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

[wwww]

Prof Drosten o kineskoj vakcini:

originalna kineska studija:

https://www.biorxiv.org/content/10.1101/2020.04.17.046375v1.full.pdf

Spoiler

Korinna Hennig: So too early to look at it. Since you have already mentioned the key word “difficult courses”. The big issue of vaccines is also very important for high-risk patients. The day before yesterday we had the headline that the first clinical vaccine study in Germany with human subjects was approved. But there is also a vaccine project in Beijing that is currently receiving attention. It's about effectiveness, not just tolerability, but in animal experiments. Simply put, eight rhesus monkeys were vaccinated and then infected with the coronavirus, albeit with a dead vaccine. So a very conventional procedure like the tetanus vaccination, right?

Christian Drosten: Yes, it is the case that something has been tried here that has been running for a long time and of which there is now a first data report in the form of a manuscript. This has received a lot of attention. We've talked about it in the past, here in the podcast: A dead vaccine is the easiest thing to do if you want to get a vaccine. You let the virus grow up in cell culture and kill it - in this case it was done by a chemical - add an adjuvant and make it into a vaccine preparation that has an uncertain effect. We discussed in previous episodes that there are certain fears when you take such a dead vaccine that there is an immune enhancement of the disease rather than protection against the disease.

 

The reason why there is such an urge to discuss it in science is that everyone actually knows you could just do a dead vaccine, and really easy. You take the virus and do it in cell culture, just make it, start clinical studies right away and start applying it. This is faster than many of the other vaccine concepts. And if it works, you know from experience with other dead vaccines that you drive well with it. At least in the early phase, you could think of something like this as the first vaccine option. But that was not considered in Germany or America, because such a dead vaccine is considered to be a risky thing. Many other variants were chosen from the outset.

Korinna Hennig: Just asked once because you said faster now: We have always held on to it, it definitely takes 12 to 18 months, no matter what vaccine we are talking about. How is that with all the risks?

Christian Drosten: First of all, a dead vaccine can be produced quickly because the virus is simply there. You have virus isolates. And one of the biggest challenges in vaccine production overall, later, when you have an approved vaccine, is that you have to make huge amounts. Many, many, many hundreds of millions of cans for populations.

Korinna Hennig: And also relatively simple. So also in countries where capacities are lower.

Christian Drosten: Exactly, then it just has to work. If you want to produce so many cans, the reflex already comes, why not take a simple production route, for example production facilities that are used to produce a polio vaccine, polio vaccine? There are many production facilities there, even in less developed countries. There are also manufacturing facilities that can produce such vaccines - even on the same production cell lines - in veterinary medicine for animal vaccines. It is therefore a consideration that one is asking oneself, a simple dead vaccine, that one could produce in huge quantities in many countries in the world at the same time. But there are also many objections to this - from bad experiences that have been made, especially with dead coronavirus vaccines, because of this immune enhancement of the disease.

Now, however, a Chinese manufacturing plant, Sinovac's name, went there and just did it. This has already been announced in the accompanying scientific literature, for example in journalistic articles in the journal "Science". Now we have the first results on the table. This study describes the accompanying animal experiments to find out if there is such an immune boost. And she says something else too.

In this study it says, phase one, human studies in China are already underway. And why was the decision made? You can see that here in the publication. It has apparently been seen beforehand based on animal experiments that such problems do not arise directly with the vaccine. You made a virus like this and first saw what happened in rodents, first in mice and rats. And you see, these animals get neutralizing antibodies quite well. These mice were vaccinated twice, on day zero and day seven, and then they watched the antibodies increase. And you get considerable neutralizing antibodies in laboratory tests, which are really good values. But now we know that test trials with such preparations in rodents actually always go quite well. And if you started to challenge such rodents with a virus, i.e. to make a stress infection, then you know from experience that they usually go very well. However, this was not done in this study. No rodents have been exposed to a stress infection. For the very simple reason that this virus does not replicate well, or not replicate, at all in rodents.

Korinna Hennig: You only looked at the antibodies.

Christian Drosten: We looked to see if antibodies were coming. Then you went one step further and infected another animal model in which the virus replicated, that is, rhesus macaques, rhesus monkeys. Four animals were vaccinated with a dead vaccine, as you would vaccinate a person: on day zero, seven and 14. So once, then the next week, then a week later. We also know three vaccinations from many dead vaccines in humans. So with many viral vaccines that are dead vaccines, there are three vaccination times. They are not always in week one, two, three. Sometimes they are today, then in 14 days and then again after two months. There are also such gaps. These are empirical values for the respective vaccine.

