Censorship continues apace

USA Today reports that Facebook will extend its censorship to anti-vaccine news. USA Today states:

‘Facebook is considering making anti-vaccination content on its site less visible amid a measles outbreak that has reignited a conversation about preventative shots.

The social media giant that’s been criticized for spreading fake news told USA TODAY it’s “taken steps to reduce the distribution of health-related misinformation on Facebook, but we know we have more to do.”

Facebook has been fighting misinformation on its platform since the 2016 presidential election after fake accounts and news stories aimed at sowing discord among users were discovered.’

Facebook, YouTube, Amazon and others announce censorship plans

Not only are social media censoring left political ideas but, now, extending this censorship to medical issues regarding vaccines and other unpopular ideas. The victims of this censorship is the left, natural medicine, and those pointing to deficiencies in current vaccines. It should be noted that we now have the technology and knowledge to make safer and more effective vaccines. Among those censoring are Facebook, YouTube, Amazon and other social media.

Those voices who normally raise concerns about censorship and demand free speech are strangely and cowardly absent today.

Small molecule nicotinamideN-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle

[**Biochemical Pharmacology**][Biochemical Pharmacology]

Available online 10 February 201

**Abstract**

Aging is accompanied by progressive declines in skeletal muscle mass and strength and impaired regenerative capacity, predisposing older adults to debilitating age-related muscle deteriorations and severe morbidity. Muscle stem cells (muSCs) that proliferate, differentiate to fusion-competent myoblasts, and facilitate muscle regeneration are increasingly dysfunctional upon aging, impairing muscle recovery after injury. While regulators of muSC activity can offer novel therapeutics to improve recovery and reduce morbidity among aged adults, there are no known muSC regenerative small molecule therapeutics. We recently developed small molecule inhibitors of nicotinamide N-methyltransferase (NNMT), an enzyme overexpressed with aging in skeletal muscles and linked to impairment of the NAD\\+ salvage pathway, dysregulated sirtuin 1 activity, and increased muSC senescence. We hypothesized that NNMT inhibitor (NNMTi) treatment will rescue age-related deficits in muSC activity to promote superior regeneration post-injury in aging muscle. 24-month old mice were treated with saline (control), and low and high dose NNMTi (5 and 10 mg/kg) for 1-week post-injury, or control and high dose NNMTi for 3-weeks post-injury. All mice underwent an acute muscle injury (barium chloride injection) locally to the tibialis anterior (TA) muscle, and received 5-ethynyl-2’-deoxyuridine systemically to analyze muSC activity. *In vivo*contractile function measurements were conducted on the injured TA muscle and tissues collected for ex-vivo analyses, including myofiber cross-sectional area (CSA) measurements to assess muscle recovery. Results revealed that muscle stem cell proliferation and subsequent fusion were elevated in NNMTi-treated mice, supporting nearly 2-fold greater CSA and shifts in fiber size distribution to greater proportions of larger sized myofibers and fewer smaller sized fibers in NNMTi-treated mice compared to controls. Prolonged NNMTi treatment post-injury further augmented myofiber regeneration evinced by increasingly larger fiber CSA. Importantly, improved muSC activity translated not only to larger myofibers after injury but also to greater contractile function, with the peak torque of the TA increased by ∼70% in NNMTi-treated mice compared to controls. Similar results were recapitulated *in vitro* with C2C12 myoblasts, where NNMTi treatment promoted and enhanced myoblast differentiation with supporting changes in the cellular NAD\\+/NADH redox states. Taken together, these results provide the first clear evidence that NNMT inhibitors constitute a viable pharmacological approach to enhance aged muscle regeneration by rescuing muSC function, supporting the development of NNMTi as novel mechanism-of-action therapeutic to improve skeletal muscle regenerative capacity and functional recovery after musculoskeletal injury in older adults

[Biochemical Pharmacology]: https://www.sciencedirect.com/science/journal/00062952
[In Press_ Accepted]: https://www.sciencedirect.com/science/journal/aip/00062952
[What]: https://service.elsevier.com/app/answers/detail/a_id/22799/supporthub/sciencedirect/
[HarshiniNeelakantan]: https://www.sciencedirect.com/science/article/abs/pii/S0006295219300462?via%3Dihub#!
[https]: https://doi.org/10.1016/j.bcp.2019.02.008
[Get]: https://s100.copyright.com/AppDispatchServlet?publisherName=ELS&contentID=S0006295219300462&orderBeanReset=true

Rotavirus vaccine reduces type 1 diabetes in children.

