforming growth factor beta (TGF-), interleukin-1 beta (IL_1), plasminogen activator inhibitor-1 (PA-I), serum leptin concentrations, and C-reactive protein of high sensitivity (hs-CRP) in all participants. The inflammatory markers were assessed using the enzyme-linked immunosorbent assay (ELISA).RESULT: The findings revealed a significant negative association between flavonoids intake and MCP-1 (P=0.024), lignans intake and MCP-1 (P=0.017), and Gal-3 (P=0.032). These significant associations were observed between other polyphenols intake and IL_1(P=0.014). There was also a significant positive association between other polyphenol intake and TGF-(P=0.008) and between phenolic acid intake and TGF-(P=0.014).CONCLUSION: Our findings suggest that a high polyphenol intake may help individuals to reduce systemic inflammation. Further large studies involving participants of different ages and genders are highly warranted.
07:23
Nobiletin alleviates myocardial ischemia-reperfusion injury via ferroptosis in rats with type-2 diabetes mellitus. GreenMedInfo
n/a PMID: Biomed Pharmacother. 2023 Jul ;163:114795. Epub 2023 May 3. PMID: 37146415 Abstract Title: Nobiletin alleviates myocardial ischemia-reperfusion injury via ferroptosis in rats with type-2 diabetes mellitus. Abstract: Susceptibility to myocardial ischemia-reperfusion (IR) injury in type-2 diabetes (T2DM) remains disputed, although studies have reported that ferroptosis is associated with myocardial IR injury. Nobiletin, a flavonoid isolated from citrus peels, is an antioxidant that possesses anti-inflammatory and anti-diabetic activities. However, it remains unknown whether nobiletin has any protective effects on susceptibility to myocardial IR injury during T2DM in rats via ferroptosis. To investigate the effects and underlying mechanisms of nobiletin on myocardial IR injury during T2DM, we induced myocardial IR model in rats at T2DM onset vs mature disease. We also established a high-fat high-glucose (HFHG) and hypoxia-reoxygenation (H/R) model in H9c2 cells to imitate abnormal glycolipid metabolism during T2DM. Myocardial injury, oxidative stress and ferroptosis towards myocardial IR in rats with mature T2DM but not at T2DM onset were increased. These changes were restored under treatment with ferrostain-1 or nobiletin. Both ferrostain-1 and nobiletin decreased the expression of ferroptosis-related proteins including Acyl-CoA synthetase long chain family member 4 (ACSL4) and nuclear receptor coactivator 4 (NCOA4) but not glutathione peroxidase 4 (GPX4) in rats with mature T2DM and cells with HFHG and H/R injury. Nobiletin strengthened the effect of si-ACSL4 on inhibiting ACSL4 expression, and also inhibited the effect of Erastin or oe-ACSL4 on increasing ACSL4 expression. Taken together, our data indicates that ferroptosis involves in susceptibility to myocardial IR injury in rats during T2DM. Nobiletin has therapeutic potential for alleviating myocardial IR injury associated with ACSL4- and NCOA4-related ferroptosis.
07:22
Naringenin and -carotene convert human white adipocytes to a beige phenotype and elevate hormone- stimulated lipolysis. GreenMedInfo
PMID: Front Endocrinol (Lausanne). 2023 ;14:1148954. Epub 2023 Apr 17. PMID: 37143734 Abstract Title: Naringenin and-carotene convert human white adipocytes to a beige phenotype and elevate hormone- stimulated lipolysis. Abstract: INTRODUCTION: Naringenin, a peroxisome proliferator-activated receptor (PPAR) activator found in citrus fruits, upregulates markers of thermogenesis and insulin sensitivity in human adipose tissue. Our pharmacokinetics clinical trial demonstrated that naringenin is safe and bioavailable, and our case report showed that naringenin causes weight loss and improves insulin sensitivity. PPARs form heterodimers with retinoic-X-receptors (RXRs) at promoter elements of target genes. Retinoic acid is an RXR ligand metabolized from dietary carotenoids. The carotenoid-carotene reduces adiposity and insulin resistance in clinical trials. Our goal was to examine if carotenoids strengthen the beneficial effects of naringenin on human adipocyte metabolism.METHODS: Human preadipocytes from donors with obesity were differentiated in culture and treated with 8M naringenin + 2M-carotene (NRBC) for seven days. Candidate genes involved in thermogenesis and glucose metabolism were measured as well as hormone-stimulated lipolysis.RESULTS: We found that-carotene acts synergistically with naringenin to boost UCP1 and glucose metabolism genes including GLUT4 and adiponectin, compared to naringenin alone. Protein levels of PPAR, PPARand PPAR-coactivator-1, key modulators of thermogenesis and insulin sensitivity, were also upregulated after treatment with NRBC. Transcriptome sequencing was conducted and the bioinformatics analyses of the data revealed that NRBC induced enzymes for several non-UCP1 pathways for energy expenditure including triglyceride cycling, creatine kinases, and Peptidase M20 Domain Containing 1 (PM20D1). A comprehensive analysis of changes in receptor expression showed that NRBC upregulated eight receptors that have been linked to lipolysis or thermogenesis including the1-adrenergic receptor and the parathyroid hormone receptor. NRBC increased levels of triglyceride lipases and agonist-stimulated lipolysis in adipocytes. We observed that expression of RXR, an isoform of unknown function, was induced ten-fold after treatment with NRBC. We show that RXRis a coactivator bound to the immunoprecipitated PPARprotein complex from white and beige human adipocytes.DISCUSSION: There is a need for obesity treatments that can be administered long-term without side effects. NRBC increases the abundance and lipolytic response of multiple receptors for hormones released after exercise and cold exposure. Lipolysis provides the fuel for thermogenesis, and these observations suggest that NRBC has therapeutic potential.
...
07:20
Naringenin attenuates cerebral ischemia/reperfusion injury. GreenMedInfo
PMID: Acta Cir Bras. 2023 ;38:e380823. Epub 2023 May 1. PMID: 37132753 Abstract Title: Naringenin attenuates cerebral ischemia/reperfusion injury by inhibiting oxidative stress and inflammatory response via the activation of SIRT1/FOXO1 signaling pathway in vitro. Abstract: PURPOSE: To explore the protection of naringenin against oxygen-glucose deprivation/reperfusion (OGD/R)-induced HT22 cell injury, a cell model of cerebral ischemia/reperfusion (I/R) injury in vitro, focusing on SIRT1/FOXO1 signaling pathway.METHODS: Cytotoxicity, apoptosis, reactive oxygen species (ROS) generation, malondialdehyde (MDA) content, 4-hydroxynonenoic acid (4-HNE) level, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities were measured by commercial kits. Inflammatory cytokines levels were determined by enzyme-linked immunosorbent assay (ELISA). The protein expressions were monitored by Western blot analysis.RESULTS: Naringenin significantly ameliorated OGD/R-induced cytotoxicity and apoptosis in HT22 cells. Meanwhile, naringenin promoted SIRT1 and FOXO1 protein expressions in OGD/R-subjected HT22 cells. In addition, naringenin attenuated OGD/R-induced cytotoxicity, apoptosis, oxidative stress (the increased ROS, MDA and 4-HNE levels, and the decreased SOD, GSH-Px and CAT activities) and inflammatory response (the increased tumor necrosis factor-, interleukin [IL]-1, and IL-6 levels and the decreased IL-10 level), which were blocked by the inhibition of the SIRT1/FOXO1 signaling pathway induced by SIRT1-siRNA transfection.CONCLUSIONS: Naringenin protected HT22 cells against OGD/R injury depending on its antioxidant and anti-inflammatory activities via promoting the SIRT1/FOXO1 signaling pathway.
07:18
Naringenin as a promising candidate against COVID-19. GreenMedInfo
PMID: J Mol Struct. 2023 Sep 5 ;1287:135642. Epub 2023 Apr 26. PMID: 37131962 Abstract Title: Targeting the vital non-structural proteins (NSP12, NSP7, NSP8 and NSP3) from SARS-CoV-2 and inhibition of RNA polymerase by natural bioactive compound naringenin as a promising drug candidate against COVID-19. Abstract: The prevalence of SARS-CoV-2-induced respiratory infections is now a major challenge worldwide. There is currently no specific antiviral drug to prevent or treat this disease. Infection with COVID-19 seriously needs to find effective therapeutic agents. In the present study, naringenin, as a potential inhibitor candidate for RNA Polymerase SARS-CoV-2 was compared with remdesivir (FDA-approved drug) and GS-441,524 (Derivative of the drug remdesivir) by screening with wild-type and mutant SARS-CoV-2 NSP12 (NSP7-NSP8) and NSP3 interfaces, then complexes were simulated by molecular dynamics (MD) simulations to gain their stabilities. The docking results displayedscores of -3.45 kcal/mol and -4.32 kcal/mol against NSP12 and NSP3, respectively. Our results showed that naringenin hadG values more negative than theG values of Remdesivir (RDV) and GS-441,524. Hence, naringenin was considered to be a potential inhibitor. Also, the number of hydrogen bonds of naringenin with NSP3 and later NSP12 are more than Remdesivir and its derivative. In this research, Mean root mean square deviation (RMSD) values of NSP3 and NSP12with naringenin ligand (5.551.58 nm to 3.450.56 nm and 0.2380.01 to 0.2420.021 nm, respectively showed stability in the presence of ligand. The root mean square fluctuations (RMSF) values of NSP3 and NSP12 amino acid units in the presence of naringenin in were 1.5 0.31 nm and 0.1180.058, respectively. Pharmacokinetic properties and prediction of absorption, distribution, metabolism, excretion, and toxicity (ADMET) properties of naringenin and RDV showed thatthese two compounds had no potential cytotoxicity.
07:16
Naringenin blocks hepatic cadmium accumulation and suppresses cadmium-induced hepatotoxicity. GreenMedInfo
PMID: Drug Chem Toxicol. 2023 Apr 19:1-9. Epub 2023 Apr 19. PMID: 37073537 Abstract Title: Naringenin blocks hepatic cadmium accumulation and suppresses cadmium-induced hepatotoxicity via amelioration of oxidative inflammatory signaling and apoptosis in rats. Abstract: Liver is one of the targets of cadmium (Cd) bioaccumulation for hepatic damage and pathologies via oxidative inflammation and apoptosis. The current study explored whether the citrus flavonoid naringenin (NAR) could prevent hepatic accumulation of Cd and Cd hepatotoxicity in a rat model. Rats in group 1 received normal saline; group 2 received NAR (50mg/kg body weight); group 3 received CdCl(5mg/kg body weight); group 4 received NAR+CdCl, for four consecutive weeks. Assays related to markers of oxidative stress, inflammation, and apoptosis were carried out using liver homogenate. Blood and liver sample analyses revealed significant elevation of blood and hepatic Cd levels coupled with prominent increases in alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) activities, whereas the albumin and total protein levels were decreased considerably. Hepatic superoxide dismutase (SOD), catalase (CAT), glutathione peroxide (GPx) activities diminished significantly compared to control followed by marked increases in malondialdehyde (MDA) levels, and dysregulation in caspase and cytokine (TNF-, IL-6, IL-4, IL-10) levels. However, it was found that in the rats administered NAR+Cd, the levels of Cd, hepatic enzymes, MDA, TNF-, IL-6, and caspases-3/-9 were prominently reduced compared to the Cd group. The hepatic SOD, CAT, GPx, IL-4, IL-10, albumin, and total protein were markedly elevated along with alleviated hepatic histopathological abrasions. Taken together therefore, NAR is a potential flavonoid for blocking hepatic Cd bioaccumulation and consequent inhibition of Cd-induced oxidative inflammation and apoptotic effects on the liver of rats.
07:13
Naringenin facilitates M2 macrophage polarization after myocardial ischemia-reperfusion. GreenMedInfo
PMID: Environ Toxicol. 2023 Jun ;38(6):1405-1419. Epub 2023 Mar 29. PMID: 36988289 Abstract Title: Naringenin facilitates M2 macrophage polarization after myocardial ischemia-reperfusion by promoting nuclear translocation of transcription factor EB and inhibiting the NLRP3 inflammasome pathway. Abstract: Myocardial ischemia-reperfusion injury (MIRI) remains an unsolved puzzle in medical circles. Naringenin (NAR) is a flavonoid with cardioprotective potential. The purpose of this article was to discuss the protective mechanism of NAR in MIRI by regulating macrophage polarization. The MIRI mouse model was established and perfused with NAR before surgery. In the in vitro experiment, macrophages RAW264.7 were treated with lipopolysaccharide to induce M1 polarization after pretreatment with NAR. Rescue experiments were carried out to validate the functions of transcription factor EB (TFEB), the NLR pyrin domain containing 3 (NLRP3) inflammasome, and autophagy in macrophage polarization. NAR reduced histopathological injury and infarction of myocardial tissues in MIRI mice, inhibited M1 polarization and promoted M2 polarization of macrophages, diminished levels of pro-inflammatory factors, and augmented levels of anti-inflammatory factors. NAR facilitated TFEB nuclear translocation and inhibited the NLRP3 inflammasome pathway. Silencing TFEB or Nigericin partly nullified the effect of NAR on macrophage polarization. NAR increased autophagosome formation, autophagy flux, and autophagy level. Autophagy inhibitor 3-methyladenine partly invalidated the inhibition of NAR on the NLRP3 inflammasome pathway. In animal experiments, NAR protected MIRI mice through the TFEB-autophagy-NLRP3 inflammasome pathway. Collectively, NAR inhibited NLRP3 inflammasome activation and facilitated M2 macrophage polarization by stimulating TFEB nuclear translocation, thus protecting against MIRI.
07:11
Nobiletin ameliorates non-alcoholic fatty liver disease. GreenMedInfo
PMID: J Agric Food Chem. 2023 May 17 ;71(19):7312-7323. Epub 2023 May 4. PMID: 37139957 Abstract Title: Nobiletin Ameliorates Nonalcoholic Fatty Liver Disease by Regulating Gut Microbiota and Myristoleic Acid Metabolism. Abstract: Disturbance of the gut microbiota plays a critical role in the development of nonalcoholic fatty liver disease (NAFLD). Increasing evidence supports that natural products may serve as prebiotics to regulate the gut microbiota in the treatment of NAFLD. In the present study, the effect of nobiletin, a naturally occurring polymethoxyflavone, on NAFLD was evaluated, and metabolomics, 16S rRNA gene sequencing, and transcriptomics analysis were performed to determine the underlying mechanism of nobiletin, and the key bacteria and metabolites screened were confirmed by in vivo experiment. Nobiletin treatment could significantly reduce lipid accumulation in high-fat/high-sucrose diet-fed mice. 16S rRNA analysis demonstrated that nobiletin could reverse the dysbiosis of gut microbiota in NAFLD mice and nobiletin could regulate myristoleic acid metabolism, as revealed by untargeted metabolomics analysis. Treatment with the bacteria,, or the metabolite myristoleic acid displayed a protective effect on liver lipid accumulation under metabolic stress. These results indicated that nobiletin might target gut microbiota and myristoleic acid metabolism to ameliorate NAFLD.
07:10
Nobiletin ameliorates hepatic steatosis through regulation of lipid alternation. GreenMedInfo
PMID: J Nutr Biochem. 2023 Aug ;118:109353. Epub 2023 Apr 27. PMID: 37116815 Abstract Title: A lipidomic study: Nobiletin ameliorates hepatic steatosis through regulation of lipid alternation. Abstract: Hepatic lipidome has been given emphasis for years since hepatic steatosis is the most remarkable character of nonalcoholic fatty liver diseases, an increasingly serious health issue worldwide. Nobiletin (NOB), one of the citrus flavonoids, exerted outstanding effect on lipid metabolism disorder. However, the underlying mechanism of NOB exerting effect on hepatic lipid alternation remains unclear. In this study, the animal model was built by feeding APOEmice with high fat diet (HFD). The results of Oil Red O-stained liver section and the biochemical assay of lipid parameters confirmed the protective effect of NOB on hepatic steatosis and global lipid metabolism disorder in APOEmice. The hepatic lipidomic study revealed a total of 958 lipids significantly altered by HFD and a total of 86, 116, 212 lipid metabolites changed by L-NOB (50 mg/kg/d NOB), M-NOB (100 mg/kg/d NOB) and H-NOB (200 mg/kg/d NOB) respectively. In the further screening analysis, an amount of 60 lipids were identified as the potential lipid markers of NOB treatment, most of which belonged to glycerophospholipids lipid categories and exhibited obvious correlation with each other and the lipid parameters related to hepatic steatosis. Taken together, our data demonstrated that glycerophospholipids metabolism played an indispensable role in the progression of hepatic steatosis and the protective effect of NOB. Besides, the modulation towards genes involved in lipid synthesis was observed after NOB administration in this study. These finding illustrated the antihepatic steatosis effect of NOB based on altering hepatic lipidome, particularly the glycerophospholipids metabolism, and provided a new insight in the pathogenesis of hepatic steatosis.
