Sunday, April 12, 2020
pregnant women have fewer places to go to deliver their babies. #coronaupdatesindia
With many hospitals across #mumbai halting admissions, shutting their OPDs over coronavirus fears or treating COVID-19 patients only, pregnant women have fewer places to go to deliver their babies.
#coronaupdatesindia #CoronaInMaharashtra #coronamumbai
A coronavirus expert from KU predicted this pandemic—here’s what he says will happen next
A coronavirus expert from KU predicted this pandemic—here’s what he says will happen next
Until recently, KU professor Anthony Fehr was one of about 100 people studying coronavirus full-time
“I had a lecture on coronaviruses last semester, in the fall, before this all happened,” he says. “I knew that there’s a lot of SARS-like viruses in China that this could happen. So I actually had a slide in my lecture that was like, ‘there are lots of SARS-like coronaviruses, we could have another outbreak within our lifetime.'”
“So I basically, you know, predicted something,” he says. “I guess I was conservative on the timeframe. But I posted that to my Facebook and everybody’s like, ‘pretty crazy!'”
Right now, Fehr is working to research conserved proteins within coronaviruses and trying to develop compounds that could inhibit them.
“We’re several years away from having anything that can be used to humans, though,” he says. “So I’m pushing my research for the next outbreak.”
And to hear Fehr tell it, there likely will be another outbreak of a coronavirus like the one currently roiling the world.
Will there be a vaccine for the novel coronavirus? Will we one day get coronavirus shots like we get flu shots? What is China’s connection to this outbreak and previous ones? Why is the disease called COVID-19 instead of SARS?
Fehr was generous enough to give us a half-hour of his time to answer these and many other questions. Some of the information is a little dense, as you might expect from one of a handful of the most knowledgable people in the world on this subject. But Fehr’s perspective is something you’ll want to hear.
Here’s a transcript of our interview, which has been edited for length and clarity.
Kansas City magazine: Can you just kind of give me a little bit of background on how you came to study the coronavirus and the typical career path of a virologist?
Dr. Anthony Fehr: I started working on coronaviruses back in 2012. Just to give you a sense of normally how academic researchers progress: We do our graduate work at one university, and when I was in graduate school, I worked on cytomegalovirus, which is a whole other virus. When you finish grad school, you go on to what’s kind of a kind of an internship where you find a lab that you want to work in for a period of several years. And then, hopefully, you do well enough there that you ultimately get some other place to like you enough that you get your own laboratory. So I went to Dr. Stanley Perlman’s lab at the University of Iowa, mostly just because I’m a trained virologist and his lab seemed very interesting. They had actually been working on coronavirus since the ’80s. It just seemed like a good lab and a good fit for me, so that’s where I did my post-doctoral work.
At the time, it was kind of iffy in terms of funding because the original SARS outbreak occurred in 2002. The money from that was starting to wane. And so there was definitely a little bit of, ‘This could be a tough career road to go down if there are no other coronavirus outbreaks in the near future.’ Well that year, actually, MERS coronavirus came out. Now with this one, the funding situation seems like it will be a lot better going forward.
I would imagine you will never worry about funding again for the rest of your career. I know that coronavirus mostly comes from animals, specifically bats. Do you mostly study animals?
I more or less study the virus. A lot of our studies are, you know, geared toward viruses in human cells. So what we do is we take these little, you could say, petri dishes. We put in human cells, and then we study how the virus replicates and that kind of thing.
But we also do quite a few mouse experiments as well. So we kind of do a combination of those. A lot of human viruses we actually have mouse models for.
From doing a little bit of reading about this, one thing that really struck me is that the ‘non-alarmist’ take was ‘It’s the flu, bro.’ You heard people saying early, and it’s, of course, not true. But from what I understand coronavirus can be the common cold—which we’ve had no ability to tackle throughout history.
So, I’ll explain that. There are a lot of different viruses that cause the common cold. Coronaviruses account for about ten to twenty percent of the common cold cases each year. And there are four different coronaviruses that can cause the common cold. So you’ve likely been infected with a coronavirus before—that is true.
And so the difference between our cold viruses and then viruses like the flu and then this SARS coronavirus 2— and SARS originally—is that the cold viruses generally get into our upper respiratory tract and that’s about as far as they go. They don’t really go any further, they kind of get in there, and cause you to cough a little bit, to sneeze, maybe give you a headache or those kinds of things. But what’s different about these viruses, they can go into the lower respiratory tract, and when they get in there and start replicating really aggressively, that can really affect your ability to breathe. And it can actually cause a lot of other damage.
