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Covid-19 / SARS-Cov2 - naučne/medicinske informacije i analize


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Dragi forumaši, molimo vas da u vreme ove krize ostanemo prisebni i racionalni i da pisanjem na ovoj temi ne dođemo u situaciju da naudimo nekome. Stoga:

 

- nemojte davati savete za uzimanje lekova i bilo kakvu terapiju, čak i ako ste zdravstveni radnik - jedini ispravni put za sve one koji eventualno osećaju simptome je da se jave svom lekaru ili na neki od telefonskih brojeva koji su za to predviđeni.

- takođe - ne uzimajte lekove napamet! Ni one proverene, ni one potencijalne - obratite se svom lekaru!

- nemojte prenositi neproverene informacije koje bi mogle nekoga da dovedu u zabludu i eventualno mu načine štetu. Znamo da je u moru informacija po pitanju ove situacije jako teško isfiltrirati one koje su lažne, pogrešne ili zlonamerne, ali potrudite se - radi se o zdravlju svih nas. Pokušajte da informacije sa kojekakvih obskurnih sajtova i sumnjivih izvora ne prenosite. Ili ih prvo proverite pre nego što ih prenesete.

- potrudite se da ne dižete paniku svojim postovima - ostanimo mirni i racionalni.

 

Budimo dostojanstveni u ovoj krizi, ovakve situacije su ogledalo svih nas. 

Hvala na razumevanju.

 

Vaš tim Vox92

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This important study from California proves what has long been suspected. Covid is much more of a vascular disease than a lung disease. This also explains the damage to the kidneys, brain and heart. The spike protein itself damages the blood vessels.

Findings also explain why the function of the brain arteries in younger people is impaired even after a slight infection. For children, this means that infection should be avoided even without lung symptoms. Older people increase their risk of dementia.

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Dugačak ali odlično napisan članak o tome kako je jedna stara medicinska definicija o tome šta je aerosol dovela do toga da je trebalo jako puno vremena da WHO i ostala medicinska tela prihvate da kovid može da se prenosi kroz vazduh

 

https://www.wired.com/story/the-teeny-tiny-scientific-screwup-that-helped-covid-kill/

 

I ne samo to, ovo pokazuje da grip isto može da se prenosi kroz vazduh, a ne samo preko zaraženih površina. To bi moglo i da objasni zašto gripa praktično nema nigde ove godine. 

 

U svakom slučaju za zatvorene prostore ključna stvar: ventilacija, ventilacija i ventilacija

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kad vec pomenu grip, Prof Drosten rece da se moze ocekivati da sledece zime grip bude jaci (jer smo ga prakticno preskocili ove sezone), te da bi bilo dobro da se vise ljudi vakcinise (verovatno ce se spremiti neka kombinovana vakcina: za osvezavanje protiv covida i za grip). Do sada su se uglavnom stariji vakcinisali protiv gripa (preko 60 godina), kaze da bi valjalo da se ta granica malcice spusti na mladje grupe, cisto zbog kombinovanog rizika.

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1 hour ago, nemanjaol said:

Dugačak ali odlično napisan članak o tome kako je jedna stara medicinska definicija o tome šta je aerosol dovela do toga da je trebalo jako puno vremena da WHO i ostala medicinska tela prihvate da kovid može da se prenosi kroz vazduh

 

https://www.wired.com/story/the-teeny-tiny-scientific-screwup-that-helped-covid-kill/

 

I ne samo to, ovo pokazuje da grip isto može da se prenosi kroz vazduh, a ne samo preko zaraženih površina. To bi moglo i da objasni zašto gripa praktično nema nigde ove godine. 

 

U svakom slučaju za zatvorene prostore ključna stvar: ventilacija, ventilacija i ventilacija

 

 

😞

Mada smo u sustini znali

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Među najbitnijim vestima godine.

 

 

 

—The viral load is so low sequencing is not possible in most
—The chance that someone could spread covid is close to zero, yet to be documented

 

Konsekvence su valjda jasne.

Edited by Laki21
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Nisu napisali da je u Izraelu vakcinacija sprovodjena prakticno uz policijski čas dok je u UAE sve funkcionisalo normalno dok je stanovnistvo vakcinisano.

