Epidemija CoViD-19

[Žika]

https://www.contagionlive.com/view/inci ... ity-groups

Spike Protein of SARS-CoV-2 Virus Alone Can Cause Damage to Lungs

figure image
A recent study conducted by investigators from the Frank Reidy Research Center for Bioelectrics at Old Dominion University has found that exposure to the spike protein on the SARS-CoV-2 virus has the potential to induce symptoms similar to COVID-19 and damage the lungs.

Results from the study are being presented at the American Society for Pharmacology and Experimental Therapeutics annual meeting, Experimental Biology 2021.

"Our findings show that the SARS-CoV2 spike protein causes lung injury even without the presence of intact virus," Pavel Solopoy, a research assistant professor at the Frank Reidy Research Center for Bioelectrics at Old Dominion University said. "This previously unknown mechanism could cause symptoms before substantial viral replication occurs."

For the study, investigators injected genetically modified mice with a segment of the SARS-CoVC-2 spike protein, and another group of mice with saline. The team then analyzed the responses the mice had after 72 hours.

Findings from the study demonstrated that the mice who were injected with the spike protein developed symptoms associated with COVID-19, including severe inflammation, an influx of white blood cells into their lungs and evidence of a cytokine storm. The mice who only received the sale shot remained normal.

The team of investigators now plan on doing further research using their mouse model to study different drugs and how they impact lung injury and COVID-19.

"These findings show that the genetically modified mouse together with just a segment of the spike protein can be used to study SARS-CoV-2 lung injury," Solopov said. "We can use this tool to develop a better understanding of how the spike protein causes lung symptoms -- even without the intact virus -- in order to develop new targets and therapeutics for COVID-19."

 

[Žika]

Journal of the American Heart Association

https://www.ahajournals.org/doi/10.1161 ... 121.318902

SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2

SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection relies on the binding of S protein (Spike glycoprotein) to ACE (angiotensin-converting enzyme) 2 in the host cells. Vascular endothelium can be infected by SARS-CoV-2,1 which triggers mitochondrial reactive oxygen species production and glycolytic shift.2 Paradoxically, ACE2 is protective in the cardiovascular system, and SARS-CoV-1 S protein promotes lung injury by decreasing the level of ACE2 in the infected lungs.3 In the current study, we show that S protein alone can damage vascular endothelial cells (ECs) by downregulating ACE2 and consequently inhibiting mitochondrial function.

We administered a pseudovirus expressing S protein (Pseu-Spike) to Syrian hamsters intratracheally. Lung damage was apparent in animals receiving Pseu-Spike, revealed by thickening of the alveolar septa and increased infiltration of mononuclear cells (Figure [A]). AMPK (AMP-activated protein kinase) phosphorylates ACE2 Ser-680, MDM2 (murine double minute 2) ubiquitinates ACE2 Lys-788, and crosstalk between AMPK and MDM2 determines the ACE2 level.4 In the damaged lungs, levels of pAMPK (phospho-AMPK), pACE2 (phospho-ACE2), and ACE2 decreased but those of MDM2 increased (Figure , i). Furthermore, complementary increased and decreased phosphorylation of eNOS (endothelial NO synthase) Thr-494 and Ser-1176 indicated impaired eNOS activity. These changes of pACE2, ACE2, MDM2 expression, and AMPK activity in endothelium were recapitulated by in vitro experiments using pulmonary arterial ECs infected with Pseu-Spike which was rescued by treatment with N-acetyl-L-cysteine, a reactive oxygen species inhibitor .

