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Monday, 24 July

02:20

Eyes of the Devil The REAL Documentary that Exposes the Horror of Child Sex Trafficking Health Impact News

by Brian Shilhavy
Editor, Health Impact News

The REAL horrors of child sex trafficking are so terrible and evil, that there is no reason to dramatize it, as Sound of Freedom does.

Tim Ballard and the O.U.R. organization admits that much of the film is dramatized, including the scene where Tim infiltrated the cartels in the jungle of Columbia by posing to be a doctor bringing in vaccines.

Tim went into a Colombian jungle by himself to rescue a little girl. FALSE

In the film, Tim poses as a doctor and goes into a jungle somewhere in Colombia to find the little boys sister, shortly after Operation Triple Take. This did not happen.

However, in real life, Tim did lead a group of O.U.R. operators, posing as doctors, into a jungle on the border of Haiti and the Dominican Republic a few years after Operation Triple Take in search for Gardy.

No one was rescued, but the operation did advance the search for Gardy, and operators were able to provide medical care to many children in need. (Source.)

As I asked in my original review of the movie after watching it, what kind of medical care did these operators who were admittedly fake doctors provide to the children in Haiti? Did they inject them with vaccines?

I continue to be attacked and ridiculed for publishing the truth about this fictional movie, with one person suggesting that I must actually support child sex trafficking if I am publishing negative reviews of Sound of Freedom.

This movie is very clearly a psyop and distraction from the REAL child sex trafficking that is occurring with young children who are also often murdered for their organs and body parts.

This is happening in Ukraine, for example, and we have exposed this evil. See:

...

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Sunday, 23 July

10:08

Exemptions To Attend School Exist Age of Autism The Rebel Alliance!

WorryNote: Back to school is stressful enough without the worries of compliance issues that do not match your family's needs.  Curious which exemptions exist in your state?  Check out www.nvic.org/law-policy-state  for information. Thank you, Cathy.

By Cathy Jameson

I wrote this several years ago on another platform in response to a letter I received.  Since we just got a similar notice, I thought Id share the post here. 

--

Late Summer 2016 - We got a reminder note from the kids' school a few weeks ago.  One of our children was "due" for a booster shot.  Documentation of that booster would be required prior to the start of the next school year.  We were not given the "...or else!" threat that's usually added to school shot notices, but the tone of the letter certainly implied it.  

I'd be lying if I said I didn't let the notice bother me much, but it did bother me.  

A lot.  

After rereading the current law - to include the section about vaccine exemptions, I wrote an email to the school nurse.  Knowing what I know about school shots (that in many states they are in fact not a requirement for school entry), I knew just how to respond to the misinformation that had been sent home with my child. 

Now, I could've gone all Encyclopedia Brown citing the law word-for-word.  Or I could've ripped her a new one for bullying my son into getting a vaccine he didn't need (the way the note was worded, he was so worried that he wouldn't be able to return to school in the fall without this booster).  But in my email, I was kind, cordial, and very respectful.  I did that not just because that's how people should be treated, but because this woman, and the staff she works with, will be the first people my child must rely on in an emergency medical situation should there be one on campus.  We need a positive working relationship with the staff, not one full of animosity.

So in my email, I simply asked for clarification.  

Will the exemption that we have on file with the school still be valid for the 2016-17 school year?  If not, I shall provide an...

10:00

How to Best Optimize Your Muscular Health Articles

This interview features two repeat guests, Georgi Dinkov, a pro-metabolic expert and a student of the late Ray Peats work, and Tyler LeBaron, Ph.D., an adjunct professor of chemistry, exercise physiology, nutrition, and sports bioenergetics. LeBaron is also the founder of the Molecular Hydrogen Institute and as an elite athlete is more than qualified for this discussion. Peat was a biologist with a specialization in physiology.

A large part of our discussion revolves around the pros and cons of eccentric versus concentric exercise, but toward the end we also delve into important topics like the metabolism of cancer, if and when baking soda can be used to treat cancer, and how molecular hydrogen helps prevent stroke damage.

Admittedly this is a dense scientific discussion on the fine details of the specifics of resistance training as a form of health. I felt it was important to bring it to the public as it is somewhat controversial, but it clearly will only be useful for a small segment of the population.

