In Early 2020, A Chinese Source Trusted By FBI Said COVID Leaked From Wuhan Lab, Sources Say

by Michael Shellenberger and Alex Gutentag via Public subsatck,

FBI’s entire 25-person Chinese intelligence squad knew of reliable human intelligence that SARS-CoV-2 Covid leaked from a lab...

Over the last several months, Public has reported on a growing body of evidence that the SARS-CoV-2 virus that caused the Covid pandemic escaped from a lab in Wuhan, China. Last year, Public and Racket were the first to report that US government officials had identified that the first patients to become sick with Covid worked at the Wuhan Institute of Virology (WIV).

Now, Public has learned from multiple sources that the FBI knew since at least March 2020 that Covid was the result of a lab leak. A Chinese national from Wuhan, working as a confidential human source (CHS) for the FBI, told their handler at the FBI’s Chinese Intelligence Squad. The sources said it was probable that the whole squad of 25 people knew.

“A person working at the Virology Institute lab in Wuhan, China was infected, left the building, and spread the virus outside the lab in Wuhan,” the CHS told the FBI, according to a source.

“It didn’t have anything to do with the wet market or the bat soup story they were going with.”

The sources asked Public to protect their identities and those of their colleagues. The sources say they are speaking up now out of concern over abuses of power within the FBI. They reached out to Public after seeing our story yesterday about how scientists, who Anthony Fauci’s National Institute of Allergy and Infectious Diseases (NIAID) had in the past funded, sought to insert a furin cleavage site right where it exists on SARS-CoV-2.

The sources added that the FBI trusted the CHS because the person’s information had been corroborated at least three times previously.

“The CHS was from Wuhan, had been vetted, and the person had provided information on three prior occasions that they were able to corroborate as true and reliable.”

Another source said the FBI had considered the information “good intel.”

...

Two sources said that the CIA may have been conflicted in investigating its origins because it didn’t want to compromise investigations of the Wuhan lab that predated the outbreak of Covid-19.

“There was a clear lack of interest in a robust analysis of Chinese military connections to WIV research, connections between Chinese military and civilian research, and connections that could be drawn between US research and WIV activity,” the whistleblower said.

Former Director of National Intelligence John Ratcliffe suggested that there could be additional reasons behind the CIA’s lack of disclosure about COVID’s origins. 

...

Fauci may have also tried to influence the FBI. 

https://www.zerohedge.com/political/early-2020-chinese-source-trusted-fbi-said-covid-leaked-wuhan-lab-sources-say

Even More on Multiple Sclerosis and EBV

 by Derek Lowe

The updates to things I've been writing about here are coming almost too quickly to catch up with, especially since I try to vary the subject matter here day by day (on the theory that if someone stops by and finds that they're not interested in today's post, that they have a good chance of finding something totally different the next time). But early this week I was writing on the latest developments in the developing story of whether multiple sclerosis (MS) is a consequence of infection by Epstein-Barr virus (EBV), and there have been more publications bearing on this already.

I had mentioned in Monday's post that one of the pieces of the puzzle seems to be that while almost everyone gets infected with EBV at some point (and that timing probably matters), obviously not everyone goes on to an immune attack on their own nervous system. There's a particular class of antibody that can be raised to a particular EBV protein, though, that can cross-react to an important protein on the surface of glial cells, and that's the connection. But in a good number of cases where that starts happening, the immune system does a last-ditch edit and tries to take out the B cells that are producing these autoreactive antibodies - and the efficiency of that process is another big determinant of someone's risk for developing MS. 

Now this paper shores up that idea, showing that indeed, if you look at the cerebrospinal fluid of MS patients, there's a lot to learn from the T cells found there. 13% of them are targeting B cells which seem to be infected with EBV. This fact has been known for some time, as part of a general association between EBV and MS, but as usual, it's difficult to sort out chickens and eggs. Does having MS make you more vulnerable to Epstein-Barr infection, or does Epstein-Barr make you more vulnerable to MS? The scales are very much tipping toward the latter. This new paper shows that if you dig deeper into that T cell population and look at the lines that have been expanded the most, the proportion of the ones that are targeting those EBV-tinged B cells is still higher (47%). That's a strong clue that this is part of the real pathology of the disease, and as the authors note, there are several possible explanations: perhaps the T cells are just there because they're targeting B cells that are straight-out infected with EBV. Or they may be going after another protein, human or viral, that cross-reacts with one or more human proteins. They could also just be recruited into the nervous system as general consequence of inflammation, making them more of a consequence of the disease rather than part of its cause. But the work I wrote about earlier this week argues that a big part of the MS story is an autoimmune war between T-cell and B-cell populations over cross-recognition of EBV and glial cell proteins, and this lands right into that framework.