So this virus is definitely not just a cold virus.
A lot of people are going to be asymptomatic, or have mild symptoms. And for those people what’s probably happening is that they’re basically controlling the virus before it gets into the lower respiratory tract.
And that’s because of antibodies they have from battling colds over the years?
No, that’s, that’s actually incorrect. The antibodies directed against the cold viruses will not be able to do anything against this virus. Probably what it is: Most healthy individuals have what’s called an innate immune response, which is where you don’t necessarily need to have previously seen this.
We all have pretty strong defenses—our cells have a lot of you know, just regular defenses that they can have all viruses. And in younger, healthy people, those defenses oftentimes are good enough to stop the virus before it gets going. Or at least delay it long enough before we can develop our own antibodies against this virus.
Oh! And so one reason that children are doing so much better with this might be that while they don’t have as many antibodies, they do have better innate defenses, because that’s kind of a way that their bodies are set up since they don’t have all those antibodies yet, but they have a more aggressive innate response?
Yeah, I mean, that’s a bit of an oversimplification. But I think, in general, you can say that the immune system between young and middle-aged people that are doing fine here is different from elderly people. Elderly people have a diminished immune response and it’s often dysregulated.
On my Twitter page, there’s a recent article quoting a lot of work from my old boss, Dr. Stanley Perlman, who had a lot of comments about what the differences could be in children.
Until I read about this, I didn’t really understand the progression of SARS. I’ve always seen this referred to as COVID-19. But now technically it’s called SARS-CoV-2, right?
Well, let me explain the naming, which is very confusing, and I kind of hate it. So, on the same day, we named two things. There’s the disease, which is COVID-19. And then there’s the virus, which is SARS-Coronavirus-2. They are distinct.
If you had the disease, and you say, ‘I had COVID-19’ that means you got a disease and you have a poor respiratory function or something like that. If you got the virus, SARS-CoV-2, that could mean a range of things. You could have no disease, you could have COVID-19. So COVID-19 is a disease whereas the virus is SARS Coronavirus-2.
It is odd. Going back 20 years to the SARS outbreak: SARS coronavirus was the original one, but the disease was named just ‘SARS.’ So, they named the virus, basically SARS coronavirus. And the disease was again Severe Acute Respiratory Syndrome—that’s what SARS stands for. And that’s the disease.
The disease caused by this virus is almost identical to SARS, so why we need to name it a different disease, I’m not quite sure. It could have easily just been called SARS as well. Because that’s what it is: It’s a Severe Acute Respiratory Syndrome.
Is the similarity to SARS something that we only learned later, or from the moment they were working on this were they saying, ‘Well, this is basically SARS?’ It seems like the major difference is that this spreads even more quickly?
In terms of the transmissibility of the virus, it is seemingly a lot more transmissible than the original SARS. But, yeah, as soon as we had the sequence of this virus, we knew that it was fairly closely related to SARS.
Getting into the sequencing. I know nothing, but from what I’ve read a lot of this stuff does tend to start in China because of the way humans and animals interact there and that’s where the genetics come from, so China is where a lot of the sequencing stuff actually happens. I was reading a Malcolm Gladwell story from the New Yorker story published in 1997 about the Spanish Flu and it mentioned Wuhan, and I’m like, “whaaaat?” I guess the current thinking is that the Spanish Flu of 1918, they think, actually originated in China. Not to politicize it or get into the racist, imperialistic ideas but as I understand it most of this work in virology involves China because of how humans and animals come into contact there. Does your work involve things that are happening in China a lot?
We don’t know exactly how this virus got into the human population, right? It’s clearly descended from a bat population—and what we do know is that there are a lot of coronaviruses in bats and a lot of SARS-like coronaviruses similar to this one and the original SARS. There’s a lot of viruses in bats in China. China has a lot of really amazing caves that are very important dwelling places for bats. Having said that, there are clearly coronaviruses in African bats—I think I saw a report where there was an Australian one. So it’s not totally just China, but there are a lot of bats with coronaviruses there.
Now, yes, the virus likely transmitted into some sort of wild animal and, yes, the fact that they do eat and sell wild animals—it could have contributed to this. But that’s also not clear, either. If we had bats with coronaviruses here, that could easily happen in the United States because we have close contact with animals. The virus might transmit in their feces or whatever. Who knows—your cat or some other animal that you interact with could certainly become infected with a virus if we had the same situation here.