Figure. SARS-CoV-2 (Severe acute respiratory syndrome coronavirus 2) Spike protein exacerbates endothelial cell (EC) function via ACE (angiotensin-converting enzyme) 2 downregulation and mitochondrial impairment.A, Representative H&E histopathology of lung specimens from 8- to 12 wk-old male Syrian hamsters 5-day post administration of pseudovirus overexpressing Spike protein (Pseu-Spike) or mock virus in control group (n=3 mice per group, 1×108 PFU). Thickened alveolar septa (red arrowhead) and mononuclear cell (red arrow). Scale bar=20 μm. B, Pseu-Spike (n=4) or mock virus (n=4)–infected hamster lungs were subjected to Western blot analysis for pAMPK (phospho-AMPK) T172, AMPK, pACE2 (phospho angiotensin-converting enzyme) S680, ACE 2, MDM2, peNOS S1176, peNOS T494, eNOS (endothelial NO synthase), and β-actin (B, i). Human pulmonary arterial EC (PAECs) were infected with Pseu-Spike or mock virus for 24 h with or without N-acetyl-L-cysteine (NAC; 5 mmol/L) pretreatment for 2 h. The protein extracts were analyzed by Western blot using antibodies against proteins as indicated (n=4; B, ii). C, Representative confocal images of mitochondrial morphology of ECs treated with human recombinant S1 protein or IgG (4 μg/mL) for 24 h (C, i) or infected with human adenovirus ACE2 S680D (ACE2-D) or ACE2 S680L (ACE2-L; 10 MOI) for 48 h (C, ii). Mitochondria were visualized using TOM20 antibody (n=4, 50 cells counted for each replicate). Scale bar=2.5 μm. Tubular: the majority of mitochondria in ECs was >10 μm in length; Intermediate: the mitochondria were <≈10 μm; Fragment: the majority of mitochondria were spherical (no clear length or width). D, Measurement of oxygen consumption rate (OCR, D, i and iii) and extracellular acidification rate (ECAR, D, ii and iv) in ECs infected with ACE2-D vs ACE2-L (10 MOI) for 48 h (n=3) or treated with IgG vs S1 protein (4 μg/mL) for 24 h (n=3). E, Real-time quantitative polymerase chain reaction analysis of the indicated mRNA levels in lung ECs from ACE2-D (n=4) and ACE2-L (n=4) knock-in mice. Eight-week-old ACE2-D and ACE2-L male mice with C57BL/6 background were used. F, Dose-response curves of acetylcholine (ACh, left)- and sodium nitroprusside (SNP, right)–mediated relaxation on the tension of phenylephrine (1 μmol/L) precontracted intrapulmonary artery stripes from Pseu-Spike-(ACh n=8, SNP n=5) or mock (ACh n=6, SNP n=5) virus–infected Syrian hamsters (1×108 PFU; F, i) and ACE2-D (n=6) or ACE2-L (n=5) mice (F, ii). The animal experiments were approved by the ethical committee of Xi’an Jiaotong University. 2-DG indicates 2-Deoxy-D-glucose; ACE2-D, a phospho-mimetic ACE2 with increased stability; ACE2-L, a dephospho-mimetic ACE2 with decreased stability; AMPK, AMP-activated protein kinase; AA/R, antimycin A&Rotenone; ENO2, enolase 2; FCCP, carbonyl cyanide-p-(trifluoromethoxy)phenylhydrazone; H&E, Hematoxylin and Eosin; HK2, hexokinase 2; HO1, heme oxygenase-1; MDM2, murine double minute 2; MOI, multiplicity of infection; NRF1, nuclear respiratory factor 1; peNOS, phospho-eNOS; PFKFB3, 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3; Resp, respiration; and TFAM, transcription factor A, mitochondrial.

We next studied the impact of S protein on mitochondrial function. Confocal images of ECs treated with S1 protein revealed increased mitochondrial fragmentation, indicating altered mitochondrial dynamics (Figure [C], i). To examine whether these mitochondrial changes were due, in part, to the decreased amount of ACE2, we overexpressed ACE2 S680D (ACE2-D, a phospho-mimetic ACE2 with increased stability) or S680L (ACE2-L, a dephospho-mimetic with decreased stability)4 in ECs. As shown in Figure [C], ii, ECs with ACE2-L had a higher number of fragmented mitochondria when compared to those with ACE2-D. Performing oxygen consumption rate and extracellular acidification rate assays, we found that ECs overexpressing ACE2-L had reduced basal mitochondrial respiration, ATP production, and maximal respiration compared to ECs overexpressing ACE2-D (Figure [D], i). Moreover, ACE2-L overexpression caused increased basal acidification rate, glucose-induced glycolysis, maximal glycolytic capacity, and glycolytic reserve (Figure [D], ii). Also, ECs incubated with S1 protein had attenuated mitochondrial function but increased glycolysis, when compared with control cells treated with IgG (Figure [D], iii and iv). We also compared the expressions of mitochondria- and glycolysis-related genes in lung ECs isolated from ACE2-D or ACE2-L knock-in mice.4 Shown in Figure [E], the mRNA levels of NRF1, HO1, and TFAM (mitochondria biogenesis-related genes) were increased, whereas those of HK2, PFKFB3, and ENO2 (glycolysis-related genes) were decreased in lung ECs in ACE2-D mice, as compared to those in ACE2-L mice.