07:07
Nobiletin improves D-galactose-induced aging mice skeletal muscle atrophy. GreenMedInfo
PMID: Nutrients. 2023 Apr 7 ;15(8). Epub 2023 Apr 7. PMID: 37111020 Abstract Title: Nobiletin Improves D-Galactose-Induced Aging Mice Skeletal Muscle Atrophy by Regulating Protein Homeostasis. Abstract: Sarcopenia, a decrease in skeletal muscle mass and function caused by aging, impairs mobility, raises the risk of fractures, diabetes, and other illnesses, and severely affects a senior's quality of life. Nobiletin (Nob), polymethoxyl flavonoid, has various biological effects, such as anti-diabetic, anti-atherogenic, anti-inflammatory, anti-oxidative, and anti-tumor properties. In this investigation, we hypothesized that Nob potentially regulates protein homeostasis to prevent and treat sarcopenia. To investigate whether Nob could block skeletal muscle atrophy and elucidate its underlying molecular mechanism, we used the D-galactose-induced (D-gal-induced) C57BL/6J mice for 10 weeks to establish a skeletal muscle atrophy model. The findings demonstrated that Nob increased body weight, hindlimb muscle mass, lean mass and improved the function of skeletal muscle in D-gal-induced aging mice. Nob improved myofiber sizes and increased skeletal muscle main proteins composition in D-gal-induced aging mice. Notably, Nob activated mTOR/Akt signaling to increase protein synthesis and inhibited FOXO3a-MAFbx/MuRF1 pathway and inflammatory cytokines, thereby reducing protein degradation in D-gal-induced aging mice. In conclusion, Nob attenuated D-gal-induced skeletal muscle atrophy. It is a promising candidate for preventing and treating age-associated atrophy of skeletal muscles.
07:05
Tangeretin could have a promising effect in counteracting lung cancer. GreenMedInfo
PMID: Life Sci. 2023 Jul 15 ;325:121749. Epub 2023 May 2. PMID: 37142089 Abstract Title: Role of NF-B/ICAM-1, JAK/STAT-3, and apoptosis signaling in the anticancer effect of tangeretin against urethane-induced lung cancer in BALB/c mice. Abstract: Lung carcinoma is one of the most prevalent and deadly neoplasia worldwide. Numerous synthetic medications have been used in the treatment of cancer. However, there are several drawbacks, such as side effects and inefficiency. The current study focused on the potential anti-cancer effectiveness of tangeretin, an antioxidant flavonoid, on lung cancer induced experimentally in BALB/c mice and explored the involvement of NF-B/ICAM-1, JAK/STAT-3, and caspase-3 signaling in its anti-cancer effect. BALB/c mice were injected with urethane (1.5 mg/kg) twice; on the first day and on the 60day of the experiment, then treated with 200 mg/kg tangeretin orally once daily for the last 4 weeks of the experiment. Compared with urethane group, tangeretin normalized oxidative stress markers; MDA, GSH, and SOD activity. Moreover, it had an anti-inflammatory effect by decreasing lung MPO activity, ICAM-1, IL-6, NF-B, and TNF-expressions. Interestingly, tangeretin decreased cancer metastasis by reducing p-JAK, JAK, p-STAT-3, and STAT-3 protein expression levels. Furthermore, it increased the apoptotic marker, caspase-3, indicating enhanced apoptosis of cancer cells. Finally, histopathology confirmed the anti-cancer effect of tangeretin. In conclusion, tangeretin could have a promising effect in counteracting lung cancer via modulation of NF-B/ICAM-1, JAK/STAT-3, and caspase-3 signaling.
07:02
Nobiletin intake attenuates hepatic lipid profiling and oxidative stress. GreenMedInfo
PMID: Molecules. 2023 Mar 12 ;28(6). Epub 2023 Mar 12. PMID: 36985541 Abstract Title: Nobiletin Intake Attenuates Hepatic Lipid Profiling and Oxidative Stress in HFD-Induced Nonalcoholic-Fatty-Liver-Disease Mice. Abstract: Nobiletin (NOB) is a naturally occurring compound, commonly found in citrus peel, that shows hepatoprotective and lipid-reducing effects. However, the lipid biomarkers and the potential improvement mechanisms have not been adequately explored. Therefore, we investigated the ameliorative effect and the molecular mechanism of NOB on NAFLD induced by a high-fat diet in mice. The results showed that supplementation with NOB over 12 weeks markedly improved glucose tolerance, serum lipid profiles, inflammatory factors, hepatic steatosis, and oxidative stress. These beneficial effects were mainly related to reduced levels of potential lipid biomarkers including free fatty acids, diacylglycerols, triacylglycerols, and cholesteryl esters according to hepatic lipidomic analysis. Twenty lipids, including DGs and phosphatidylcholines, were identified as potential lipid biomarkers. Furthermore, RT-qPCR and Western blot analysis indicated that NOB inhibited the expression of lipogenesis-related factors such as SREBP-1c, SCD-1, and FAS, and upregulated the expression of lipid oxidation (PPAR) and well as antioxidation-related factors (Nucl-Nrf2, NQO1, HO-1, and GCLC), indicating that NOB intake may reduce lipid biosynthesis and increase lipid consumption to improve hepatic steatosis and oxidative stress. This study is beneficial for understanding the ameliorative effects of NOB on NAFLD.
06:57
Suppressing NLRP3 activation and PI3K/AKT/mTOR signaling ameliorates amiodarone-induced pulmonary fibrosis. GreenMedInfo
PMID: Inflammopharmacology. 2023 Jun ;31(3):1373-1386. Epub 2023 Mar 22. PMID: 36947298 Abstract Title: Suppressing NLRP3 activation and PI3K/AKT/mTOR signaling ameliorates amiodarone-induced pulmonary fibrosis in rats: a possible protective role of nobiletin. Abstract: Amiodarone (AMD), a medicine used to treat life-threatening arrhythmias, is frequently linked to pulmonary fibrosis (PF). Despite the involvement of NLRP3 inflammasome and PI3K/Akt/mTOR axis in fibrosis modulation and development, their significance in the etiology of AMD-induced PF remains uncertain. Nobiletin (NOB), a citrus flavonoid, has recently gained attention for its ability to reduce fibrotic processes in a variety of organs through inhibiting NLRP3-associated inflammation and suppressing PI3K/AKT/mTOR fibrotic pathway. Therefore, this research aimed to investigate the possible beneficial impact of NOB against AMD-induced PF, taking into account the roles of NLRP3 and PI3K/AKT/mTOR axis in its pathogenesis. Twenty-four rats were randomly specified into Vehicle; NOB 20 mg/kg; AMD 30 mg/kg, and NOB+AMD. All treatments were administered orally once a day for 4 weeks. The lung oxidant/antioxidant status, as well as the expression of inflammatory and fibrotic markers were all assessed. The results revealed that NOB, by improving Nrf2/HO-1 pathway, could reduce ROS production and NLRP3 activation, which in turn hindered IL-1release, prohibited TGF-1-related PI3K/AKT/mTOR cascade, suppressed-SMA expression, and impeded collagen deposition. These findings point to a novel strategy by which NOB may alleviate the AMD-prompted NLRP3 inflammatory responses and associated PF through blocking PI3K/AKT/mTOR signaling.
06:55
Citrus aurantium can participate in the treatment of NSCLC through multiple targets and pathways. GreenMedInfo
PMID: Biomed Res Int. 2023 ;2023:6407588. Epub 2023 Jan 23. PMID: 36726839 Abstract Title: The Effect ofon Non-Small-Cell Lung Cancer: A Research Based on Network and Experimental Pharmacology. Abstract: PURPOSE: To screen the main active components ofthrough a network pharmacology approach, construct a component-disease target network, explore its molecular mechanism for the treatment of non-small-cell lung cancer (NSCLC), and validate it experimentally.METHODS: The active ingredients inand the targets ofand NSCLC were collected through the Traditional Chinese Medicine Systematic Pharmacology Database and Analysis Platform (TCMSP), GeneCards, and OMIM databases. The protein interaction network was constructed using the STRING database, and the component-disease relationship network graph was analyzed using Cytoscape 3.9.1. The Metascape database can be used for GO and KEGG enrichment analyses. The Kaplan-Meier plotter was applied for overall survival analysis of key targets ofin the treatment of NSCLC. Real-time PCR (RT-PCR) and Western blotting were used to determine the mRNA and protein levels of key targets offor the treatment of NSCLC.RESULTS: Five active ingredients ofwere screened, and 54 potential targets for the treatment of NSCLC were found, of which the key ingredient was nobiletin and the key targets are TP53, CXCL8, ESR1, PPAR-, and MMP9. GO and KEGG enrichment analyses indicated that the mechanism of nobiletin in treating NSCLC may be related to the regulation of cancer signaling pathway, phosphatidylinositol-3 kinase (PI3K)/protein kinase B (Akt) signaling pathway, lipid and atherosclerosis signaling pathway, and neurodegenerative signaling pathway. The experimental results showed that nobiletin could inhibit the proliferation of NSCLC cells and upregulate the levels of P53 and PPAR-and suppress the expression of MMP9 (
06:51
Berberine activates PPAR and promotes gut microbiota-derived butyric acid to suppress hepatocellular carcinoma. GreenMedInfo
PMID: Phytomedicine. 2023 Jul ;115:154842. Epub 2023 Apr 28. PMID: 37148713 Abstract Title: Berberine activates PPARand promotes gut microbiota-derived butyric acid to suppress hepatocellular carcinoma. Abstract: BACKGROUND: Peroxisome proliferator-activated receptors (PPARs) are a family of ligand-inducible transcription factors that govern various essential metabolic activities in the liver and other organs. Recently, berberine (BBR) has been characterized as a modulator of PPARs; however, the matter of whether PPARs are involved in the inhibitory effect of BBR on hepatocellular carcinoma (HCC) is not well understood.PURPOSE: This study aimed to investigate the role of PPARs in the suppressive effect of BBR on HCC and to elucidate the relative mechanism.METHODS: We studied the role of PPARs in the anti-HCC effects of BBR both in vitro and in vivo. The mechanism whereby BBR regulated PPARs was studied using real-time PCR, immunoblotting, immunostaining, luciferase, and a chromatin immunoprecipitation coupled PCR assay. Additionally, we used adeno-associated virus (AAV)-mediated gene knockdown to address the effect of BBR more effectively.RESULTS: We demonstrated that PPARplayed an active role in the anti-HCC effect of BBR, rather than PPARor PPAR. Following a PPAR-dependent manner, BBR increased BAX, cleaved Caspase 3, and decreased BCL2 expression to trigger apoptotic death, thereby suppressing HCC development both in vitro and in vivo. It was noted that the interactions between PPARand the apoptotic pathway resulted from the BBR-induced upregulation of the PPARtranscriptional function; that is, the BBR-induced activation of PPARcould mediate the binding with the promoters of apoptotic genes such as Caspase 3, BAX, and BCL2. Moreover, gut microbiota also contributed to the suppressive effect of BBR on HCC. We found that BBR treatment restored the dysregulated gut microbiota induced by the liver tumor burden, and a functional gut microbial metabolite, butyric acid (BA), acted as a messenger in the gut microbiota-liver axis. Unlike BBR, the effects of BA suppressing HCC and activating PPARwere not potent. However, BA was able to enhance the efficacy of BBR by reducing PPARdegradation through a mechanism to inhibit the proteasome ubiquitin system. Additionally, we found that the anti-HCC effect of BBR or a combination of BBR and BA was much weaker in mice with AAV-mediated PPARknockdown than those in the control mice, suggesting the critical role of PPAR.CONCLUSION: In summary, this study is the first to report that a liver-gut microbiota-PPARtrilogy contributes to the anti-HCC effect of BBR. BBR not only directly activated PPARto trigger apoptotic death but also promoted gut microbiota-derived BA production, which could reduce PPARdegradation to enhance the efficacy o...
06:47
Berberine stimulates lysosomal AMPK independent of PEN2 and maintains cellular AMPK activity through inhibiting the dephosphorylation regulator UHRF1. GreenMedInfo
PMID: Front Pharmacol. 2023 ;14:1148611. Epub 2023 Apr 18. PMID: 37144221 Abstract Title: Berberine stimulates lysosomal AMPK independent of PEN2 and maintains cellular AMPK activity through inhibiting the dephosphorylation regulator UHRF1. Abstract: AMPK is the key regulatory kinase mediating the effect of berberine (BBR) and metformin on metabolic improvement. The present study investigated the mechanism of BBR on AMPK activation at low doses, which was different from that of metformin.Lysosomes were isolated, and AMPK activity assay was performed. PEN2, AXIN1 and UHRF1 were investigated through gain/loss of function approaches, including overexpression, RNA interfering and CRISPR/Cas9-mediated gene knockout. Immunoprecipitation was utilized for detecting the interaction of UHRF1 and AMPK1 after BBR treatment.BBR activated lysosomal AMPK, but weaker than metformin. AXIN1 mediated BBR's effect on lysosomal AMPK activation, while PEN2 did not. BBR, but not metformin, decreased UHRF1 expression by promoting its degradation. BBR reduced the interaction between UHRF1 and AMPK1. And overexpression of UHRF1 abolished the effect of BBR on AMPK activation.BBR activated lysosomal AMPK as dependent on AXIN1, but not PEN2. BBR maintained cellular AMPK activity by reducing UHRF1 expression and its interaction with AMPK1. The mode of action of BBR was different from that of metformin on AMPK activation.
06:43
Berberine affects the proliferation, migration, invasion, cell cycle, and apoptosis of bladder cancer cells. GreenMedInfo
PMID: Arch Esp Urol. 2023 Mar ;76(2):152-160. PMID: 37139621 Abstract Title: Berberine Affects the Proliferation, Migration, Invasion, Cell Cycle, and Apoptosis of Bladder Cancer Cells T24 and 5637 by Down-Regulating the HER2/PI3K/AKT Signaling Pathway. Abstract: OBJECTIVE: To assess the anticancer effect, target, and mechanism of berberine on bladder cancer.METHODS: Bladder cancer T24 and 5637 cells were treated with different concentrations of berberine. Then, cell proliferation was assessed by cell counting kit-8 (CCK8) measure, cell migration and invasion were assessed by transwell method, cell cycle and apoptosis were assessed by flow cytometry, and the expression of human epidermal growth factor receptor-2/PhosphoInositide-3 Kinase/AKT Serine/Threonine Kinase (HER2/PI3K/AKT) proteins were assessed by Western blot. Berberine molecular docking and HER2 target were performed using the AutoDock Tools 1.5.6. Finally, HER2 inhibitors CP-724714 and berberine were used independently or in combination to detect AKT and P-AKT protein downstream changes by Western blot.RESULTS: Berberine inhibited the proliferation of T24 and 5637 bladder cancer cells in a concentration-dependent and time-dependent manner. Berberine can significantly inhibit the migration, invasion, and cell cycle progression of T24 and 5637 bladder cancer cells, promote their apoptosis, and down-regulate the expression of HER2/PI3K/AKT proteins. Berberine showed good docking with HER2 molecular target and had a similar and synergistic effect with HER2 inhibitor in T24 and 5637 bladder cancer cells.CONCLUSIONS: Berberine inhibited the proliferation, migration, invasion, and cell cycle progression of T24 and 5637 bladder cancer cells and promoted their apoptosis by down-regulating HER2/PI3K/AKT signaling pathway.
06:41
Berberine ameliorates chronic kidney disease through inhibiting the production of gut-derived uremic toxins in the gut microbiota. GreenMedInfo
PMID: Acta Pharm Sin B. 2023 Apr ;13(4):1537-1553. Epub 2022 Dec 20. PMID: 37139409 Abstract Title: Berberine ameliorates chronic kidney disease through inhibiting the production of gut-derived uremic toxins in the gut microbiota. Abstract: At present, clinical interventions for chronic kidney disease are very limited, and most patients rely on dialysis to sustain their lives for a long time. However, studies on the gut-kidney axis have shown that the gut microbiota is a potentially effective target for correcting or controlling chronic kidney disease. This study showed that berberine, a natural drug with low oral availability, significantly ameliorated chronic kidney disease by altering the composition of the gut microbiota and inhibiting the production of gut-derived uremic toxins, including-cresol. Furthermore, berberine reduced the content of-cresol sulfate in plasma mainly by lowering the abundance ofand inhibiting the tyrosine--cresol pathway of the intestinal flora. Meanwhile, berberine increased the butyric acid producing bacteria and the butyric acid content in feces, while decreased the renal toxic trimethylamine-oxide. These findings suggest that berberine may be a therapeutic drug with significant potential to ameliorate chronic kidney disease through the gut-kidney axis.
06:38
Berbamine suppresses intestinal SARS-CoV-2 infection. GreenMedInfo
PMID: Emerg Microbes Infect. 2023 Dec ;12(1):2195020. PMID: 36951188 Abstract Title: Berbamine suppresses intestinal SARS-CoV-2 infection via a BNIP3-dependent autophagy blockade. Abstract: SARS-CoV-2, the causative virus of COVID-19, continues to threaten global public health. COVID-19 is a multi-organ disease, causing not only respiratory distress, but also extrapulmonary manifestations, including gastrointestinal symptoms with SARS-CoV-2 RNA shedding in stool long after respiratory clearance. Despite global vaccination and existing antiviral treatments, variants of concern are still emerging and circulating. Of note, new Omicron BA.5 sublineages both increasingly evade neutralizing antibodies and demonstrate an increased preference for entry via the endocytic entry route. Alternative to direct-acting antivirals, host-directed therapies interfere with host mechanisms hijacked by viruses, and enhance cell-mediated resistance with a reduced likelihood of drug resistance development. Here, we demonstrate that the autophagy-blocking therapeutic berbamine dihydrochloride robustly prevents SARS-CoV-2 acquisition by human intestinal epithelial cells via an autophagy-mediated BNIP3 mechanism. Strikingly, berbamine dihydrochloride exhibited pan-antiviral activity against Omicron subvariants BA.2 and BA.5 at nanomolar potency, providing a proof of concept for the potential for targeting autophagy machinery to thwart infection of current circulating SARS-CoV-2 subvariants. Furthermore, we show that autophagy-blocking therapies limited virus-induced damage to intestinal barrier function, affirming the therapeutic relevance of autophagy manipulation to avert the intestinal permeability associated with acute COVID-19 and post-COVID-19 syndrome. Our findings underscore that SARS-CoV-2 exploits host autophagy machinery for intestinal dissemination and indicate that repurposed autophagy-based antivirals represent a pertinent therapeutic option to boost protection and ameliorate disease pathogenesis against current and future SARS-CoV-2 variants of concern.