So, if you arent interested in resistance training then let me reinforce right at the start, as we do mention it in the interview, but it is buried at the end, that the most important exercise you can do is regular movement throughout the day. If you are a wearing an Oura ring or step counter, you should be shooting for five to seven miles (10,000 to 15,000 steps) per day.

There was a compelling study published earlier this year that showed that moderate activity was far more important than vigorous activity at decreasing mortality. Ideally you can do this activity outside during the middle of the day with minimal clothing on so you can also get your daily sun exposure full of UVB, and near IR to optimize your health.

Since this interview has limited practical use for most of us, I am reposting my new summary of why KAATSU is likely the most important resistance training you can do after 40 to 50 years old. I would also encourage you to read the free article on Substack as it has all the specific details you need to know about KAATSU. If you are interested in purchasing the KAATSU please use the 10% off link that is in the Substack article.

...

Why Molecular Hydrogen Is a Superior Antioxidant Articles

In this interview, repeat guest Tyler LeBaron, MSc., Ph.D., reviews some of the many benefits of molecular hydrogen (H2). Perhaps most importantly, molecular hydrogen acts as a selective antioxidant, meaning it doesn't indiscriminately suppress free radicals.

It uses your body's own biological systems and feedback loops to identify where and when you're under oxidative stress, and when found, antioxidant genes are stimulated and key antioxidants are transcribed from your DNA. So, molecular hydrogen is not in and of itself a direct radical-scavenging antioxidant. Rather, it helps your body make its own endogenous antioxidants. This is what makes molecular hydrogen so unique.

This is crucial because excessive antioxidants use can be deleterious and molecular hydrogen serves as a redox regulator, so, just like Goldilocks, you get just the right amount, not too much and not too little, which makes your cells very happy.

H2 Activates Nrf2 Pathway

One of the pathways activated by H2 when free radicals are present is the Nrf2 pathway. LeBaron explains:

"In your cell you have this protein, Nrf2, and it's attached to Keap1. They're always attached together. But when you get oxidative stress it can cleave off.

[Oxidative stress] causes the cleaving off of the Nrf2 and the Keap1, and the Nrf2 can then diffuse into the nucleus [where] it binds to the ARE, the antioxidant response element of the DNA. [This triggers] the production of all these endogenous antioxidants Phase 2 enzymes of detoxification and antioxidation and there are over 200 of them."

This is one of the primary benefits of molecular hydrogen. It's also what makes molecular hydrogen so useful for such a wide variety of conditions. According to LeBaron, it's been shown to have therapeutic benefits in more than 170 different animal disease models.

"What this means is, for example, there are lots of ways to induce diabetes in an animal model. Using these different models, we can show molecular hydrogen has therapeutic effects. And, yes, the Nrf2 in some cases seems to be extremely important. In fact, by using gene knockout or or interfering RNA, you can blunt the benefits of molecular hydrogen. So, the Nrf2 is very important," LeBaron says.

Molecular Hydrogen Is an Important Nrf2 Regulator

Sulforaphane, found in broccoli, is another well-studied Nrf2 activator. But in contrast to sulforaphane (as well as other Nrf2 activators), molecular hydrogen does not disturb redox homeostasis within the cell by adding too many antioxidants.

R...

Evidence-Based Homeopathic Family Medicine Articles

Editor's Note: This article is a reprint. It was originally published December 2, 2018.

Homeopathy has been a form of medicine for hundreds of years. Dana Ullman, whose father was a medical doctor, a pediatrician and allergist, has dedicated a significant portion of his professional life to the practice of homeopathy. Ullman was introduced to this medical art as a junior at University of California (UC) Berkeley, in 1973.

"A Stanford-trained doctor and a male midwife created a group of people to study homeopathy together: three doctors, two nurses, two yoga teachers, a dentist and several laypeople. We met weekly for five years. Towards the end of that, I was honored to be arrested for practicing medicine without a license. That was in 1976.

We won an important court case settlement by differentiating medical care from health care. We made it clear that I wasn't treating a disease. I was treating a person with a disease.

The courts agreed that was a reasonable interpretation, and that as long as I have written contracts with my patients that differentiate medical care from health care, as long as I refer patients for medical care, which is not what I am providing, then it can work out. I've been doing that ever since," Ullman says.