SARS-CoV-2 infection induces EC inflammation, leading to endotheliitis.1,5 Because S protein decreased ACE2 level and impaired NO bioavailability, we examined whether S protein entry is indispensable for dysfunctional endothelium. As shown in Figure [F], i, the endothelium-dependent vasodilation induced by acetylcholine was impaired in pulmonary arteries isolated from Pseu-Spike-administered hamsters, whereas the endothelium-independent vasodilation induced by sodium nitroprusside was not affected. We also compared the acetylcholine- and sodium nitroprusside–induced vasodilation of pulmonary vessels from ACE2-D or ACE2-L mice. As anticipated, acetylcholine-induced vasodilation was hindered in pulmonary arteries isolated from ACE2-L mice in comparison to ACE2-D mice (Figure [F], ii). There was, however, little difference in sodium nitroprusside–induced vasodilation between ACE2-D and ACE-L animals.

Although the use of a noninfectious pseudovirus is a limitation to this study, our data reveals that S protein alone can damage endothelium, manifested by impaired mitochondrial function and eNOS activity but increased glycolysis. It appears that S protein in ECs increases redox stress which may lead to AMPK deactivation, MDM2 upregulation, and ultimately ACE2 destabilization.4 Although these findings need to be confirmed with the SARS-CoV-2 virus in the future study, it seems paradoxical that ACE2 reduction by S protein would decrease the virus infectivity, thereby protecting endothelium. However, a dysregulated renin-angiotensin system due to ACE2 reduction may exacerbate endothelial dysfunction, leading to endotheliitis. Collectively, our results suggest that the S protein-exerted EC damage overrides the decreased virus infectivity. This conclusion suggests that vaccination-generated antibody and/or exogenous antibody against S protein not only protects the host from SARS-CoV-2 infectivity but also inhibits S protein-imposed endothelial injury.

 

[Žika]

https://scitechdaily.com/covid-19-is-a- ... lar-level/

COVID-19 Is a Vascular Disease: Coronavirus’ Spike Protein Attacks Vascular System on a Cellular Level


Salk researchers and collaborators show how the protein damages cells, confirming COVID-19 as a primarily vascular disease.

Scientists have known for a while that SARS-CoV-2’s distinctive “spike” proteins help the virus infect its host by latching on to healthy cells. Now, a major new study shows that they also play a key role in the disease itself.

The paper, published on April 30, 2021, in Circulation Research, also shows conclusively that COVID-19 is a vascular disease, demonstrating exactly how the SARS-CoV-2 virus damages and attacks the vascular system on a cellular level. The findings help explain COVID-19’s wide variety of seemingly unconnected complications, and could open the door for new research into more effective therapies.

“A lot of people think of it as a respiratory disease, but it’s really a vascular disease,” says Assistant Research Professor Uri Manor, who is co-senior author of the study. “That could explain why some people have strokes, and why some people have issues in other parts of the body. The commonality between them is that they all have vascular underpinnings.”

Salk researchers collaborated with scientists at the University of California San Diego on the paper, including co-first author Jiao Zhang and co-senior author John Shyy, among others.

While the findings themselves aren’t entirely a surprise, the paper provides clear confirmation and a detailed explanation of the mechanism through which the protein damages vascular cells for the first time. There’s been a growing consensus that SARS-CoV-2 affects the vascular system, but exactly how it did so was not understood. Similarly, scientists studying other coronaviruses have long suspected that the spike protein contributed to damaging vascular endothelial cells, but this is the first time the process has been documented.

In the new study, the researchers created a “pseudovirus” that was surrounded by SARS-CoV-2 classic crown of spike proteins, but did not contain any actual virus. Exposure to this pseudovirus resulted in damage to the lungs and arteries of an animal model—proving that the spike protein alone was enough to cause disease. Tissue samples showed inflammation in endothelial cells lining the pulmonary artery walls.