Science Daily
Possible link between rotavirus vaccine and decline in type 1 diabetes
Date:
January 22, 2019
Source:
Walter and Eliza Hall Institute
Summary:
A drop in the number of young children diagnosed with type 1 diabetes could be associated with the introduction of routine rotavirus vaccination of Australian infants.


A drop in the number of young children diagnosed with type 1 diabetes could be associated with the introduction of routine rotavirus vaccination of Australian infants, according to a new study by Melbourne researchers.

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The researchers investigated the number of Australian children diagnosed with type 1 diabetes from 2000 to 2015 and found that type 1 diabetes diagnoses in children aged 0-4 years declined from 2007 — the year that rotavirus vaccine was introduced as a routine infant vaccination.

This is the first time the rate of type 1 diabetes in young children in Australia has fallen since the 1980s. While not conclusively linking the rotavirus vaccine with protection against type 1 diabetes, the discovery builds on earlier research suggesting natural rotavirus infection may be a risk factor for type 1 diabetes.

The study, a collaboration led by the Murdoch Children’s Research Institute and Walter and Eliza Hall Institute clinician scientists, was published in JAMA Pediatrics today.

Decline in type 1 diabetes

Since the 1980s, the incidence of type 1 diabetes has steadily increased in Australia and worldwide, but the reasons for this increase are poorly understood. Type 1 diabetes is a serious, lifelong autoimmune condition, in which the body’s immune system destroys cells in the pancreas that produce insulin, a hormone that controls the level of glucose in the blood.

By investigating the number of Australian children diagnosed with type 1 diabetes each year since 2000, the research team observed that after 2007 the rate of type 1 diabetes decreased in children aged 0-4 years, said study lead Dr Kirsten Perrett from the Murdoch Children’s Research Institute.

“The significant decrease in type 1 diabetes that we detected in young children after 2007 was not seen in older children aged 5-14. This suggests the young children could have been exposed to a protective factor that didn’t impact older children,” Dr Perrett said.

“We observed the decline in the rate of type 1 diabetes in children born after 2007 coincided with the introduction of the oral rotavirus vaccine onto the Australian National Immunisation Program in 2007.”

The rotavirus vaccine is routinely given to Australian infants aged 2 and 4 months to protect them against a severe, potentially life-threatening form of diarrhoea.

Exploring the connection

Professor Len Harrison from the Walter and Eliza Hall Institute, who is the study senior author, said the discovery followed on from earlier research implicating rotavirus infection in the development of type 1 diabetes.

“Twenty years ago our team revealed an association between the appearance of immune markers of type 1 diabetes in children and rotavirus infection. Subsequent studies in laboratory models suggested rotavirus infection of pancreatic cells can trigger an immune attack against the insulin-producing cells — similar to what occurs in type 1 diabetes,” he said.

“While not conclusive, our latest study suggests that preventing rotavirus infection in Australian infants by vaccination may also reduce their risk of type 1 diabetes. We will be continuing this research to look more closely at the correlation, by comparing the health records of young children with or without type 1 diabetes.

“At this stage we don’t yet know whether the reduction in type 1 diabetes is a permanent effect or transient, and it may only be relevant to Australian children,” Professor Harrison said.

The research was supported by the National Health and Medical Research Council (ECF APP1054394), a Melbourne Children’s Clinician-Scientist Fellowship, a Murdoch Children’s Research Institute grant, the Colin North Diabetes Fund and the Victorian Government.

Story Source:

Materials provided by Walter and Eliza Hall Institute. Note: Content may be edited for style and length.

Journal Reference:

Kirsten P. Perrett, Kim Jachno, Terry M. Nolan, Leonard C. Harrison. Association of Rotavirus Vaccination With the Incidence of Type 1 Diabetes in Children. JAMA Pediatrics, 2019; DOI: 10.1001/jamapediatrics.2018.4578
Cite This Page:
MLA
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Chicago
Walter and Eliza Hall Institute. “Possible link between rotavirus vaccine and decline in type 1 diabetes.” ScienceDaily. ScienceDaily, 22 January 2019. <www.sciencedaily.com/releases/2019/01/22

Make Vaccines Safe

  • Vaccines contain chemicals and other ingredients that are carcinogenic.

  • The biggest class of carcinogenic additives in vaccines are heavy metals with mercury being the most dangerous. Even minute amounts of mercury affect every system of the body: the endocrine, the neurological system, the digestive system, the epithelial tissue.