So the wet animal markets are not the issue?
I think they might have possibly have contributed here. But I was talking to people that, you know, go to China a lot and that’s a pretty rare thing in China. Actually, they don’t have a lot of these wet animal markets, the vast majority of people there just go to the store, they don’t actually go to these markets. But it could have been one or two people that did it and, you know, started this outbreak.
So, compared to the original SARS, what are we doing right this time? And what did we do wrong? How is it different in the original SARS outbreak?
With the original SARS outbreak, China was less than forthcoming about telling the world that there was an outbreak. The technology also was dramatically slower back then, so we didn’t know what the virus was in that case—and I would have to say, “we” with quotation marks because I was barely in college at that time. But you can imagine the sequencing technology and the speed at which these things can get done or just is somewhat greater today than it was in 2000.
So, the great thing that happened here is that we got the sequence immediately, we could develop diagnostic tests very quickly. And considering the speed at which the virus transmits through the human population, had we not had that, China might have had quadruple or ten times more cases than they actually had—if not more that. That was a great thing. They were able to basically stop this outbreak.
What we’re not doing? It’s hard to say because, you know, there are a lot of hard decisions that have to be made when you talk about forcing quarantine and forcing people to stay in their houses and canceling lots of events, and I don’t know if I would have made the right decisions at the end of the day. But you look back at it probably the moment this virus got out of China and into some of these other countries and it was more than just a couple of cases in these other countries, we should have probably shut down our borders to any international travel. I don’t know if that would have solved it, because this virus is extremely tricky to stop from spreading. We don’t really have a clue how many people are actually infected in this country right now. I look at the numbers every day, and it’s like, there’s 10,000 now, but it could easily be five times that many—or more.
Yeah, I mean, that I find those numbers to be a little bit funny. I remember someone in Ohio said, ‘Well, actually, we probably have 100,000 cases,’ but every case is being reported by the media as ‘There’s a new case in Jackson County!‘ I obviously have no idea, but it seems possible that there are several thousand cases in Jackson County right now. Because you know all of these things that other people don’t know, what do you do that most people don’t do in your daily life? Do you wash your hands for 40 seconds?
I probably do the same thing as everybody else does. I mean, I guess I’m concerned about it. But at the same time, you know, these things are really hard. You spend your whole life like doing all these cleaning things, and it’s still not a guarantee.
Do you think you’re going to get it? I mean, are we all going to get it?
That’s a great question. And—I don’t think we will. Even if you multiply the number of cases in China, by ten, that’s still less than one percent of their whole population. So even if they underestimated their numbers by ten, that’s still probably like, maybe like a percent of the whole population. So, that indicates that the large majority of us may or may not get it, you know, depending on how effectively we can stop it through the current measures. And so, we’ll see.
And I’m hopeful that perhaps this will kind of diminish with the season as the other coronaviruses do. I would not guarantee that—that’s certainly not something that’s guaranteed by any stretch of the imagination. But I’m hopeful that will be the case and that we’ll have time to maybe get a vaccine out by the time we hit cold season next year.
The common cold, unlike the flu, is basically impossible to develop a vaccine for because it changes so quickly. Isn’t that something that we have to worry about with this?
So, as I said, coronavirus counts for about twenty percent of common colds but the vast majority of the other cases are what are called rhinoviruses. Rhinoviruses mutate very rapidly and you can’t really make a vaccine against those things.
Coronaviruses don’t mutate quite as rapidly. They still mutate rapidly, but they don’t move quite as rapidly as other RNA viruses, because they have what’s called “proofreading.” So they can actually “proofread” their genome when they make new copies, for errors.
Now, that’s not a foolproof system. They’re still going to make mutations. It’s not clear how long a vaccine would work—it could be like a flu where you have to kind of take the current strain and take your best guess at it. But at the same point, I don’t think it’s going to be an every year type of thing. It might be that it’s every five years or something like that, that you’ll see that your immunity might wane to this virus.
At the very least, it might have some partial immunity that can mitigate and take the lethality rate down from three or four percent to a more manageable number.
So do you think that getting a coronavirus shot is going to become like getting a flu shot after this?