Srbija je negde izmedju bila, pa su i brojke izmedju 

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Large clinical trial to study repurposed drugs to treat COVID-19 symptoms

 

 

"Nacionalni zavod za zdravlje finansiraće veliko, randomizirano, placebom kontrolisano kliničko ispitivanje faze 3, kako bi se testiralo nekoliko postojećih lekova na recept i bez recepta za ljude, koji se mogu sami primenjivati u lečenju simptoma COVID-19. Deo javno-privatnog partnerstva za ubrzavanje terapijskih intervencija i vakcina COVID-19 (ACTIV), cilj ACTIV-6 je da pruži mogućnosti lečenja zasnovane na dokazima za većinu odraslih pacijenata sa COVID-19 koji imaju blage do umerene simptome i nisu dovoljno bolesni da bi bili hospitalizovani. NIH će obezbediti početno ulaganje od 155 miliona dolara u finansiranje suđenja.

 

„Iako radimo dobar posao u lečenju hospitalizovanih pacijenata sa teškom bolešću, trenutno nemamo odobreni lek koji se može sam primenjivati kako bi se olakšali simptomi ljudi koji pate od blage bolesti kod kuće i smanjio rizik od njihove kojima je potrebna hospitalizacija “, rekao je direktor NIH Francis S. Collins, dr. med., dr. „ACTIV-6 će proceniti da li određeni lekovi koji obećavaju u malim ispitivanjima mogu da prođu strogost većeg ispitivanja.“

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Be well: A potential role for vitamin B in COVID-19

 

"Vitamin B ne samo da pomaže u izgradnji i održavanju zdravog imunološkog sistema, već može potencijalno da spreči ili smanji simptome COVID-19 ili da leči SARS-CoV-2 infekciju. Loš nutricionistički status ljude lakše predisponira na infekcije; stoga je uravnotežena ishrana neophodna za imunokompetentnost. Potrebni su bezbedni i ekonomični pomoćni ili terapijski pristupi za suzbijanje aberantne imunološke aktivacije, koja može dovesti do oluje citokina, i za delovanje protiv tromboze. Odgovarajući unos vitamina neophodan je za pravilno funkcionisanje tela i jačanje imunološkog sistema. Vitamin B modulira imunološki odgovor smanjujući regulaciju pro-inflamatornih citokina i upale, smanjujući otežano disanje i gastrointestinalne probleme, sprečavajući hiperkoagulabilnost, potencijalno poboljšavajući ishode i smanjujući dužinu boravka u bolnici za pacijente sa COVID-19."

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  • 1 month later...

Why no one is sure if Delta is deadlier

 

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We keep trying to pigeonhole specific variants as “more dangerous,” “more deadly,” or “more problematic,” but viral evolution is a humbling, haphazard mess—a plot-twisting story we have to watch play out in real time. “We cannot be complacent about ‘Oh, this is the end of the mutations,’” Akiko Iwasaki, a virologist and immunologist at Yale, told me. 

As long as the virus has hosts to infect, it will keep shape-shifting in ways we can’t fully predict. That biological caprice makes it harder to anticipate the next pandemic hurdles we’ll need to clear, and assess the dangers still ahead. But our role in this relationship matters too: What the virus can accomplish also depends a great deal on us, which means its evolution does as well.

As desperately as we want to purge it, the coronavirus’s main objective is to get closer to us. Its biological imperative is to enmesh itself into a suitable host, reproduce, and disperse, then begin the process anew.

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These different possibilities can be teased apart in experiments in laboratory cells and animals, but they all converge on a single principle, Angela Rasmussen, a virologist at the Vaccine and Infectious Disease Organization in Saskatchewan, Canada, told me: “What we’re seeing is a virus that’s becoming more efficient at making more viruses.” Given sufficient time with a new host, most viruses can be expected to trend more transmissible; the coronavirus is probably no exception.