06:35
Bisphenol P exposure in C57BL/6 mice caused gut microbiota dysbiosis and induced intestinal barrier disruption. GreenMedInfo
PMID: Environ Int. 2023 May ;175:107949. Epub 2023 Apr 25. PMID: 37126915 Abstract Title: Bisphenol P exposure in C57BL/6 mice caused gut microbiota dysbiosis and induced intestinal barrier disruption via LPS/TLR4/NF-B signaling pathway. Abstract: Despite being one of the most world's widely used and mass-produced compounds, bisphenol A (BPA) has a wide range of toxic effects. Bisphenol P (BPP), an alternative to BPA, has been detected in many foods. The effects of BPP dietary exposure on gut microbiota and the intestinal barrier were unclear. We designed three batches of animal experiments: The first studied mice were exposed to BPP (30 g/kg BW/day) for nine weeks and found that they gained weight and developed dysbiosis of the gut microbiota. The second, using typical human exposure levels (L, 0.3 g/kg BW/day BPP) and higher concentrations (M, 30 g/kg BW/day BPP; H, 3000 g/kg BW/day BPP), caused gut microbiota dysbiosis in mice, activated the Lipopolysaccharide (LPS) /TLR4/NF-B signaling pathway, triggered an inflammatory response, increased intestinal permeability, and promoted bacterial translocation leading to intestinal barrier disruption. The third treatment used a combination of antibiotics and alleviated intestinal inflammation and injury. This study demonstrated the mechanism of injury and concentration effects of intestinal damage caused by BPP exposure, providing reference data for BPP use and control and yielding new insights for human disease prevention.
06:31
Exposure to bisphenol A induces neurotoxicity associated with synaptic and cytoskeletal dysfunction in neuro-2a cells. GreenMedInfo
PMID: Toxicol Ind Health. 2023 Jun ;39(6):325-335. Epub 2023 Apr 25. PMID: 37122122 Abstract Title: Exposure to bisphenol A induces neurotoxicity associated with synaptic and cytoskeletal dysfunction in neuro-2a cells. Abstract: Bisphenol A (BPA) has been reported to injure the developing and adult brain. However, the underlying mechanism still remains elusive. This study used neuro-2a cells as a cellular model to investigate the neurotoxic effects of BPA. Microtubule-associated protein 2 (MAP2) and tau protein maintain microtubule normal function and promote the normal development of the nervous system. Synaptophysin (SYP) and drebrin (Dbn) proteins are involved in regulating synaptic plasticity. Cells were exposed to the minimum essential medium (MEM), 0.01% (v/v) DMSO, and 150 M BPA for 12, 24, or 36 h. Morphological analysis revealed that the cells in the BPA-treated groups shrank and collapsed compared with those in the control groups. CCK-8 and lactate dehydrogenase assay (LDH) assays showed that the mortality of neuro-2a cells increased as the BPA treatment time was prolonged. Ultrastructural analysis further revealed that cells demonstrated nucleolar swelling, dissolution of nuclear and mitochondrial membranes, and partial mitochondrial condensation following exposure to BPA. BPA also decreased the relative protein expression levels of MAP2, tau, and Dbn. Interestingly, the relative protein expression levels of SYP increased. These results indicated that BPA inhibited the proliferation and disrupted cytoskeleton and synaptic integrity of neuro-2a cells.
06:26
BPA exposure enhances the metastatic aggression of ovarian cancer. GreenMedInfo
PMID: Food Chem Toxicol. 2023 Jun ;176:113792. Epub 2023 Apr 18. PMID: 37080528 Abstract Title: BPA exposure enhances the metastatic aggression of ovarian cancer through the ER/AKT/mTOR/HIF-1signaling axis. Abstract: Long-term exposure to bisphenol A (BPA) in humans may promote ovarian cancer development. In present study, the mechanisms by which BPA mediates the aggression metastatic behavior of ovarian cancer were investigated in vitro/in vivo. The results showed that BPA (10 M) significantly promoted the proliferation, migration and invasion of human ovarian cancer cells (ES-2 and OVCAR-3 cells); moreover, it promoted ES-2 and OVCAR-3 cell glucose uptake, lactic acid release and intracellular ATP synthesis. After administration of 5 g/kg/day BPA, tumor volume was increased compared with that in control group. KEGG and GO enrichment analyses showed that the genes from ES-2 cell in 10 M BPA-treated group were enriched mainly in central carbon metabolism and PI3K-AKT signaling pathway. Then, qRTPCR and western blotting results showed that BPA (10 M) increased the mRNA and protein expression levels of glycolysis-related genes and mTOR, p-AKT HIF-1and ERin vitro/vivo; whereas this effect was reduced after treatment with the ERinhibitor methyl-piperidino-pyrazole. Furthermore, coimmunoprecipitation and mass spectrometry showed that BPA promoted the direct interaction of ERwith lactate dehydrogenase A. These results show that BPA directly promoted the proliferation, migration and invasion of ovarian cancer cells through the ER/AKT/mTOR/HIF-1signaling axis to enhance glycolysis.
06:20
Red grape juice extract prevents BPA-induced vascular damage modulating specific intracellular mechanisms. GreenMedInfo
PMID: Toxics. 2023 Apr 21 ;11(4). Epub 2023 Apr 21. PMID: 37112618 Abstract Title: Protective Effects of a Red Grape Juice Extract against Bisphenol A-Induced Toxicity in Human Umbilical Vein Endothelial Cells. Abstract: Human exposure to bisphenol A (BPA) occurs through the ingestion of contaminated food and water, thus leading to endothelial dysfunction, the first signal of atherosclerosis.L. (grape) juice is well known for its health-promoting properties, due to its numerous bioactive compounds among which are polyphenols. The aim of this study was to evaluate the protective effect of a red grape juice extract (RGJe) against the endothelial damage induced by BPA in human umbilical vein endothelial cells (HUVECs) as an in vitro model of endothelial dysfunction. Our results showed that RGJe treatment counteracted BPA-induced cell death and apoptosis in HUVECs, blocking caspase 3 and modulating p53, Bax, and Bcl-2. Moreover, RGJe demonstrated antioxidant properties in abiotic tests and in vitro, where it reduced BPA-induced reactive oxygen species as well as restored mitochondrial membrane potential, DNA integrity, and nitric oxide levels. Furthermore, RGJe reduced the increase of chemokines (IL-8, IL-1, and MCP-1) and adhesion molecules (VCAM-1, ICAM-1, and E-selectin), caused by BPA exposure, involved in the primary phase of atheromatous plaque formation. Overall, our results suggest that RGJe prevents BPA-induced vascular damage modulating specific intracellular mechanisms, along with protecting cells, owing to its antioxidant capability.
06:15
Influence of gut microbiota on metabolism of bisphenol A. GreenMedInfo
PMID: Toxics. 2023 Mar 31 ;11(4). Epub 2023 Mar 31. PMID: 37112567 Abstract Title: Influence of Gut Microbiota on Metabolism of Bisphenol A, a Major Component of Polycarbonate Plastics. Abstract: Bisphenol A (BPA) is a major component of polycarbonate plastics and epoxy resins. While many studies have investigated the effect BPA exposure has upon changes in gut microbial communities, the influence of gut microbiota on an organism's ability to metabolize BPA remains comparatively unexplored. To remedy this, in this study, Sprague Dawley rats were intermittently (i.e., at a 7-day interval) or continuously dosed with 500g BPA/kg bw/day for 28 days, via oral gavage. In the rats which underwent the 7-day interval BPA exposure, neither their metabolism of BPA nor their gut microbiota structure changed greatly with dosing time. In contrast, following continuous BPA exposure, the relative level ofandin the rats' guts significantly increased, and the alpha diversity of the rats' gut bacteria was greatly reduced. Meanwhile, the mean proportion of BPA sulfate to total BPA in rat blood was gradually decreased from 30 (on day 1) to 7.4% (by day 28). After 28 days of continuous exposure, the mean proportion of BPA glucuronide to total BPA in the rats' urine elevated from 70 to 81%, and in the rats' feces the mean proportion of BPA gradually decreased from 83 to 65%. Under continuous BPA exposure, the abundances of 27, 25, and 24 gut microbial genera were significantly correlated with the proportion of BPA or its metabolites in the rats' blood, urine, and feces, respectively. Overall, this study principally aimed to demonstrate that continuous BPA exposure disrupted the rats' gut microbiota communities, which in turn altered the rats' metabolism of BPA. These findings contribute to the better understanding of the metabolism of BPA in humans.
06:00
Protective effects of selenium nanoparticles against bisphenol A-induced toxicity in porcine intestinal epithelial cells. GreenMedInfo
PMID: Int J Mol Sci. 2023 Apr 14 ;24(8). Epub 2023 Apr 14. PMID: 37108405 Abstract Title: Protective Effects of Selenium Nanoparticles against Bisphenol A-Induced Toxicity in Porcine Intestinal Epithelial Cells. Abstract: Bisphenol A (BPA) is widely used to harden plastics and polycarbonates and causes serious toxic effects in multiple organs, including the intestines. Selenium, as an essential nutrient element for humans and animals, exhibits a predominant effect in various physiological processes. Selenium nanoparticles have attracted more and more attention due to their outstanding biological activity and biosafety. We prepared chitosan-coated selenium nanoparticles (SeNPs) and further compared the protective effects, and investigated the underlying mechanism of SeNPs and inorganic selenium (NaSeO) on BPA-induced toxicity in porcine intestinal epithelial cells (IPEC-J2). The particle size, zeta potential, and microstructure of SeNPs were detected by using a nano-selenium particle size meter and a transmission electron microscope. IPEC-J2 cells were exposed to BPA alone or simultaneously exposed to BPA and SeNPs or NaSeO. The CCK8 assay was performed to screen the optimal concentration of BPA exposure and the optimal concentration of SeNPs and NaSeOtreatment. The apoptosis rate was detected by flow cytometry. Real-time PCR and Western blot methods were used to analyze the mRNA and protein expression of factors related to tight junctions, apoptosis, inflammatory responses and endoplasmic reticulum stress. Increased death and morphological damage were observed after BPA exposure, and these increases were attenuated by SeNPs and NaSeOtreatment. BPA exposure disturbed the tight junction function involved with decreased expression of tight junction protein Zonula occludens 1 (ZO-1), occludin, and claudin-1 proteins. Proinflammatory response mediated by the transcription factor nuclear factor-k-gene binding (NF-B), such as elevated levels of--,--,--,--, and tumor necrosis-(-expression was induced at 6 and 24 h after BPA exposure. BPA exposure also disturbed the oxidant/antioxidant status and led to oxidative stress. IPEC-J2 cell apoptosis was induced by BPA exposure, as indicated by increased BCL-2-associated X protein (Bax), caspase 3, caspase 8, and caspase 9 expression and decreased B-cell lymphoma-2 (Bcl-2) and Bcl-xl expression. BPA exposure activated the endoplasmic reticulum stress (ERS) mediated by the receptor protein kinase receptor-like endoplasmic reticulum kinase (PERK), Inositol requiring enzyme 1 (IRE1), and activating transcription factor 6 (ATF6). We found that treatment with SeNPs and NaSeOcan alleviate the intestinal damage caused by BPA. SeNPs were superior to NaSeOand counteracted BPA-induced tight junction function injury, proinflammatory response, oxidative stre...
05:53
Patients Are Still Being Misinformed About Electroconvulsive Therapy Mad In America
From Psychology Today/John Read, PhD: Two years ago I reported, here, on our survey of patient information leaflets about electroconvulsive therapy (ECT) in England. On the basis of leaflets from 36 of 51 clinics (71%), we concluded that informed consent is not being complied with, because: Patients are being misled about the risks they are taking and the limited nature of ECTs benefits.
This month sees the publication of two follow up papers. The first1 is a replication of our first audit, in ECT clinics in Northern Ireland, Scotland and Wales . . . The idea for the study came from our co-author Lisa Morrison who has had 96 ECTs herself.
The results were almost as disappointing as the England audit. The number of accurate statements (out of a possible 29) ranged from seven to 20, with an average of 16.9. The most frequently omitted crucial pieces of information were: cardiovascular risks (included by only five leaflets), that it is not known how ECT works (3), risk of mortality (2), risks from multiple general anaesthetic procedures (2), how to access a legal advocate (2), and that that there is no evidence of long-term benefits (1).
The leaflets also made between six and nine inaccurate statements (out of 11) with an average of 7.0. Nineteen minimised memory loss, blamed the memory loss on depression, claimed that ECT is the most effective treatment, and asserted it has very high response rates without mentioning similar placebo response rates. All 23 leaflets told patients that ECT saves lives, although almost all studies either find no difference between ECT and non-ECT groups, or that the ECT group has higher suicide rates.
***
Back to Around the Web
The post Patients Are Still Being Misinformed About Electroconvulsive Therapy appeared first on Mad In America...
05:49
Induction of reproductive injury by bisphenol A and the protective effects of cyanidin-3-O-glucoside and protocatechuic acid. GreenMedInfo
PMID: Sci Total Environ. 2023 Jul 20 ;883:163615. Epub 2023 Apr 25. PMID: 37105472 Abstract Title: Induction of reproductive injury by bisphenol A and the protective effects of cyanidin-3-O-glucoside and protocatechuic acid in rats. Abstract: Bisphenol A (BPA) has attracted growing attention as a well-known environmental pollutant due to its high risk of male reproductive toxicity. In this study, transcriptomics profiling combined with metabolomic techniques was applied to explore the intervention effects of BPA-induced male reproductive toxicity. We demonstrated that cyanidin-3-O-glucoside (C3G) and its main metabolite protocatechuic acid (PCA) significantly increased testosterone and luteinizing hormone (LH) levels in the serum of rats, and improved sperm quality. Furthermore, we identified and screened differentially expressed genes (DEGs) and metabolites (DMs) that functionally enriched in the steroidogenesis-related pathways. Next, the validated results found that C3G and PCA significantly up-regulated the gene expressions of Star, Cyp11a1, Cyp17a1, Cyp19a1, Cyp7a1, Hsd3b1, Hsd3b2, Hsd17b3, Scrab1, and Ass1 in testicular. In Leydig cells, C3G and PCA dramatically alleviated apoptosis, ROS accumulation, and cell cycle arrest caused by BPA. In addition, molecular docking and simulation results implied that C3G and PCA competitively with BPA bind to the estrogen receptorsand(ERand ER) and shared common key amino acids. The main interaction modes between small molecules and estrogen receptors included-stacking, salt bridges, hydrogen bonds, and hydrophobic interactions. Therefore, our study sheds light on C3G and PCA supplementation can protect male reproduction from BPA-induced injury.
05:36
Low dose prenatal bisphenol A exposure on adiposity in male and female ICR offspring. GreenMedInfo
PMID: Ecotoxicol Environ Saf. 2023 Jun 1 ;257:114946. Epub 2023 Apr 25. PMID: 37105096 Abstract Title: In vivo effects of low dose prenatal bisphenol A exposure on adiposity in male and female ICR offspring. Abstract: BACKGROUND: Bisphenol A (BPA) is known to exhibit endocrine disrupting activities and is associated with adiposity. We examined the obesogenic effect of prenatal BPA exposure in the present study.METHODS: Pregnant ICR mice were exposed to vehicle or BPA via the drinking water at a dose of 0.5 g/kgd throughout the gestation. Obesity-related indexes were investigated in the 12-wk-old offspring. Primary mouse embryonic fibroblasts (MEFs) collected from treated embryos were used to test effects of BPA on adipocyte differentiation.RESULTS: Offspring presented a significantly higher rate of weight gain than the control, with impaired insulin sensitivity and increased adipocyte size. Differentiation of MEFs from BPA-treated mice showed a higher propensity for the adipocyte commitment as well as up-regulation of genes enriched in lipid biosynthesis. TGF-signaling pathway was found to modulate obesogenic effect of BPA in MEF model, but estrogen signaling pathway had no effect.CONCLUSIONS: The present study provides strong evidence of the association between prenatal exposure to low dose of BPA and a significant increase in body weight in the offspring mice with a critical role played by TGF-signaling pathway. The potential interactions modulating the binding of BPA and TGF-that activate its obesogenic effects need to be examined.
05:32
A grape juice supplemented with natural grape extracts is well accepted by consumers and reduces brain oxidative stress. GreenMedInfo
PMID: Antioxidants (Basel). 2021 Apr 26 ;10(5). Epub 2021 Apr 26. PMID: 33926060 Abstract Title: A Grape Juice Supplemented with Natural Grape Extracts Is Well Accepted by Consumers and Reduces Brain Oxidative Stress. Abstract: Neurodegenerative diseases pose a major health problem for developed countries. Stress, which induces oxidation in the brain, has been identified as the main risk factor for these disorders. We have developed an antioxidant-enriched drink and have examined its protective properties against acute oxidative stress. We found that addition of red grape polyphenols and MecobalActiveto grape juice did not provoke changes in juice organoleptic characteristics, and that the pasteurization process did not greatly affect the levels of flavonoids and vitamin B12. Out of all combinations, grape juice with red grape polyphenols was selected by expert judges (28.6% selected it as their first choice). In vivo, oral administration of grape juice supplemented with red grape polyphenols exerted an antioxidant effect in the brain of stressed mice reducing two-fold the expression of genes involved in inflammation and oxidation mechanisms and increasing three-fold the expression of genes related to protection against oxidative stress. In addition, we found that this drink augmented antioxidant enzyme activity (17.8 vs. 8.2 nmol/mg), and prevented lipid peroxidation in the brain (49.7 vs. 96.5 nmol/mg). Therefore, we propose supporting the use of this drink by the general population as a new and global strategy for the prevention of neurodegeneration.