Another suprising bit of the story comes from the distant past. This Nature article is an overview of a series of data-rich genomics papers the journal has recently published. These are part of a big push in recent years to unravel the prehistory of Europe and Asia through genomic markers and sequencing of ancient remains, work which is bringing that era into focus in a way that nothing else could do. It's become clearer that there were at least three distinct waves of migration into Europe from Eurasia starting about 45,000 years ago (give or take a few thousand). First there were hunter-gatherers from Asia (who encountered Neaderthals and such on arrival), followed by farming cultures from the Middle East about 11,000 years ago, who were then overlaid by a third wave of animal herders from the eastern steppes about 5,000 years back. It's a complex story that integrates both genomic and archaeological evidence, and you may be wondering what the heck it has to do with multiple sclerosis.

Well, this latest work suggests that genes that are known to confer increased risk for MS actually expanded during this period, and that this (and other genomic signatures) are not (or certainly not all) due to these populations mixing and adapting over the years. Instead, different waves tended to go to different parts of Europe and more or less take over (Denmark, in particular, seems to have gone through some population changes so complete and drastic that genocidal conquest comes to mind as a likely explanation). The MS susceptibility genes came in with that last wave of pastoralist herders, and then became even more common in the northern regions where they settled. This suggests that there was some selection pressure amplifying a favorable trait, which means that there could be some immune advantage here that we aren't appreciating. In addition, I would think that many cases of MS may not strike hard enough and early enough to have a strong effect on sexual selection and childbearing, allowing whatever benefits there are to these immune responses (perhaps more resistance to viruses derived from the domesticated animals?) to outweigh the downsides even more, evolutionarily.

It's an active field, for sure! And the next few years should seen even more puzzle pieces falling into place. I'm glad to be able to witness it all in real time.

https://www.science.org/content/blog-post/even-more-multiple-sclerosis-and-ebv

EBV and Multiple Sclerosis: More of the Story

 by Derek Lowe

I wrote a year ago about evidence for a connection between Epstein-Barr virus (EBV) and multiple sclerosis. Since then, I’m glad to report that the evidence has become even stronger.

The first new advance was the discovery of a region of an EBV protein (EBNA1) that could well be the site of the problem. Antibodies that are raised to the 386-405 part of the EBNA1 protein also recognize a particular epitope (amino acids 370-385) of a protein in human glial cells. This GlialCAM protein seems to be essential for glial cells to perform one of their key functions, producing and maintaining the myelin sheath around neurons, and demyelination is the exact defect that is seen in MS. If you infuse such antibodies into normal mice, they come with MS-like symptoms and nerve damage. In addition, this team found that CD8+ T cells from MS patients that recognize EBNA1 also recognize GlialCAM, while EBNA1-recognizing T cells from control patients are more selective and don’t bind GlialCAM. (That same protein, by the way, is also of interest in glioblastoma).

Coupled with the epidemiology noted earlier (see the earlier blog post linked above), this is very strong evidence for the hypothesis. But the huge majority of people who are infected with EBV (almost everyone is!) don’t develop MS. Fine, you might say, that’s because they don’t develop those particular antibodies to the EBNA1 epitope, the ones that seem to be causing all the trouble. Unfortunately for that explanation, there are indeed people who have been infected with EBV, and who develop those exact antibodies in response, and who still don’t develop multiple sclerosis.

An explanation for that might now be at hand. This new paper shows that this autoreactivity is subject to several controls of its own, and that these can vary widely between individuals. Other cell-destroying components of the immune system (NK “natural killer” cells) appear to eliminate the B cells that are turning out the autoreactive antibodies. There really need to be some feedback mechanisms like this in the system, because autoreactivity of your own tissues to your own immune system is both bad news and not all that uncommmon, either. And the authors also show that whether or not these B cells survive being culled depends on HLA-E expression, a key mediator for recognition by the patrolling NK cells, which itself depends on several other variable factors. Taken together, they calculate that individuals who have the B cells expressing the glial-targeting antibodies can have their risks for MS vary by up to 250-fold, depending on how HLA-E expression lines up.