 

But here the animals were vaccinated in one and the next and the week after next. And overall you have seen very good antibody production, a tired production of neutralizing antibodies. So the level of neutralizing antibodies is lower than in the rodents. But that's not so surprising. Also in humans in the natural infection this is a very low level compared to other infections. And you chose two different cans, that's not important in detail now. But you can say there was a group of monkeys that got more and one that got less vaccine.

What was then done is a stress infection, with an unbelievable concentration of virus, as we as humans in a natural infection will certainly not get. The monkey has been given a million infectious units of the virus with a tube directly into the trachea. This is done under anesthetic in the animals. They are given a brief anesthetic. Then you insert a small tube into the windpipe and put the virus in there. These are very special animal experiments. I have never observed such an animal experiment in my entire career. I didn't even watch it. This is something for specialists in vaccine research who, as the ultimate ratio - if it really matters - do such ape experiments. So not that the listeners think, things like that are constantly being done in research laboratories everywhere. It is really an exception. You can also see this from the fact that only four animals were taken. In experiments in laboratory mice, these are larger numbers of animals, so that one can also make average values.

Korinna Hennig: But there was a control group because you mentioned eight animals at the beginning.

Christian Drosten: Yes, that's right. Of course there are control groups. What I emphasize here is the group that is observed correctly. It just got infected here. What has been seen is that there was clear protection in both the group that received a lot and the group that received little virus - even against this very high exposure dose of virus. So much more than a human patient would get in a natural infection. You could say that in the small dose, in the three microgram group, microgram is a measure of protein concentration, and you could still see a little bit of virus replication. So from the stress virus, but only temporarily, without that having made any illness in the animals. The animals were then sacrificed and dissected. This means that they are killed under anesthesia and the lungs are closely examined and all other organs of the animals, so that precise data can be obtained from these experiments if one sacrifices such animals as monkeys for such a vaccine study. And there it is, the lungs were completely protected while a little virus was still seen in the laboratory test. And in the high dose of the vaccine there was no virus left, not even a hint of a virus replication. There is also no evidence of any immune enhancement in the laboratory. There are clear signs that can be obtained with laboratory tests, i.e. certain immune tests on immune cells. They were made too. No evidence of enhancement in the sense of an antibody-dependent enhancement observation, as has been seen in the past with other such coronavirus vaccines.

Korinna Hennig: So the dangerous reaction of the immune system, the overreaction.

Christian Drosten: Exactly. As a scientist, you can now start criticizing certain details of it. I have not now summarized the full scope of the study. There are secondary aspects that are interesting. For example, one looked: do the neutralizing antibodies that are produced also work against viruses from all over the world? Because in the meantime the viruses have diverged a bit in evolution. Yes, they work against viruses from all over the world. That can also be said here. At the end of this study, you are a bit amazed. I am sure that this will spark discussions in the vaccine development scene, but also in society beyond. You have to take a closer look at that now. It is not necessarily much faster to make a dead vaccine. From a seed virus, from an initial virus to a preparation that could then be used in animal experiments and so on to go into initial clinical trials, that too takes time. But the fact that production facilities for such a vaccine are already very widely available in the world, even in countries that are not so highly developed, there are such production facilities. Such production facilities also exist in veterinary medicine. It's a worthwhile consideration whether you don't want to go this route.

 

Korinna Hennig: That means things could go quickly from the time of approval. We are talking about production, where the decisive advantage can be gained?

Christian Drosten: Starting up to a very large production - many, many million cans, and in many countries at the same time. Not that a manufacturer's vaccine is produced and sold centrally from somewhere in two or three countries, but that many countries are able to produce such a vaccine. The know-how for this is not difficult know-how. Many countries have the knowledge.

Ukratko:

Kinezi rade na jednoj vakcini s mrtvim covid-19 virusom, poceli testove na ljudima u Kini. Prvi rezultati na rezus majmunima pokazali da nece doci do preterane reakcije imunog sistema (sto je obicno problem ovog tipa vakcina) i da se stvori dovojno pravih antitela. Ova vakcina funkcionise protiv svih varijanti covid-19 koje su sada aktuelne u svetu. Prednost ovog tipa vakcine je sto se moze praviti u mnogim zemljama sveta (pa i u zemljama u razvoju), tako da kad dobiju dozvolu onda se moze vrlo brzo nastancovati dovoljno vakcina.

 

o nemackoj vakcini:

Spoiler

Korinna Hennig: The German vaccine that hit the headlines the day before yesterday is about a genetically engineered variant. Is it actually conceivable, sometimes for the layperson, that it boils down to this: in the end we have different approaches and then really different variants of vaccines against the SARS coronavirus-2?