The team then replicated this process in the lab, exposing healthy endothelial cells (which line arteries) to the spike protein. They showed that the spike protein damaged the cells by binding ACE2. This binding disrupted ACE2’s molecular signaling to mitochondria (organelles that generate energy for cells), causing the mitochondria to become damaged and fragmented.

Previous studies have shown a similar effect when cells were exposed to the SARS-CoV-2 virus, but this is the first study to show that the damage occurs when cells are exposed to the spike protein on its own.

“If you remove the replicating capabilities of the virus, it still has a major damaging effect on the vascular cells, simply by virtue of its ability to bind to this ACE2 receptor, the S protein receptor, now famous thanks to COVID,” Manor explains. “Further studies with mutant spike proteins will also provide new insight towards the infectivity and severity of mutant SARS CoV-2 viruses.”

The researchers next hope to take a closer look at the mechanism by which the disrupted ACE2 protein damages mitochondria and causes them to change shape.

Reference: “SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2” by Yuyang Lei, Jiao Zhang, Cara R. Schiavon, Ming He, Lili Chen, Hui Shen, Yichi Zhang, Qian Yin, Yoshitake Cho, Leonardo Andrade, Gerald S. Shadel, Mark Hepokoski, Ting Lei, Hongliang Wang, Jin Zhang, Jason X.-J. Yuan, Atul Malhotra, Uri Manor, Shengpeng Wang, Zu-Yi Yuan and John Y-J. Shyy, 31 March 2021, Circulation Research.
DOI: 10.1161/CIRCRESAHA.121.318902

Other authors on the study are Yuyang Lei and Zu-Yi Yuan of Jiaotong University in Xi’an, China; Cara R. Schiavon, Leonardo Andrade, and Gerald S. Shadel of Salk; Ming He, Hui Shen, Yichi Zhang, Yoshitake Cho, Mark Hepokoski, Jason X.-J. Yuan, Atul Malhotra, Jin Zhang of the University of California San Diego; Lili Chen, Qian Yin, Ting Lei, Hongliang Wang and Shengpeng Wang of Xi’an Jiatong University Health Science Center in Xi’an, China.

The research was supported by the National Institutes of Health, the National Natural Science Foundation of China, the Shaanxi Natural Science Fund, the National Key Research and Development Program, the First Affiliated Hospital of Xi’an Jiaotong University; and Xi’an Jiaotong University.

 

[Пантограф]

Astrazeneka i Fajzer uspešno sprečavaju delta soj koronavirusa

Studija sa univerziteta Oksford pokazala je da su vakcine za kovid 19 koje je napravila Astrazeneka i Fajzer Biontek veoma efikasne protiv delta i kapa varijanti virusa.

Линк:

https://www.b92.net/zdravlje/vesti.php?yyyy=2021&mm=06&dd=23&nav_id=1879835

 

[Žika]

Njima only 84 hospitalised predstavlja nešto preko 10% vakcinisanih sa obe doze. Što kaže Šekler kao gripić.
Još je rano za procenu smrtnosti a ko voli nek malo izgugla koje su starosne grupe izloženije ovom virusu.
Inače ovaj soj je u Indiji napravio haos u mlađoj populaciji.

https://www.gov.uk/government/news/conf ... fied-in-uk

Public Health England (PHE) releases weekly updates on the number of confirmed new cases of variants of concern and variants under investigation identified in the UK.

Delta variant cases continue to rise
PHE’s weekly COVID-19 variant cases data show that numbers of the Delta (VOC-21APR-02) variant in the UK have risen by 33,630 since last week to a total of 75,953. The most recent data show 99% of sequenced and genotyped cases across the country are the Delta variant.

Data show an increased risk of hospitalisation with Delta compared to Alpha, although PHE’s analysis shows that 2 doses of vaccine gives a high degree of protection against hospitalisation, estimated to be more than 90%.

According to PHE’s latest variant technical briefing, as of 14 June, a total of 806 people have been hospitalised with the Delta variant, an increase of 423 since last week. Of these, 527 were unvaccinated, and only 84 of the 806 had received both doses.

