Virus

konjski nil wrote:kako si tačno zamislio da rade kada kvislinzi u službi kronista prerađuju virus ko mutavi 24/7/365 zasipaju nas novim sojevima svaki dan usput zahtevaju da se ispoštuju šestomesečni bezbednosni protokoli i kad vakcine zastare imaju obraza da nadrabaju haha što vam vakcine ne rade 
btw ja bih se zabrinuo da sam crnogorčina

ps
avax lažovi nemaju granica sad su stigli do trogodišnjih švedskih lokdauna

https://twitter.com/Gronnet/status/1703739709615181939

MNE wrote:naravno da je to problem, ali kako to objasniti vama paničarima

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https://covid19.rs/

Moramo da se naviknemo da živimo sa koronom

A third of long COVID patients sustained damage to multiple organs five months after infection, a study has found.

Scans of patients who were treated in hospital for COVID-19 showed higher rates of damage to the lungs, brain and kidneys compared with the non-COVID control group.

Lung injuries were almost 14 times higher among long COVID patients, while abnormal findings involving the brain and kidneys were three and two times higher respectively.

How badly the organs were affected was often due to the severity of their infection, their age and other diseases in the body.

konjski nil wrote:te tzv blage mutacije su trojanska konjušina kako bi se razbarušeni nehajnici nastavili izlagati dok ih reinfekcije ne izrešetaju do imunodeficijencije lvl aids

Globally, recent studies have revealed a significant correlation between COVID-19 and peptic ulcer disease. In the United States, Safari et al, 8 demonstrated that COVID-19 uses angiotensin-converting enzyme 2 (ACE2) as an entry receptor to interact with cells of the host.

COVID-19 rampant among musicians despite “end of the pandemic”

James McDonald 24 September 2023

A remarkable number of musicians—from Ringo Starr to Harry Styles—have canceled concerts and other appearances in the past year due to acknowledged cases of COVID-19 or, more frequently, due to undisclosed illnesses. While governments have averted their eyes from the COVID pandemic, halting its reporting of cases and other crucial data, observable phenomena such as an epidemic of canceled shows demonstrate that the deadly, highly contagious disease is still very much with us.

juče bio na nekom domjenku i bude par forica u fzn haha ko još veruje u koronu nameštaljka ser kenj prd ofc ja se pravim mutav jer sam strpljiv i volim da svako iskoristi šansu da sazna na najbolji mogući način tj putem samospoznaje

Looks like SARS Cov 2 was the cause of the hepatitis in Kids https://t.co/dVc8J6dzw3 https://t.co/PiXXFkaJYu pic.twitter.com/dfB7Md5PAF

— AJ Leonardi, MBBS, PhD (@fitterhappierAJ) September 30, 2023

Cause of increased heart risk from COVID infection revealed
1 October 2023

Researchers from New York University have uncovered an explanation for why infection with the virus that causes COVID-19 can increase the risk of heart attacks and strokes: it triggers an immune response in fatty plaques.

These plaques are fat deposits within the arteries, which accumulate over time, reduce blood flow and lead to complications like coronary heart disease and atherosclerosis.  

Since the pandemic, health researchers have warned of the potential connection between COVID-19 and several inflammatory heart problems including myocarditis and pericarditis, and heightened risk of heart attack and stroke for a year after infection.  

The researchers from NYU’s Grossman School of Medicine have now learnt how this increased risk occurs within certain COVID-19 patients, though they also note their research only applies to those versions of SARS-CoV-2 in circulation in New York from May 2020-21.

The researchers took tissue samples from the arteries of eight people who died from severe COVID-19 in the first year of the pandemic – each with previously diagnosed heart disease and three or more cardiovascular risk factors such as high blood pressure – they used an AI program and microscope analysis to detect sites of viral infection.  

They found the virus infects both arterial cells and macrophages (a type of white blood cell) involved in guarding against excess plaque within the heart. Macrophages surrounded by plaque were more likely to attract the virus than those that weren’t, and infection caused them to release a range of cytokines – inflammatory proteins that facilitate the body’s immune response – including interleukins previously linked to heart attacks.  

With fat-laden macrophages unable to perform their job, the risk of further plaque build-up risks prolonging the effects of COVID-19 and cardiovascular complications.

“The virus creates a highly inflammatory environment that could make it easier for plaque to grow, rupture, and block blood flow to the heart, brain, and other key organs,” says Dr Natalia Eberhardt, an immunologist at NYU Langone Health who led the study published in Nature Cardiovascular. “Our findings provide for the first time a direct mechanistic link between COVID-19 infection and the heart complications it provokes.”

Eberhardt and her colleagues highlight how SARS-CoV-2 can infect a range of cells in the body to cause inflammation and elicit an immune response. Severe inflammatory responses dubbed ‘cytokine storms’ occur when a flood of cytokines creates an extreme immune response that attacks the body’s healthy tissues as well as clearing away infections.

6 Vials of SmallPox Left Unguarded for Decades Found In Government Research Lab: and this is just the stuff we know about... pic.twitter.com/TSy8KyUMwf

— Chris Turnbull (@EnemyInAState) October 24, 2023