Definition of Homeopathy

The principles of homeopathy were originally developed by Dr. Samuel Hahnemann (1755-1843), a German physician to the Royal family, and are based in the law of similars, also known as "like cures like."

"Homeopathy is a type of natural medicine that uses nano-doses, really small doses of plants, minerals, animals and chemicals," Ullman explains. "We look to find whatever toxicological symptoms that substance causes. Once you know what syndrome or symptom a substance causes in the toxic dose, you can use specially prepared nano-sized doses of that substance to treat the syndrome that it causes.

The logic of that [is that] your body does whatever it can to survive. Your symptoms are not the result of breakdown. Your symptoms are the result of that doctor inside of you that is trying to defend you and is trying to heal you. Your symptoms are part of your defenses.

And the very word, 'symptom' means sign or signal, and symptoms are just that. They're signaling us that something's wrong. Instead of turning off that signal, in homeopathy, you turn into the skid.

One of the things that your driver's education teacher probably taught you is that when you skid, you turn into t...

09:35

Geoengineering Watch Global Alert News, July 22, 2023, #415 Geoengineering Watch

Dane Wigington GeoengineeringWatch.org "Four Times More Toxic": How Wildfire Smoke Ages Over Time, that's the headline from a new European Commission report. So what changes occur with smoke over time? It becomes far more toxic due to oxidation and atmospheric chemical reactions. Will "official sources" ever address the ongoing geoengineering atmospheric particulate spraying that is taking place

07:14

Hollywood Actor Jim Caviezel Said that Hes Jesus and that Trump is Moses in Child Trafficking Medical Kidnap

by Brian Shilhavy
Editor, Health Impact News

The frenzy surrounding the Sound of Freedom fictional movie has gone from hype, to insanity, to now blasphemy.

Hollywood actor Jim Caviezel appeared on Fox News and stated that we have to do a lot more to rescue children being trafficked, and that Donald Trump was the one who was going to rescue trafficked children.

Im still Jesus, but he (Trump) is Moses.

This is on our Bitchute channel:

If you are a true disciple of Jesus Christ, then you know that taking a stand for Truth means to go against the crowd.

Well, the crowd in the U.S. today, at least in the Christian Right, is following false apostles and prophets claiming to be saviors of children who are trafficked.

But this is what Paul wrote to the disciples of Jesus in the First Century:

We ought always to thank God for you, brothers, and rightly so, because your faith is growing more and more, and the love every one of you has for ea...

07:13

Hollywood Actor Jim Caviezel Said that Hes Jesus and that Trump is Moses in Child Trafficking Vaccine Impact

by Brian Shilhavy
Editor, Health Impact News

The frenzy surrounding the Sound of Freedom fictional movie has gone from hype, to insanity, to now blasphemy.

Hollywood actor Jim Caviezel appeared on Fox News and stated that we have to do a lot more to rescue children being trafficked, and that Donald Trump was the one who was going to rescue trafficked children.

Im still Jesus, but he (Trump) is Moses.

This is on our Bitchute channel:

If you are a true disciple of Jesus Christ, then you know that taking a stand for Truth means to go against the crowd.

Well, the crowd in the U.S. today, at least in the Christian Right, is following false apostles and prophets claiming to be saviors of children who are trafficked.

But this is what Paul wrote to the disciples of Jesus in the First Century:

We ought always to thank God for you, brothers, and rightly so, because your faith is growing more and more, and the love every one of you has for ea...

06:59

Hollywood Actor Jim Caviezel Said that Hes Jesus and that Trump is Moses in Child Trafficking Health Impact News

by Brian Shilhavy
Editor, Health Impact News

The frenzy surrounding the Sound of Freedom fictional movie has gone from hype, to insanity, to now blasphemy.

Hollywood actor Jim Caviezel appeared on Fox News and stated that we have to do a lot more to rescue children being trafficked, and that Donald Trump was the one who was going to rescue trafficked children.

Im still Jesus, but he (Trump) is Moses.

This is on our Bitchute channel:

If you are a true disciple of Jesus Christ, then you know that taking a stand for Truth means to go against the crowd.

Well, the crowd in the U.S. today, at least in the Christian Right, is following fals...

Saturday, 22 July

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...

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...

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...

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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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 (

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

Article

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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.

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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.

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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.

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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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