USA: NIH National Institutes of Health news - latest ME/CFS webinar 14 Jan 2025

Dakota15 said:
“And that’s why nobody trusts the NIH,” Harris responded.
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Adding some important context for that statement from Harris:
Medhill on the Hill said:
Later in the hearing, Harris questioned the NIH’s biological research involving transgender individuals, asking Bertagnolli whether the agency would report a transgender woman as a biological male or female.

“We assign them according to the biological research question we are trying to answer,” Bertagnolli said. “We’re not going to say they’re a man or they’re a woman. We are going to base it off the science and the scientific question we’re trying to answer.”

“And that’s why nobody trusts the NIH,” Harris responded.
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https://medillonthehill.medill.nort...director-over-vaccine-rhetoric-racial-equity/
 
Sharing today from NIH Director Dr. Monica Bertagnolli at today NASEM's webinar:

https://twitter.com/user/status/1860042597995336036


MB: "Every year I give my priorities to the President. Individual diseases sometimes end up in those priorities as well. We do have the ability to do that, but it depends. President Biden's two big health priorities were Cancer & Women's Health. The budget reflected that."
 
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Jay Bhattacharya to head the NIH.

Authored the Great Barrington Declaration, calling to let the virus spread, in October 2020. The signing was celebrated with champagne whilst ICUs were overflowing with the dying and we did not yet have treatments, vaccines or an understanding of the virus.
 
MD PhD would typically be the type of person that would take a NIH academic role. But the reality is he is extremely poor at interpreting evidence, and does his best to shoehorn in his beliefs into his.

It appears he never completed a residency, and went straight to economics after medical school. The man opines about health, but has never held responsibility for anyone's care in his life. He has zero clinical experience.
 
11/6/24, NIH: 'The Office of Autoimmune Disease Research Announces 2024 R56 Awardees'

'In the application “Antibodies in the Neurologic Effects of COVID-19,” supported by OADR-ORWH and NINDS, Lena Al-Harthi, Ph.D., proposes to study aberrant antibodies in the context of COVID-19 disease to understand how they trigger inflammation and autoreactivity. This research aims to elucidate the role of inflammatory antibodies in the acute and chronic neurological manifestations of COVID-19. This work may advance the scientific understanding of both COVID-19 complications that significantly affect quality of life, and other forms of autoimmune encephalitis."

"Dr. Al-Harthi is the Vice Dean of Research and a Professor and Chair in the Department of Microbial Pathogens and Immunity at RUSH Medical College. Dr. Al-Harthi earned her Ph.D. in microbiology from The George Washington University. Her dissertation was conducted under the mentorship of Suresh Arya, Ph.D., in the laboratory of Robert Gallo, M.D., co-discoverer of HIV. From there, Dr. Al-Harthi continued postdoctoral training in HIV immunology as a Mark Weiss Fellow of infectious diseases at RUSH University Medical Center, where she joined the faculty in 2000. Her research has focused on defining mechanisms of neurocognitive disturbance associated with chronic viral infections—particularly HIV-associated neurocognitive disorder, which is a collection of thinking, movement, and mood complications experienced by people with HIV. More recently, Dr. Al-Harthi has been applying her vast expertise to the neuroinflammatory complications of HIV to better understand the long-term neurological sequelae of COVID-19'
 
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(mods just sharing but I understand if this is not needed)

4/15/22, 'Pondering the Effects of HIV and COVID-19 on the Brain with Avi Nath'

Nath: "..so we scanned a lot of brains and we got exquisite anatomy from the human brain that nobody had ever seen before..what we started seeing was that there are these blood vessels that look abnormal in the brain and that the areas around the blood vessels looked abnormal and they would sometimes see small clots in there, other times we would see that the blood vessel wall was very abnormal, and sometimes you were seeing little what looked like little hemorrhages around the blood vessels."

"my guess is that what I would be interested in because the pathologies on the endothelial cells...what I would like to do is put these proteins on these endothelial cells and see if it disrupts those tight junctions.."