  • Antibodies that are stimulated by the body from vaccines are not always enough to provide lifelong protection from a disease. For example, people who had Chicken Pox often still get Shingles later in life.

  • Vaccines include foreign RNA and DNA from animals, aborted fetal tissue, formaldehyde, antifreeze-like compounds. If you added these same ingredients to a baby’s bottle you would be charged with attempted murder.

Gonorrhea Protection From Vaccine

Serogroup B meningococcal vaccine Bexsero reported to elicit antibodies to Neisseria Gonorrhea

December 21st, 2018 – New research indicates that the meningococcal B vaccine Bexero may offer cross-protection against gonorrhea.

Bexsero, which is FDA-approved to prevent invasive disease caused by Neisseria meningitidis serogroup B, for individuals 10 to 25 years of age, includes the MeNZB OMV component plus 3 recombinant antigens, NadA, fHBP-GNA2091 and NHBA-GNA1030.

This research found there is a high level of sequence identity between MeNZB OMV and Bexsero OMV antigens, and gonococcal proteins in test rabbits.

This study’s conclusion said ‘the anti-gonococcal antibodies induced by MeNZB-like OMV proteins could explain the previously seen decrease

And, the high level of anti-gonococcal-NHBA antibodies generated by Bexsero vaccination in humans may result in additional cross-protection against gonorrhea.

Gonorrhea is the 2nd most commonly reported notifiable disease in the USA.

Gonorrhea is a sexually transmitted disease caused by infection with the Neisseria gonorrhoeae bacterium.

N. gonorrhea infects the mucous membranes of the reproductive tract, including the cervix, uterus, and fallopian tubes in women, and the urethra in women and men, according to the US Centers for Disease Control and Prevention (CDC).

This new study builds on a 2017 report that the outer membrane vesicle (OMV) meningococcal B vaccine, MeNZB, was reported to be associated with reduced rates of gonorrhea following a mass vaccination campaign in New Zealand.

To probe the basis for this protection we assessed cross-reactivity to N. gonorrhea of serum raised to the meningococcal vaccine Bexsero, which contains the MeNZB OMV component plus three recombinant antigens (NadA, fHBP-GNA2091, and NHBA-GNA1030).

This new information is important since gonorrhea is becoming increasingly difficult due to widespread antibiotic resistance, says the CDC.

In 2017, 555,608 cases of gonorrhea were reported to CDC.

While vaccines are routinely used for N.meningitidis, no vaccine is available for N.gonorrhea.

“We have all the knowledge and technology to make a real gonorrhea vaccine,” said the producer of Bexero, GSK, in an interview during November 2018.

This study’s results may lead to human clinical trials.

These Australian researchers included Evgeny A Semchenko, Aimee Tan, ay Borrow, and Kate L Seib, Institute for Glycomics, Griffith University, Gold Coast, Australia.

Veteran killed by Veteran’s Hospital policeman in Kansas City during routine traffic stop! Family suing for wrongful death

**Veteran died after confrontation at Kansas City VA hospital. Senators demand answers**

BY ANDY MARSO

DECEMBER 11, 2018 05:30 AM

A man named Dale Farhner died in May after a confrontation with Kansas City VA Medical Center police. The VA has declined to provide any information about his death.

Two U.S. senators are seeking answers about the death of a veteran following an altercation at the Kansas City \[VA Medical Center\]\[\]. VA officials have declined for months to provide information to The Star.

Dale Farhner of Kingston, Mo., died in May, and since then The Star has sought details about what happened. ButVA officials have withheld information, saying the matter remains under review.

U.S. Sen. Claire McCaskill, a Missouri Democrat, and U.S. Sen. Roy Blunt, a Missouri Republican, sent a joint letter to U.S. Veterans Affairs Secretary Robert Wilkie last week, asking for answers.

“We certainly appreciate the requirements of an investigation, but hope that after over six months some initial information can be forthcoming,” the letter reads. “The health and well-being of our veterans have been among our highest shared priorities in Congress. Please release any information that can be made public regarding Mr. Farhner, and if not, please explain the reasons why.”

The Star received an anonymous tip that on May 10 Farhner had a confrontation with VA police outside the entrance to the medical center’s emergency department, at 4801 Linwood Blvd. The tipster said Farhner was comatose following the confrontation and was taken to the University of Kansas Hospital, where he was diagnosed with a brain hemorrhage.

