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#covid

132 posts113 participants24 posts today
Continued thread

Update. "More Than $110 Million in #NIH Grants to #Harvard, Affiliated Hospitals Terminated Since Late February"
thecrimson.com/article/2025/4/

"All of the grants were terminated before the #Trump administration announced a $9 billion review of funding to Harvard and affiliated health care centers. At least four grants to Harvard-affiliated scholars — specifically those related to research on Covid-19 — have since been temporarily reinstated as the White House battles court challenges. The affected projects had more than $43 million in undisbursed funds at the time of cancellation…All of the canceled projects prominently featured themes of #gender and #sexualidentity, #Covid-19 and its #vaccine, or health disparities."

#Academia #Censorship #DefendResearch #Funding #Medicine #USPol #USPolitics
@academicchatter

www.thecrimson.comMore Than $110 Million in NIH Grants to Harvard, Affiliated Hospitals Terminated Since Late February | News | The Harvard CrimsonThe National Institutes of Health has terminated research grants worth more than $110 million to Harvard University and its affiliated hospitals since late February, according to public Department of Health and Human Services filings reviewed by The Crimson.

Повернення після поразки? 🤔 Колишній губернатор-демократ з Невади Стів Сісолак, який втратив посаду через критику щодо COVID-обмежень, розмірковує над можливим камбеком! Чи зможе він подолати негатив, який призвів до його поразки? Читайте статтю, щоб дізнатися більше про його плани та шанси на успіх! 📰
#політика #США #Невада #вибори #COVID #поверненнявладу #демократи

Детальніше: newsua.us/politics/kolyshniy-h

New US research:

Identifying commonalities & differences between EHR representations of #PASC & ME/CFS in the RECOVER EHR cohort

nature.com/articles/s43856-025

"These findings suggest symptom management approaches to these illnesses could overlap"

@mecfs
#MyalgicEncephalomyelitis #ChronicFatigueSyndrome #MEcfs #CFS #PwME @longcovid
#LongCovid #PwLC #postcovid #postcovid19 #LC #Covidlonghaulers #longhaulers #COVIDBrain #NeuroPASC
@covid19 #Coronavirus
#COVID19 #COVID #COVID_19 #COVIDー19 #SARSCoV2

Covid is no worse than the flu?

I know, I have now led dozens of posts over the past few years with this sarcastic question. But now, with the pandemic officially declared over by the politicians and the majority of the public behaving as though Covid19 is no longer a threat, it seems particularly apropos in light of the reasons for declaring the pandemic over: to get people back to work and back to consuming. Yet, as the data from this study show, Long Covid has had an enormous negative impact on the income and quality of life for millions of Americans, particularly the poor and working class, and particularly for African Americans and women.

*Nearly 1 in 7 working-age adults in the U.S. had experienced Long Covid by the end of 2023
*Socially disadvantaged adults were 152% more likely to suffer from Long Covid
*Groups with higher risk for Long Covid include being Black, LGBTQ, Hispanic, Female, or low income
*In 2022, people with Long Covid lost $211 billion in wages
*In 2023, people with Long Covid lost $218 billion in wages

One reason for the disproportionate effect of Long Covid on marginalized communities, particularly BIPOC and poor people, is that these groups suffer disproportionately from chronically elevated levels of the stress hormone, Cortisol, due to the stress caused by racism, sexism, homophobia, and poverty. Elevated Cortisol levels are also associated with increased risk of heart disease, hypertension, and diabetes, as well as impaired immune function.

For a really good documentary on the Social Determinants of Health and the relationship between racism and poverty on stress/cortisol levels and negative health outcomes, please see the Unnatural Causes video series

cidrap.umn.edu/covid-19/studie

CIDRAPStudies: 1 in 7 US working-age adults report long COVID, with heaviest burden on the poor

A surprise work lunch appears. You don't *have* to go, but it's awkward if you don't. You have been wearing an #N95 at work for over a year.