Christian Drosten: In countries like Germany, it will certainly be the case that there will be a whole range of vaccines that may be available at this time next year. Maybe the first ones will be available a little earlier than next year at this time. I do not want to make any precise statements now.

Korinna Hennig: But hope.

Christian Drosten: I'm not a vaccine researcher, that's not my field at all. The virology itself is a bit in the middle of all the problems here. On the one hand, epidemiology to mathematical modeling and on the other hand, vaccine research. These are all special subjects. As virologists we can understand a little bit of everything. But we can’t do everything. So here it will be that there will be different vaccines. And what we have in clinical trials first in Germany is the other side of the spectrum. These are the state-of-the-art vaccines that certainly have a perspective. But where it may not be as easy to say as with a dead vaccine, it can be produced all over the world.

ovo su sofisticiranije vakcine i ne mogu se proizvoditi bas svuda u svetu jer treba posebna tehnologija. Inace, ocekuje da ce biti vise razlicitih vakcina u Nemackoj, od razlicitih proizvodjaca.

 

o ispitivnju T-celija, sto mozda moze dati odgovor zasto neki imaju blazi oblik bolesti a neki se mozda ni ne zaraze:

 

Spoiler

In Charité, you also dealt with one of the big questions in your team. Why are there so many mild gradients? And why do some people apparently do not become infected despite close contact with infected people? At Charité, you looked at the importance of regulatory T cells, which may play a role. So blood cells that serve the immune system. What did you find out? What are the indications?

Christian Drosten: Yes, there is also a special discipline, immunology. This is not the same as virology. We only contributed a little to this study. This is actually Andreas Thiel's laboratory here at the Charité, they did an interesting study. That is, T helper cells were examined for their reactivity to this new corona virus. Firstly, in patients who had just survived this SARS-2 infection. It is expected that not only are there antibodies - this is a department of the adaptive immune response - but that there must also be T cells that indicate cellular immunity, but also influence and improve the ability of antibody formation. They are central to the immune response. But you can't measure them by simple antibody tests. The studies that are discussed in public are simple antibody tests. They have something for themselves, they can be made from large numbers of blood samples in mass throughput. But you can also take a closer look at the adaptive immune response. This is what immunologists do using T cells, T cell studies.

What is done here: Pieces of the SARS-2 virus are artificially produced in the laboratory - peptides, we say. These peptides are of a size that is suitable for covering certain structures on the surface of the T cells and being recognized by these T cells so that they begin to send signals. These signals are measured in a laboratory test. The reactivity of these T cells can actually be expected when you have this disease behind you.

What was also asked in the study is: What about patients who have not yet had this disease? So for T cells that were collected from patients before this epidemic. And surprisingly - or perhaps not so surprisingly for many who are familiar with it - it has been seen that 34 percent of the patients have reactive T cells, although these patients have never been in contact with the SARS-2 virus. Now it is possible to predict these T cell stimulating sections of such a virus. And you can compare them to similar sections in other viruses, especially human cold corona viruses. There are four of them. And that has been done. In fact, it has to be said that there are such sections in the human cold corona viruses. They could stimulate such T cells and at the same time they are to some extent consistent between the common cold coronavirus and the SARS-2 virus.

 

Korinna Hennig: Does that mean that an explanation could be what is going on under the keyword background immunity? If I have been infected with another corona cold virus, can it also protect me from infection with the SARS-CoV-2?

Christian Drosten: Yes, as you say, that's exactly right. It can be. It is not the case that one can say: We have observed this phenomenon, i.e. this possible background immunity, in this study in 34 percent of the patients, so 34 percent of the population are immune. So we can subtract the number from our 70 percent of the population who have to become infected. So it is clear that the pandemic is over earlier, hooray.

Korinna Hennig: That would be nice.

Christian Drosten: It's not like that. This is a typical fallacy. We may have to imagine that this is already priced in, as stock marketers would say. The fact is that we observe that although this is a virus that many people die from, there are also many mild or even completely unnoticed cases. We also need to find explanations why these cases are so mild. One explanation could be that the mild cases may have received less virus at the beginning of the infection. Or overall they are in a better constitution. You can put it all together. Maybe that's all true. But this influence, which we are now discussing, is likely to add to this: that there is a certain background immunity in the population. But that doesn't change the number of patients who die. Because the number of patients who die is an observation of reality. In this reality there is already a background immunity. But now we are beginning to recognize this part of reality.