05:10
RFK Jr. Proves HHS is in Violation of Vaccine Safety Requirements Under the Law Mandate for Safer Childhood Vaccines Children's Health Defense
In 1986, Congress passed one of the most troubling pieces of legislation in modern history, the National Childhood Vaccine Injury Act (NCVIA), which shields vaccine manufacturers from almost all state-law tort liability. See 42 U.S.C 300aa22 as interpreted by Bruesewitz v. Wyeth LLC, 562 U.S. 223 (2011). One feature of the bill that gave at least some hope to vaccine safety advocates was the inclusion of a stipulation titled Mandate for Safer Childhood Vaccines, which placed responsibility for vaccine safety directly in the hands of the Secretary of the U.S. Department of Health and Human Services (HHS). See 42 U.S.C. 300aa27. Part of this Mandate required that HHS submit a report to Congress every two years detailing the agencys research and other efforts to improve the safety of vaccines given to children.
In May 2017, Robert F. Kennedy Jr. invited Del Bigtree, Aaron Siri and Lyn Redwood to a meeting with Dr. Anthony Fauci, Dr. Francis Collins and several other public health officials at the Executive Office of the National Institutes of Health (NIH). For many years, Kennedy had been loudly pointing out that the Department of Health and Human Services (HHS) had not only neglected to conduct large-scale vaccinated versus unvaccinated research, but they had also failed to test the seventy-one doses of vaccines on the childhood schedule against inert placebos. Kennedy directly asked Fauci and Collins for evidence of true placebo controlled studies using inert placebos which neither could produce. During the meeting, Kennedy and his team became concerned that HHS might not be fulfilling the obligations placed upon the agency under 42 U.S.C. 300aa-27.
The Informed Consent Action Network (ICAN) filed a Freedom of Information Act request in Aug. 2017 seeking the biennial reports that HHS was to have submitted to Congress starting in 1989 as stipulated by the Mandate for Safer Childhood Vaccines. In April of 2018, having still heard nothing as a result of the FOIA request, Kennedy and attorney Aaron Siri...
04:37
Sage retracting three dozen articles for compromised peer review Retraction Watch
Sage Publishing is retracting 37 articles from an engineering journal after finding indicators of third party involvement in the peer review process.
The publishers investigation continues, and more papers may be retracted, a spokesperson for the company told Retraction Watch.
A single retraction notice lists the links of the 37 papers to be retracted from Proceedings of the Institution of Mechanical Engineers, Part E: Journal of Process Mechanical Engineering. The notice states:
After an internal investigation Sage became aware that the peer-review process for these articles had been compromised and contains indicators of third-party involvement.
As these were accepted because of a peer-review process that did not meet Sages expectations of high quality and ethical peer-review, the publisher cannot uphold the integrity of the research. In line with COPE guidelines and Sage policies, these articles are retracted.
The authors have been informed of this decision using the email addresses provided at submission.
Ooi Kim Tiow, the journals editor in chief and an associate provost at Nanyang Technological University in Singapore, has not responded to our request for comment.
Only one of the papers has attracted notice on PubPeer. In June of last year, sleuth Alexander Magazinov commented that Applications of fractional derivatives in MHD free-convective oscillating flow of a blood based CNTs nanofluid across a porous medium contained A hollow sentence with a bulk citation to the benefit of a certain YM Chu.
Early this year, Sage became aware of concerns with the journals content after one article showed indicators of third party activity and compromised peer review, a spokesperson...
03:04
So Long, Psych Meds: Escaping the Medication Maze Mad In America
There are as many different ways to approach this story as there are stories and tales within the story. This is more of a chronology and a first attempt to begin to put a narrative on a time that defied all logic and almost led me to my death on myriad occasions in myriad ways. It is by no means an exhaustive tale and the number of both contributing and resulting variables is vast.
There are many tales yet to be told. They are currently tangled together in a long-confused brain but the hope is that with the writing and the telling begins the unravelling of the confusion.
The evening of June 27th 2023 marked the two-year anniversary since I choked down my final offering of psychiatric medication. It was a small quarter of a tablet of lithium maybe 100mg, maybe 50mg. How lucky I feel to not be able to remember exactly what strengths they come in. There was a time when I could think of nothing else but pills and prescriptions, pain and panic. Psychiatry shrank my world. It eradicated vision and possibility. It was time-consuming and energy consuming. It served as the ultimate distraction. Ive come across the quote about drugging our poets and prophets but Id go one step further to ask whether we are drugging our humanity, our very essence and our ability to function in the world in any meaningful way.
I was introduced to psychiatric medications following a severe back injury in...
02:10
7 Ways to Use Free Electrons to Stop Inflammation (rapidly and dramatically) The Healthy Home Economist
The many ways to harness the power of free electrons to dramatically and rapidly reduce silent or painful systemic bodily inflammation. Inflammation is arguably one of the most if not the most common reasons for the epidemic of chronic disease today. Hence, keeping body tissues free of inflammation is of paramount importance and a key
The post 7 Ways to Use Free Electrons to Stop Inflammation (rapidly and dramatically) appeared first on The Healthy Home Economist.
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Friday, 21 July
21:50
The Dog Days of Summer Are Donation Days for Age of Autism Age of Autism The Rebel Alliance!
Autism doesn't take a V-A-C-A-T-I-O-N and neither do we. Thanks for considering a tax deductible donation. Donorbox is safe and secure. Paper checks to PO Box 110546 Trumbull CT 06611. Thank you! Kim
21:00
Childhood Vaccination Rates Move (Slowly) in the Right Direction Science-Based Medicine
Childhood vaccination rates worldwide tanked during the first two years of the pandemic. A recently released report from the UN revealed that 2022 was better, but the improvements weren't seen everywhere. And we still have a long way to go.
The post Childhood Vaccination Rates Move (Slowly) in the Right Direction first appeared on Science-Based Medicine.11:30
Potential protective effects of red grape seed extract in a rat model of malathion-induced neurotoxicity. GreenMedInfo
PMID: Vet World. 2023 Feb ;16(2):380-385. Epub 2023 Feb 26. PMID: 37042003 Abstract Title: Potential protective effects of red grape seed extract in a rat model of malathion-induced neurotoxicity. Abstract: BACKGROUND AND AIM: Exposure to pesticide mixtures used in agricultural practice poses a grave risk to non-target animals. This study aimed to determine whether red grape seed extract (RGSE, which is 95% bioflavonoids and equal to 12,000 mg of fresh red grape seed, and 150 mg of vitamin C) alleviated the changes in brain-derived neurotrophic factor (BDNF) level, acetylcholinesterase activity, oxidative stress, and apoptosis induced by orally administered malathion in a rat model of malathion-induced neurotoxicity.MATERIALS AND METHODS: Thirty-two adult male Wistar albino rats were divided into four groups and exposed to malathion with or without 4 weeks of RGSE treatment, treated with RGSE alone, or left untreated as controls. The animals were euthanized 24 h after last treatment. Brain samples were collected to measure acetylcholinesterase, superoxide dismutase (SOD), and caspase 3 activity, total antioxidant capacity (TAC), and BDNF levels.RESULTS: Malathion significantly reduced acetylcholinesterase and SOD activity and TAC and significantly increased caspase 3 activity. In comparison, acetylcholinesterase and SOC activity, BDNF level, and TAC were improved and caspase 3 activity was decreased in the malathion-RGSE group, indicating that RGSE corrected the alterations detected in these biochemical parameters.CONCLUSION: Oxidative stress and apoptosis in the brains of rats exposed to oral malathion were substantially controlled by RGSE treatment.
11:27
Grape seed proanthocyanidin extract attenuates cigarette smoke extract-induced lung inflammation and emphysema. GreenMedInfo
PMID: Food Chem Toxicol. 2023 Jul ;177:113795. Epub 2023 Apr 26. PMID: 37116776 Abstract Title: GSPE attenuates CSE-induced lung inflammation and emphysema by regulating autophagy via the reactive oxygen species/TFEB signaling pathway. Abstract: Cigarette smoke can enhance reactive oxygen species (ROS) production in inflammatory and epithelial cells. Subsequently, ROS enhance autophagy-induced inflammation due to alveolar macrophages (AMs), the primary source of cytokines implicated in chronic obstructive pulmonary disease (COPD) pathogenesis. Therefore, we hypothesized that grape seed proanthocyanidin extract (GSPE), an effective antioxidant, could inhibit emphysema and airway inflammation by ameliorating cigarette smoke extract (CSE)-induced autophagy via suppressing oxidative stress in macrophages. We observed that GSPE significantly attenuated histological changes observed in CSE-induced emphysema and airway inflammation in the lungs of mice. Moreover, GSPE ameliorated lung inflammation by reducing the number of cells, macrophages, and neutrophils and the tumor necrosis factor (TNF)-, interleukin (IL)-1, and IL-6 levels measured in bronchioloalveolar lavage fluid. ROS levels increased after CSE instillation and significantly decreased with in vitro GSPE treatment. GSPE decreased transcription factor EB (TFEB) oxidation by reducing ROS, inhibiting TFEB nuclear translocation. Furthermore, GSPE inhibited ROS-induced autophagy in RAW 264.7 cells, bone marrow-derived macrophages, and AMs. Inhibiting autophagy through GSPE treatment diminishes CSE-induced lung inflammation by inhibiting the NLRP3 inflammasome. This study demonstrates that GSPE can ameliorate CSE-induced inflammation and emphysema via autophagy-induced NLRP3 inflammasome regulation through the ROS/TFEB signaling pathway in a COPD mouse model.
11:10
Grape seed proanthocyanidins inhibit replication of the dengue virus. GreenMedInfo
PMID: Viruses. 2023 Mar 30 ;15(4). Epub 2023 Mar 30. PMID: 37112864 Abstract Title: Grape Seed Proanthocyanidins Inhibit Replication of the Dengue Virus by Targeting NF-kB and MAPK-Mediated Cyclooxygenase-2 Expression. Abstract: Dengue virus (DENV) infection is a serious global health issue as it causes severe dengue hemorrhagic fever and dengue shock syndrome. Since no approved therapies are available to treat DENV infection, it is necessary to develop new agents or supplements that can do this. In this study, grape seed proanthocyanidins extract (GSPE), which is widely consumed as a dietary supplement, dose-dependently suppressed the replication of four DENV serotypes. The inhibitory mechanism demonstrated that GSPE downregulated DENV-induced aberrant cyclooxygenase-2 (COX-2) expression, revealing that the inhibitory effect of the GSPE on DENV replication involved targeting DENV-induced COX-2 expression. Mechanistic studies on signaling regulation have demonstrated that GSPE significantly reduced COX-2 expression by inactivating NF-B and ERK/P38 MAPK signaling activities. Administrating GSPE to DENV-infected suckling mice reduced virus replication, mortality, and monocyte infiltration of the brain. In addition, GSPE substantially reduced the expression of DENV-induced inflammatory cytokines associated with severe dengue disease, including tumor necrosis factor-, nitric oxide synthase, interleukin (IL)-1, IL-6, and IL-8, suggesting that GSPE has potential as a dietary supplement to attenuate DENV infection and severe dengue.
10:51
Stearoyl-CoA desaturases1 accelerates non-small cell lung cancer metastasis. GreenMedInfo
PMID: Int J Mol Sci. 2023 Apr 6 ;24(7). Epub 2023 Apr 6. PMID: 37047797 Abstract Title: Stearoyl-CoA Desaturases1 Accelerates Non-Small Cell Lung Cancer Metastasis by Promoting Aromatase Expression to Improve Estrogen Synthesis. Abstract: Metastases contribute to the low survival rate of non-small cell lung cancer (NSCLC) patients. Targeting lipid metabolism for anticancer therapies is attractive. Accumulative evidence shows that stearoyl-CoA desaturases1 (SCD1), a key enzyme in lipid metabolism, enables tumor metastasis and the underlying mechanism remains unknown. In this study, immunohistochemical staining of 96 clinical specimens showed that the expression of SCD1 was increased in tumor tissues (
10:48
'Once You Start Censoring, Youre on Your Way to Dystopia and Totalitarianism,' RFK Jr. Tells House Committee GreenMedInfo
RFK Jr. testified before a U.S. House hearing organized by the Subcommittee on the Weaponization of the Federal Government
10:47
'Once You Start Censoring, Youre on Your Way to Dystopia and Totalitarianism,' RFK Jr. Tells House Committee GreenMedInfo
Originally published on www.childrenshealthdefense.org by Michael
Nevradakis, Ph.D.
In a hearing marred by contentious interruptions and attempts by House Democrats to remove him as a witness, Robert F. Kennedy Jr., CHD chairman on leave from Children's Health Defense testified before a U.S. House hearing organized by the Subcommittee on the Weaponization of the Federal Government.
10:22
Effect of grape seed extract on oxidative stress and pathological changes of aorta in rats with chronic periodontitis and arteriosclerosis. GreenMedInfo
PMID: Shanghai Kou Qiang Yi Xue. 2022 Dec ;31(6):597-601. PMID: 36970794 Abstract Title: [Effect of grape seed extract on oxidative stress and pathological changes of aorta in rats with chronic periodontitis and arteriosclerosis]. Abstract: PURPOSE: To investigate the effect of grape seed extract on pathological changes of aorta in rats with chronic periodontitis and arteriosclerosis, and to analyze the possible mechanism.METHODS: Fifteen SPF male rats with chronic periodontitis and arteriosclerosis were randomly divided into three groups, i.e., model group(n=5), low dose of grape seed extract group (n=5), high dose of grape seed extract group (n=5) , and control group (n=10). The rats in the low and high dose groups were treated with 40 mgkg-1d-1 and 80 mgkg-1d-1 for 4 weeks respectively, while the rats in the normal control group and the model group were treated with the same amount of normal saline at the same time. The maximal intima-media thickness(IMT) of abdominal aorta was measured by H-E staining, the activity of SOD and the content of MDA in serum were measured by colorimetry, the content of GSH-px in serum and serum levels of inflammatory factor (TNF-) and interleukin-6(IL-6) were detected by ELISA. p38 mitogen-activated protein kinase/nuclear transcription factor Kappa B p65(p38 MAPK/NF-B p65) pathway was detected by Western blotting. SPSS 20.0 software package was used for statistical analysis.RESULTS: In the model group, the intima of abdominal aorta was irregularly thickened, with a lot of inflammatory cell infiltration, and arterial lesions appeared. In the low-and high-dose groups of grape seed extract, the plaque of abdominal aorta intima decreased and inflammatory cells reduced significantly, arterial vascular disease was improved, and the improvement was more obvious in high dose group than in low dose group. Compared with the control group, the levels of IMT, serum MDA, TNF-, IL-6, p-p38MAPK/p38MAPK, NF-B p65 and serum SOD and GSH-px in the model group were increased, while those in the model group were decreased(P0.05); the levels of IMT, serum MDA, TNF-, IL-6, p-p38MAPK/p38MAPK, NF-B p65 and SOD, GSH-px were decreased in the low and high dose groups(P0.05).CONCLUSIONS: Grape seed extract can inhibit the oxidative stress level and inflammatory reaction in serum of chronic periodontitis with arteriosclerosis rats, thus improving the intimal lesion of aorta, possibly by inhibiting the activation of p38MAPK/NF-B p65 pathway.
10:19
Sound of Freedom: A Movie About Child Trafficking Produced by Child Traffickers? Medical Kidnap
by Brian Shilhavy
Editor, Health Impact News
I have been vehemently attacked and criticized by some people for daring to publish critical articles about the Sound of Freedom movie, especially the article about the people who funded the movie. See:
Sound of Freedom Movie Allegedly Funded by Billionaire Philanthropists with Ties to Human Trafficking
A Kevin J wrote this comment about that article:
What a ridiculous article. Conclusions are based on allegedly and might have ties to this or that, and guilt-by-association darts. So a guy who allegedly helped fund the film (in other words, rumor has it) might have ties to cartels and the Clintons. No evidence anywhere this guy helped fund the movie.
But the source for this funding is Tim Ballard himself, who stated who was funding the movie in an interview in Utah 5 years ago on Fox News. Here is the clip from Fox 13 News in Utah. The original interview is here.
This same local news outlet, Fox 13 News Utah, also reported in 2020 that Tim Ballards organization, Operation Underground Railroad, was under criminal investigation for its fundraising methods.
Some people have also attacked me for referring to Sound of Freedom as a fictional movie, and not a documentary.
But again, the source of this information is Tim Ballard himself, who...
10:18
Sound of Freedom: A Movie About Child Trafficking Produced by Child Traffickers? Vaccine Impact
by Brian Shilhavy
Editor, Health Impact News
I have been vehemently attacked and criticized by some people for daring to publish critical articles about the Sound of Freedom movie, especially the article about the people who funded the movie. See:
Sound of Freedom Movie Allegedly Funded by Billionaire Philanthropists with Ties to Human Trafficking
A Kevin J wrote this comment about that article:
What a ridiculous article. Conclusions are based on allegedly and might have ties to this or that, and guilt-by-association darts. So a guy who allegedly helped fund the film (in other words, rumor has it) might have ties to cartels and the Clintons. No evidence anywhere this guy helped fund the movie.