PHE now publishes the number of deaths among people who have tested positive for Delta within the past 28 days. The case fatality rate remains low for Delta. However, deaths tend to happen some weeks after infection and the majority of cases were confirmed less than 28 days ago. It is therefore too early to judge the case fatality of Delta compared to Alpha or other variants.

Dr Jenny Harries, Chief Executive, UK Health Security Agency said:

Cases are rising rapidly across the country and the Delta variant is now dominant. The increase is primarily in younger age groups, a large proportion of which were unvaccinated but are now being invited to receive the vaccine. It is encouraging to see that hospitalisations and deaths are not rising at the same rate but we will continue to monitor it closely. The vaccination programme and the care that we are all taking to follow the guidance are continuing to save lives.

Please make sure that you come forward to receive both doses of the vaccine as soon as you are eligible. Don’t drop your guard – practise ‘hands, face, space, fresh air’ at all times.

 

[Zuma]

Sve nas interesuje šta dalje možemo očekivati. Evo jednog drugačijeg pristupa koji do sada nisam video.

Gledajući dosadašnje dijagrame toka epidemije, teško je ne videti ne samo da se talasi periodično ponavljaju, nego i da međusobno prilično liče jedan na drugi. Jasno je da postoji i neka unutrašnja dinamika pojave, rasta i nestajanja svakog talasa koja ih uobličava u uglavnom pravilnu i ponavljajuću formu zvonastog oblika. Zato bi moglo biti interesantno direkno ih uporediti i videti da li tu postoje prve naznake nekih pravilnosti. Naravno, uz svest da to ne mora baš ništa da znači jer se nepoznate zakonitosti koje ih formiraju uvek mogu promeniti već sledeći put, a i da je svega četri primerka nedovoljno za zaključak da postoji pravilna serija.

Evo dva dijagrama poređenja oblika i trajanja dosadašnja četri talasa. Na X osi su dani, a na Y osi je normalizovani broj slučajeva, tj broj slučajeva infekcije skaliran tako da svi talasi imaju sličnu veličinu, pošto to olakšava poređenje njihovog oblika i zavisnosti od vremena.

Jedna stvar upada u oči. Talas je prvo bio uzak, a mirni period između talas kratak. Kako vreme prolazi, talasi traju duže, tj razvlače se sve više, ali zato i period između njih duže traje. Nažalost četri maksimuma i tri doline su isuviše malo za zaključke, pogotovo što je treća dolina atipična jer se broj slučajeva nije ni spustio do malih vrednosti (pošto je bila sredina zime, januar), već prešao u sledeći talas. Ipak i tu se vidi da je brzina promene bila manja, što se slaže sa prepostavkom o tendenciji "razvlačenja" talasa i mirnog perioda između njih. Moguće objašnjenje ove pojave je što smo u početku imali strogi lokdaun, što je brzo preseklo veliki rast. Kako je vreme prolazilo, ljudi su se opuštali i manje vodili računa o izolaciji, a Vučić je zbog straha od nemira i svoje fokusiranosti na ekonomiju prećutno prešao na neki kvazi-Švedski i veoma liberalan model reagovanja. Delom zbog toga, a delom zbog postepenog akomuliranja imuniteta u narodu, brzina promene broja zaraženih počinje da biva sve manja (Pošto virus ima sve manje nezaštićenih osoba na raspolaganju za dalje širenje. To ne smanjuje broj konačno zaraženih, jer još nezaraženih kandidata i dalje ima sasvim dovoljno, ali ipak smanjuje brzinu širenja i opadanja. Rezultat je isti, ali sve zajedno duže traje). Naravno, sasvim su moguća i druga objašnjanja.

Neka vrsta predikcije izvučena iz ovih trendova bi bila da će trenutni miran period trajati od jedan do dva meseca, tj tokom leta, ali ne duže od toga. Onda se vraćamo na istu priču. Sem ako se nekom magijom do jeseni ne vakciniše više od 60% stanovništva, što će se teško desiti posle svih pisanja koja su u najvećem delu trajanja epidemije žestoko forsirala paranoju kao opšti pogled na svet, na ovom i na svim drugim forumima. To se tek sada donekle promenilo, ali nažalost kasno.

 

[Žika]

 

[GOJE]

@Žika,

Meni je potpuno neverovatno da ti uporno kačiš argumente koji pobijaju tvoje stavove. Neprevaziđeno.