Probably not. You know, these highly lethal coronaviruses are zoonotic events. We don’t have one like the flu that goes around every year. Maybe this one will become that—we really don’t know. This SARS Coronavirus-2 could be one of those that mutates enough that it reoccurs every year, or maybe every two or three years, and because it transmits so well we can’t really ever get rid of it. That’s certainly a possibility. The other possibility is we get a vaccine, it sort of goes away, and then we’re waiting for the next one.
And that is something that will happen again because there’s just so much genetic material out there in all of these bat populations around the world, if I understand correctly.
I think it’s likely. I think based on what happened this year they’re going to start really regulating markets in China. Again, a lot of this is just chance. And you know, maybe it’ll be five years from now, maybe it’ll be 50 years from now.
Something a lot of people don’t know that there was a big outbreak of a coronavirus just two years ago in China, in pigs. There was a pig virus that emerged from bats. Bats actually infected pigs and that moved into the pig population in China. Just two years ago.
So, again, that just re-emphasizes that this happens somewhat frequently.
I know from reading about past pandemics like the Spanish Flu that the second wave—when it comes back either slightly mutated or when people have their guard down—has been one of the tougher times.
I’ve never heard of that—the second wave being worse. It’ll be interesting to see how this happens. Will it come back? If it does go away during the summer—and that’s a big ‘if’—when does it come back, does it come back with basically the same sequence, so if you already had it you’re gonna be completely immune? Or will you only be partially immune? How many people will not get it because they had it asymptomatically that we just don’t know about? So there’s a lot of questions that come about from that.
Are they getting plasma with antibodies in it from people who have recovered to give to our top officials?
I’ve heard a bit about that. You know, if you recover from this, you’ll likely have antibodies that could be neutralizing or could inhibit the virus. And that’s a common way to treat patients—basically, give them these antibodies from another person. Now, you have to be careful because you have to have a blood match. So it’s not necessarily ideal, but I think it has the potential to work.
I know that there are many other infections where we do that and it can be helpful. All of these things that we’re throwing out there have not been tested. So I’m just saying it has worked in other viruses but that doesn’t necessarily mean it’s going to work here.
I have to ask about the reaction from your friends and family who probably thought ‘he’s doing this weird nerdy work on this virus, SARS, from 20 years ago.’ Have people that are close to you suddenly been like, ‘So tell me everything you know about coronavirus’?
Yeah, I’ve definitely had a few more friends come out of the woodwork that normally don’t talk to you that want to talk. But I take it all in stride. I feel like it’s our obligation as scientists to inform the public as best as we can, whenever people ask. They definitely seem to take more of an interest in my work now
Saturday, April 11, 2020
Wednesday, April 8, 2020
under study:- Nitric Oxide Gas Inhalation for Severe Acute Respiratory Syndrome in COVID-19.
COVID-19 is an emerging, rapidly evolving situation.
Get the latest public health information from CDC: https://www.coronavirus.gov.
Get the latest public health information from CDC: https://www.coronavirus.gov.
Get the latest research information from NIH:
https://www.nih.gov/coronavirus.
Nitric Oxide Gas Inhalation for Severe Acute Respiratory Syndrome in COVID-19. (NOSARSCOVID)
|
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. |
| ClinicalTrials.gov Identifier: NCT04290871 |
Recruitment Status :
Withdrawn
(A new coordinating center has been defined (Massachusetts General Hospital))
First Posted : March 2, 2020
Last Update Posted : March 24, 2020
|
Sponsor:
Xijing Hospital
Collaborators:
Massachusetts General Hospital
Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico
Information provided by (Responsible Party):
chonglei, Xijing Hospital
- Study Details
- Tabular View
- No Results Posted
- Disclaimer
- How to Read a Study Record
Study Description
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Brief Summary:
The investigators will enroll 102
patients with a confirmed diagnosis of COVID-19. Patients will be
randomized to receive either inhaled nitric oxide (per protocol) or
placebo. ICU Standards of care will be the institution's own protocols
(such as ventilation strategies and use and dose of antivirals and
antimicrobials, steroids, inotropic and vasopressor agents).
| Condition or disease | Intervention/treatment | Phase |
|---|---|---|
| Coronavirus SARS (Severe Acute Respiratory Syndrome) | Drug: Nitric Oxide Gas | Phase 2 |
Detailed Description:
2019-new
Coronavirus (2019-nCoV) infection (COVID-19) is highly contagious and
responsible for thousands of casualties. Originated in Wuhan (China),
the 2019-nCoV is spreading to many countries, including Italy, Korea and
Japan. While no targeted-treatment against 2019-nCoV virus is available
to-date, inhaled nitric oxide gas (NO) has shown antiviral activity
against Coronavirus during the 2003 SARS outbreak. The investigators
designed this study to assess whether inhaled NO improves survival in
patients affected with severe COVID-2019.