Korinna Hennig: But that can be an explanation for the individual. So if I live in a household with four other people in a family and two just don't become infected, even though others are infected, then it may stay that way.

Christian Drosten: Exactly. Even at this so-called secondary attack rate, where we make the observation, that's maybe 15 percent who are infected in the household in one observation period. One of the explanations why the rest is not infected could be that they have some background immunity. But there are certainly other reasons. Maybe they didn't have that much contact in the infectious time. Or it was no coincidence that they got an infectious dose from the virus. If one extended this observation period by imagining that the infectious time for the first patient would be longer, then they would still get infected. All such statistical effects are certainly also important.

It can only be that this T cell immunity also provides protection. For example, we recently discussed this good study in the Italian village where half of the patients were already infected, but they were completely asymptomatic. There, too, one could look for an explanation that these might be patients with background immunity. However, it must also be said that it was another finding in this study that symptomatic and asymptomatic patients excrete and pass on the same virus concentration, so that this is probably unrelated to the infection process.

I have to say something else. There are cases where there is even a T-cell reactivity that is in the background, disease-enhancing and not disease-protecting. You can't say that here either. It is just a very interesting immunological observation at the moment. The first observation made in this direction worldwide and a very good basis for further elucidating this in the context of observational studies. Now it is clear, the technology is in place, we can do it now. And now we can start asking questions. For example, ask: If we know there is a family and we have collected these T cells from the whole family. Now the virus is coming and we ask ourselves: Who is actually infected? Then you can go back to the stored samples and ask: He got infected, what did the T cells look like at the time? And the other one wasn't infected. What did its T cells look like? An example of a study approach that is now possible.

 

Korinna Hennig: But if we think about it from an individual point of view: If I'm in the family and the father has become infected, two children may even have been infected with mild symptoms. But not the mother. Can I assume that if such an approach is actually confirmed, it will not get it anymore? She can then visit her grandparents again at some point, even though she hasn't gone through the illness. Or is that entirely hypothetical?

Christian Drosten: It can be, but it can also be that she gets it, just has no symptoms. It is also possible. We are already thinking in the direction that this pre-existing T cell reactivity even helps to produce antibodies particularly well and quickly. We have a wide range of antibody production there too. Some patients produce very high levels of antibodies or titers, and some do not have as high at the same infection load. This variation could also be explained by pre-existing background immunity. This could also explain the very wide range of variation in the neutralizing antibodies. It could be that patients with pre-existing antibodies generate neutralizing antibodies in a better and faster way.

Korinna Hennig: But when it comes to the question of whether you can be a carrier, has that not been finally clarified?

Christian Drosten: Not at all. Not at all. I also say this a little to prevent such studies - including this study here - from being misinterpreted. It is not the case that such simple scientific information can always be used to infer something about the course of the epidemic and the fate of the pandemic in Germany.

 

 

Ukratko: otkrili su da t-celije iz uzraka krvi ljudi koji se nikada nisu sreli s covid-19 (uzeti pre pojave virusa) u 34% slucajeva su reagovali na virus. Ovo moze da znaci da mozda ti ljudi imaju neki osnovni imunitet, odnosno da ce brze reagovati na pojavu covid-19 pa ce imati blazi oblik bolesti. Ali moze da znaci i da ce prejako reagovati. Ne zna se jos. Za sada su samo utvrdili da neki ljudi imaju t-celije koje reaguju na covid-19 iako nisu bili zarazeni njime. Dalja istrazivanja slede.

evo je studija:

https://www.medrxiv.org/content/10.1101/2020.04.17.20061440v1

 

 

[ciao]

Institut Pasteur je objavio rezultate svojih analiza koje rade na prvom "klasteru" u Francuskoj, to je jedna gimnazija u blizini Pariza (na severu) gde je jedan profesor bio medju prvim zrtvama jos u februaru. Napravili su ispitivanje na dobrovoljcima : iz gimnazije - ucenici i profesori a i njihove familije - ukupno 661 osoba (320 ucenici i profe i 341 njihove familije). Rezultat je da je oko 40% u grupi ucenika i profana bilo zarazeno, medjutim interesantno da je medju njihovim familijama bilo samo 11% zarazenih, sto je vrlo neobican rezultat, kao da izvesni ljudi imaju vec neki imunitet, nemaju pojma zbog cega.