"now one possibility is that the viral proteins are coming out, but not the virus themselves. The other possibility is that you may be forming antibodies to these spike proteins, the antibodies can then form what is called anti-idiotypic antibodies and so you have an antibody against the antibody that idiotypic antibody can look exactly like the spike protein and then that can go and bind to the ACE2 receptor and cause damage. Our hypothesis is this latter pathway....that is our hypothesis that there are anti-idiotypic antibodies to the spike protein that are causing the damage.."

"there is a fair bit of microglial activation and because of that you get neurolophagia, which is these might activated microglia can then chew up the neurons and cause neuronal damage."

"If you can understand how a virus manipulates the immune system then you can have the ways of being able to block that. So, checkpoint inhibitor is another good example - it will cause exhaustion of immune system, viral infections - the same thing about cancers - they exhaust the immune system - so you have these cells circulating but they're no longer doing their job and that is because it induces the expression of these molecules called checkpoints - now if you block those, then they become active again. So, it's an interesting concept."
 
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(Mods just sharing here but if you don't think this is informative feel free to clean up)

5/8/23, 'MedNews Week Conference - Dr. Avindra Nath (NIH) - COVID-19 & the Brain'

Nath: "So from these blood vessels - you can see this dark stuff here, these are this fibrinogen leaking from the blood vessels and also in the olfactory bulbs and in these blood vessels we found these small platelets that were sticking to them and that's how they were occluding these blood vessels that's how it's causing all these clots - okay so there's something abnormal about the endothelial cells as to why these platelets are sticking there and what we found was that it these endothelial cells expressed this molecule called PECAM-1 and this is a very sticky molecule and we think this is being expressed because antibodies are binding to it and that's what is really doing - once it gets activated then number of things can happen so the platelets can stick and cause clots or the blood vessels themselves can get leaky and things can go through them and when they go through then these inflammatory cells come in - these macrophages they enter the brain because they're going in there to clean up the mess, the problem is they are really bad guests when they go in, they never leave and they keep destroying the tissue around them, okay so causes this chronic inflammation - I think some of the long COVID symptoms are probably related to this..."

"Our hypothesis then is that the antibodies attack these blood vessels - these cells come in over here, the macrophages - you get leakage of these proteins into the parenchyma and all these cells come in to clean it up, they get activated they automatically kill the neuron and form blood clots over here...”
 
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Interesting videos, thanks @Dakota15. I note that there's not a whiff of BPS theories, nothing about effort preference or a need for behavioural modifications in relation to Long Covid, and Dr Nath notes the similarities with ME/CFS, chronic Lyme, and Gulf War Illness. Dr Nath comes across as very sympathetic to the debilitating nature of Long Covid and aware that it is affecting millions of people.
 
12/17/24, “A conversation with Monica Bertagnolli, director of the National Institutes of Health”

MB: “Another example that comes from COVID demonstrates where we’re in trouble if we don’t have critical basic science — the issue of long COVID. Now we’ve got a vaccine, but so many people are having serious health challenges in the form of persistent symptoms postinfection, and here we are really missing some things that fundamental science could provide us. We do not have a good handle yet on the basic biology of what that virus is doing to produce those long-term effects. We don’t have a diagnostic test; we don’t have evidence from fundamental science showing how to identify a replication-competent virus within a person, which is a leading hypothesis that can show where to focus development of treatment.

With the same new disease, we have a great example of how fundamental science investment paid off tremendously and also where, if we don’t have fundamental science investment, we can really be behind in the tools we need to move forward for health.”
 
From: NIH MECFS Information <NIH-MECFS_INFORMATION@LIST.NIH.GOV> On Behalf Of NIH MECFS Information List
To: NIH-MECFS_INFORMATION@LIST.NIH.GOV
Subject: News from NIH: Registration now open for the NIH ME/CFS Webinar on Jan 14 at 2pm ET


NIH’s next ME/CFS Webinar will be held on January 14, 2025 from 2:00 – 3:00 pm ET. The webinar will include updates from NIH on ME/CFS-related research activities and a presentation by Vikram Chib, PhD, and Agostina Casamento-Moran, PhD, from Johns Hopkins University. Please register in advance.