 

[marrecar]

Žika » 23 Jun 2021 01:48 pm[/url]":3rlycibv]

marrecar » Sre Jun 23, 2021 9:43 am[/url]":3rlycibv]Meni su konstantno zanimljivi ti Sejšeli, otvorili se za turiste i eto odjednom bum korona. A ne mogu nigde naći podatke ko je u stvari zaražen, da li lokalno vakcinisano stanovništvo ili turisti, jer oni moraju ostati svakako tu dok se ne izleče. I ko radi uopšte to ukrštanje podataka, kao veliki broj zaraženih na Sejšelima, a tamo svi vakcinisani, pa kao to odmah znači da su vakcinisani zaraženi, dakle ne valja vakcina.

Pisao sam u vezi Sejšela, ludilo sa koronom je krenulo sa vakcinacijom i kako rastu procenti vakcinisanih tako rastu i brojevi obolelih.
U aprilu su cifre već krenule nenormalno za zemlju koja je u 2020. bila bez korone ???
37 % obolelih su vakcinisani sa dve doze , veliki prcenat, 20% vakcinisanih su završili u bolnici dakle nisu lakši slučajevi.
Oni i dalje očekuju turiste i da će njihov udeo u bolesnom stanovništvu biti oko 10%.
U avion bez PCR testa ne može , zar ne ?
Nemaju evidenciju koji su sojevi dominantni.

Britanija i Indijski soj ?

Da, na tvoje pisanje sam se najviše pozvao, jer opet nismo mogli nigde da ustanovimo ko se to zaista zarazio, odnosno ko je ušao u tu statistiku. Ako piše da se naglo povećao broj zaraženih, da je stanovništvo vakcinisano, onda se mogao izvući pogrešan zaključak da je vakcinisano stanovništvo zaraženo. Dok je u realnosti možda taj broj zaraženih u stvari od turista koji, iako imaju pcr test, ne znači da nisu zaraženi niti da se ne mogu zaraziti tamo. Ako se tamo zaraze, ne mogu otići odatle, pa onda ulaže u statistiku te države. Isto kao što se u Srbiji vodi statistika o vakcinisanima, a dolaze stranci da se vakcinišu, pa je procenat vakcinacije (trajno naseljenog) stanovništva u realnosti manji.

 

[Zuma]

Evo još jedne priče kao iz drama Dušana Kovačevića. Već drugi put grupe građana napadaju ekipe koje sa zemlje zaprašuju komarce. Lajtmotiv: "Otkuda ja znam čime nas vi to prskate?" Samo što sada imamo i poučan video snimak. To je potpuno ista tema kao i ove kojima se ovde zamajavamo već godinu dana: "Otkuda ja znam šta ima u vakcinama?", "Odakle je virus?", "Šta se zaista dešava u bolnicama?" ...

Ponovo napad na vozilo koje prska komarce, jer - "prska koronom" VIDEO
https://www.b92.net/lokal/beograd/hroni ... eo-1879787

Vest na B92 je senzacionalistički predstavljena, pa moram da kažem da imam izvesnog razumevanja za ove što se bune. Ustvari, čak i za teoretičare zavera. Mislim da u konkretnom slučaju epidemije korone greše, da su lenji, nefleksibilni u razmišljanju, da ne žele da uče, i da društvu prave ogromnu štetu, ali kad je u pitanju njihov osnovni motiv za sumnjičavost, ne mogu im puno zameriti. Izvor nepoverenja je ekstremna verzija neoliberalizma u kojoj Američki desničari narod (dakle sve koji rade kod nekoga, a nemaju SVOJU firmu) vide prosto kao dokazano nesposobnu st.ku koja je dobra samo za klanicu i iskorišćavanje, dok je pod Trampom i sam koncept istine bio maltene isčezao. Pa kad vas neko stalno laže, normalno je da na kraju, bez zaista dobrog opšteg obrazovanja, više nećete verovati nikome. Međutim to je put u destrukciju društva. Ako smo i u Srbiji stigli do toga da lokalni "čuvari zdravlja" osećaju potrebu da na ulici proveravaju specifikaciju i hemijsku formulu sredstva za zaprašivanje komaraca, o čemu naravno ne znaju ništa, onda je apsurdni svet iz drama Dušana Kovačevića veoma blizu. Ili smo tamo već odavno.