But the source for this funding is Tim Ballard himself, who stated who was funding the movie in an interview in Utah 5 years ago on Fox News. Here is the clip from Fox 13 News in Utah. The original interview is here.
This same local news outlet, Fox 13 News Utah, also reported in 2020 that Tim Ballards organization, Operation Underground Railroad, was under criminal investigation for its fundraising methods.
Some people have also attacked me for referring to Sound of Freedom as a fictional movie, and not a documentary.
But again, the source of this information is Tim Ballard himself, who...
10:18
Targeting Nrf2 signaling pathway and oxidative stress by resveratrol for Parkinson's disease. GreenMedInfo
PMID: Mol Biol Rep. 2023 Jun ;50(6):5455-5464. Epub 2023 May 8. PMID: 37155008 Abstract Title: Targeting Nrf2 signaling pathway and oxidative stress by resveratrol for Parkinson's disease: an overview and update on new developments. Abstract: Parkinson's disease (PD) as a prevalent neurodegenerative condition impairs motor function and is caused by the progressive deterioration of nigrostriatal dopaminergic (DAergic) neurons. The current therapy solutions for PD are ineffective because they could not inhibit the disease's progression and they even have adverse effects. Natural polyphenols, a group of phytochemicals, have been found to offer various health benefits, including neuroprotection against PD. Among these, resveratrol (RES) has neuroprotective properties owing to its capacity to protect mitochondria and act as an antioxidant. An increase in the formation of reactive oxygen species (ROS) leads to oxidative stress (OS), which is responsible for cellular damage resulting in lipid peroxidation, oxidative protein alteration, and DNA damage. In PD models, it's been discovered that RES pretreatment can diminish oxidative stress by boosting endogenous antioxidant status and directly scavenging ROS. Several studies have examined the involvement of RES in the modulation of the transcriptional factor Nrf2 in PD models because this protein recognizes oxidants and controls the antioxidant defense. In this review, we have examined the molecular mechanisms underlying the RES activity and reviewed its effects in both in vitro and in vivo models of PD. The gathered evidence herein showed that RES treatment provides neuroprotection against PD by reducing OS and upregulation of Nrf2. Moreover, in the present study, scientific proof of the neuroprotective properties of RES against PD and the mechanism supporting clinical development consideration has been described.
10:09
Resveratrol inhibits restenosis through suppressing proliferation, migration and trans-differentiation of vascular adventitia fibroblasts. GreenMedInfo
PMID: Curr Med Chem. 2023 May 5. Epub 2023 May 5. PMID: 37151061 Abstract Title: Resveratrol inhibits restenosis through suppressing proliferation, migration and trans-differentiation of vascular adventitia fibroblasts via activating SIRT1. Abstract: AIM: After the balloon angioplasty, vascular adventitia fibroblasts (VAFs), which proliferate, trans-differentiate to myofibroblasts and migrate to neointima, are crucial in restenosis. Resveratrol (RSV) has been reported to protect the cardiovascular by reducing restenosis and the mechanism remains unclear.METHOD: This study was dedicated to investigate the effect of RSV on VAFs in injured arteries and explore the potential mechanism. In this work, carotid artery balloon angioplasty was performed on male SD rats to ensure the injury of intima and VAFs were isolated to explore the effects in vitro. The functional and morphological results showed the peripheral delivery of RSV decreased restenosis of the injured arteries and suppressed the expression of proliferation, migration and transformation related genes. Moreover, after being treated with RSV, the proliferation, migration and trans-differentiation of VAFs were significantly suppressed and exogenous TGF-1 can reverse this effect.RESULT: Mechanistically, RSV administration activated SIRT1 and decreased the translation and expression of TGF-1, SMAD3 and NOX4, and reactive oxygen species (ROS) decreased significantly after VAFs treated with RSV.CONCLUSION: Above results indicated RSV inhibited restenosis after balloon angioplasty through suppressing proliferation, migration and trans-differentiation of VAFs via regulating SIRT1- TGF-1-SMAD3-NOX4 to decrease ROS.
10:00
Documentary Stare Into the Lights, My Pretties Articles
Editor's Note: This article is a reprint. It was originally published April 14, 2018.
Technology didn't come about by accident, it's a reflection of human will, or so claims the intriguing documentary, "Stare Into the Lights My Pretties." Yet, with the rate of technological development continuing to grow exponentially, it's unclear if anyone envisioned how society would become obsessed with staring at screens, such that our waking hours are dominated by them in one form or another.
In the beginning, there were only a few ways to get new technology funded, known as the ABCs. "A," for armed forces, included ARPA, the Advanced Research Projects Agency, which commissioned the work that started the internet.
"B," for bureaucracy, refers to innovations such as government sites intended to deliver information and services, including online tax returns. "C," or corporate power, made up the third arm, which drove the development of new products to draw in new markets.
According to Lelia Green, a professor and senior lecturer at the school of communications at Edith Cowan University, Perth, Australia, who is featured in the film, "Google would offer many examples of corporate power driven development."1 Yet, social engagement is the new driver of technology that has taken off more so in recent years. Green notes that distributed collaborators and everyday innovators are now an important driver of technology.
"The acknowledgement of distributed networks of collaborators allows recognition of the creative power of harnessing the hive;' the community of people engaged in a shared activity," she says. "We see these alliances of enthusiasts working creatively and productively in gaming contexts, in wikis and on fan fiction sites to name but a few," but what does all of this mean, and what will happen if this technological culture is left to continue unchecked?
Are Machines Running Our Lives?
At the foundation of the documentary is the unsettling question of who's really in control: the machines or us? The film gives some unsettling statistics of how integrated technology has become in our 21st century lives:
- Over 3.8 billion people have access to the internet
- There are 2 billion active Facebook users every month
- The average adult spends more than eight hours a day with screens (more time than sleep)
- Within the first 15 minutes of waking up, 4 out of 5 smartphone users check their phones
- By the time the average person reaches 70, they will have spent the equivalent of 10 to 15 years of their life watching television, more than fo...
The video above features a lecture that Del Bigtree gave in early 2023 in California. Bigtree is the founder and CEO of the Informed Consent Action Network (ICAN) and hosts the internet talk show The Highwire.
When the COVID pandemic hit, antivaxxers were suddenly named as one of the Top 10 health threats worldwide. Thats when Bigtree realized we were really getting somewhere, and public trust in Big Pharma and our health authorities has continued to dwindle since then, as more and more truth is getting out.
What I can prove is what matters to me, and what I'm really obsessed with is putting Tony Fauci and Deborah Birx and all the rest of these people in prison, he says.
So what I'm going to lay out for you today is sort of my court case on what took place here, and why I believe we will win a case of crimes against humanity. This is our best case going forward.
Bigtrees Background
Bigtree got his start in journalism as an Emmy Award-winning producer on the CBS TV show The Doctors, where he focused on outing dangerous drugs and toxins like Monsantos RoundUp weedkiller.
In his speech, he tells the story of how he ended up leaving CBS and joining a team that was working on Vaxxed, a documentary by Dr. Andrew Wakefield that featured a Centers for Disease Control and Prevention whistleblower named Dr. William Thompson, who admitted the agency had covered up evidence linking the MMR vaccine with autism among Black infant boys.
After finishing Vaxxed, Bigtree founded ICAN to continue his investigation into medical fraud. He brought attorney Aaron Siri onboard, and started suing the CDC, the Food and Drug Administration, the Department of Health and Human Services and the National Institutes of Health to get to the truth about what these agencies do and do not know about vaccine safety.
They kept winning cases, but none of the mainstream media outlets were reporting about these cases. So, Bigtree launched The Highwire to fill that void and report on things that MSM refuse to discuss, such as the fact that as the childhood vaccination schedule has expanded, the health of American children has plummeted.
Greatest Decline in Human Health in Recorded History
Bigtree says:
America's kids are 70% more likely to die before adulthood than kids in other rich countries. We suck at what we do here. If health is what we're going for, we are underachieving in a major way. And ... we're one of the most vaccinated nations in the world ...
In 1986, prior to giving [drug companies] liability protection, we were getting about 11 vaccines by the time we were 18 years old ... By 2017...
Psychological Warfare: A Bag of Tricks Articles
This story is about being stronger than any monsters psychological tricks.
Introduction
In the medical freedom movement, we often discuss psychological trickery in the context of the technocrats and their attempt at the not-so-great reset but of course, the need for good people to effectively counter dark-hearted liars is as old as the world. In the course of human history, there has been no lack of contenders for the role of super predators.
There has been no lack of dark-hearted, cold-blooded individuals seeking power over others though illegitimate means: taking what doesnt belong to them, distorting reality (a.k.a. lying), turning people into zombies, tricking people into acting against their own self-interests, etc. We are not the first ones to deal with this kind of shameless scoundrels, and we probably wont be the last ones!
Watching Out for Tricks Without Fear
Staying vigilant in a spiritually honest way is important because the wicked ones are extremely crafty in their use of psychological tricks. They look for weaknesses in peoples emotional "armor" in real time and attack where they see holes whether its a lack of situational awareness, ideological addiction, anxiety, pride, insecurity, fear, anger, or being blinded by pain.
And yes, todays technological tools allow them to lie on an industrial scale but the core methods are still the same!
"There is a misconception that only "stupid" people get duped. Not true at all! There are methods to dupe highly intelligent people. There are methods to dupe the ones with pure hearts ("prey naivete"). There are methods to dupe people who are vain or insecure.
There are methods to dupe the wounded and the angry. There are methods to dupe the poor, and methods to dupe the rich. Really, the moment we decide that we are some kind of intellectual geniuses or super successful achievers, we make ourselves vulnerable to tricks."
Types of "Exploits"
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The vain can be tricked into acting against their interests very effectively by either provoking them with insult and triggering a self-sabotaging response that costs them a chunk of their reputation or by leading them on with a promise of a "statusy" reward. Very often, when we suddenly feel very insulted and want to just act hot-headed and let it all out, the desire to act hot-headed may not be coming from us. It very well could be various the tricksters at work, waving their metaphorical magic wand and giving people hot-headed thoughts. That is a... |
09:59
Resveratrol inhibits autophagy against myocardial ischemia-reperfusion injury. GreenMedInfo
PMID: Eur J Pharmacol. 2023 Jul 15 ;951:175748. Epub 2023 May 5. PMID: 37149277 Abstract Title: Resveratrol inhibits autophagy against myocardial ischemia-reperfusion injury through the DJ-1/MEKK1/JNK pathway. Abstract: Resveratrol (RES), a natural polyphenolic compound found in red wine and grape skins, has attracted significant attention due to its cardioprotective properties. DJ-1, a multifunctional protein that participated in transcription regulation and antioxidant defense, was shown to provide a significant protective impact in cardiac cells treated with ischemia-reperfusion. We created a myocardial ischemia-reperfusion (I/R) model in vivo and in vitro by ligating the left anterior descending branch of rats and subjecting H9c2 cells to anoxia/reoxygenation (A/R) to investigate whether RES reduces myocardial ischemia-reperfusion injury by upregulating DJ-1. We discovered that RES dramatically enhanced cardiac function in rats with I/R. Subsequently, we found that RES prevented the rise in autophagy (P62 degradation and LC3-II/LC3-I increase) induced by cardiac ischemia-reperfusion in vitro and in vivo. Notably, the autophagic agonist rapamycin (RAPA) eliminated RES-induced cardioprotective effects. In addition, Further data showed that RES significantly increased the expression of DJ-1 in the myocardium with the treatment of I/R. At the same time, pretreatment with RES reduced phosphorylation of MAPK/ERK kinase kinase 1 (MEKK1) and Jun N-terminal Kinase (JNK) stimulated by cardiac ischemia-reperfusion, and Beclin-1 mRNA and protein levels while decreasing lactate dehydrogenase (LDH) and improving cell viability. However, the lentiviral shDJ-1 and JNK agonist anisomycin disrupted the effects of RES. In summary, RES could inhibit autophagy against myocardial ischemia-reperfusion injury through DJ-1 modulation of the MEKK1/JNK pathway, providing a novel therapeutic strategy for cardiac homeostasis.
09:40
Sound of Freedom: A Movie About Child Trafficking Produced by Child Traffickers? Health Impact News
by Brian Shilhavy
Editor, Health Impact News
I have been vehemently attacked and criticized by some people for daring to publish critical articles about the Sound of Freedom movie, especially the article about the people who funded the movie. See:
Sound of Freedom Movie Allegedly Funded by Billionaire Philanthropists with Ties to Human Trafficking
A Kevin J wrote this comment about that article:
What a ridiculous article. Conclusions are based on allegedly and might have ties to this or that, and guilt-by-association darts. So a guy who allegedly helped fund the film (in other words, rumor has it) might have ties to cartels and the Clintons. No evidence anywhere this guy helped fund the movie.
But the source for this funding is Tim Ballard himself, who stated who was funding the movie in an interview in Utah 5 years ago on Fox News. Here is the clip from Fox 13 News in Utah. The original interview is here.
This same local news outlet, Fox 13 News Utah, also reported in 2020 that Tim Ballards organization, Operation Underground Railroad, was under criminal investigation for its fundraising methods.
09:29
Protective effect of resveratrol and tannic acid combination on aluminium chloride induced neurotoxicity. GreenMedInfo
PMID: Nutr Neurosci. 2023 May 5:1-13. Epub 2023 May 5. PMID: 37144738 Abstract Title: Protective effect of resveratrol and tannic acid combination on aluminium chloride induced neurotoxicity in rats. Abstract: OBJECTIVE: Alzheimer's disease is a progressive neurodegenerative disease and one of the most common causes of dementia. Despite recent advancements, there exists an unmet need for a suitable therapeutic option. This study aimed to evaluate the protective effects of the combination of resveratrol (20mg/kg/day p.o.) and tannic acid (50mg/kg/day p.o.) to reduce aluminium trichloride-induced Alzheimer's disease in rats.METHODS: Wistar rats weighing 150-200g were administered with aluminium chloride (100mg/kg/day p.o.) for 90 days to induce neurodegeneration and Alzheimer's disease. Neurobehavioral changes were assessed using novel object recognition test, elevated plus maze test, and Morris water maze test. Histopathological studies were performed using H&E stain and Congo Red stains to check amyloid deposits. Further oxidative stress was measured in brain tissue.RESULTS: Aluminium trichloride treated negative control group showed cognitive impairment in the Morris water maze test, novel object recognition test, and elevated plus maze test. Further, the negative control group showed significant oxidative stress, increase amyloid deposits, and severe histological changes. Treatment with the combination of resveratrol and tannic acid showed significant attenuation in cognitive impairment. The oxidative stress markers and amyloid plaque levels were significantly attenuated with the treatment.CONCLUSION: The present study indicates the beneficial effects of resveratrol-tannic acid combination in AlClinduced neurotoxicity in rats.
09:26
Resveratrol attenuates the disruption of lipid metabolism observed in amyloid precursor protein. GreenMedInfo
PMID: Neuroscience. 2023 Jun 15 ;521:134-147. Epub 2023 May 3. PMID: 37142180 Abstract Title: Resveratrol Attenuates the Disruption of Lipid Metabolism Observed in Amyloid Precursor Protein/Presenilin 1 Mouse Brains and Cultured Primary Neurons Exposed to A. Abstract: To examine whether resveratrol (RSV), an activator of silent mating-type information regulation 2 homolog 1 (SIRT1), can reverse the disruption of lipid metabolism caused by-amyloid peptide (A), APP/PS1 mice or cultured primary rat neurons were treated with RSV, suramin (inhibitor of SIRT1), ZLN005, a stimulator of peroxisome proliferator-activated receptorcoactivator-1(PGC-1), or PGC-1silencing RNA. In the brains of the APP/PS1 mice, expressions of SIRT1, PGC-1, low-density lipoprotein receptor (LDLR) and very LDLR (VLDLR) were reduced at the protein and, in some cases, mRNA levels; while the levels of the proprotein convertase subtilisin/kexin type 9 (PCSK9), apolipoprotein E (ApoE), total cholesterol and LDL were all elevated. Interestingly, these changes were reversed by administration of RSV, while being aggravated by suramin. Furthermore, activation of PGC-1, but inhibition of SIRT1, decreased the levels of PCSK9 and ApoE, while increased those of LDLR and VLDLR in the neurons exposed to A, and silencing PGC-1, but activation of SIRT1, did not influence the levels of any of these proteins. These findings indicate that RSV can attenuate the disruption of lipid metabolism observed in the brains of APP mice and in primary neurons exposed to Aby activating SIRT1, in which the mechanism may involve subsequently affecting PGC-1.
09:23
Resveratrol inhibits ferroptosis via activating NRF2/GPX4 pathway in mice with spinal cord injury. GreenMedInfo
PMID: Microsc Res Tech. 2023 May 2. Epub 2023 May 2. PMID: 37129001 Abstract Title: Resveratrol inhibits ferroptosis via activating NRF2/GPX4 pathway in mice with spinal cord injury. Abstract: Ferroptosis is a newly defined form of cell death involved in neurologic disease. Resveratrol is a non-flavonoid polyphenolic compound with anti-inflammatory and antioxidant properties, but its potential therapeutic mechanism in spinal cord injury (SCI) remains unknown. Therefore, this study evaluates the mechanism by which resveratrol promotes neurological and motor function recovery in mice with SCI. The motor function of mice was evaluated using the Basso Mouse Scale score and footprint test. The effect of resveratrol on the neuronal cell state was observed using NeuN, fluoro-Jade C, and Nissl staining. The expression of iron content in injured segments was observed using Perls blue and Diaminobenzidine staining. The effect of resveratrol on the levels of malondialdehyde, glutathione, Fe, and glutathione peroxidase 4 enzyme activity was also investigated. The mitochondrial ultrastructures of injured segment cells were observed using transmission electron microscope, while the protein levels of ferroptosis-related targets were detected using Western blot. Our findings show that resveratrol improves motor function after SCI and has certain neuroprotective effects; in ferroptosis-related studies, resveratrol inhibited the expression of ferroptosis-related proteins and ions. Resveratrol improved changes in mitochondrial morphology. Mechanistically, the Nrf2 inhibitor ML385 reversed the inhibitory effect of resveratrol on ferroptosis-related genes, indicating that resveratrol inhibits ferroptosis through the Nrf2/GPX4 pathway. Our findings elucidate that resveratrol promotes functional recovery, inhibits ferroptosis post-SCI, and provides an experimental basis for subsequent clinical translational research.
