Recent comments in /f/science

EmpyreanFantasy t1_j8wkdw6 wrote

As a result of dog domestication they are the most successful species of canine by THOUSANDS of miles. There are millions and millions of dogs. Nowhere near that many wolves. This mutualism was mutually beneficial for humanity and canis familiaris, more than their ancestors could ever dream of.

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dumnezero t1_j8wjlfu wrote

From the paper:

>Also referred to as the neutrophil chemotactic factor, IL-8 recruit’s neutrophils and NK-cells to sites of inflammation where they can clear infected cells and promote wound healing.

>It is possible that the apparent lack of IL-8 in long-COVID patients may be responsible for at least some of the debilitating symptoms including post-exertional malaise, fatigue, and persistent cough, shortness of breath and chest pain.

>In this scenario, the acute SARS-CoV-2 infection damages the lungs, the cytokine milieu unfolds as described above, recruiting cells to the site of damage where the cells can either (a) help control the infection and induce a wound healing environment and the individual recovers normally; or (b) the infection causes abundant cellular infiltration leading to a high concentration of immune cells in a relatively small physical space, ultimately causing more tissue damage, which is not efficiently repaired in the absence of IL-8.

>Predictably, under scenario ‘b’ the individual remains having difficulty with oxygen transfer from the lungs into the blood stream. Therefore, if the macrophages and other cells that secrete IL-8 become exhausted or are otherwise incapable of secreting IL-8, neutrophils will not be recruited to assist in the wound healing process in the lung once the infection has been cleared [63]. Scenario ‘b’ therefore emerges as a potential model to explain certain long-COVID complications based on lack of IL-8.

>IFNγ is secreted by the innate immune Natural Killer cells (NK) and Natural Killer T cells (NKT) as well as the adaptive immune CD4+ Th1 and CD8+ Cytotoxic T Lymphocytes (CTL) after the development of antigen-specific immunity [64]. Together with IL-12, IFNγhelps drive the differentiation of Th1 cells, which in turn can secrete IL-2, TNFα, and IFNγ [65]. The observed lack of circulating IFNγ (Figure 1 and Table 2) in the plasma of patients suggests either severe immune dysfunction or exhaustion.

The war in the lungs is over, but there are too many soldiers still there, hanging out, causing drama. What's not happening: they need to be transported away and the engineering+construction crews need to come in to start rebuilding.

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dumnezero t1_j8wigeu wrote

The important part is:

>Based on our results we propose that immune exhaustion perpetuates long-COVID due to the seemingly complete reduction of IFNγ and IL-8, as well as significant decreases in IL-2, IL-4, IL-6, IL-13, and IL-17. Identifying these and other deficiencies will provide clues towards methods to intervene and possibly restore immune function in the context long-COVID. Although functional assays that test the ability of immune cells from individuals with long-COVID to respond to pathogenic stimuli will be required to support this theory.

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nyet-marionetka t1_j8wfzg6 wrote

Cats tend to do this too, pee in the bathtub or sink. I am not sure why. Maybe drain odors smell to them like “this is the place to urinate”, or maybe it’s something about the smooth surface, though I would think carpet would seem better to pee on.

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Ok-Training-7587 t1_j8wetcp wrote

I asked ChatGPT to simplify the results of this study for me so I could understand it. Here's what it wrote. If someone is a scientist and understands this study, I'd love to hear if there are anything chatgpt got wrong. Here's the output:

"The study looked at 12 people who had long-lasting symptoms after having COVID-19, and compared them to 15 healthy people. They measured certain chemicals in their blood called cytokines, which help the body fight infections. They found that most of the cytokines were lower in the people with long-lasting symptoms compared to the healthy people. The cytokines that were the most different were Interferon Gamma (IFNγ) and IL-8, which were completely absent in the people with long-lasting symptoms. They also found that IL-6, IL-2, IL-17, and IL-13 were also lower in people with long-lasting symptoms, but not as much as IFNγ and IL-8.All of the people with long-lasting symptoms were women, so the researchers wanted to see if there was a difference between men and women in the healthy group. They found that there was no significant difference in cytokine levels between healthy men and women, except for one cytokine (IL-2) which was lower in healthy men than in healthy women. When they compared the women with long-lasting symptoms to the women in the healthy group, they found that the levels of IFNγ, IL-8, IL-6, IL-2, and IL-13 were lower in the women with long-lasting symptoms, but not IL-1β, IL-12, IL-10, IL-5, or TNFα. The decrease in IL-5 levels in women with long-lasting symptoms was only significant when comparing to other women, but not when comparing to men and women together."

