Shiroc posted:

I'm not gonna try to find the rest of this to inflict it on me but does he ever fully realize he's the bad guy in this or is it just a quirky anecdote for him?

https://www.mdpi.com/1648-9144/60/1/164 posted:

Abstract
COVID-19 is primarily a respiratory disease, but numerous studies have indicated the involvement of various organ systems during the course of illness. We conducted a comprehensive review of atypical complications of COVID-19 with their incidence range (IR) and their impact on hospitalization and mortality rates. We identified 97 studies, including 55 research articles and 42 case studies. We reviewed four major body organ systems for various types of atypical complications: (i) Gastro-intestinal (GI) and hepatobiliary system, e.g., bowel ischemia/infarction (IR: 1.49–83.87%), GI bleeding/hemorrhage (IR: 0.47–10.6%), hepatic ischemia (IR: 1.0–7.4%); (ii) Neurological system, e.g., acute ischemic stroke/cerebral venous sinus thrombosis/cerebral hemorrhage (IR: 0.5–90.9%), anosmia (IR: 4.9–79.6%), dysgeusia (IR: 2.8–83.38%), encephalopathy/encephalitis with or without fever and hypoxia (IR: 0.19–35.2%); (iii) Renal system, e.g., acute kidney injury (AKI)/acute renal failure (IR: 0.5–68.8%); (iv) Cardiovascular system, e.g., acute cardiac injury/non-coronary myocardial injury (IR: 7.2–55.56%), arrhythmia/ventricular tachycardia/ventricular fibrillation (IR: 5.9–16.7%), and coagulopathy/venous thromboembolism (IR: 19–34.4%). This review encourages and informs healthcare practitioners to keenly monitor COVID-19 survivors for these atypical complications in all major organ systems and not only treat the respiratory symptoms of patients. Post-COVID effects should be monitored, and follow-up of patients should be performed on a regular basis to check for long-term complications.
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2. Purpose of Article
This review was intended (1) to summarize a large number of research studies and case reports on various atypical complications of the COVID-19 virus in major organ systems, (2) to assemble the data on the range of their incidence, and (3) to gather information on the impact of these complications on hospitalization and mortality rates.
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4.1. Gastrointestinal System
4.1.1. Complications
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_{Figure 1. Prevalence of gastrointestinal complications among COVID-19 patients (prevalence represents the maximum percentage reported in the literature).}
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4.1.2. Underlying Pathophysiology
The underlying pathophysiology related to GI damage among COVID-19 patients is most likely multifactorial. The most credible mechanism is direct virus-mediated tissue damage due to the existence of ACE2 receptors in the glandular cells of the intestine, in addition to the assimilation of the viral nucleocapsid protein among the epithelial cells of the stomach, duodenum, and rectum, as well as glandular enterocytes. Additionally, diffused endothelial inflammation among the submucosal vessels of the small intestine in histopathological evidence and mesenteric ischemia suggest microvascular small-bowel injury. The existence of infiltrating lymphocytes and plasma cells and interstitial edema in the gastric, duodenal, and rectal lamina propria of COVID-19 patients provides support for tissue damage mediated by inflammation. It has also been suggested that the GI manifestations and severe disease progression are contributed by the modification of the intestinal flora caused by the virus.
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4.2. Neurological System
4.2.1. Complications
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_{Figure 2. Prevalence of neurological complications among COVID-19 patients (prevalence represents maximum percentage reported in the literature).}
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4.2.2. Underlying Pathophysiology
The underlying pathophysiological mechanisms proposed include direct invasion of neural parenchyma cells by the virus. The central nervous system is assessed by SARS-CoV-2 through the lamina cribrosa, olfactory bulb, and nasal mucosa or transport through the retrograde axonal. In the respiratory tree, ACE2 receptors are highly expressed in nasal epithelial cells, which may justify the symptoms of modified smell or taste mostly reported in outpatients retrospectively with SARS-CoV-2. The other complications are attributed to the neurovirulence of SARS-CoV-2, which reflects the prothrombotic and proinflammatory cascade resulting in cytokine storm, which in turn produces effects on the blood–brain barrier and brain vasculature. This has been particularly observed in critical patients experiencing toxic–metabolic prolongation of multi-organ dysfunction.
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4.3. Renal System
4.3.1. Complications
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_{Figure 3. Prevalence of renal complications among COVID-19 patients (prevalence represents maximum percentage reported in the literature).}
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4.3.2. Underlying Pathophysiology
Several possible pathophysiological mechanisms have been identified for renal abnormalities. Firstly, the virus may infect the renal cells directly, as evidenced by the existence of ACE2 receptors on them and histopathological findings. Secondly, microvascular dysfunction is incidental to endothelial damage as demonstrated by renal lymphocytic endothelialitis, and moreover to the inclusion of particles of the virus in the endothelium of glomerular capillary cells. Thirdly, cytokine storm may have a vital role in the immunopathology of AKI. Another likely mechanism for glomerular injury is arbitrated by specific immunological effector mechanisms induced by the virus or viral antigen immunocomplexes. In addition, proteinuria is not considered the classic manifestation of AKI; short-term heavy albuminuria might arise from direct podocyte injury or endothelial dysfunction. Other causative etiologies for renal injury include acute respiratory distress syndrome, interstitial nephritis, volume depletion, and rhabdomyolysis.
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4.4. Cardiovascular System
4.4.1. Complications
(..)