The clinical spectrum of
symptomatic patients ranges from mild upper respiratory syndrome to
severe diffuse viral pneumonia in the context of severe multiorgan
dysfunction leading to death. In China, overall reported fatality rate
is between 2.2% in patients with proven infection. In hospitalized
patients with COVID-19, about 25% required admission to ICU. Of these,
61% of patients met clinical criteria for acute respiratory distress
syndrome (ARDS). In another retrospective study in Wuhan (China) on 52
critically ill patients with COVID-19, the incidence of patients with
pneumonia meeting ARDS criteria was 67%. ICU mortality reached 63%, with
various profiles of combined organ failure in deceased patients (81%
with ARDS, 37.5% with AKI, 28% with cardiac injury and 28% with liver
failure).
In 2004, during the
Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) outbreak, it
was demonstrated that treatment with NO reversed pulmonary hypertension,
improved severe hypoxia and shortened the length of ventilatory support
as compared to matched control patients with SARS-CoV. In a subsequent
in-vitro study, NO donors (e.g. S-nitroso-N-acetylpenicillamine) greatly
increased the survival rate of SARS-CoV-infected eukaryotic cells,
suggesting direct antiviral effects of NO. Coronavirus responsible for
SARS-CoV shares most of the genome of COVID-19 indicating potential
effectiveness of inhaled NO therapy in these patients.
Here, the investigators
propose a randomized clinical trial aimed to prevent progression of the
disease in patients with severe acute respiratory syndrome.
Control group: the
institutional standard of care will be delivered. Treatment group: in
addition to standard therapy, the subjects will receive inhalation of
NO. Inspired NO/N2 will be delivered at 80 parts per million (ppm) in
the first 48 hours of enrollment. After that, NO levels will be
decreased to 40 ppm until severe hypoxia resolves. Weaning from NO will
start when patients improves the level of oxygenation to a PaO2/FiO2
> 300 mmHg or SpO2 > 93% for more than 24 hours consecutively.
Physician will follow their own institutional weaning protocols. In the
absence of institutional protocols, NO will be reduced every 4 hours in
step-wise fashion starting from 40 ppm to 20, 10, 5, 3, 2 and 1 ppm. If
hypoxemia (SpO2 < 93%) or acute hypotension (systolic blood pressure
< 90 mmHg) occurs during weaning, NO should be increased to a prior
higher concentration.
Safety: prolonged
treatment with inhaled NO can lead to increased methemoglobin levels.
Blood levels of methemoglobin will be monitored via a non-invasive
CO-oximeter or MetHb levels in blood. If methemoglobin levels rise above
5% at any point of the study, inhaled NO concentration will be halved.
Study Design
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| Study Type : | Interventional (Clinical Trial) |
| Actual Enrollment : | 0 participants |
| Allocation: | Randomized |
| Intervention Model: | Parallel Assignment |
| Masking: | Triple (Participant, Care Provider, Outcomes Assessor) |
| Primary Purpose: | Treatment |
| Official Title: | Nitric Oxide Gas Inhalation Therapy for Severe Acute Respiratory Syndrome Due to COVID-19. |
| Estimated Study Start Date : | March 23, 2020 |
| Estimated Primary Completion Date : | March 1, 2021 |
| Estimated Study Completion Date : | March 1, 2022 |
Resource links provided by the National Library of Medicine
MedlinePlus related topics:
Coronavirus Infections
Drug Information available for:
Nitric oxide
Arms and Interventions
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| Arm | Intervention/treatment |
|---|---|
| Experimental: Treatment Group
Nitric Oxide gas will be administered in the ventilatory circuit.
|
Drug: Nitric Oxide Gas
Inspired NO will be
delivered at 80 parts per million (ppm) in the first 48 hours of
enrollment. After that, NO levels will be decreased to 40 ppm until
severe hypoxia resolves. Weaning from NO will start when patients
improves the level of oxygenation to a PaO2/FiO2 > 300 mmHg or SpO2
> 93% for more than 24 hours consecutively. Physician will follow
their own institutional weaning protocols. In the absence of
institutional protocols, NO will be reduced every 4 hours in step-wise
fashion starting from 40 ppm to 20, 10, 5, 3, 2 and 1 ppm.
