Between January 1st, 2020 and December 31st, 2021, 3,814,479 participants were included in the study (888,463 cases and 2,926,016 controls). After matching, the COVID-19 cohort exhibited significantly higher risks of rheumatoid arthritis (aHR:2.98, 95% CI:2.78–3.20), ankylosing spondylitis (aHR:3.21, 95% CI:2.50–4.13), systemic lupus erythematosus (aHR:2.99, 95% CI:2.68–3.34), dermatopolymyositis (aHR:1.96, 95% CI:1.47–2.61), systemic sclerosis (aHR:2.58, 95% CI:2.02–3.28), Sjögren's syndrome (aHR:2.62, 95% CI:2.29–3.00), mixed connective tissue disease (aHR:3.14, 95% CI:2.26–4.36), Behçet's disease (aHR:2.32, 95% CI:1.38–3.89), polymyalgia rheumatica (aHR:2.90, 95% CI:2.36–3.57), vasculitis (aHR:1.96, 95% CI:1.74–2.20), psoriasis (aHR:2.91, 95% CI:2.67–3.17), inflammatory bowel disease (aHR:1.78, 95%CI:1.72–1.84), celiac disease (aHR:2.68, 95% CI:2.51–2.85), type 1 diabetes mellitus (aHR:2.68, 95%CI:2.51–2.85) and mortality (aHR:1.20, 95% CI:1.16–1.24).

Conditions that affect erythrocyte turnover influence HbA1c concentrations and the International Expert Committee has warned clinicians to be aware of any conditions that could affect the turnover of red blood cells. Although many forms of anemia are associated with lowering of HbA1c, iron deficiency has been shown to shift HbA1c slightly upward. The exact mechanism through which iron deficiency anemia affects HbA1c levels, however still remains unclear. The explanations provided above are merely speculations, warranting further studies to confirm and elucidate the role of these factors. As little work has been done in this field so future and large scale studies are required which may address HbA1c enhancing effect and the mechanism of increased HbA glycation in iron deficiency properly.

Plausible, need to reread.

Inflammation can trigger lasting phenotypes in immune and non-immune cells. Whether and how human infections and associated inflammation can form innate immune memory in hematopoietic stem and progenitor cells (HSPC) has remained unclear. We found that circulating HSPC, enriched from peripheral blood, captured the diversity of bone marrow HSPC, enabling investigation of their epigenomic reprogramming following coronavirus disease 2019 (COVID-19). Alterations in innate immune phenotypes and epigenetic programs of HSPC persisted for months to 1 year following severe COVID-19 and were associated with distinct transcription factor (TF) activities, altered regulation of inflammatory programs, and durable increases in myelopoiesis. HSPC epigenomic alterations were conveyed, through differentiation, to progeny innate immune cells. Early activity of IL-6 contributed to these persistent phenotypes in human COVID-19 and a mouse coronavirus infection model. Epigenetic reprogramming of HSPC may underlie altered immune function following infection and be broadly relevant, especially for millions of COVID-19 survivors.

Former Harvard Researcher Faked Sleep Apnea Study

Posted: April 13, 2009

A former Harvard researcher has admitted falsifying a medical study. According to Boston.com, Dr. Robert Fogel has been disciplined by the Department of Health and Human Services (HHS) for faking data in a sleep apnea study funded by federal research grants.

This is the second time in recent months that a medical researcher has been caught falsifying a study. As we reported last month, medical journals have been asked to retract <"https://www.yourlawyer.com/practice_areas/defective_drugs">drug studies involving Vioxx, Celebrex, Lyrica and other drugs that were conducted by Dr. Scott S. Reuben of Baystate Medical Center.

Because of Reuben’s “research”, it had become routine for doctors to combine the use of painkillers like Celebrex and Lyrica for patients undergoing common procedures such as knee and hip replacements. Not surprisingly, Reuben has strong ties with the pharmaceutical industry. According to the Journal, he had been a paid speaker on behalf of Pfizer – the maker of Lyrica and Celebrex – and it paid for some of his research. Wyeth provided $10,000 in grant money to. Reuben from 2001 to 2003, the Journal said. Merck also funded some of Reuben’s work.

Fogel also has ties to the pharmaceutical industry. Since leaving Harvard, Fogel has been employed by Merck Research Laboratories, where he is now director of clinical research at its respiratory and allergy division in Rahway, N.J.

According to The Wall Street Journal, in 2006 Fogel apparently confessed to his former supervisor at Harvard’s Brigham and Women’s Hospital that he had falsified data in the 2003 sleep apnea study. According to the Office of Research Integrity at HHS, Fogel:

• Changed/falsified roughly half of the physiologic data
• Fabricated roughly 20% of the anatomic data that were supposedly obtained from Computed Tomography (CT) images
• Changed/falsified 50 to 80 percent of the other anatomic data
• Changed/falsified roughly 40 to 50 percent of the sleep data so that those data would better conform to his hypothesis.
• Published some of the falsified and fabricated data in an abstract in the journal Sleep in 2001.

According to Boston.com, Fogel falsified the data so that it would conform with his hypothesis. The falsified paper concluded that the shape and volume of a person’s airway combines with obesity to make those patients more likely to suffer sleep apnea.

According to the Office of Research Integrity at HHS, Fogel has entered into a voluntary disciplinary settlement, in which he agreed, among other things, to be excluded from research funded by the US Public Health Service for three years unless he is actively supervised.

Fogel told the publication The Scientist that since his admission, Harvard’s office of research integrity reviewed 30 studies in which he was involved. He told The Scientist that the 2003 sleep apnea study was the only one that included fake data.

“What I did was obviously horrendously wrong,” Fogel told the magazine. “I never really thought through the consequences, and once I did this I got myself into a loop that I found I couldn’t get out of.”

It would be interesting if the reason fat people have worse cancer outcomes is not just because we’re forced to wait too long to access healthcare, but because anti-fatness made us consume more sucralose.

Conclusions
Long-COVID patients suffer prolonged, diffuse symptoms and poorer health. Vascular transformation blood biomarkers were significantly elevated in Long-COVID, with angiogenesis markers (ANG-1/P-SEL) providing classification accuracy of 96%. Vascular transformation blood biomarkers hold potential for diagnostics, and modulators of angiogenesis may have therapeutic efficacy.

Collection of links.