_{Figure 4. Prevalence of cardiovascular complications among COVID-19 patients (prevalence represents maximum percentage reported in the literature).}
(..)
4.4.2. Underlying Pathophysiology
The underlying pathophysiology of CV complications is most likely multifactorial. ACE2 is highly expressed in endothelial cells, fibroblasts, and myocytes of the CV tissue, and direct viral injury is one possible mechanism. Myocarditis, MI, and circulatory failure may develop due to viral load and inflammatory infiltrates, as evidenced by some autopsy studies and pathological reports. In addition, endothelial damage mediated by viruses and cytokine storms can be another assumed underlying mechanism for myocardial injury. In general, viral infections further predispose patients to MI, and this risk is elevated in COVID-19 patients, with evidence of unjustifiably escalated hypercoagulability, which induces MI mediated by thrombotic events. Furthermore, isolated right ventricular malfunction may arise due to pulmonary thromboembolism and increased pulmonary vascular pressures due to ARDS.
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https://www.cell.com/cell-host-microbe/fulltext/S1931-3128(24)00006-4 posted:

Highlights
• Gut microbiota composition influences severity of respiratory viral infection
• Gut-restricted segmented filamentous bacteria reprograms lung macrophages
• Expression levels of complement and Notch4 expression impact viral infection severity
• Transplant of lung macrophages transfers proneness to respiratory viral infection

Summary
Susceptibility to respiratory virus infections (RVIs) varies widely across individuals. Because the gut microbiome impacts immune function, we investigated the influence of intestinal microbiota composition on RVI and determined that segmented filamentous bacteria (SFB), naturally acquired or exogenously administered, protected mice against influenza virus (IAV) infection. Such protection, which also applied to respiratory syncytial virus and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was independent of interferon and adaptive immunity but required basally resident alveolar macrophages (AMs). In SFB-negative mice, AMs were quickly depleted as RVI progressed. In contrast, AMs from SFB-colonized mice were intrinsically altered to resist IAV-induced depletion and inflammatory signaling. Yet, AMs from SFB-colonized mice were not quiescent. Rather, they directly disabled IAV via enhanced complement production and phagocytosis. Accordingly, transfer of SFB-transformed AMs into SFB-free hosts recapitulated SFB-mediated protection against IAV. These findings uncover complex interactions that mechanistically link the intestinal microbiota with AM functionality and RVI severity.

Graphical abstract

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https://www.medicalnewstoday.com/articles/gut-microbiota-may-protect-against-respiratory-viruses posted:

• A new study in mice suggests the presence of certain gut bacteria transforms alveolar macrophages into respiratory virus neutralizers.
  
• The results show that the macrophages disabled respiratory illnesses like COVID-19, RSV, and the flu.
  
• The mechanisms behind this discovery are unclear, and the researchers are planning human trials to determine whether the findings can be replicated.