Other Name: Nitric Oxide inhalation
|
| Sham Comparator: Control Group
The delivery system will be set up anyway without study gas administration
|
Drug: Nitric Oxide Gas
Inspired NO will be
delivered at 80 parts per million (ppm) in the first 48 hours of
enrollment. After that, NO levels will be decreased to 40 ppm until
severe hypoxia resolves. Weaning from NO will start when patients
improves the level of oxygenation to a PaO2/FiO2 > 300 mmHg or SpO2
> 93% for more than 24 hours consecutively. Physician will follow
their own institutional weaning protocols. In the absence of
institutional protocols, NO will be reduced every 4 hours in step-wise
fashion starting from 40 ppm to 20, 10, 5, 3, 2 and 1 ppm.
Other Name: Nitric Oxide inhalation
|
Outcome Measures
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Primary Outcome Measures :
- SARS-free patients at 14 days [ Time Frame: 14 days since beginning of treatment ]Percentage of patients that have a PaO2/FiO2 ratio steadily > 300 in ambient air
Secondary Outcome Measures :
- Survival at 28 days [ Time Frame: 28 days ]
- Survival at 90 days [ Time Frame: 90 days ]
- SARS-free days at 28 days [ Time Frame: 28 days ]Composite outcome in which: Death=0, Days of treatment =1
- SARS -free days at 90 days [ Time Frame: 90 days ]Composite outcome in which: Death=0, Days of treatment =1
- Renal Replacement Therapy [ Time Frame: 28 days ]Incidence
- Liver Failure [ Time Frame: 28 days ]Incidence
- Mechanical Support of Circulation [ Time Frame: 28 days ]Incidence of patients requiring VA-ECMO, LVAD, IABP
- PaO2/FiO2 ratio in ambient air [ Time Frame: daily for 28 days ]In ambient air if possible
Eligibility Criteria
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Information from the National Library of Medicine
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies.
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies.
| Ages Eligible for Study: | 18 Years and older (Adult, Older Adult) |
| Sexes Eligible for Study: | All |
| Accepts Healthy Volunteers: | No |
Criteria
Inclusion Criteria:
- Age ≥18 years
- Laboratory (RT-PCR) confirmed infection with 2019-nCoV
- PaO2/FiO2 < 300 or SpO2 below 93% breathing ambient air
Exclusion Criteria:
- Physician makes a decision that trial involvement is not in the patient's best interest, or any condition that does not allow the protocol to be followed safely
- Pregnant or positive pregnancy test in a pre-dose examination
- Use of high flow nasal cannula
Contacts and Locations
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Information from the National Library of Medicine
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT04290871
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT04290871
Sponsors and Collaborators
Xijing Hospital
Massachusetts General Hospital
Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico
Investigators
| Principal Investigator: | Chong Lei, MD, PhD | Fourth Military Medical University | |
| Principal Investigator: | Lorenzo Berra, MD | Massachusetts General Hospital |
More Information
Go to
Publications:
| Responsible Party: | chonglei, Chong Lei, MD, PhD, Xijing Hospital |
| ClinicalTrials.gov Identifier: | NCT04290871 History of Changes |
| Other Study ID Numbers: | NO-SARS-COVID-19 |
| First Posted: | March 2, 2020 Key Record Dates |
| Last Update Posted: | March 24, 2020 |
| Last Verified: | March 2020 |
| Studies a U.S. FDA-regulated Drug Product: | Yes |
| Studies a U.S. FDA-regulated Device Product: | No |
| Product Manufactured in and Exported from the U.S.: | No |
Additional relevant MeSH terms:
| Coronavirus Infections Severe Acute Respiratory Syndrome Syndrome Disease Pathologic Processes Respiratory Tract Diseases Coronaviridae Infections Nidovirales Infections RNA Virus Infections Virus Diseases Respiratory Tract Infections Nitric Oxide Bronchodilator Agents |
Autonomic Agents Peripheral Nervous System Agents Physiological Effects of Drugs Anti-Asthmatic Agents Respiratory System Agents Free Radical Scavengers Antioxidants Molecular Mechanisms of Pharmacological Action Neurotransmitter Agents Endothelium-Dependent Relaxing Factors Vasodilator Agents Gasotransmitters Protective Agents |
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