The tipster said Farhner died May 12 at KU Hospital. That much is confirmed by \[online obituaries\]\[\], which said he was 66 and from Kingston. Efforts to reach his next-of-kin, as identified by his funeral home, were not successful.

**HELP LIFT A BURDEN FOR THOSE WHO SERVE**

Military families—even those with VA benefits—often face health care bills they can’t pay, raising their risk for depression, substance abuse and suicide.

That’s why we’ve launched The War Within Initiative to abolish millions in military medical debt. Every dollar our readers contribute to RIP Medical Debt, a 501(c)(3) nonprofit, forgives $100 in unpaid medical bills.

The Star sought comment in May from Dwayne Rider, who was then the spokesman for the Kansas City VA Medical Center.

Rider responded via email on May 31, saying “due to privacy restrictions, we cannot release additional information at this time.”

The Star filed a formal request under the Freedom of Information Act that same day.

The VA responded on July 7 with an emailed letter saying it had identified “nine documents totaling 18 pages of written records, and one video, and one audio recording” relevant to the request.

But VA records manager Laura Hughes wrote that she was withholding all of it “based on the open/pending status of the Veterans Health Administration Office of Security & Law Enforcement review.”

“Due to the open/pending status the documents are pre-decisional to VHA’s findings and decision regarding this incident,” Hughes said. “Based upon the information available to me I believe release of the records could potentially impair the deliberative process as release of the pre-decisional document to the public would likely negatively impact a frank discussion on matters of policy between subordinates and supervisors.”

The Star lodged a formal appeal of that decision on July 20.

As of Monday, the VA’s appeals office had provided no response. Tracy Knight, an information specialist in the Washington, D.C., office of the VA’s general legal counsel, said she could give no time line for a decision.

“The attorney who’s working it has been in contact with his deputy and they’ve got to go back and forth and do some additional work,” Knight said.

On Monday, Kansas City VA staff once again rebuffed requests for comment on Farhner’s death.

The Jackson County Medical Examiner’s office performed Fahrner’s autopsy, but Marshanna Hester, a spokeswoman for the office, said no information could be released because the case is still open.

“All documents prepared by and in the custody of the Jackson County Medical Examiner’s Office relating to this matter are investigative reports of a law enforcement agency and are thus closed records until the investigation becomes inactive,” Hester said Friday via email.

Study links frequent red meat consumption to high levels of chemical associated with heart disease

NEWS RELEASES
Monday, December 10, 2018

Findings reveal tripling of blood levels of TMAO from red meat diet, but dietary effects can be reversed

Researchers have identified another reason to limit red meat consumption: high levels of a gut-generated chemical called trimethylamine N-oxide (TMAO), that also is linked to heart disease. Scientists found that people who eat a diet rich in red meat have triple the TMAO levels of those who eat a diet rich in either white meat or mostly plant-based proteins, but discontinuation of red meat eventually lowers those TMAO levels.

TMAO is a dietary byproduct that is formed by gut bacteria during digestion and is derived in part from nutrients that are abundant in red meat. While high saturated fat levels in red meat have long been known to contribute to heart disease—the leading cause of death in the United States—a growing number of studies have identified TMAO as another culprit. Until now, researchers knew little about how typical dietary patterns influence TMAO production or elimination.

The findings suggest that measuring and targeting TMAO levels—something doctors can do with a simple blood test—may be a promising new strategy for individualizing diets and helping to prevent heart disease. The study was funded largely by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health. It will be published Dec. 10 in the European Heart Journal, a publication of the European Society of Cardiology.

“These findings reinforce current dietary recommendations that encourage all ages to follow a heart-healthy eating plan that limits red meat,” said Charlotte Pratt, Ph.D., the NHLBI project officer for the study and a nutrition researcher and Deputy Chief of the Clinical Applications & Prevention Branch, Division of Cardiovascular Sciences, NHLBI. “This means eating a variety of foods, including more vegetables, fruits, whole grains, low-fat dairy foods, and plant-based protein sources such as beans and peas.”

“This study shows for the first time what a dramatic effect changing your diet has on levels of TMAO, which is increasingly linked to heart disease,” said Stanley L. Hazen, M.D., Ph.D., senior author of the study and section head of Preventive Cardiology & Rehabilitation at the Cleveland Clinic. “It suggests that you can lower your heart disease risk by lowering TMAO.”

Hazen estimated that as many as a quarter of middle-aged Americans have naturally elevated TMAO levels, which are made worse by chronic red meat consumption. However, every person’s TMAO profile appears to be different, so tracking this chemical marker, Hazen suggested, could be an important step in using personalized medicine to fight heart disease.