09:19
Resveratrol reliefs DEHP-induced defects during human decidualization. GreenMedInfo
PMID: Ecotoxicol Environ Saf. 2023 Jun 15 ;258:114931. Epub 2023 Apr 28. PMID: 37121080 Abstract Title: Resveratrol reliefs DEHP-induced defects during human decidualization. Abstract: Di-(2-Ethylhexyl) phthalate (DEHP) is widely used as an additive in many plastic products. Studies have revealed that DEHP persistent exposure can affect embryonic development and lead to adverse female reproductive disorders. The establishment of pregnancy involves extensive changes in the endometrial tissue, including massive extracellular matrix (ECM) remodeling. Decidualization of the endometrium provides a suitable environment for subsequent growth by causing changes in the morphology of the uterine stromal cells, is a key process in human pregnancy. Resveratrol (RSV) is a natural polyphenolic plant antitoxin with a wide range of pharmacological effects. Growing evidence indicates that RSV has therapeutic effects on certain female reproductive disorders. In this study, the effect of DEHP on cell viability was investigated by cell proliferation assay. Cell decidualization was induced in vitro, and the downregulation of molecules associated with decidualization was confirmed through quantitative real-time PCR and western blot analysis. Immunofluorescence analysis revealed alteration in cell morphology, and found that administration of DEHP sufficiently induced ERentry into the nucleus. The effect of DEHP on cells was fully verified by RNA-seq analysis. Interestingly, an upregulation of decidual molecules was observed after rescue with RSV, which was confirmed by RNA-seq transcriptome analysis and quantitative real-time PCR assay. Additionally, the expression of ECM remodeling-related genes was significantly restored by RSV administration. The study revealed the potential mechanisms of DEHP-induced decidualization defects and the functional relieving roles of RSV while providing a perspective therapeutic candidate for alleviating the DEHP-induced deficiencies in decidualization.
09:15
Resveratrol protects against cadmium-induced cerebrum toxicity. GreenMedInfo
PMID: J Sci Food Agric. 2023 Apr 28. Epub 2023 Apr 28. PMID: 37115015 Abstract Title: Resveratrol protects against cadmium-induced cerebrum toxicity through modifications of the cytochrome P450 enzyme system in microsomes. Abstract: BACKGROUND: Cadmium (Cd), known as a vital contaminant in the environment, penetrates the blood-brain barrier and accumulates in the cerebrum. Acute toxicosis of Cd, which leads to lethal cerebral edema, intracellular accumulation and cellular dysfunction, remains to be illuminated with regard to the exact molecular mechanism of cerebral toxicity. Resveratrol (RES), present in the edible portions of numerous plants, is a simply acquirable and correspondingly less toxic natural compound with neuroprotective potential, which provides some theoretical bases for antagonizing Cd-induced cerebral toxicity.RESULTS: This work was executed to research the protective effects of RES against Cd-induced toxicity in chicken cerebrum. Markedly, these lesions were increased in the Cd group, which also exhibited a thinner cortex, reduced granule cells, vacuolar degeneration, and an enlarged medullary space in the cerebrum. Furthermore, Cd induced CYP450 enzyme metabolism disorders by disrupting the nuclear xenobiotic receptor response (NXRs), enabling the cerebrum to reduce the ability to metabolize exogenous substances, eventually leading to Cd accumulation. Meanwhile, accumulated Cd promoted oxidative damage and synergistically promoted the damage to neurons and glial cells.CONCLUSION: RES initiated NXRs (especially for aromatic receptor and pregnancy alkane X receptor), decreasing the expression of CYP450 genes, changing the content of CYP450, maintaining CYP450 enzyme normal activities, and exerting antagonistic action against the Cd-induced abnormal response of nuclear receptors. These results suggest that the cerebrum toxicity caused by Cd was reduced by pretreatment with RES.2023 Society of Chemical Industry.
09:11
Natural polyphenols-resveratrol, quercetin, magnolol, and -catechin-block certain aspects of heroin addiction. GreenMedInfo
PMID: Toxics. 2023 Apr 17 ;11(4). Epub 2023 Apr 17. PMID: 37112606 Abstract Title: Natural Polyphenols-Resveratrol, Quercetin, Magnolol, and-Catechin-Block Certain Aspects of Heroin Addiction and Modulate Striatal IL-6 and TNF-. Abstract: We have examined the effects of four different polyphenols in attenuating heroin addiction using a conditioned place preference (CPP) paradigm. Adult male Sprague Dawley rats received heroin (alternating with saline) in escalating doses starting from 10 mg/kg, i.p. up to 80 mg/kg/d for 14 consecutive days. The rats were treated with distilled water (1 mL), quercetin (50 mg/kg/d),-catechin (100 mg/kg/d), resveratrol (30 mg/kg/d), or magnolol (50 mg/kg/d) through oral gavage for 7 consecutive days, 30 min before heroin administration, starting on day 8. Heroin withdrawal manifestations were assessed 24 h post last heroin administration following the administration of naloxone (1 mg/kg i.p). Heroin CPP reinstatement was tested following a single dose of heroin (10 mg/kg i.p.) administration. Striatal interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-) were quantified (ELISA) after naloxone-precipitated heroin withdrawal. Compared to the vehicle, the heroin-administered rats spent significantly more time in the heroin-paired chamber (
08:54
Double-loaded doxorubicin/resveratrol polymeric micelles providing low toxicity on cardiac cells and enhanced cytotoxicity on lymphoma cells. GreenMedInfo
PMID: Pharmaceutics. 2023 Apr 19 ;15(4). Epub 2023 Apr 19. PMID: 37111772 Abstract Title: Double-Loaded Doxorubicin/Resveratrol Polymeric Micelles Providing Low Toxicity on Cardiac Cells and Enhanced Cytotoxicity on Lymphoma Cells. Abstract: The anthracycline antibiotic doxorubicin is a well-known antitumour agent, however its cardiotoxicity is a significant obstacle to therapy. The aim of the present study was to improve the safety of doxorubicin through its simultaneous encapsulation with a cardioprotective agent (resveratrol) in Pluronic micelles. The formation and double-loading of the micelles was performed via the film hydration method. Infrared spectroscopy proved the successful incorporation of both drugs. X-ray diffraction analyses revealed that resveratrol was loaded in the core, whereas doxorubicin was included in the shell. The double-loaded micelles were characterised by a small diameter (26 nm) and narrow size distribution, which is beneficial for enhanced permeability and retention effects. The in vitro dissolution tests showed that the release of doxorubicin depended on the pH of the medium and was faster than that of resveratrol. In vitro studies on cardioblasts showed the opportunity to reduce the cytotoxicity of doxorubicin through the presence of resveratrol in double-loaded micelles. Higher cardioprotection was observed when the cells were treated with the double-loaded micelles compared with referent solutions with equal concentrations of both drugs. In parallel, treatments of L5178 lymphoma cells with the double-loaded micelles revealed that the cytotoxic effect of doxorubicin was enhanced. Thus, the study demonstrated that the simultaneous delivery of doxorubicin and resveratrol via the micellar system enabled the cytotoxicity of doxorubicin in lymphoma cells and lowered its cardiotoxicity in cardiac cells.
08:54
Medicine Is Plagued by Untrustworthy Clinical Trials. How Many Studies Are Faked or Flawed? Mad In America
From Nature: For years, a number of scientists, physicians and data sleuths have argued that fake or unreliable trials are frighteningly widespread. Theyve scoured RCTs in various medical fields, such as womens health, pain research, anaesthesiology, bone health and COVID-19, and have found dozens or hundreds of trials with seemingly statistically impossible data. Some, on the basis of their personal experiences, say that one-quarter of trials being untrustworthy might be an underestimate. If you search for all randomized trials on a topic, about a third of the trials will be fabricated, asserts Ian Roberts, an epidemiologist at the London School of Hygiene & Tropical Medicine.
The issue is, in part, a subset of the notorious paper-mill problem: over the past decade, journals in many fields have published tens of thousands of suspected fake papers, some of which are thought to have been produced by third-party firms, termed paper mills.
But faked or unreliable RCTs are a particularly dangerous threat. They not only are about medical interventions, but also can be laundered into respectability by being included in meta-analyses and systematic reviews, which thoroughly comb the literature to assess evidence for clinical treatments. Medical guidelines often cite such assessments, and physicians look to them when deciding how to treat patients.
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08:46
Cardioprotective role of a magnolol and honokiol complex in the prevention of doxorubicin-mediated cardiotoxicity. GreenMedInfo
PMID: Mol Cell Biochem. 2023 Apr 19. Epub 2023 Apr 19. PMID: 37074505 Abstract Title: Cardioprotective role of a magnolol and honokiol complex in the prevention of doxorubicin-mediated cardiotoxicity in adult rats. Abstract: Doxorubicin (DOXO) induces marked cardiotoxicity, though increased oxidative stress while there are some documents related with cardioprotective effects of some antioxidants against organ-toxicity during cancer treatment. Although magnolia bark has some antioxidant-like effects, its action in DOXO-induced heart dysfunction has not be shown clearly. Therefore, here, we aimed to investigate the cardioprotective action of a magnolia bark extract with active component magnolol and honokiol complex (MAHOC; 100 mg/kg) in DOXO-treated rat hearts. One group of adult male Wistar rats was injected with DOXO (DOXO-group; a cumulative dose of 15 mg/kg in 2-week) or saline (CON-group). One group of DOXO-treated rats was administered with MAHOC before DOXO (Pre-MAHOC group; 2-week) while another group was administered with MAHOC following the 2-week DOXO (Post-MAHOC group). MAHOC administration, before or after DOXO, provided full survival of animals during 12-14 weeks, and significant recoveries in the systemic parameters of animals such as plasma levels of manganese and zinc, total oxidant and antioxidant statuses, and also systolic and diastolic blood pressures. This treatment also significantly improved heart function including recoveries in end-diastolic volume, left ventricular end-systolic volume, heart rate, cardiac output, and prolonged P-wave duration. Furthermore, the MAHOC administrations improved the structure of left ventricles such as recoveries in loss of myofibrils, degenerative nuclear changes, fragmentation of cardiomyocytes, and interstitial edema. Biochemical analysis in the heart tissues provided the important cardioprotective effect of MAHOC on the redox regulation of the heart, such as improvements in activities of glutathione peroxidase and glutathione reductase, and oxygen radical-absorbing capacity of the heart together with recoveries in other systemic parameters of animals, while all of these benefits were observed in the Pre-MAHOC treatment group, more prominently. Overall, one can point out the beneficial antioxidant effects of MAHOC in chronic heart diseases as a supporting and complementing agent to the conventional therapies.
08:38
A review of the use of honokiol in lung cancer therapy. GreenMedInfo
PMID: J Asian Nat Prod Res. 2023 Apr 3:1-9. Epub 2023 Apr 3. PMID: 37010929 Abstract Title: Use of honokiol in lung cancer therapy: a mini review of its pharmacological mechanism. Abstract: Honokiol (3',5-di-(2-propenyl)-1,1'-biphenyl-2,2'-diol) is a biologically active natural product derived fromand has been shown to have excellent biological activities. This paper discusses research progress on the use of honokiol in the treatment of lung cancer, as studies have confirmed that honokiol can exert anti-lung-cancer effects through multiple pathways and multiple signaling pathways, such as inhibiting angiogenesis, affecting mitochondrial function and apoptosis, regulating of autophagy and epithelial-mesenchymal transition (EMT). In addition, honokiol combined with other chemotherapy drugs is also a way in which it can be applied.
08:30
Honokiol prevents chronic cerebral hypoperfusion induced astrocyte A1 polarization to alleviate neurotoxicity. GreenMedInfo
PMID: Free Radic Biol Med. 2023 Jun ;202:62-75. Epub 2023 Mar 28. PMID: 36997099 Abstract Title: Honokiol prevents chronic cerebral hypoperfusion induced astrocyte A1 polarization to alleviate neurotoxicity by targeting SIRT3-STAT3 axis. Abstract: Alzheimer's Dementia (AD) and Vascular Dementia (VaD) are two main types of dementias for which no specific treatment is available. Chronic Cerebral Hypoperfusion (CCH) is a pathogenesis underlying AD and VaD that promotes neuroinflammatory responses and oxidative stress. Honokiol (HNK) is a natural compound isolated from magnolia leaves that can easily cross blood brain barrier and has anti-inflammatory and antioxidant effects. In the present study, the effects of HNK on astrocyte polarization and neurological damage in in vivo and in vitro models of chronic cerebral hypoperfusion were explored. We found that HNK was able to inhibit the phosphorylation and nuclear translocation of STAT3, A1 polarization, and reduce conditioned medium's neuronal toxicity of astrocyte under chronic hypoxia induced by cobalt chloride; STAT3 phosphorylation inhibitor C188-9 was able to mimic the above effects of HNK, suggesting that HNK may inhibit chronic hypoxia-induced A1 polarization in astrocytes via STAT3. SIRT3 inhibitor 3-TYP reversed, while Sirt3 overexpression mimicked the inhibitory effects of HNK on oxidative stress, STAT3 phosphorylation and nuclear translocation, A1 polarization and neuronal toxicity of astrocyte under chronic hypoxic conditions. For in vivo research, continuous intraperitoneal injection of HNK (1 mg/kg) for 21 days ameliorated the decrease in SIRT3 activity and oxidative stress, inhibited astrocytic STAT3 nuclear translocation and A1 polarization, and prevented neuron and synaptic loss in the hippocampal of CCH rats. Besides, HNK application improved the spatial memory impairment of CCH rats, as assessed with Morris Water Maze. In conclusion, these results suggest that the phytochemical HNK can inhibit astrocyte A1 polarization via regulating SIRT3-STAT3 axis, thus improving CCH-induced neurological damage. These results highlight HNK as novel treatment for dementia with underlying vascular mechanisms.
08:28
Honokiol reduces fungal burden and ameliorate inflammation lesions of Aspergillus fumigatus keratitis. GreenMedInfo
PMID: Int Immunopharmacol. 2023 May ;118:109849. Epub 2023 Mar 16. PMID: 36933490 Abstract Title: Honokiol reduces fungal burden and ameliorate inflammation lesions of Aspergillus fumigatus keratitis via Dectin-2 down-regulation. Abstract: PURPOSE: To screen and identify the mechanism of honokiol on anti-fungi and anti-inflammation in fungal keratitis (FK) through bioinformatic analysis and biological experiments.METHODS: Transcriptome profile demonstrated differential expression genes (DEGs) of Aspergillus fumigatus keratitis between PBS-treated and honokiol-treated groups via bioinformatics analyses. Inflammatory substances were quantified by qRT-PCR, Western blot and ELISA, and macrophage polarization was examined by flow cytometry. Periodic acid Schiff staining and morphological interference assay were used to detect hyphal distribution in vivo and fungal germination in vitro, respectively. Electron microscopy was to illustrate hyphal microstructure.RESULTS: Illumina sequencing demonstrated that compared with the honokiol group, 1175 up-regulated and 383 down-regulated genes were induced in C57BL/6 mice Aspergillus fumigatus keratitis with PBS treatment. Through GO analysis, some differential expression proteins (DEPs) played major roles in biological processes, especially fungal defense and immune activation. KEGG analysis provided fungus-related signaling pathways. PPI analysis demonstrated that DEPs from multiple pathways form a close-knit network, providing a broader context for FK treatment. In biological experiments, Dectin-2, NLRP3 and IL-1were upregulated by Aspergillus fumigatus to evaluate immune response. Honokiol could reverse the trend, comparable to Dectin-2 siRNA interference. Meanwhile, honokiol could also play an anti-inflammatory role via promoting M2 phenotype polarization. Moreover, honokiol reduced hyphal distribution in the stroma, delayed germination, and destroyed the hyphal cell membrane in-vitro.CONCLUSIONS: Honokiol possesses anti-fungal and anti-inflammatory effects in Aspergillus fumigatus keratitis and may develop a potential and safe therapeutic modality for FK.