So if this holds up, then the etiology of MS would go like this: first, a person is infected with the Epstein-Barr virus (and that’s a large percentage of the population). Second, that person’s immune response features clonal expansion of antibodies towards a particular epitope of the EBNA1 viral protein, which cross-reacts with the GlialCAM protein on the surface of glial cells in the nervous system. I’m not sure what proportion of EBV-infected people express these, but this eventually leads to demyelination and immune cell infiltration into the nervous tissue, the hallmarks of the MS disease state. There is also a T-cell population that has this same cross-reactivity problem. And finally, the patient apparently must also have an insufficient B-cell quality control response to the cells that are producing these antibodies, with not enough of them being attacked by NK cells and destroyed. The T cells mentioned above that have a selectivity problem of their own might be getting their antigen presentation from the same pathways that produce those B cells; I don’t know if that’s clear yet.

This whole story is turning into a classic of modern immunology. There are still some details to be worked out, but a lot of strong evidence is coming together. That of course leads to thoughts of disease prevention, and it will be very interesting to watch the progress of the (several) vaccine candidates against EBV. Now that we know more about what to look for, we should be able to monitor what the immunological state is after vaccination and what the effect might be on prevention of MS.

A key issue is when a person becomes infected with EBV. The epidemiological study indicated that the risk of developing MS is much higher in people who are infected only after reaching adulthood as opposed to infancy, and there’s still a lot of work to be done to understand what leads to this (and where a vaccinated patient will land on that scale). The hope is that infant vaccination could cause multiple sclerosis to outright disappear as a disease, but it’s also possible that other factors could partially cancel that out or possibly even make things worse. But we’re getting the tools to find that out - we’ve never had them before.

https://www.science.org/content/blog-post/ebv-and-multiple-sclerosis-more-story

Low-frequency ultrasound can improve oxygen saturation in blood

 Research conducted by a team of scientists from Kaunas universities, Lithuania, revealed that low-frequency ultrasound influences blood parameters. The findings suggest that ultrasound's effect on haemoglobin can improve oxygen's transfer from the lungs to bodily tissues.

The research was undertaken on 300 blood samples collected from 42 pulmonary patients.

The samples were exposed to six different low-frequency ultrasound modes at the Institute of Mechatronics of Kaunas University of Technology (KTU).

The changes in 20 blood parameters were registered using the blood analysing equipment at the laboratories of the Lithuanian University of Health Sciences (LSMU). For the prediction of ultrasound exposure, artificial intelligence, i.e. analysis of variance (ANOVA), non-parametric Kruskal-Wallis method and machine learning algorithms were applied.

The calculations were made at the KTU Artificial Intelligence Centre.

The use of non-pharmaceutical treatment improves oxygen circulation and reduces blood pressure

KTU professors Vytautas Ostasevicius and Vytautas Jurenas say that the ongoing research papers are related to blood platelet aggregation.

The research of the KTU team revealed that the ultrasound's impact on blood parameters is not limited to the platelet count -- it also affects red blood cells (RBC), which can result in better oxygen circulation and lowered blood pressure.

"During exposure to low-frequency ultrasound, aggregated RBCs are dissociated into single RBCs, whose haemoglobin molecules interact with oxygen over the entire surface area of RBCs, which is larger than that of aggregated RBCs and improves oxygen saturation in blood. The number of dissociated single RBCs per unit volume of blood decreases due to the spaces between them, compared to aggregates, which reduces blood viscosity and affects blood pressure," explains Prof Ostasevicius, the Head of KTU Institute of Mechatronics.

The scientists claim that the effect of ultrasound on the haemoglobin in RBCs was higher than its impact on platelet aggregation, which is responsible for blood clotting.

Their findings have been supported by an additional analysis made at the LSMU Laboratory of Molecular Cardiology.

"This means that low-frequency ultrasound can be potentially used for improving oxygen saturation in lungs for pulmonary hypertension patients. Keeping in mind the recent COVID-19 pandemic, we see a huge potential in exploring the possibilities of our technology further," says Prof Ostasevicius.

Partnership between medical and engineering scientists

In medicine, high-frequency ultrasound from 2 to 12 MHz is used for both diagnostic and therapeutic purposes.