#COVID #CovidIsNotOver #WearAMask

Do you:

#Lauterbach verbreitet weiter krasse Lügen 😠: „Die Wahrheit ist doch: Es hat noch nie eine Impfung gegeben in der Geschichte der Menschheit, die so intensiv untersucht wurde wie die Corona-Impfung.“ berliner-zeitung.de/politik-ge
FALSCH‼️
#Kekulé korrigierte: Das meiste Wissen gibt es bei Impfungen, die es schon lange eingesetzt werden.
#FAKT: Die #COVID-Impfstoffe erhielten Notzulassungen. Der reguläre Weg wurde nie beschritten, sondern die Abkürzung der Studien dauerhaft erlaubt 😧 >> #WISSENSLÜCKEN 😮

Virologe Hendrik Streeck sitzt für die CDU im neuen Bundestag.
Berliner Zeitung · Hendrik Streeck über Corona bei Markus Lanz: „Da wurde viel zu viel mit der Angst gespielt“By Jens Blankennagel

Reiterating: negative pressure zones completely contained aerosolized virus. They could not detect ANY virus in the air of areas that were upstream of negative-pressure COVID-19 care!

So yes, home isolation protocols that include negative pressure zones absolutely are well founded!

Folks who have worked in or around remediation that uses the same principle might not be surprised.

sciencedirect.com/science/arti

This preprint seems so good!

goals were: a) to detect viral load in indoor air in different areas and floors of a separate COVID building in a hospital [...], b) to evaluate the effect of an air-cleaner in the reduction of viral load in the presence of patients, and c) to examine the correlation between viral presence in the air and particle matter burden.

their methodology is making me happy!

Their system separated aerosols into > 2.5 μm, 1.0 to 2.5 μm, 0.5 to 1.0 μm, 0.25 to 0.50 μm, and < 0.25 μm, and found

SARS-CoV-2 was detected in all different fractions and the highest viral loads were detected at stages A (> 2.5 μm) and B (1 - 2.5 μm).

however this was in open-window conditions, ie. low CO2 and higher airflow; sampling with the same equipment in households, they found

the highest amount was detected in Stage 4 (0.25 - 0.5 μm)

The data is mostly PCR but they did do some sequencing, and positively confirmed the dominant variants were stable through the study, and not confounding.

Note the air cleaner was a "Airocide (APS GCS-25 model) air purifier" which uses "photocatalytic oxidation technology" as well as 254nm UV, with no HEPA or other mechanical filter.

Also, this is vindicating for those of us pleading with folks to not immediately de-mask in the hallway:

the highest concentration was detected in COVID clinic rooms displaying a high peak of 1123 copies/m3, whereas at the corridor area showed 481 copies/m3

Also highly of note, they could not detect any virus in the areas that were upstream of negative-pressure COVID-19 care. So yes, home isolation protocols that emphasize negative pressure zones absolutely are well founded!

sciencedirect.com/science/arti via aus.social/@Sidherian

These findings support the “Broken Bridge Syndrome” hypothesis, positing that structural disconnections between the brainstem and cerebellum contribute to PCS [Long COVID] symptomatology. Furthermore, we propose that chronic activation of the Extended Autonomic System (EAS), encompassing the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system, may perpetuate these symptoms

In this high quality brain volume data,

Significant volume loss was observed in the superior cerebellar peduncle (SCP) in LC patients compared to healthy controls (LC: 219.74 mm³ vs. controls: 347.03 mm³, p < .001, Hedges’ g = 3.31). Furthermore, reduced volumes were evident in the dorsal raphe (DR) and
midbrain reticular formation (mRt) (p < .001)

It was not metabolism-marker scanning, but volumentric, so they were able to capture:

Three-dimensional reconstructions revealed deformities in the 4th ventricle and cerebellar peduncles, suggesting impaired cerebrospinal fluid dynamics [...] Importantly, these volume reductions and FA changes correlated with motor deficits,
proprioceptive dysfunction, and autonomic dysregulation

TLDR?