 

[Žika]

GOJE » Sre Jun 23, 2021 3:08 pm[/url]":21s88c43]@Žika,

Meni je potpuno neverovatno da ti uporno kačiš argumente koji pobijaju tvoje stavove. Neprevaziđeno.

Koje stavove ?

 

[chiko]

Zuma » Sre Jun 23, 2021 5:55 pm[/url]":1rek9rti]Evo još jedne priče kao iz drama Dušana Kovačevića. Već drugi put grupe građana napadaju ekipe koje sa zemlje zaprašuju komarce. Lajtmotiv: "Otkuda ja znam čime nas vi to prskate?" Samo što sada imamo i poučan video snimak. To je potpuno ista tema kao i ove kojima se ovde zamajavamo već godinu dana: "Otkuda ja znam šta ima u vakcinama?", "Odakle je virus?", "Šta se zaista dešava u bolnicama?" ...

Moderni ludisti.

 

[Bender Rodriguez]

Moderni ludisti su nesto drugo. Ludista strahuje od gubitaka poslova usled alavosti velikih poslodavaca.

Ovi su samo cuknuti u glavu.

 

[Zuma]

Šta smo preživeli i šta se na jesen i zimu može očekivati, nastavak.

Kad se podaci iz prethodne poruke predstave kao dijagram kompletnog toka epidemije, ali sa jasno markiranim trajanjima talasa i trajanjima mirnih perioda između talasa, onda se dobija ovo.

Ili isto to predstavljeno kao pregledna tabela trajanja talasa i zatišja između njih.

Ovde se jasno vidi pravilna tendencija produžavanja trajanja talasa, tj postepenog prokužavanja stanovništva uz verovatno sve manji trud oko zaštite, a možda i produžavanja perioda između njih, mada za ovo poslednje nema dovoljno podataka i veliko je pitanje da li ta pravilnost postoji. Plave vrednosti su one koje bi se dobile za očekivani peti talas kad bi se ovi trendovi razvlačenja trajanja talasa nastavili isto kao i do sada. Naravno, ne treba očekivati da se matematički niz može tek tako slepo i mehanički nastaviti, i da će zaista tako biti, pošto verovatno neće (tri i po meseca za 5. talas, tj cela jesen?). To sam stavio samo informativno, pošto se iz više brojnih vrednosti lakše vidi dosadašnja tendencija. Svetlija crvena boja je kratkotrajno i delimično januarsko popuštanje između trećeg i četvrtog talasa, u sred zime, tj jedini broj koji je zbog toga izvan pravilne sekvence rasta svih ostalih vrednosti.

 

[Zuma]

I da ne promakne ako nije posebno naglašeno: Svi ovakvi računi koji su prosto nastavci starih trendova podrazumevaju da nije uveden neki sasvim novi faktor koji ranije nije postojao. Recimo novi delta soj virusa, ako on ima BITNO drugačije epidemiološke karakteritike. U sprotnom sve postaje još neizvesnije.

 

[termicar]

Ako je nekome interesantno juce sam radio analize krvi (zbog svojih boljki) pa sam uradio iz ciste znatizelje i test za antitela i evo ga rezultat:

Vakcinisan drugom dozom 20.02. Sinopharm vakcina; referentna vrednost je 50 (sve preko 50 je pozitivno) moj rezultat je 225; imam 55+ godina.

 

[molder]

Neki ekonomisti imaju stav, da se priča o povratku Korone na jesen ciljano plasira preko medija zbog "bump" ekonomije koja je potrebna svetu ovog leta. Svako od nas ima ljude u okruženju koje ovo leto doživljavaju kao poslednje, pa se masovno izlazi,kupuje, putuje, i to često bez ikakvog ekonomskog pokrića...

 

[Kailan]

Неки економисти су имали став и да интернет неће имати већи значај за глобалну економију од факс машине

Корона није нигде нестала да би се "вратила", ту је и остаће и биће претња за свакога ко нема или не може да створи имунитет на њу док цела популација не створи довољан имунитет на њу да би њена тежина била у равни сезонских грипова. Као што је случај и са другим коронавирусима.