"Acoustic waves emitted by high-frequency ultrasound have a limited penetration depth into the body, so external tissues are more affected by high-frequency ultrasound than internal organs. Low-frequency ultrasound acoustic waves, penetrate deeper into the internal organs with a more uniform sound pressure distribution," explains Prof Jurenas.

There are numerous applications for ultrasound in medical settings.

"For example, focused ultrasonic waves are used to break kidney stones, and to kill cancer cells. Maybe ultrasound can be used to activate certain medications. Or, to alleviate the delivery of antibiotics to the inflamed areas?" says Prof Jurenas.

The technology used in the above-described study is only one illustration of many successful working partnerships between engineers and physicians.

For example, just recently, the researchers of KTU Institute of Mechatronics have created the frame for immobilising the Gamma Knife radiosurgery patients at the Clinics of the Lithuanian University of Health Sciences.

"We believe, that using the know-how of different areas one can achieve greater results," say KTU researchers about interinstitutional and interdisciplinary cooperation.

Journal Reference:

1. Vytautas Ostasevicius, Agnė Paulauskaite-Taraseviciene, Vaiva Lesauskaite, Vytautas Jurenas, Vacis Tatarunas, Edgaras Stankevicius, Agilė Tunaityte, Mantas Venslauskas, Laura Kizauskiene. Prediction of Changes in Blood Parameters Induced by Low-Frequency Ultrasound. Applied System Innovation, 2023; 6 (6): 99 DOI: 10.3390/asi6060099

https://www.sciencedaily.com/releases/2024/01/240122120139.htm

Walgreens to explore sale of Shields Health for over $4 b

 Walgreens Boots Alliance is exploring a sale of specialty pharmacy company Shields Health Solutions, Bloomberg News reported on Tuesday, citing people familiar with the matter.

The sale could be valued at more than $4 billion, the report added.

https://finance.yahoo.com/news/walgreens-explore-sale-shields-health-234607974.html

Mechanism linking anxiety to testosterone

 A groundbreaking study has unveiled a significant link between anxiety disorders and a brain receptor known as TACR3, as well as testosterone.

Prof. Shira Knafo, head of the Molecular Cognitive Lab at Ben-Gurion University, led the research published last month in the journal Molecular Psychiatry.

Anxiety is a common response to stress, but for those dealing with anxiety disorders, it can significantly impact daily life.

Clinical evidence has hinted at a close connection between low testosterone levels and anxiety, particularly in men with hypogonadism, a condition characterized by reduced sexual function.

However, the precise nature of this relationship has remained unclear until now.

Prof. Knafo discovered male rodents exhibiting exceedingly high anxiety levels had notably lower levels of a specific receptor called TACR3 in their hippocampus.

The hippocampus is a brain region closely associated with learning and memory processes.

TACR3 is part of the tachykinin receptor family and responds to a substance known as neurokinin.

This observation piqued the researchers' curiosity and was the foundation for an in-depth investigation into the link between TACR3 deficiency, sex hormones, anxiety, and synaptic plasticity.

The rodents were classified based on their behavior in a standard elevated plus maze test measuring anxiety levels.

Subsequently, their hippocampi were isolated and underwent gene expression analysis to identify genes with varying expressions between rodents with extremely low anxiety and those with severe anxiety.

One gene that stood out was TACR3. Previous research had revealed that mutations in genes associated with TACR3 led to a condition known as "congenital hypogonadism," resulting in reduced sex hormone production, including testosterone.

Notably, young men with low testosterone often experienced delayed sexual development, accompanied by depression and heightened anxiety.

This pairing led researchers to investigate the role of TACR3 further.

Prof. Knafo and her team were aided in their research by two innovative tools they crafted themselves.

The first, known as FORTIS, detects changes in receptors critical for neuronal communication within living neurons.

By utilizing FORTIS, they demonstrated that inhibiting TACR3 resulted in a sharp increase in these receptors on the cell surface, blocking the parallel process of long-term synaptic strengthening, known as LTP.

The second pioneering tool employed was a novel application of cross-correlation to measure neuronal connectivity within a multi-electrode array system.

This tool played a pivotal role in uncovering the profound impact of TACR3 manipulations on synaptic plasticity.

Synaptic plasticity refers to the ability of synapses, the connections between brain cells, to change their strength and efficiency.