 

Inace i ovo istrazivanje je pokazalo veliku razliku izmedju pusaca i nepusaca ( oko 4 puta vise medju nepusacima). Francuzi se izgleda skroz izbezumili zbog uticaja nikotina, navalili da kupuju nikotinske patcheve, sad su ih povukli iz apoteke iz slobodne kupovine i stalno upozoravaju da nepusaci ne treba da koriste patcheve nikotina kao prevenciju jer nikotin ima i negativnih dejstva a pogotovo cigarete itd

 

 

Edited April 25, 2020 by ciao

[Tomiprunet]

Sve je to super ta istrazivanja, ali i jos jednom da napisem, da bi se to trebalo objavljivati u nekim specijalizovanim sajtevima, ne da bude dostupno svima kao informacija. Nista jos nije potvrdjeno, i vidite ljudi navalili na nikotinske paceve, pa onda na hlorokin, pa na ispijanje tecnosti za dezinfekciju, .... Umesto da su ljudi postajali sve pametniji oni postaju sve gluplji i gluplji.

 

[Jataganac]

https://www.jpost.com/health-science/israeli-covid-19-treatment-with-100-percent-success-rate-tested-on-us-patient-624653?utm_source=jpost&utm_medium=facebook&utm_campaign=boost&utm_content=04-14-20

 

[Mama_mia]

4 hours ago, I, Ja Sam Laki said:

i vidite ljudi navalili na nikotinske paceve, pa onda na hlorokin, pa na ispijanje tecnosti za dezinfekciju, .... Umesto da su ljudi postajali sve pametniji oni postaju sve gluplji i gluplji.

 

 

pa ne moras bas ni da budes mnogo pametan da bi znao da nije normalno ispijati/ubrizgavati nekakvu wc dezinfekcionu tvar

dovoljno je da se bude `odlepljen`, onda gutas svasta...tako i savete cime da se lecis...

 

nego ovo sam htela da nalepim, oko simptoma misleci da pise nesto sto nismo znali od pocetka, ali znali smo,

zar nismo?

 

As part of its efforts, the Center for Disease Control and Prevention in the United States (CDC) published six new symptoms to the list of possible signs of infection with the coronavirus.

The new signs, which were determined following the gathering of much information from doctors about the patients' reports of the disease, have been added to the list of symptoms reported in recent months - fever, cough and shortness of breath.

The agency is now adding another six possible symptoms of the coronavirus, so that the complete list is: fever, cough, shortness of breath or difficulty breathing, chills, repeated shivers from chills, muscle pain, headache, sore throat and loss of taste or smell.

The document also states that rashes often appear along with the disease, but nonetheless sneezing is not yet considered a symptom of the virus infection.

"People with COVID-19 have reported a wide range of symptoms - from mild symptoms to severe illness," the CDC website states. According to the agency, each of the nine symptoms of the updated list will most likely appear 2-14 days after exposure to the virus.

 

 

 

[wwww]

19 minutes ago, Mama_mia said:

nego ovo sam htela da nalepim, oko simptoma misleci da pise nesto sto nismo znali od pocetka, ali znali smo,

zar nismo?

 

 fever, cough, shortness of breath or difficulty breathing, chills, repeated shivers from chills, muscle pain, headache, sore throat and loss of taste or smell.

The document also states that rashes often appear along with the disease, but nonetheless sneezing is not yet considered a symptom of the virus infection.

"each of the nine symptoms of the updated list will most likely appear 2-14 days after exposure to the virus.

Da, ovo smo sve znali vec nekoliko sedmica, ako ne i citav mesec.

[Sunshine State]

https://www.ncbi.nlm.nih.gov/pubmed/32252338

 

https://clinicaltrials.gov/ct2/show/NCT04344041

 

Vitamin D supplementation is mentioned as a potentially interesting treatment for SARS-Cov-2 infection but on a scientific basis with a low level of evidence until now.

We hypothesize that high-dose vitamin D supplementation improves the prognosis of older patients diagnosed with COVID-19 compared to a standard dose of vitamin D.

[handys]

https://www.acsh.org/news/2020/04/24/why-failure-remderivir-deeply-disturbing-14743

[Angelia]

4 minutes ago, handys said:

https://www.acsh.org/news/2020/04/24/why-failure-remderivir-deeply-disturbing-14743

Ovo jeste veliko razocarenje jer se racunalo da je to sigurica.

[Angelia]

Interesatna ideja, i kontra argumenti:

 

That process could get a push from the Israeli study, which surfaced this week on MedRxiv, a website where researchers share their preliminary work.

Matthew Liao, who directs the Center for Bioethics at New York University, said the impulse to find a shortcut out of the pandemic is entirely reasonable.

“But it’s a bad idea,” he said of the Israeli proposal. To embrace such a strategy as a way to lessen the population’s economic suffering “is a bit of a false dilemma,” he said. Beside risking lives to engage in a population-wide medical experiment, “there are a lot of other ways to reduce the economic impact” of a prolonged campaign of social distancing, he said.