During the webinar, attendees will have the opportunity to ask questions out loud or submit written questions in the Zoom Q&A box. For those on the phone, please dial *9 to raise/lower your hand and *6 to mute/unmute. Additional instructions for joining by phone are on the Zoom support website. We regret that we may not be able to respond to all questions that we receive, but we will try to answer as many as possible in the time allotted. The webinar will be recorded and posted on the NIH ME/CFS website after the event.


Regards,

The Trans-NIH ME/CFS Working Group

https://twitter.com/user/status/1869400929105231908
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Dakota15 said:
'Insight into mechanisms of ME/CFS'
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Just a summary of the NIH ME/CFS study
People with PI-ME/CFS had higher heart rates throughout the day and a smaller drop in their nighttime heart rate than healthy volunteers. This suggests that the autonomic nervous system, which controls unconscious bodily functions, is disrupted in PI-ME/CFS. Heart and lung function were also less able to respond to exercise in people with PI-ME/CFS.
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I think this bit got a bit garbled -
In one test, participants were repeatedly given the choice of performing either an easy task for a low reward or a hard task for a higher reward. Those with PI-ME/CFS were less likely to choose the hard task than the healthy volunteers, suggesting less ability to exert effort. The healthy volunteers had reduced muscle function and brain motor cortex activity after repeated tasks. But people with PI-ME/CFS did not. Brain scans during one task found that those with PI-ME/CFS had lower activity in a brain region called the temporoparietal junction. These findings suggest that the fatigue of those with PI-ME/CFS might be caused by dysfunction in the way the brain decides how to exert effort.

When the team analyzed cerebrospinal fluid, they found that participants with PI-ME/CFS had reduced levels of chemicals called catechols. Catechols help regulate the nervous system. Catechol levels correlated with effort preference and motor function in people with PI-ME/CFS, but not in healthy volunteers. This suggests that altered catechol signaling in the brains of people with PI-ME/CFS may give rise to their altered effort.
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The team examined immune function as well. They found differences in B cells, which make antibodies to help fight pathogens. People with PI-ME/CFS had more naïve B cells, which can be activated by any foreign substance. But they had fewer switched memory B cells, which respond to a specific pathogen that the body has encountered before. B cell dysfunction was more prominent in women. These findings suggests that the immune system continues to be activated in the absence of infection.

Taken together, the results suggest that PI-ME/CFS may be caused by immune system dysfunction that is triggered by infections. This may lead to chemical changes in the central nervous system that affect certain brain functions to cause ME/CFS symptoms.
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Walitt's infamous quote gets another run:
“Rather than physical exhaustion or a lack of motivation,” says first author Dr. Brian Walitt, “fatigue may arise from a mismatch between what someone thinks they can achieve and what their bodies perform.”
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—by Brian Doctrow, Ph.D.
 
11/8/24, 'Monica Bertagnolli - Current Priorities for the US NIH'

MB: "The cardiovascular institute receives much funding in collaboration with NIAID for its work in the effects of COVID on the heart and lungs and cardiovascular system.."

MB: "I wish we could have a better say, frankly, over exactly how much money is spent where..."

MB: "I spend, 30% of my time, 40% of my time at Congress - that's my biggest job. Talking, arguing, advocating, describing, explaining - and I get just as much support - I get equal support - from both parties, I can say that completely..."
 
Interesting to listen to that video.
For me it confirms just how much Jonathan Swift is worth re-reading. The NIH is Lilliput in all its glory - an obsession with minutiae and social protocol.

US medical science was not always like that. It had Hench and Alport and Kunkel and more - but it faded out in the 1990s. If the ME/CFS study is worthy of a mention for 'promising findings of 2024' pickings must have been slim.
 
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