This dynamic process is fundamental for the brain's adaptation to the environment.

Through synaptic plasticity, the brain can reorganize its neural circuitry in response to new experiences.

This flexibility allows for the modification of synaptic connections, enabling neurons to strengthen or weaken their communication over time.

Essentially, synaptic plasticity is a key mechanism by which the brain encodes and stores information, adapting continuously to the ever-changing external stimuli and internal states.

Importantly, it revealed that deficiencies stemming from TACR3 inactivity could be efficiently rectified through testosterone administration, offering hope for novel approaches to address challenges related to anxiety associated with testosterone deficiency.

TACR3 is seemingly a central player in bridging anxiety and testosterone.

The researchers have unraveled the complex mechanisms behind anxiety and opened avenues for novel therapies, including testosterone treatments, that could improve the quality of life for individuals grappling with sexual development disorders and associated anxiety and depression.

Prof. Knafo is a member of the Department of Physiology and Cell Biology in the Faculty of Health Sciences as well as The National Institute for Biotechnology in the Negev.

The research was supported by the Israel Science Foundation (Grant no. 536/19).

Journal Reference:

1. Magdalena Natalia Wojtas, Marta Diaz-González, Nadezhda Stavtseva, Yuval Shoam, Poonam Verma, Assaf Buberman, Inbar Izhak, Aria Geva, Roi Basch, Alberto Ouro, Lucia Perez-Benitez, Uri Levy, Erika Borcel, Ángel Nuñez, Cesar Venero, Noa Rotem-Dai, Isana Veksler-Lublinsky, Shira Knafo. Interplay between hippocampal TACR3 and systemic testosterone in regulating anxiety-associated synaptic plasticity. Molecular Psychiatry, 2023; DOI: 10.1038/s41380-023-02361-z

https://www.sciencedaily.com/releases/2024/01/240122144432.htm

Good and bad news on low back pain

 Low back pain is a major cause of disability around the globe, with more than 570 million people affected. In the United States alone, health care spending on low back pain was $134.5 billion between 1996 and 2016, and costs are increasing.

"The good news is that most episodes of back pain recover, and this is the case even if you have already had back pain for a couple of months," University of South Australia Professor Lorimer Moseley says.

"The bad news is that once you have had back pain for more than a few months, the chance of recovery is much lower. This reminds us that although nearly everyone experiences back pain, some people do better than others, but we don't completely understand why."

The systematic review and meta-analysis, conducted by an international team of researchers, included 95 studies with the goal of understanding the clinical course of acute (< 6 weeks), subacute (6 to less than 12 weeks) and persistent (12 to less than 52 weeks) low back pain.

For people with new back pain, pain and mobility problems lessened significantly in the first 6 weeks, but then recovery slowed.

This study filled a gap in a 2012 paper from the same research team, with new findings showing that many people with persistent low back pain (more than 12 weeks) continue to have moderate-to-high levels of pain and disability.

"These findings make it clear that back pain can persist even when the initial injury has healed," Prof Moseley says.

"In these situations, back pain is associated with pain system hypersensitivity, not ongoing back injury. This means that if you have chronic back pain -- back pain on most days for more than a few months -- then it's time to take a new approach to getting better."

He notes that there are new treatments based on training both the brain and body that "focus on first understanding that chronic back pain is not a simple problem, which is why it does not have a simple solution, and then on slowly reducing pain system sensitivity while increasing your function and participation in meaningful activities."

The authors state that identifying slowed recovery in people with subacute low back pain is important so that care can be escalated and the likelihood of persistent pain reduced.

Further research into treatments is needed to help address this common and debilitating condition, and to better understand it in people younger than 18 and older than 60 years.

Journal Reference:

1. Sarah B. Wallwork, Felicity A. Braithwaite, Mary O’Keeffe, Mervyn J. Travers, Simon J. Summers, Belinda Lange, Dana A. Hince, Leonardo O.P. Costa, Luciola da C. Menezes Costa, Belinda Chiera, G. Lorimer Moseley. The clinical course of acute, subacute and persistent low back pain: a systematic review and meta-analysis. Canadian Medical Association Journal, 2024; 196 (2): E29 DOI: 10.1503/cmaj.230542

https://www.sciencedaily.com/releases/2024/01/240122182806.htm