In an actual controlled avalanche, safety experts engineer the periodic release of a mountainside’s buildup of snow to keep the valley below from becoming entombed.

In the coronavirus version, the Israeli researchers propose to recruit waves of healthy volunteers in their 20s, 30s and 40s who are willing to be deliberately infected. In numbers that never exceed Israel’s healthcare capacity, the volunteers would weather any symptoms, recover, and rejoin a growing population of immune compatriots. The rest of the country would remain locked down.

If 80% of eligible Israelis sign up to be infected, virtually all of these “controlled avalanche” graduates would join the ranks of those who recovered from unintentional infections, the authors calculate. Applying age-specific death rates tallied in Wuhan, China, to Israel's population, the team estimated that 2,540 of those volunteers would die from COVID-19. But within roughly 200 days, they say, somewhere between 40% and 71% of Israel’s population of 8.9 million would gain immunity from the virus the old-fashioned way.

At that point, the coronavirus would run up against so many immune Israelis that its spread would virtually stop. This collective state of herd immunity would protect those, including the old and vulnerable, who had stayed at home as the controlled avalanches tumbled down outside.

Compared to a strategy in which all Israelis are urged to stay inside and practice social distancing, the controlled avalanche strategy would reduce overall deaths by 43%, the researchers calculate. The benefits of herd immunity after the lockdown ends would save the lives of Israelis who are more vulnerable to the virus. And that point would come faster, cutting deaths further.

Cumulatively, implementing a controlled avalanche strategy would drive down the maximum number of people who need intensive hospital care by 62%, the study authors said. And half of the people at low risk of becoming ill could leave their homes and go back to work two months earlier.

“Implementation of the controlled avalanche policy is thus the safest among all the possible options,” the authors conclude.

Johns Hopkins University bioethicist Jeffrey Kahn said the new research is problematic because it relies on facts about the virus’ behavior and impact that are still in dispute.

The idea that those between 20 and 49 would die of COVID-19 in such small numbers has been countered by later studies and by many case reports, Kahn said.

So has the belief that reinfection doesn’t happen after a person has recovered. One study released this week suggested that as many as 30% of those who have recovered produce very low levels of protective antibodies, and in 10% of cases the levels were too low to be detectable, calling their immunity into question.

The World Health Organization went further in a scientific brief released Friday. Pushing back against proposals by some countries to issue "immunity passports" to those who have recovered, the WHO warned that even people with coronavirus antibodies may be vulnerable to a second infection.

Researchers are a long way from having the data in hand to pinpoint the level of population immunity necessary for the pandemic to fizzle, Kahn added.

 

https://news.yahoo.com/could-controlled-avalanche-stop-coronavirus-212135278.html

[Jataganac]

Cjepivo za koronu na tržištu u listopadu? Indijci ga proizvode i neće ga patentirati

 

https://www.index.hr/mobile/clanak.aspx?category=vijesti&id=2178236

 

 

[Sunshine State]

Nasi lekari na poslu pisu:

 

One thing I heard from my discussion with friends who are treating patients in ICU: Intubation seems to be causing more lung damage and scaring, while early proning + hyperbaric oxygen seems to help with recovery.

[ciao]

Institut Paster (Pariz) napravio test za antitela i to test koji pokazuje kolika je otpornost pojedinca na virus tj imunitet tj koliko su antitela koja pojedinac ima ako ih ima efikasna - postoje tri nivoa tj odgovora na test - nezasticen, slabo zasticen, vrlo zasticen; Ne mogu da kazu ni za koga da je sto posto zasticen; u  dosadasnjim testiranjima se pokazalo 98% pouzdano. Test jos uvek nije spreman za masovnu prozivodnju; treba da prodje jos poprilicno overa itd. Za slucaj da virus mutira, sve ispocetka

Edited April 27, 2020 by ciao

[handys]

https://theness.com/neurologicablog/index.php/hydroxychloroquine-not-looking-good-for-covid-19/#more-12010

[Angelia]

Aj sad svi u apoteke za Pepsid  Salim se naravno, nemoj da me neko ozbiljno shvatio

 

Over the past few weeks researchers have been discreetly studying a new potential treatment for COVID-19 -- and it might not be what you expect.

The treatment in question is called famotidine, and it's the active ingredient in Pepcid, an over-the-counter medication commonly used to alleviate heartburn.