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discotititis t1_j8wcddm wrote

As someone who works in immunology, your explanation is very inaccurate. When an unknown virus invades the host, special cells known as dendritic cells (not antibodies or bacteria—antibodies can’t even be produced until B cells are activated) take up bits of the virus and travel to lymph nodes (not the thymus—the thymus is where T cells mature).

In the lymph node, a single T cell with a matching receptor recognizes the bit of the virus the dendritic cell is presenting. When it recognizes the virus, the T cell divides and multiplies. Certain kinds of T cells—killer T cells—destroy infected cells. Other kinds of T cells—helper T cells—activate B cells, which produce antibodies that neutralize virus. All the multiplication of T cells and activation of B cells occurs in the lymph nodes—it’s why doctors check to feel if they’re swollen when you’re sick to see if there’s an infection on.

Cytokines like IFNy and IL-8 (among others mentioned in this paper) are produced by a wide array of immune and non-immune cells when they recognize viral infection. (Not the thymus, though. Once again, the thymus is just where T cells develop.) They activate dendritic cells to take up bits of virus and travel to the lymph node. They also direct T cells to develop in a certain way and for B cells to produce the right kind of antibodies. They also encourage migration of other kinds of immune cells to the site of infection to eliminate the virus.

The authors here believe that immune exhaustion is the cause of long COVID. Once cells stop producing these necessary cytokines, the immune system simply cannot function as it should anymore. This exhaustion doesn’t come from initial underreaction, though—it’s overreaction of the immune system that causes it.

Tons of studies have proven that high levels of pro-inflammatory cytokines like the ones in this paper actually correlate with worse outcomes. The inflammation they cause, when unchecked, can be very damaging to tissues. On the other hand, lack of reaction at all is also very dangerous. The immune system has to walk a tight line between over- and underreaction or risk either scenario. Long COVID is essentially dysfunction of this balance, likely due to initial overreaction.

I recommend How the Immune System Works by Lauren Sompayrac as a great primer to immunology. Cause it doesn’t work like how this person is describing it.

TL;DR: This explanation is absolute BS and any doctor or scientist would laugh their ass off about any number of things in it. Bacteria and antibodies taking virus to the thymus? Doesn’t happen and goes against the entire logic of how the immune system works. The thymus dying? The thymus shrinks with age, but that doesn’t cause what we see in long COVID. It usually just causes a weaker immune system in old age.

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Wagamaga OP t1_j8wbjkj wrote

The rare and unusual life of an anchoress, a woman who devoted her life to prayer while living in seclusion, has been unearthed by the University of Sheffield and Oxford Archaeology, thanks to a skeletal collection now held at the University.

Analysis of the collection, which includes a staggering 667 complete skeletons dated to the Roman, Medieval, and Civil War era, has revealed one in particular that is likely Lady Isabel German, an important anchoress - or type of religious hermit - who is documented to have lived at All Saints Church in Fishergate, York during the 15th century.

As an anchoress, Lady German would have chosen to live a life of seclusion. Living inside a single room of the church without direct human contact, she would have devoted herself to prayer and accepted charity to survive.

Skeleton SK3870 was discovered in 2007 during excavations at what was once All Saints Church on the site of the famous York Barbican. Not found in the cemetery alongside the others skeletons in the collection, this medieval woman was buried in a tightly crouched position within the apse of the church foundations, a small room located behind the altar.

Only clergy, or the very rich were buried inside churches at this time, so the new study suggests the location of this highly unusual burial makes SK3870 a prime candidate to be that of the All Saints’ anchoress, Lady German.

Dr Lauren McIntyre, University of Sheffield Alumna and Osteoarchaeologist at Oxford Archaeology Limited, conducted the analysis of the historical and osteoarchaeological evidence, which included using radiocarbon dating and isotopic investigation to examine skeleton SK3870.

https://www.tandfonline.com/doi/full/10.1080/00766097.2022.2129682?forwardService=showFullText&journalCode=ymed20&tokenAccess=VKG3PM4WXMT95DSUCPKE&tokenDomain=eprints&target=10.1080%2F00766097.2022.2129682

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