Our findings reveal significant structural and functional alterations in the brainstem and cerebellar peduncles of LC patients

medrxiv.org/content/10.1101/20

via
#SARSCoV2 #COVID #COVID19 #COVIDIsNotOver #AirborneAware #CovidCompetent

medRxiv · Brainstem Reduction and Deformation in the 4th Ventricle Cerebellar Peduncles in Long COVID Patients: Insights into Neuroinflammatory Sequelae and "Broken Bridge Syndrome"Post-COVID Syndrome (PCS), also known as Long COVID, is characterized by persistent and often debilitating neurological sequelae, including fatigue, cognitive dysfunction, motor deficits, and autonomic dysregulation (Dani et al., 2021). This study investigates structural and functional alterations in the brainstem and cerebellar peduncles of individuals with PCS using diffusion tensor imaging (DTI) and volumetric analysis. Forty-four PCS patients (15 bedridden) and 14 healthy controls underwent neuroimaging. Volumetric analysis focused on 22 brainstem regions, including the superior cerebellar peduncle (SCP), middle cerebellar peduncle (MCP), periaqueductal gray (PAG), and midbrain reticular formation (mRt). Significant volume reductions were observed in the SCP (p < .001, Hedges' g = 3.31) and MCP (p < .001, Hedges' g = 1.77), alongside decreased fractional anisotropy (FA) in the MCP, indicative of impaired white matter integrity. FA_Avg fractional anisotropy average tested by FreeSurfer Tracula, is an index of white matter integrity, reflecting axonal fiber density, axonal diameter and myelination. These neuroimaging findings correlated with clinical manifestations of motor incoordination, proprioceptive deficits, and autonomic instability. Furthermore, volume loss in the dorsal raphe (DR) and midbrain reticular formation suggests disruption of pain modulation and sleep-wake cycles, consistent with patient-reported symptoms. Post-mortem studies provide supporting evidence for brainstem involvement in COVID-19. Radtke et al. (2024) reported activation of intracellular signaling pathways and release of immune mediators in brainstem regions of deceased COVID-19 patients, suggesting an attempt to inhibit viral spread. While viral genetic material was detectable, infected neurons were not observed. Matschke et al. (2020) found that microglial activation and cytotoxic T lymphocyte infiltration were predominantly localized to the brainstem and cerebellum, with limited involvement of the frontal lobe. This aligns with clinical observations implicating the brainstem in PCS pathophysiology. Cell specific expression analysis of genes contributing to viral entry (ACE2, TMPRSS2, TPCN2, TMPRSS4, NRP1, CTSL) in the cerebral cortex showed their presence in neurons, glial cells, and endothelial cells, indicating the potential for SARS-CoV-2 infection of these cell types. Associations with autoimmune diseases with specific autoantibodies, including beta 2 and M 2 against G protein coupled alpha 1, beta 1, beta 2 adrenoceptors against angiotensin II type 1 receptor or M1,2,3 mAChR, among others, voltage-gated calcium channels (VGCC) are known (Blitshteyn et al. 2015 and Wallukat and Schminke et al. 2014). These findings support the "Broken Bridge Syndrome" hypothesis, positing that structural disconnections between the brainstem and cerebellum contribute to PCS symptomatology. Furthermore, we propose that chronic activation of the Extended Autonomic System (EAS), encompassing the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system, may perpetuate these symptoms (Goldstein, 2020). Perturbations in this system may relate to the elevation of toxic autoantibodies AABs (Beta 2 and M 2), specific epitopes of the COVID virus's SPIKE protein and Cytokine storm of IL-1, IL-6, and IL-8 in their increased numbers (1,000->10,000) Further research is warranted to elucidate the underlying neuroinflammatory mechanisms, EAS dysregulation, and potential therapeutic interventions for PCS. Keywords: Long COVID, Brainstem, Cerebellar Peduncles, Diffusion Tensor Imaging, Neuroinflammation, Broken Bridge Syndrome, Extended Autonomic System (EAS) ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This study was funded by OTTO Research Group ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: 2022-100867-BO-ff 1. Ethics approval was granted by the Ethics Committee of the Hamburg Medical Association, Germany, on September 5, 2022, under the title "MRI Biomarkers in Chronic Fatigue," by Prof. Dr. Rolf Stahl. 2. The project complies with the ethical and professional requirements. The Ethics Committee approves the project. The Ethics Committee operates on the basis of German law and professional regulations, as well as in accordance with ICH-GCP. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes All data produced in the present study are available upon reasonable request to the authors All data produced in the present work are contained in the manuscript