Since March 13, researchers at Northwell Health, a network of hospitals in New York, have been enrolling patients hospitalized with COVID-19 into their study of famotidine, which is being delivered through an IV in megadoses nine times greater than the typical over-the-counter dose. The drug is being given in combination with the much-touted antimalarial hydroxychloroquine.

Researchers said some data on safety will be available "in a few weeks," but did not say when data will be available showing whether the drug combination is effective.

 

https://news.yahoo.com/popular-heartburn-medicine-being-studied-treatment-coronavirus-024500582.html

[Sunshine State]

2 hours ago, Angelia said:

Aj sad svi u apoteke za Pepsid  Salim se naravno, nemoj da me neko ozbiljno shvatio

 

Over the past few weeks researchers have been discreetly studying a new potential treatment for COVID-19 -- and it might not be what you expect.

The treatment in question is called famotidine, and it's the active ingredient in Pepcid, an over-the-counter medication commonly used to alleviate heartburn.

Since March 13, researchers at Northwell Health, a network of hospitals in New York, have been enrolling patients hospitalized with COVID-19 into their study of famotidine, which is being delivered through an IV in megadoses nine times greater than the typical over-the-counter dose. The drug is being given in combination with the much-touted antimalarial hydroxychloroquine.

Researchers said some data on safety will be available "in a few weeks," but did not say when data will be available showing whether the drug combination is effective.

 

https://news.yahoo.com/popular-heartburn-medicine-being-studied-treatment-coronavirus-024500582.html

 

Kako uopste dodju na ideju da probaju, recimo, bas famotidin, bas hlorokvin, bas copaxone....?

Ako pricamo o famotidinu, leku iz grupe histamin-2 blokera, sto ne probaju, recimo, ranitidine ili cimetidine?

 

[Angelia]

2 minutes ago, Sunshine State said:

 

Kako uopste dodju na ideju da probaju, recimo, bas famotidin, bas hlorokvin, bas copaxone....?

Ako pricamo o famotidinu, leku iz grupe histamin-2 blokera, sto ne probaju, recimo, ranitidine ili cimetidine?

 

I ja se to pitam sve vreme dok objavljuju sta sve pokusavaju.

Racunam da znaju nesto o virusu sto mi ne znamo, od kako su mu provalili kod. A drugo verovatno da iz predthodnih iskustava znaju odlike corona virusa pa pokusavaju stvari koje su vec predpostavljene.

[Sunshine State]

1 minute ago, Angelia said:

I ja se to pitam sve vreme dok objavljuju sta sve pokusavaju.

Racunam da znaju nesto o virusu sto mi ne znamo, od kako su mu provalili kod. A drugo verovatno da iz predthodnih iskustava znaju odlike corona virusa pa pokusavaju stvari koje su vec predpostavljene.

Ma ok, ovi "viri" lekovi, to je jasno zbog njihovog antivirusnog dejstva....ali, imamo 3 common H2 blokera, i oni probaju famotidine...

[Angelia]

Just now, Sunshine State said:

Ma ok, ovi "viri" lekovi, to je jasno zbog njihovog antivirusnog dejstva....ali, imamo 3 common H2 blokera, i oni probaju famotidine...

Pa objasnjavaju u textu da smatraju da ce velike kolicine da "skrenu paznju" virusu, otkud znam, dal ce mase crvenom maramom 

Samo sad cekam navalu u apotekama

[Sunshine State]

11 minutes ago, Angelia said:

Pa objasnjavaju u textu da smatraju da ce velike kolicine da "skrenu paznju" virusu, otkud znam, dal ce mase crvenom maramom 

Samo sad cekam navalu u apotekama

 

Sad cu malo da pretrazim net da vidim sta kazu koji je to mehanizam dejstva famotidina, a sto ne drugi H2 blokeri

[ciao]

1 hour ago, Sunshine State said:

 

Kako uopste dodju na ideju da probaju, recimo, bas famotidin, bas hlorokvin, bas copaxone....?

Ako pricamo o famotidinu, leku iz grupe histamin-2 blokera, sto ne probaju, recimo, ranitidine ili cimetidine?

 

Za hloroquin znam da su ga kinezi u Wuhanu koristili i navodno smatrali ga najuspesnijim od raznih lekova koje su pokusavali. Mozda su ostali ti koje navodis?