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https://www.cidrap.umn.edu/misc-emerging-topics/three-fourths-adults-have-hidden-infectious-illness-work-travel-or-socialize posted:

Three fourths of adults have hidden infectious illness to work, travel, or socialize, surveys suggest
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Participants said they would consider concealment when the illness was described as being moderately transmissible and as having mild symptoms.
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"Healthy people forecasted that they would be unlikely to hide harmful illnesses—those that spread easily and have severe symptoms—but actively sick people reported high levels of concealment regardless of how harmful their illness was to others," said Wilson N. Merrell, a doctoral candidate and lead author of the study, in a press release from the Association for Psychological Science, which publishes the journal.

quote:

"Results of our determinant analyses are consistent with managers using RTO mandates to reassert control over employees and blame employees as a scapegoat for bad firm performance," the authors wrote. "Also, our findings do not support the argument that managers impose mandates because they believe RTO increases firm values."

The researchers analyzed public RTO data from 137 S&P 500 firms and determined that RTO mandates were more common for firms that had poor prior stock market performance. RTO mandates were more common for firms with "male and powerful CEOs." The authors found no significant impact of RTO mandates on stock returns or firm profitability.

fosborb posted:

god this is cathartic

Return-to-office mandates aren't making companies more valuable and productive, study finds

Steve Yun posted:

productivity was never the concern. it’s the real estate value of their office

Pingui posted:

Pingui posted:

quote:

Only 5% of participants across all studies said they had concealed a COVID-19 infection.

https://www.frontiersin.org/articles/10.3389/fped.2024.1325562/abstract posted:

Background and objective: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has broad tissue tropism and high transmission, which are likely to perpetuate the pandemic. The study aim to analyze the clinicopathogenic characteristics in paediatric patients.In this single-centre study, we retrospectively included all confirmed cases infected by SARS-CoV-2 infection at Xi'an Children's Hospital, China, from 1 December to 31 December 2022. The demographic, clinical, laboratory, and radiological features of the patients were analysed.

Results: A total of 4,520 paediatric patients with SARS-CoV-2 omicron variant infections were included. Of these, 3,861 (85.36%) were outpatients, 659 (14.64%) were hospitalised patients, and nine patients (0.20%) died. Of the nine patients who died, five were diagnosed with acute necrotising encephalopathy (ANE). The most common symptoms were fever in 4275 (94.59%) patients, cough in 1320 (29.20%) patients, convulsions in 610 (13.50%) patients, vomiting in 410 (9.07%) patients, runny nose/coryza in 277 (6.13%) patients, hoarseness of voice in 273 (6.04%) patients. A blood cell analysis showed a slight elevation of monocytes (mean: 11.140.07%). The main diagnoses for both outpatients and inpatients were respiratory infection with multisystem manifestations. A high incidence of convulsions is a typical characteristic of children infected with SARS-CoV-2. Five of the nine COVID-19 fatalities were associated with ANE. This indicates that nervous system damage in children with SARS-CoV-2 infection is more significant.

fosborb posted:

god this is cathartic

Return-to-office mandates aren't making companies more valuable and productive, study finds

Insanite posted:

what i enjoy is that the school i'll be sending my kid to in the fall is literally falling apart. it's actually closed right now while, idk, some folks slap some rubber cement on the crumbling ceilings or whatever.

the $40k/year private school a half mile away had UV lighting added to its state of the art ventilation system in december of 2020. lol.

same story at most of the ~nice~ schools around here.

super sweet best pal posted:

The ideal corporate strategy would be to reject RtO, downsize to a smaller office for any onsite operations that aren't covered by remote work and just outsource everything else to countries where you can pay fractions of pennies on the dollar for expensive white collar jobs.

NeonPunk posted:

This is weird, almost as if Covid does something to our immune system

https://twitter.com/JoIsSummer/status/1752429790890475828

Already got his measles vaccination and still got it

Hellequin posted:

His youngest sister was frequently the target of bullying and snarky remarks regarding her mental health/living conditions/etc. in pieces he wrote for the New Yorker and when she killed herself he wrote a lovely self pitying piece. He is scum.

NeonPunk posted:

This is weird, almost as if Covid does something to our immune system

https://twitter.com/JoIsSummer/status/1752429790890475828

Already got his measles vaccination and still got it

Pittsburgh Fentanyl Cloud posted:

There is a certain shitlib aesthetic that's all about knowing that you're very smart and clever and making sure that everyone else knows how smart and clever you are, too, and he's the standard-bearer for that poo poo.