For the study, researchers enrolled 113 healthy men and women in a clinical trial to examine the effects of dietary protein—in the form of red meat, white meat, or non-meat sources—on TMAO production. All subjects were placed on each diet for a month in random order. When on the red meat diet, the participants consumed roughly the equivalent of about 8 ounces of steak daily, or two quarter-pound beef patties. After one month, researchers found that, on average, blood levels of TMAO in these participants tripled, compared to when they were on the diets high in either white meat or non-meat protein sources.

While all diets contained equal amounts of calories, half of the participants were also placed on high-fat versions of the three diets, and the researchers observed similar results. Thus, the effects of the protein source on TMAO levels were independent of dietary fat intake.

Importantly, the researchers discovered that the TMAO increases were reversible. When the subjects discontinued their red meat diet and moved to either a white meat or non-meat diet for another month, their TMAO levels decreased significantly.

The exact mechanisms by which TMAO affects heart disease is complex. Prior research has shown TMAO enhances cholesterol deposits into cells of the artery wall. Studies by the researchers also suggest that the chemical interacts with platelets—blood cells that are responsible for normal clotting responses—in a way that increases the risk for clot-related events such as heart attack and stroke.

TMAO measurement is currently available as a quick, simple blood test first developed by Hazen’s laboratory. In recent published studies, he and his colleagues reported development of a new class of drugs that are capable of lowering TMAO levels in the blood and reducing atherosclerosis and clotting risks in animal models, but those drugs are still experimental and not yet available to the public.

The study was supported by grants from the NHLBI and the Office of Dietary Supplements (HL103866, HL126827, HL106003, HL130819) and the National Institute of Diabetes and Digestive and Kidney Diseases (DK106000). The study was also supported by UCSF Clinical and Translational Science Unit.

Part of the National Institutes of Health, the National Heart, Lung, and Blood Institute (NHLBI) plans, conducts, and supports research related to the causes, prevention, diagnosis, and treatment of heart, blood vessel, lung, and blood diseases; and sleep disorders. The Institute also administers national health education campaigns on women and heart disease, healthy weight for children, and other topics. NHLBI press releases and other materials are available online at https://www.nhlbi.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892

Guillain-Barré Syndrome

Medically reviewed by Debra Sullivan, PhD, MSN, RN, CNE, COI

What is Guillain-Barré syndrome?


Guillain-Barré syndrome is a rare but serious autoimmune disorder in which the immune system attacks healthy nerve cells in your peripheral nervous system.

This leads to weakness, numbness, and tingling. It can eventually cause paralysis.

The cause of this condition is unknown, but it’s typically triggered by an infectious illness, such as the stomach flu or a lung infection.

Guillain-Barré is rare, affecting only about 1 in 100,000 Americans, according to the National Institute of Neurological Disorders and Stroke.

There’s no cure for the syndrome, but treatment can reduce the severity of your symptoms and shorten the duration of the illness.

There are multiple types of Guillain-Barré, but the most common form is acute inflammatory demyelinating polyradiculoneuropathy (AIDP). It results in damage to myelin.

Other types include Miller Fisher syndrome, which affects the cranial nerves.

What causes Guillain-Barré syndrome?
The precise cause of Guillain-Barré is unknown.

According to the Centers for Disease Control and Prevention (CDC), about two-thirds of people with Guillain-Barré develop it soon after they’ve been sick with diarrhea or a respiratory infection.

This suggests that the disorder may be triggered by an improper immune response to the previous illness. Learn more about autoimmune disease here.

Campylobacter jejuni infection has been associated with Guillain-Barré. Campylobacter is one of the most common bacterial causes of diarrhea in the United States. It’s also the most common risk factor for Guillain-Barré.

Campylobacter is often found in undercooked food, especially poultry.

The following infections have also been associated with Guillain-Barré:

influenza
cytomegalovirus, which is a strain of the herpes virus
Epstein-Barr virus infection, or mononucleosis
mycoplasma pneumonia, which is an atypical pneumonia caused by bacteria-like organisms
HIV or AIDS
Anyone can get Guillain-Barré, but it’s more common among older adults.

In extremely rare cases, people can develop the disorder days or weeks after receiving a vaccination.

The CDC and the U.S. Food and Drug Administration (FDA) have systems in place to monitor the safety of vaccines, detect early warning signs of side effects, and record any cases of Guillain-Barré that develop following a vaccination.