 

Mozemo na spisak da dodamo i biljku artemisia - najnoviji lek otkriven i zvanicno proklamovan kao lek za covid na Madagaskaru - to je koliko sam shvatila prirodan lek tj caj od biljke artemisia koja raste na Madagaskaru a i jos negde valjda. Zasto artemisia : - za vreme rata u Vijetnamu sa obe strane se umiralo izgleda vise od malarije nego od rata, onda su ameri poceli da koriste chloroqin i malarija im vise nije bila problem a vijetnamci su umirali i dalje masovno od malarije, onda su im kinezi rekli da od biljke artemisie prave caj i da to leci od malarije - izgleda btw da je tacno. Elem, kad su na Madagaskaru culi da je chloroquin lek za coronu naravno logicno je da je onda i artemisia,; Znaci caj od artemisia = lek za koronu zvanicno na madagskaru. Pretpostavljam da nema sekundarnih efekata jer je samo caj a koliko leci - to niko ne zna jer valjda na Madagskaru i nema corone. Oni su pokusavali da ubede francuze da proglase artemisia za lek za koronu i da ga zajedno prave, tj unovce ali za sada nista od toga

Edited April 27, 2020 by ciao

[Angelia]

Evo sad ovo

It came as new results from antibody testing revealed that 24.7 percent of New York City residents tested positive. 

If accurate, it means that more than 2million of the city's 8.4million population have become infected, and that the death rate - when calculated using the 11,460 confirmed COVID-19 deaths, is 0.5 percent. 

 

Pa  znaci NYC je najblizi heard immunity.

 

Sve ovo sa testiranjem na antibodies nas dovodi do cinjenice da virus i nije tako smrtonosan.

[Angelia]

16 hours ago, Sunshine State said:

 

Sad cu malo da pretrazim net da vidim sta kazu koji je to mehanizam dejstva famotidina, a sto ne drugi H2 blokeri

Sta sam rekla? Danas CVS i Amazon, prijavili vec da Pepcid leti sa rafova, i dolaze u opasnost nedostatka.

[Angelia]

Six monkeys given a vaccine developed by the University of Oxford are said to be coronavirus-free 28 days after sustained exposure to the virus.

The result is a promising early sign for the vaccine, which is also undergoing human trials. A working human version, however, remains months away even in the best-case scenario.

 

https://news.yahoo.com/6-monkeys-given-experimental-coronavirus-094138199.html

 

A potential coronavirus treatment just suffered a setback, as researchers narrowed a clinical trial of the drug Kevzara after an early review of how the treatment was working.

The early look at study data led researchers to change the study to exclusively focus on critically ill coronavirus patients. The drugmakers Regeneron and Sanofi are testing Kevzara, an arthritis drug, against COVID-19, the disease caused by the novel coronavirus. 

......

Researchers are also testing a similar treatment from Swiss drugmaker Roche, called Actemra. Both drugs have the same target, called the IL-6 cytokine. Roche's study began enrolling patients earlier this month, with results expected in early summer.

https://news.yahoo.com/potential-coronavirus-treatment-just-suffered-134800624.html

 

 

[wwww]

16 hours ago, Angelia said:

Evo sad ovo

It came as new results from antibody testing revealed that 24.7 percent of New York City residents tested positive. 

If accurate, it means that more than 2million of the city's 8.4million population have become infected, and that the death rate - when calculated using the 11,460 confirmed COVID-19 deaths, is 0.5 percent. 

 

Pa  znaci NYC je najblizi heard immunity.

 

Sve ovo sa testiranjem na antibodies nas dovodi do cinjenice da virus i nije tako smrtonosan.

Do ovog rezultata su dosli tako sto su testirali ljude na koje su naisli na ulici (oni koji su isli u supermarket ili na posao itd.). Mislim da im izorak nije reprezentativan (cula sam/procitala i takav komentar negde) jer je za pretpostaviti da je % onih koji su prelezali covid-19 a koji su zabarikadirani u kucama  (ukljucujuci i decu), ipak znatno manji.

 

Ja cekam rezultate neke studije u Minhenu, gde bi trebalo da su ispravno odabrali uzorak od 3000 ljudi za isti tip testiranja (na antitela).

 

Inace, u Nemackoj nisu radili obdukcije preminulih od covid-19 do sada (RKI preporucio da se ne rade da bi se zastitili oni koji vrse obdukciju). Do sada su samo u Hamburgu i delimicno u Lajpcigu odradili neke obdukcije. Izostanak obdukcija je kritikovan, posto se propustilo da se bolje upozna bolest i kako ona utice na pojedine organe. Sad je RKI promenio misljenje i od sad ce se raditi obdukcije, ali jos nisu osmislili neki plan da saveznom nivou (nadam se da ce neko ipak sve ovo da koordinira, kao i  da ce svi relevantni lekari imati pristup dobijenim rezultatima).

Edited April 28, 2020 by wwww