Не постоји апсолутно ниједан разлог зашто не би било новог таласа са сезонама вирусних инфекција, поготово не у земљама где се мање од половине популације вакцинисало

 

[MC_]

Vakcinisan sam pre 2 meseca kineskom vakcinom. Sada sam uradio test. U laboratoriji gde sam bio se radi izvesni "test reaktivnosti na sike protein".
Granicna vrednost je 0.8, kod mene je 4.8.
medjutim kineska vakcina se pokazal kao nikakava na Sejselima bez obzira na antitela.

 

[molder]

Kailan » 24 Jun 2021 09:37 am[/url]":3gvwdxks]
Корона није нигде нестала да би се "вратила", ту је и остаће и биће претња за свакога ко нема или не може да створи имунитет на њу док цела популација не створи довољан имунитет на њу да би њена тежина била у равни сезонских грипова. Као што је случај и са другим коронавирусима.

Bez ovog wikipedia copy paste pojasnjenja, koje nema nikakve veze sa pricom, bi mi propao dan, ovako necu umreti u neznanju

 

[Пантограф]

Koliko je opasan lambda soj?

Dok naučnici u Nemačkoj upozoravaju na opasnost od soja delta, već se širi sledeća varijanta virusa. Koliko je opasan soj lambda, koji se ubrzano širi pre svega po Latinskoj Americi?

L(ambda)ink:https://www.b92.net/zdravlje/vesti.php?yyyy=2021&mm=06&dd=23&nav_id=1879756

 

[Kailan]

molder » Чет Јун 24, 2021 12:13 pm[/url]":1r6u4q90]

Kailan » 24 Jun 2021 09:37 am[/url]":1r6u4q90]
Корона није нигде нестала да би се "вратила", ту је и остаће и биће претња за свакога ко нема или не може да створи имунитет на њу док цела популација не створи довољан имунитет на њу да би њена тежина била у равни сезонских грипова. Као што је случај и са другим коронавирусима.

Bez ovog wikipedia copy paste pojasnjenja, koje nema nikakve veze sa pricom, bi mi propao dan, ovako necu umreti u neznanju

А шта ти је "прича", да зли рептили шире лажи о могућности новог таласа коронавируса кад крене сезона вируса у земљама без адекватне заштите са злом намером да подстакну иначе јако штедљив народ да троши паре? У скоро свим земљама света ниси могао мотком да натераш људе да седе кући, сад кад мисле да је пандемија прошла мора неко да их слаже како би ишли на летовања, по кафићима, клубовима, трошили и сл

Глупости

 

[chiko]

Ali to je jedna bas lepa teorijica zavere.
Nemoj da kvaris zabavu.

 

[Bender Rodriguez]

Sve je teorija zavere.

I sve je govor mrznje.

 

[Bender Rodriguez]

Sad sam bio u pošti da pomognem nekome oko ovog cirkusa sa digitalnim sertifikatom o vakcinaciji. Naravno, nismo ništa uspeli da uradimo, ali ne zbog krivice ljudi u Pošti. I gledam taj pičvajz koji su napravili i jedna stvar mi nije jasna.

Ako je država bila spremna i sposobna da ljudima isplaćuje po 100, pa 60, pa 30 evra samo i samo na osnovu JMBG i broja lične karte... u čemu je toliki jbni problem da se i za zeleni sertifikat napravi sistem tako da dođeš, daš JMBG i broj LK, sistem se poveže sa sistemom RFZO i bazom gde su vakcinisani, i lepo ako tj. kad te nađe u spisku vakcinisanih, da ti izda prokleti sertifikat?

Ali ne. Moraš da praviš naloge na eUpravi, na ConsentID, da čekaš 24 sata da obrade zahtev, da proveravaš email, da se loguješ i tek onda da ideš do Pošte da ti ga izdaju. A ovamo su nam svima po 3, 4, nekome i 5 puta DAVALI PARE samo na osnovu JMBG I broja lične karte. Znači, pare mogu samo uz JMBG i LK, a jedno papirče o potvrdi vakcinacije... to ne može. Za to mora postupak ko da otvaraš svoju banku ili stranku. :kafa:

Ona izreka je stvarno tačna, gde prestaje logika, tu počinje Srbija.