08:26
Honokiol acts as an AMPK complex agonist therapeutic in non-alcoholic fatty liver disease and metabolic syndrome. GreenMedInfo
PMID: Chin Med. 2023 Mar 17 ;18(1):30. Epub 2023 Mar 17. PMID: 36932412 Abstract Title: Honokiol acts as an AMPK complex agonist therapeutic in non-alcoholic fatty liver disease and metabolic syndrome. Abstract: BACKGROUND: Non-alcoholic fatty liver (NAFLD) and its related metabolic syndrome have become major threats to human health, but there is still a need for effective and safe drugs to treat these conditions. Here we aimed to identify potential drug candidates for NAFLD and the underlying molecular mechanisms.METHODS: A drug repositioning strategy was used to screen an FDA-approved drug library with approximately 3000 compounds in an in vitro hepatocyte model of lipid accumulation, with honokiol identified as an effective anti-NAFLD candidate. We systematically examined the therapeutic effect of honokiol in NAFLD and metabolic syndrome in multiple in vitro and in vivo models. Transcriptomic examination and biotin-streptavidin binding assays were used to explore the underlying molecular mechanisms, confirmed by rescue experiments.RESULTS: Honokiol significantly inhibited metabolic syndrome and NAFLD progression as evidenced by improved hepatic steatosis, liver fibrosis, adipose inflammation, and insulin resistance. Mechanistically, the beneficial effects of honokiol were largely through AMPK activation. Rather than acting on the classical upstream regulators of AMPK, honokiol directly bound to the AMPK1 subunit to robustly activate AMPK signaling. Mutation of honokiol-binding sites of AMPK1 largely abolished the protective capacity of honokiol against NAFLD.CONCLUSION: These findings clearly demonstrate the beneficial effects of honokiol in multiple models and reveal a previously unappreciated signaling mechanism of honokiol in NAFLD and metabolic syndrome. This study also provides new insights into metabolic disease treatment by targeting AMPK1 subunit-mediated signaling activation.
08:22
Honokiol showed promising preclinical potential as a multiple target drug for Amyotrophic lateral sclerosis treatment. GreenMedInfo
PMID: Acta Pharm Sin B. 2023 Feb ;13(2):577-597. Epub 2022 Aug 10. PMID: 36873166 Abstract Title: Honokiol alleviated neurodegeneration by reducing oxidative stress and improving mitochondrial function in mutant SOD1 cellular and mouse models of amyotrophic lateral sclerosis. Abstract: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting both upper and lower motor neurons (MNs) with large unmet medical needs. Multiple pathological mechanisms are considered to contribute to the progression of ALS, including neuronal oxidative stress and mitochondrial dysfunction. Honokiol (HNK) has been reported to exert therapeutic effects in several neurologic disease models including ischemia stroke, Alzheimer's disease and Parkinson's disease. Here we found that honokiol also exhibited protective effects in ALS disease models bothand. Honokiol improved the viability of NSC-34 motor neuron-like cells that expressed the mutant G93A SOD1 proteins (SOD1-G93A cells for short). Mechanistical studies revealed that honokiol alleviated cellular oxidative stress by enhancing glutathione (GSH) synthesis and activating the nuclear factor erythroid 2-related factor 2 (NRF2)-antioxidant response element (ARE) pathway. Also, honokiol improved both mitochondrial function and morphologyfine-tuning mitochondrial dynamics in SOD1-G93A cells. Importantly, honokiol extended the lifespan of the SOD1-G93A transgenic mice and improved the motor function. The improvement of antioxidant capacity and mitochondrial function was further confirmed in the spinal cord and gastrocnemius muscle in mice. Overall, honokiol showed promising preclinical potential as a multiple target drug for ALS treatment.
08:09
Honokiol alleviates diabetic nephropathy pathogenesis possibly by attenuating ER stress and Rock pathway. GreenMedInfo
PMID: Life Sci. 2023 May 1 ;320:121543. Epub 2023 Mar 4. PMID: 36871934 Abstract Title: Nephroprotective effects of honokiol in a high-fat diet-streptozotocin rat model of diabetic nephropathy. Abstract: AIMS: Diabetic nephropathy (DN) is the foremost basis of end-stage kidney failure implicating endoplasmic reticulum (ER) stress and dysregulation of Rho kinase/Rock pathway. Magnolia plants are used in traditional medicine systems in Southeast Asia owing to bioactive phytoconstituents. Earlier, honokiol (Hon) exhibited therapeutic potential in experimental models of metabolic, renal, and brain disorders. In the present study, we evaluated potential of Hon against DN and possible molecular mechanisms.MAIN METHODS: In the existing experiments, high-fat diet (HFD) (17 weeks) and streptozotocin (STZ) (40 mg/kg once) induced DN rats were orally treated with Hon (25, 50, 100 mg/kg) or metformin (150 mg/kg) for 8 weeks.KEY FINDINGS: Hon attenuated albuminuria, blood biomarkers (e.g., urea nitrogen, glucose, C-reactive protein, and creatinine) and ameliorated lipid profile, electrolytes levels (Na/K), and creatinine clearance against DN. Hon significantly decreased renal oxidative stress and inflammatory biomarkers against DN. Histomorphometry and microscopic analysis revealed nephroprotective effects of Hon marked by a decrease in leukocyte infiltration, renal tissue damage, and urine sediments. RT-qPCR showed that Hon treatment attenuated mRNA expression of transforming growth factor-1 (TGF-1), endothelin-1 (ET-1), ER stress markers (GRP78, CHOP, ATF4, and TRB3), and Rock 1/2 in DN rats. Data from ELISA supported a decrease in levels of TGF-1, ET-1, ER stress markers, and Rock1/2 by Hon.SIGNIFICANCE: Hon attenuated hyperglycemia, redox imbalance, and inflammation and improved renal functions in rats. Hon alleviates DN pathogenesis possibly by attenuating ER stress and Rock pathway.
08:00
Happy Hour Spirit of the Antichrist series Pt 3 with JB Hixson Dr. Tenpenny
07-20-2023 Listen to audio here. If you prefer to watch rather than listen, click on the video below: https://drtenpenny.b-cdn.net/2023/07-20-23-HHr-JBHixson-Pt3.mp4 Spirit of the Antichrist: The Gathering Cloud of Deception This []
07:54
Honokiol suppresses the aberrant interactions between renal resident macrophages and tubular epithelial cells in lupus nephritis. GreenMedInfo
PMID: Cell Death Dis. 2023 Mar 1 ;14(3):174. Epub 2023 Mar 1. PMID: 36859530 Abstract Title: Honokiol suppresses the aberrant interactions between renal resident macrophages and tubular epithelial cells in lupus nephritis through the NLRP3/IL-33/ST2 axis. Abstract: Lupus nephritis (LN) is a type of immune-complex nephritis caused by systemic lupus erythematosus and is a major contributor to mortality and morbidity. Honokiol (HNK) has been found to have a therapeutic effect on LN, but its action mechanism remains unclear. In this study, we first demonstrated that HNK attenuates kidney injury in MRL/lpr mice. Results from RNA sequencing combined with ingenuity pathway analysis suggested that HNK plays an anti-LN role through inhibition of the NLRP3 inflammasome and IL33. GEO chip data, single-cell data, and clinical samples from LN patients demonstrated that the pyroptosis and IL-33/ST2 pathways are abnormally activated during the stage of LN. In vivo, similar to the results of the AAV-mediated NLRP3 shRNA MRL/lpr model, HNK downregulated serum and renal IL-33 levels, and suppressed NLRP3 inflammasome and the IL-33/ST2 axis in the kidney. In vitro, co-culturing NLRP3-overexpressing or IL-33 knocked-down rat renal macrophages with NRK-52E cells confirmed that NLRP3 activation in resident macrophages directly upregulates IL-33, which in turn mediates the IL-33/ST2/NF-B pathway to promote the inflammatory response of renal tubular epithelial cells. Furthermore, a molecular docking model and surface plasmon resonance analysis were utilized to demonstrate a direct interaction between HNK and NLRP3. In conclusion, this study provides a novel anti-LN treatment strategy in which HNK plays a preventive and therapeutic role against LN by suppressing the abnormal crosstalk between renal resident macrophages and renal tubular epithelial cells by inhibiting the activation of the NLRP3/IL-33/ST2 axis.
07:05
Kiwi fruit essence reduces radiation-induced lung injury. GreenMedInfo
PMID: Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2023 Apr ;39(4):332-338. PMID: 37087551 Abstract Title: [Kiwi fruit essence reduces radiation-induced lung injury by down-regulating TNF-and PDGF-B in rats]. Abstract: Objective To observe the role of tumor necrosis factor-(TNF-) and platelet-derived growth factor-B (PDGF-B) in kiwi fruit essence-mediated protection of radiation-induced lung injury (RILI) in rats. Methods 96 male healthy Sprague-Dawley rats were divided into normal control group, model group, and kiwi fruit essence treatment group(60 and 240 mg/kg) by the random number table method, with 24 animals in each group. The whole lungs underwent 6 MV X-ray irradiation (18 Gy) to induce RILI animal models in rats of the latter three groups. On the next day after irradiation, rats in the latter two groups were intragastrically administrated with 60 or 240 mg/kg kiwi fruit essence, once a day. The rats in the normal control and model groups were treated with 9 g/L sodium chloride solution. Eight rats in the latter three groups were randomly sacrificed on days 14, 28, and 56, while normal control rats were sacrificed on day 56 as the overall control. Blood samples were collected and separated. Serum concentrations of TNF-and PDGF-B were detected using ELISA. The lung tissues were isolated for HE and Masson staining to evaluate alveolitis and pulmonary fibrosis (PF). The hydroxyproline (HYP) content in lung tissues was detected. The mRNA and protein expression of pulmonary TNF-and PDGF-B were determined by quantitative real-time PCR and immunohistochemistry. Results Compared with the model group, treatment with 60 and 240 mg/kg kiwi fruit essence group significantly reduced alveolitis on days 14 and 28 as well as PF lesions on days 28 and 56. Compared with the normal control group, HYP content in the lung tissue of the model group increased on day 28 and day 56, while TNF-and PDGF-B levels in the serum and lung tissues increased at each time point. Compared with the model group during the same period, 60 and 240 mg/kg kiwi fruit essence element treatment group reported the diminished levels of serum and pulmonary TNF-on day 14 and day 28. Consistently, the lung tissue HYP content and serum and pulmonary PDGF-B levels on day 28 and day 56 were reduced. In addition, the above indicators in the 240 mg/kg kiwi fruit essence treatment group were lower than those for the 60 mg/kg kiwi fruit essence treatment group. Conclusion Kiwi fruit essence can alleviate RILI in rats, which is related to the down-regulation of TNF-expression at the early stage and decreased PDGF-B level at the middle and late stages.
06:48
Doctor and councillor calling for fluoride to be added to all of Nottinghamshires tap water Fluoride Action Network
Councillor Dr John Doddy, who is also Chairman of the Health & Wellbeing Board at Nottinghamshire County Council, said he is the pied piper of a campaign for water fluoridation in the county.
He said it is insanity that fluoride has not been added to water across the whole country yet.
Fluoride is a naturally occurring mineral found in some soils, food and drink which strengthens the outer surface of teeth, making them more resistant to decay.
It is added to dental products including many toothpastes, but can also be put into tap water so it reaches whole populations.
The World Health Organisation recommends water fluoridation as an effective and safe public health intervention.
Some areas of Nottinghamshire, including Mansfield, Bassetlaw, Ashfield and some parts of Newark and Sherwood have had fluoride in their tap water since the 1970s.
A Department of Health and Social Care spokesperson said it wants more of the country to benefit from water fluoridation.
Opponents of flouridation have raised concerns over dental fluorosis a brown discolouration which can appear on a childs teeth if they are exposed to too much flouride while still developing.
The NHS says it is uncommon in the UK for fluorosis to be severe enough to seriously affect the appearance of teeth, because fluoride levels in water are carefully monitored by the Drinking Water Inspectorate and adjusted if necessary.
As of 2022, the Secretary of State for Health and Social Care has responsibility for water fluoridation, as opposed to local authorities and water companies.
A motion by Cllr Doddy was passed at Nottinghamshire County Council full council on July 13 supporting water fluoridation in the entire county.
He told the Local Democracy Reporting Service: The reason it has become so important is the post-Covid deterioration in the oral health of the children of Nottingham.
We knew there were problems before Covid, but it is clear there has been no bounce back in the ability to access a dentist.
It coincides with a national feeling that there is a problem with the teeth of the nation.
From my point of view, its simple, putting fluoride in the water is the single most effective public health measure that exists for reducing dental decay.
Cllr Doddy said the chemical makes a 35 per cent reduction in rotten teeth and questioned why it hasnt been added to water locally for 40 years.
He said in the areas which have fluoride in their water, there is a dental decay rate of around 18 per cent in children, compared to 37 per cent in other areas of the county.
Cllr Doddy added: The simple reality is in 40 years there hasnt been a single side effect.
I will get councils in the East Midlands to agree that we want it and then go down to London and hand them the evidence.
Ive spoken personally to (the healt...
06:23
Doctor reveals gross reason you need to change your pillow every two years Healthy Holistic Living
How many of us are guilty of ignoring those yellow stains on our pillows? They might just look gross, but according to Dr. Karan Raj, an NHS surgeon in the UK, these tell-tale signs should not be overlooked.
Who is Dr. Karan Raj?
Dr. Raj has become something of an internet sensation with 3 million followers on TikTok, where he explains complex medical concepts in an easily understandable way. His expertise spans a wide array of topics from the inner workings of the placebo effect to the cause of hair loss during chemotherapy. However, its his video on the topic of changing pillows that has left many of his followers stunned.
@dr.karanr Change your pillows! #wonderwaterwhip #learnontiktok #schoolwithdrkaran #sleep Steven Universe L.Dre
The Unsettling Truth about Yellow Stains
The yellow stains on your pillows arent just unsightly theyre indicative of a buildup of sweat and body oils. Dr. Raj breaks down the science behind these discolorations, explaining that the moisture trapped in pillows can encourage the growth of mold and bacteria.
...
06:01
Exploration of bioactive molecules from Tinospora cordifolia and Actinidia deliciosa as an immunity modulator. GreenMedInfo
PMID: Nat Prod Res. 2023 Jan 9:1-5. Epub 2023 Jan 9. PMID: 36622893 Abstract Title: Exploration of bioactive molecules fromandas an immunity modulatormolecular docking and molecular dynamics simulation study. Abstract: andare the widely used plant in Ayurvedic systems of medicine. Both plants are well known for their immunomodulatory activity. In the current study, in silico exploration was performed using advanced computational techniques such as molecular docking and molecular dynamics simulation approach. Bioactive molecules from theandwere docked against the Human IL-2. Out of all the docked bioactive molecules, Pygenic acid-B (PubChem CID:146157192) showed the highest negative binding affinity.
05:59
Effect of Tinospora cordifolia on gestational diabetes mellitus and its complications. GreenMedInfo
PMID: Women Health. 2023 ;63(5):359-369. Epub 2023 Apr 20. PMID: 37080903 Abstract Title: Effect ofon gestational diabetes mellitus and its complications. Abstract: Ayurvedic system of medicine uses giloy or guduchi, also known as(TC), to treat diabetes and related diseases like hyperglycemia and hyperlipididemia. However, its usage in gestational diabetes mellitus (GDM) is not well studied. The primary objective of the study was to examine the effects of water extract of TC called satva, essential oil, and hydroalcoholic (HA) extract on GDM and its complications and to explore their mechanism of action using mice model. We used streptozotocin-induced diabetes in pregnant mice as murine model and tested TC preparations for anti-GDM activities. Blood glucose, insulin, litter size, and placental weight were assessed. ELISA method was used to measure plasma insulin level to compute homeostatic model assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), and homeostatic model assessment for assessing beta cell function (HOMA-Beta) levels to estimate insulin resistance, insulin sensitivity, and beta cell function respectively. TC-treated groups had significantly higher serum insulin levels, QUICKI, average litter size, and lower placental weight (
05:51
Consumption of 2 green kiwifruits daily improves constipation and abdominal comfort. GreenMedInfo
PMID: Am J Gastroenterol. 2023 Jun 1 ;118(6):1058-1068. Epub 2022 Dec 20. PMID: 36537785 Abstract Title: Consumption of 2 Green Kiwifruits Daily Improves Constipation and Abdominal Comfort-Results of an International Multicenter Randomized Controlled Trial. Abstract: INTRODUCTION: Consumption of green kiwifruit is known to relieve constipation. Previous studies have also reported improvements in gastrointestinal (GI) comfort. We investigated the effect of consuming green kiwifruit on GI function and comfort.METHODS: Participants included healthy controls (n = 63), patients with functional constipation (FC, n = 60), and patients with constipation-predominant irritable bowel syndrome (IBS-C, n = 61) randomly assigned to consume 2 green kiwifruits or psyllium (7.5 g) per day for 4 weeks, followed by a 4-week washout, and then the other treatment for 4 weeks. The primary outcome was the number of complete spontaneous bowel movements (CSBM) per week. Secondary outcomes included GI comfort which was measured using the GI symptom rating scale, a validated instrument. Data (intent-to-treat) were analyzed as difference from baseline using repeated measures analysis of variance suitable for AB/BA crossover design.RESULTS: Consumption of green kiwifruit was associated with a clinically relevant increase of1.5 CSBM per week (FC; 1.53, P
05:42
Chemopreventive effects and anti-tumorigenic mechanisms of Actinidia arguta. GreenMedInfo
PMID: Genes Environ. 2022 Dec 9 ;44(1):26. Epub 2022 Dec 9. PMID: 36494703 Abstract Title: Chemopreventive effects and anti-tumorigenic mechanisms of Actinidia arguta, known as sarunashi in Japan toward 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)- induced lung tumorigenesis in a/J mouse. Abstract: BACKGROUND: Previously, we reported the inhibitory effect of Actinidia arguta juice, known as sarunashi juice (sar-j) in Japan, on mutagenesis, inflammation, and mouse skin tumorigenesis. The components of A. arguta responsible for the anti-mutagenic effects were identified to be water-soluble, heat-labile phenolic compounds. We proposed isoquercetin (isoQ) as a candidate anticarcinogenic component. In this study, we sought to investigate the chemopreventive effects of A. arguta juice and isoQ on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in A/J mice, and identify the possible mechanisms underlying the anti-tumorigenic effects of A. arguta.RESULTS: The number of tumor nodules per mouse lung in the group injected with NNK and administered A. arguta juice orally was significantly lower than that in the group injected with NNK only. Oral administration of isoQ also reduced the number of nodules in the mouse lungs. As expected, the mutagenicity of NNK and 1-methyl-3-nitro-1-nitrosoguanidine (MNNG) detected using S. typhimurium TA1535 decreased in the presence of sar-j. However, NNK and MNNG mutagenicity detected using S. typhimurium YG7108, a strain lacking the O-methylguanine DNA methyltransferases (ogtand ada) did not decrease in the presence of sar-j suggesting that sar-j may mediate its antimutagenic effect by enhancing the DNA damage repair by ogtand ada. Phosphorylation of Akt, with or without epidermal growth factor stimulation, in A549 cells was significantly decreased following sar-j and isoQ treatment, indicating that components in sar-j including isoQ suppressed the PI3K/AKT signaling pathways.CONCLUSIONS: Sar-j and isoQ reduced NNK-induced lung tumorigenesis. Sar-j targets both the initiation and growth/progression steps during carcinogenesis, specifically via anti-mutagenesis, stimulation of alkyl DNA adduct repair, and suppression of Akt-mediated growth signaling. IsoQ might contribute in part to the biological effects of sar-j via suppression of Akt phosphorylation, but it may not be the main active ingredient.