The Oldest Man posted:

time to do a murder so i have something to write about in the atlantic

*touches earpiece*

im sorry im being informed that joke was deprecated when that lady wrote about killing the dog she adopted to entertain her during wfh

spiritual bypass posted:

we do not joke about killing dogs itt

DominoKitten posted:

David Sedaris in the New Yorker:

Deep Dish Fuckfest posted:

confirmed: vaccines don't work

Fansy posted:

That Sedaris-style pressure to unmask is a relic of 2022. I had a guy at the museum ask "are you sick?" the other day and my kid's teachers still say, "oh we love to see her beautiful smile!" but people have stopped overtly asking us to unmask.

fosborb posted:

I still lol about "you're so brave" every few days

U-DO Burger posted:

My family is enrolled in a Covid study that takes regular blood draws, and tests us every week for Covid/flu/RSV. CDC just pulled the funding so the study is concluding more than a year before it was supposed to lol

Pulvis Sumus posted:

Feels like I found a bit of a gem.

Pulvis Sumus posted:

Feels like I found a bit of a gem.

NeonPunk posted:

Connective tissues issues? Like joints? Because our workplace has quite several folks falling over on the bus lately. Like one of them said that for some reason their ankle or knee just out of nowhere just stopped working and they just couldn't even stand on it anymore

Long COVID symptoms lead to hEDS diagnosis in small study posted:

SARS-CoV-2 infection can lead to long COVID

Infection by SARS-CoV-2 can lead to prolonged and diverse symptoms, colloquially known as “long COVID.” Besides the lungs being affected, other symptoms include fatigue, cognitive disturbances, and both neurogenic and musculoskeletal pain. Patients may also experience postural orthostatic tachycardia syndrome, which causes dizziness and a fast heart rate when getting up from lying down.

Notably, these symptoms are also characteristic of hEDS and HSD. Both these conditions involve hypermobile joints and stretchy skin, with HSD occurring in patients for whom EDS has been excluded as a diagnosis.

Here, a group of clinicians at Tulane University School of Medicine, in New Orleans, described the outcomes of five women, ages 33 to 51, who did not have a history of a hypermobility disorder.

Up to 15 months after getting COVID-19, all patients developed persistent and debilitating fatigue, accompanied by cognitive dysfunction, joint pain, and dysautonomia, which is a group of disorders caused by abnormalities in the autonomic nervous system that governs involuntary body functions like heartbeat and breathing.

“This constellation of symptoms aligned with those familiarly seen in patients at our institution’s Ehlers-Danlos Syndrome/Hypermobility Spectrum Disorder Clinic, prompting referrals,” the researchers wrote.

All 5 women fulfilled criteria for hypermobility spectrum disorder

After physical tests and evaluation of generalized joint hypermobility, all patients fulfilled criteria for HSD. The five women had genetic variants in an enzyme (methylenetetrahydrofolate reductase) linked to the development of hEDS and HSD. Taking into account clinical and lab findings, four women were diagnosed with hEDS and one with HSD.

A mast cell disorder, a condition marked by an excess of immune mast cells, was suspected or confirmed in four of the five women. These patients were advised to supplement with vitamin B9 (also known as folate) and a plant-based antioxidant called quercetin.

The onset of hEDS could be due to the activation of immune responses within connective tissues triggered by the SARS-CoV-2 infection, according to the clinicians.

Overall, “the presence of SARS-CoV-2 itself may trigger a misdirected host immune response to traumatized connective tissue in such patients with preexisting joint hypermobility and may yet represent another possible mechanism for new-onset or worsening connective tissue symptoms within the post-acute infection period,” the scientists concluded.

NeonPunk posted:

Connective tissues issues? Like joints? Because our workplace has quite several folks falling over on the bus lately. Like one of them said that for some reason their ankle or knee just out of nowhere just stopped working and they just couldn't even stand on it anymore

CGI Stardust posted:

just did a quick search, and there's an n=5 case study on Ehlers-Danlos Syndrome developing as a result of COVID

admittedly this is too small to draw any conclusions from, but interesting and worth keeping an eye on