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A more contagious virus might, at first pass, seem like a deadlier virus: Its enhanced invasion capabilities might allow it to grip more tightly onto its host, building up to levels high enough to overwhelm the body. “In that case, you could have transmissibility and virulence increasing in lockstep,” Paul Turner, an evolutionary biologist and virologist at Yale, told me—a neat, simple story. Some researchers have hypothesized that this could be the narrative behind the Alpha and Delta variants, both of which have been linked to bumps in hospitalization. But those patterns haven’t yet been conclusively nailed down, Turner said, and no evidence so far suggests that the coronavirus is systematically evolving to become more malicious. Viruses are microscopic entities hungry for spread, not carnage; the suffering of their host is not an imperative for them to persist. If a surge in virulence happens, it’s often incidental—collateral damage from an increase in contagiousness.

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With vaccines on the rise in many parts of the world, and fewer hosts to infect, the virus is starting to hit roadblocks and slowly sputter out. “By vaccinating, we’re making it less likely that new variants will emerge,” Çevik told me. Eventually, as our collective defenses build, SARS-CoV-2 might become no more a nuisance than a common-cold coronavirus, causing only fleeting and inconsequential symptoms in most people, whose bodies have seen some version of the pathogen before, Jennie Lavine, an epidemiologist and virologist at Emory University, told me. That, of course, makes equitable access to vaccines all the more important, so mutational hot spots don’t arise in unprotected places.

Left to its own devices, the virus could hypothetically bridle itself. But it may have no incentive to. “Counting on the virus to become less virulent on its own is a bad bet,” like waiting for an enemy to slacken its offense, Yale’s Iwasaki told me. The better move is to double down on our defense, the tools we already know best.In years to come, we’ll probably have to tinker with our vaccine recipes to keep pace with the fast-changing virus. But every vaccine we debut has the potential to block a route the virus might have otherwise taken. Viral genomes aren’t infinitely mutable—they can edit only the starting material they’ve been given, and they can’t make certain changes without hamstringing their precious capacity to spread. With time, we might be able to use shots strategically, to force SARS-CoV-2 onto more predictable evolutionary paths, Turner told me: “That’s the way we gain control.” If we’re going to live with this virus long-term—as we absolutely must—then vaccines are our key to building a sustainable relationship, one in which we turn the tables. We can make the virus’s evolution react to us, and not the other way around.

 

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  • 1 month later...

Da li je neko od clanova foruma imao ovaj novi Delta soj i koji su simptomi, da li se razlikuju?

 

Imam temperaturu vec 2 dana, skoci na 37.8, evo sada cak i 38.1, pa je oborim na 37. Sinoc sam se pokrio do glave, jeza me uhvatila, hladno mi je bilo, preznojao sam se koliko nikada u zivotu, majica kao da sam ispod tusa bio. Ja sam do sada mislio da je ovo u vezi sa nekom infekcijom koja mi se javi kad mi padne imunitet, potraje par dana i sve se vrati na normalu ali nije bilo ovoliko temperature. 


Nikakve druge simptome nemam, mogu normalno da disem, ni neki kasalj ni grlo (to povremeno ionako imam), samo ta neka malaksalost, pospanost, bol u misicima/telu. 

 

Znam da ovo treba da ispricam lekaru, ali ne bih da pravim laznu uzbunu za nesto sa cime inace zivim. 

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30 minutes ago, djura.net said:

@Kooineeperk

Trebao si da uradis brzi test, 

mozda ni sad nije kasno. Jesi li bio u nekom rizicnom kontaktu, jel neko od tvojih imao virus ovih dana?

 

Pa nisam bio u rizicnom kontaktu da sad znam da su ti ljudi zarazeni. 

 

Evo me ok sam. Bice da je to proradila ta moja infekcija ali me malo jace uhvatila temp nego ranije. 

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Ne moze ni sa testom da se zasigurno zna da li je korona. U ogromnom broju slucajeva brzi test bude negativan i ako ste bolesni. PCR je nesto precizniji mada i kod njega ima odredjeni broj false pozitivnih i negativnih. 

 

S obzirom da je proslo vec nedelju dana mozes ds uradis test na antitela da vidis da li je prisutna infekcija, sto takodje ume da bude neprecizno.... 

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brzi test je veoma pouzdan, procenjuje se da je u 95.1% rezultat rapid testa tacno dijagnostifikovao prisustvo/odsustvo infekcije.

antigenski testovi iz krvi su prilicno nepouzdani metod pronalazenja infekcije, a mislim da se kod nas oni najcesce i primenjuju.

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