05:37
Inflammatory foods and dementia there may be a link Skeptical Raptor
The Skeptical Raptor, stalking pseudoscience in the internet jungle.
A new study shows that foods with a high inflammatory index may be linked to dementia and Alzheimer's disease.
05:05
The Simple Cleaning Hack To Remove Yellow Stains From Pillows Healthy Holistic Living
As temperatures rise and the sweltering heat of summer nights intensify, many people find solace in their fresh, white linen sheets. The sleep may be rejuvenating, but the aftermath on the pillows is far from pleasant. If you too have found the yellowed stains on your once-pristine pillows a constant irritant, fear not. The solution may be cheaper and easier than youve ever thought possible.
Why Do We Get Yellow Stains on Our Pillows
The discoloration or yellowing of pillows is primarily due to perspiration. This issue is more relatable for those who tend to be hot sleepers, but its a universal problem that can occur unnoticed.
Primary reasons our pillows turn yellow:
Perspiration
The primary culprit behind these stains is a chemical component found in our sweat known as urea. Urea is a harmless metabolic byproduct that our bodies also excrete in much larger volumes in our urine. Over time, urea decomposes and reverts into ammonia. For those who want a deeper understanding, its technically the resultant ammonia that triggers the appearance of these yellow stains on pillows.
Damp Hair
Night-time shower enthusiasts who retire to bed with wet hair can inadvertently cause their pillows to turn yellow. The moisture from your hair seeps into the pillow, gradually causing yellow discoloration over time. If you use hair care products like leave-in conditioners, they might exacerbate pillow stains as they transfer from your hair onto the pillow.
Saliva
Although it might be uncomfortable to admit, most of us drool to some extent during sleep. Over time, saliva can also lead to the yellowing of your pillow. While it may not be the primary factor, saliva, in combination with sweat and other forms of moisture, can contribute to discoloration.
Natural Body Oils and Dead Skin Cells
Your bodys natural oils and the dead skin cells that we all shed can add to the yellowing process. Similar to sweat, these oils eventually pass through your pillowcase and settle on your pillow.
Topical Beauty and Skin Care Products
Lastly, lotions, face creams, and other beauty products applied
before bedtime stand as the second major cause of pillow yellowing.
Like sweat, these products tend to transfer onto pillows relatively
quickly. Applying these products an hour or two before bedtime
allows for better absorption, thus minimizing the amount
transferred onto your pillow.
Before delving into our pillow-cleaning solution, its worth noting
that regular washing is crucial. Experts suggest washing pillows at
least twice a year. However, if youre pressed for time or have
persistent, stubborn stains, youre going to love our efficient
solution.
Is It Okay to Sleep on a Pillow with Yellow Stains?
While having a pillow with a few yellow stains might not be aesthetically pleasing, its generally...
04:34
Trojan Horse Nanoparticles Kill Cancer Cells Without Drugs Healthy Holistic Living
In the ceaseless quest for finding more efficient methods of treating cancer, scientists have made an unprecedented breakthrough. Theyve engineered a Trojan horse mechanism that deploys anticancer nanoparticles into cancer cells, causing them to self-destruct without needing any drugs. The term Trojan horse hails from the ancient Greek tale, employed here as a metaphor to describe the method by which these nanoparticles infiltrate cancer cells. Although research is still in the early stages, this innovative approach has shown remarkable effectiveness in destroying cancer cells in a petri dish and reducing tumor growth in mice.
Innovation at Nanyang Technological University Singapore (NTU
Singapore)
Researchers at NTU Singapore have skillfully developed their Trojan horse by impregnating an anti-cancer nanoparticle with a specific amino acid, known as L-phenylalanine. This amino acid is crucial for the growth of cancer cells, making it the perfect disguise for the anticancer nanoparticle. As the cancer cells seek to absorb the L-phenylalanine, they unknowingly allow the deadly nanoparticle into their structure, subsequently leading to their self-destruction.
The Power of Nano-pPAAM
The nano-sized Trojan horse is known as Nano-pPAAM. This ultrasmall particle, with a diameter of just 30 nanometers, possesses excellent intrinsic anticancer and cancer-selective properties, as...
03:06
Blood Clots: the Common Killer You Might Be Ignoring Healthy Holistic Living
Blood clotting is a natural and vital part of the bodys healing process. When you sustain an injury, blood clots form to stem bleeding, allowing the wound to heal. However, when clots form within the veins without a corresponding injury, this can signal a serious health issue. To safeguard your health, its crucial to recognize the early signs of such internal blood clots. Early detection allows for prompt treatment, helping to prevent the clot from developing into a life-threatening condition.
What is a Blood Clot?
Blood clots form when platelets and proteins in the plasma (the liquid part of the blood) bind together to create a clot over an injury site, preventing excessive bleeding. This vital process protects against dangerous blood loss that could lead to death 1.
Typically, your body naturally dissolves the blood clot once the
injury heals. However, sometimes, clots form inside vessels without
any injury or fail to dissolve on their own. Such clotting can be
perilous 1.
Types of Blood Clots and Their Health Implications
Blood clots c...
03:00
ChatGPT Changes Its Mind: Maybe Antidepressants Do More Harm Than Good Mad In America
Last week, in my chat with ChatGPT, I sought to see whether it could produce evidence supporting the long-term use of antipsychotics. I imagined the chat as a simulation of questions that could be asked of a prominent biological psychiatrist at a debate. In the end, ChatGPT couldnt identify a single longitudinal study that told of better long-term outcomes for psychotic patients who regularly took antipsychotic medication than for those who stopped taking such medication.
This week, I wanted to see what ChatGPT would have to say about the long-term impact of antidepressants. In particular, I wanted to see whether it would point to the STAR*D study as evidence of their benefit. When Joanna Moncrieff and colleagues published their 2022 paper debunking the low-serotonin theory of depression, The New York Times and other outlets responded by writing that this didnt mean the drugs werent effective, citing the STAR*D study, with its purported 67% remission rate, as evidence of that effectiveness. In truth, nothing like that happened in the study. The published finding of 67% is better described as scientific fraud, and so, in this chat, with ChatGPT sitting in for an imagined psychiatrist on the debate stage, I wondered how it would respond if it cited STAR*D and I pointed out evidence of that fraud.
Our chat:
Robert Whitaker: Write an essay on the long-term effects of antidepressants as a treatment for depression.
ChatGPT
Title: Unveiling the...
02:27
FDAs Lab Test Power-Grab Continues Alliance for Natural Health USA Protecting Natural Health
More FDA protectionism that works against patient interests. Action Alert!
The FDA has announced its intent to issue a proposed rule this coming August that would extend the agencys power over laboratory developed tests (LDTs). This is a critical threat, as LDTs are crucial tools used in personalized medicine because labs can create custom diagnostic tests for all sorts of health conditions. We cannot allow the FDA to stifle innovation and best medical practice (including Functional Data Analysis the other type of FDA) in this sector and regulate these tests out of existence, as the agency has been trying to do for decades.
If the FDA is successful, your ability to get the personalized care you need from your doctor or healthcare provider will be compromised. LDTs are diagnostic tests developed and performed by local labs. They are important tools used by healthcare providers to diagnose and manage a wide range of conditions. They are widely usedthousands of different LDTs are availableand include genetic tests, heavy metal tests, tests for rare conditions, nutritional status tests, and hormone tests. They can be tailored to meet specific patient needs and can be used to respond rapidly to emerging threats like COVID-19. Currently, laboratories have the flexibility to adapt and modify tests based on evolving scientific knowledge and patient requirements. That could all change if the FDA wins.
LDTs are regulated by the Centers for Medicare and Medicaid Services (CMS). The rule hasnt been published yet so we dont know specifics, but what the FDA has been trying to do for years is to claim the authority to regulate LDTs as medical devices, which in many cases will mean they will require pre-market approval.
Weve spoken to a leading laboratory that offers many crucial tests that integrative healthcare providers rely on. Without being able to talk specifics since we dont know what the FDAs proposed rule looks like yet, their view was that the majority of their tests would be safe from FDA scrutiny because they use standardized methodologies and are low-risk. As any new regulatory framework adopted by the FDA will likely be a tiered, risk-based approach, low-risk tests would probably not face the same scrutiny as higher-risk tests (i.e., tests that could lead to patient harm if there is an error because the test is the primary means of diagnosing a disease).
We still think theres reason to worry about access, though, because the FDA has consistently demonstrated antipathy towards natural health and integrative medicine. The agency has, over the years, taken an adversarial stance against...
02:27
WHO Admission: Aspartame Possibly Carcinogenic Alliance for Natural Health USA Protecting Natural Health
yet the FDA, responsible for protecting our health and making sure our food is safe, continues to go to bat for Big Food. Action Alert!
Would you be concerned if you and your children were consuming a possible carcinogen every day? One that Big Food and the FDA has said is a safe way of avoiding sugar?
Late last week, the WHOs International Agency for Research on Cancer (IARC) labeled the artificial sweetener aspartame (marketed as NutraSweet and Equal) as possibly carcinogenic to humans. Predictably, Big Food has attacked the IARCs findings, creating an entirely new industry-funded front group that continues to try to defend aspartame in the face of mounting evidence showing its dangerous. The FDA was also quick to dig in on aspartames safety despite years of evidence demonstrating the cancer link. The fact that the food industry and the agency responsibility for regulating that industry are in lockstep when it comes to defending a possible carcinogen that millions of Americans are consuming every day is yet another example of the crony capitalism that is threatening our health and the health of our children. We must act now to stop it.
The IARCs conclusion that there is limited evidence of carcinogenicity for aspartame was based on studies showing a positive association between consumption of artificially sweetened beverages containing aspartame and cancer. Despite the IARCs classification, the Joint FAO/WHO Expert Committee on Food Additives announced that recommended daily limits for consumption of the sweetener would not change.
In response to the news of aspartames new classification, the FDA sprang into actionin defense of Big Food. In its response, the agency states that it disagrees with the IARCs conclusion and that FDA scientists do not have any safety concerns with aspartame.
Those following the research know that the IARCs classification of aspartame as a possible carcinogen has been a long time coming. Starting in the early 2000s, research from the prestigious Ramazzini Institute in Italy ...
02:10
24 Ways We Should Fundamentally Transform Our Healthcare System Alliance for Natural Health USA Protecting Natural Health
From Ronald Hoffman, MD
Its time to fundamentally transform our healthcare system. The fact is, we spend way more per capita on healthcare than any other country in the world, and our health outcomes rank behind those of many poorer countries; virtually everyone agrees that the status quo cant remain without the prospect of an unsustainable disease burden and fiscal disaster.
What is needed is a very fundamental re-ordering of our healthcare priorities and elimination of the perverse incentives which lead to more people undergoing costly sick-care. Only then can our healthcare system be saved from implosion, and the costly toll of degenerative diseases on our society and our economy be alleviated.
Here are some of the reforms I propose:
- Eliminate inequity by offering health coverage for all Americans based on means-tested eligibility. No one should die from lack of rudimentary medical care; nor should they suffer medical bankruptcy.
- Create competition and diversity in health insurance. Plans should be available ranging from bare-bones/high deductible to platinum coverage. Innovative companies should be allowed to compete for health-conscious applicants by offering a wide range of integrative medicine benefits.
- Foster a return to direct-pay of doctors which eliminates pricey insurance and government bureaucrats as arbiters of correct medical care.
- HSAs (tax-incentivized health savings accounts) should be encouraged, and expanded to cover supplements, gym memberships, yoga, and treatment by alternative practitioners.
- Medical education needs to be completely reformed. While pharmacology and surgery now dominate curricula, reflecting the priorities of BigPharma and device makers, young doctors need to be mobilized to become the vanguard for prevention via diet and lifestyle.
- Expand post-graduate education opportunities for doctors in integrative medicine and nutrition. Most doctors pursuing these careers must do so outside of traditional residency programs, at great cost to them.
- Put an end to state medical boards prosecution of doctors merely for providing integrative services.
The post 24 Ways We Should Fundamentally Transform Our Healthcare System first appeared on Alliance for Natural Health USA - Protecting Natural Health.
02:03
Superfoods for a Super You Dr. Tenpenny
There are so many supplements we can take. How do you know which ones to choose, and how do you prevent taking 25 pills every day? One of the best []
Go Back:30 Days | 7 Days | 2 Days | 1 Day
Thursday, 20 July
16:26
14:24
06:50
Calgary water fluoridation delayed again as implementation cost rises Fluoride Action Network
The re-introduction of fluoride into Calgarys drinking water is expected to take longer and cost more than originally anticipated.
Calgary city council voted in favour of adding fluoride to the citys water supply in November 2021, after a plebiscite during the municipal election resulted in 62 per cent of Calgarians voting in support.
The project was originally slated to be completed sometime this year but was extended until June 2024. The latest timeline from the City of Calgary now anticipates the work to be completed by September 2024.
The implementation cost for infrastructure at the two water treatment plants has also grown to $28.1 million, from original estimates of $10.1 million.According to city officials, the new cost estimates account for inflation, and the additional project scope.
We had a lot more information about the project that included some inflationary impacts, City of Calgary utilities delivery manager Tanner Fellinger told Global News. It also included some scope of work that one of our facilities requires an additional building as a result just to safely house the equipment and materials.
Fluoride was removed from the citys drinking water in 2011, and city officials said the infrastructure was decommissioned and removed following the decision to stop fluoridation.
The delay has prompted a group of 22 pediatricians to pen a letter to city manager David Duckworth outlining their frustrations with the timeline, including the significant decline in oral health since fluoride was removed from the citys drinking water.
The lack of water fluoridation affects everyone and especially children of low socioeconomic status, the letter said. For many vulnerable Calgary children, water fluoridation was their only form of dental protection.
Juliet Guichon, presid...
01:37
How to survive a depression or anxiety crisis: 17 Chipur tipurs Chipur
Its not uncommon and it calls for action, not shame. Depression, anxiety, mania, stress, substances - sometimes we live on the edge. And it comes at a cost. How to survive a depression or anxiety crisis? Lets talk
The post How to survive a depression or anxiety crisis: 17 Chipur tipurs first appeared on Chipur.
Thursday, 13 July
05:16
US DOJ and EPA reach settlement with JR Simplot over Idaho phosphate plant Fluoride Action Network
HOUSTON (ICIS)The US Department of Justice (DOJ) and the US Environmental Protection Agency (EPA) have announced a settlement with the JR Simplot Company involving their Don Plant phosphate manufacturing facility located near Pocatello, Idaho.
The agencies said the settlement resolves allegations primarily under the Resource Conservation and Recovery Act (RCRA) at the facility, including that Simplot failed to properly identify and manage certain waste streams as hazardous wastes.
The settlement requires Simplot to implement process modifications designed to enable greater recovery and reuse of phosphate. It also requires the company to ensure that financial resources will be available when the time comes for environmentally sound closure of the facility.
Simplot will also pay a civil penalty of $1.5m.
The Don Plant facility manufactures products for agriculture and industry including phosphoric acid and phosphate fertilizer with the results generating large quantities of acidic wastewater and a solid material called phosphogypsum.
The phosphogypsum is deposited in a large pile known as a gypstack, and acidic wastewater is discharged to the gypstack, which has a capacity to hold several billion gallons of acidic wastewater.
It was fully lined in 2017 in accordance with a previous consent orders Simplot entered into with the state of Idaho and the US.
The settlement also resolves alleged violations of the Clean Air Act (CAA) that relate to fluoride emissions from the facility, and of the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) and the Emergency Planning and Community Right-to-Know Act (EPCRA) that relate to reporting and notification requirements for hazardous substances and toxic chemicals.
Under the terms Simplot has agreed to implement specific waste management measures it has valued at nearly $150m.
These measures include extensive new efforts to recover and reuse the phosphate content within these wastes and avoid their disposal in the gypstack.
Simplot will also implement requirements that ensure gypstack stability and containment that will protect the environment even should climate change result in more severe weather events.
The settlement also includes a detailed plan setting the terms for the future closure and long-term care of the gypstack and requires Simplot to immediately secure and maintain approximately $108m dedicated to being available when the facility is eventually closed.
The company has further agreed to cease operation of the facilitys cooling towers no later than 27 June 2026, and replace them with one or more newly constructed cooling ponds, which will significantly reduce fluoride emissions to the air.
It will also submit revised Toxic Release Inventory forms for the years 2004-2013 that include estimates of certain metal compounds manufactured, processed or other...