Can touching a barbell in the gym get you sick with the coronavirus?

Masks help quite a bit.
Of course the ones made out of fabric aren't 100% effective, but 50-60% effectiveness ain't bad for something so cheap and readily available.
Anyone who is not wearing a mask is a total covIDIOT.



Great!
Less French people and more HCQ supply.




Great!
Less liberals and more HCQ supply left for us. How can that not be great?



Less than 1% of the population has been infected.
If herd immunity is for real, that's still too far away now.

Liberals can settle for having herd mentality while herd immunity arrives.



Great!
Less French (from not taking HCQ) and more supplies are left for us.
Why is trump taking HCQ if he doesn't
have coronavirus, and it doesn't prevent it?
Don't believe for one minute that he has EVER taken even one small dose of ANY drug. This is a jackass who is even afraid to take Tylenol. Here's his strategy. He wants everyone to think he took a drug that every expert has stated would not only be useless with the coronavirus, it is extremely dangerous because of side effects that could cause heart and other issues. Him and his defiant macho attitude. He wants everyone to think he's tough and invincible. What he doesn't want anyone to dwell on is that in fact in a recent NEW YORK TIMES commentary, he does own a piece of one of the manufacturers of Hydroxichlouriquin. Gee what a surprise!

So the other day he stated that he had been on this drug for a couple of weeks and now he's off it. He said SEE, I TOOK IT AND I'M OK. SO IF YOU CAN GET THEN TAKE IT BECAUSE IT WORKS. This guy will do or say anything. But the bottom line however is that all of this horseshit, is nothing more than deflection from the pandemic and the devastating daily news that he doesn't want to talk about.

All he knows how to do is LIE LIE LIE. Pick a subject and he'll concoct some bullshit story about it. This country is a mess medically and financially and it's becoming painfully obvious that this mental pigmy has absolutely no idea how to right the ship. He still has NO FEDERAL PLAN for this pandemic nor any plan for restoring the economy. He has never had any managerial skills even dating back to his business. He operated as a dictator would. He never was capable of taking advice. No business he has ever been affiliated with, has ever been successful. Six (6) Bankruptcies should paint the real picture of this con artist whose only tool is HOW GOOD CAN HE LIE! ( from Quora)
 
If you guys though you saw a primate in a tree in the woods (partially instructed view) and nobody was around to verify it, would you actually believe your eyes?
Not crazy. Just high on some filthy green :D:p i saw it north of that location, near the New Hampshire border. (If I in fact saw the monkey) wonder if it has covid?Screenshot_20200529-071824.png
 
[OA] Covid-19: The challenges facing endocrinology.

The Covid-19 pandemic has hit the planet like a tidal wave, imperiling the lives of thousands and threatening health systems with collapse. In this issue of the Annals of Endocrinology, Alexandre et al. [1] remind us that the gateway to Sars-CoV-2 is the angiotensin II converting enzyme (ACE2), physiological regulator of the renin-angiotensin system (RAS).

Angiotensin II stimulates the secretion of aldosterone via the AT1 receptor of the adrenal gland (glomerulated zone) and has its own vasoconstrictive, pro-fibrosing, pro-inflammatory activity. ACE2 converts angiotensin II-[1–8] to angiotensin-[1–7], which has properties opposite to those of angiotensin II, and is therefore a negative regulator of the RAS.

The legitimate question raised by the authors is whether the prescription of converting enzyme inhibitor [1–10] (ACEi) and angiotensin receptor type 1 blockers (ARAII), very widely used in hypertension treatment, may increase the risk of developing severe acute respiratory syndrome in Covid-19-infected patients.

It is convincingly explained why, on the basis of the available evidence, scientific societies do not recommend discontinuation of hypertension treatment by ACEi and ARAIIs in Covid-19+ patients. Therapeutic prospects and the first trials of the use of the soluble form of ACE2 as a virus trap are underway.

Covid-19 challenges the endocrinologist in many ways. Three in particular are worth raising here:

· the relative protection of children, presumed to be healthy carriers, and the lower incidence of death in women (1/3) suggest that the hormonal environment and genetic aspects are factors for surviving Covid-19. We know for example that the TLR7 gene present on the X chromosome is a receptor which influences antiviral response [2]. Paradoxically, as immune response is stronger in women, contributing to greater susceptibility to autoimmune disease, this flaw becomes an advantage over viral infection. In men, who make up more than two-thirds of deaths from Covid-19, risk is higher after 50 years and even more after 70 years. But age is not the only factor; a context of metabolic syndrome with overweight, diabetes and hypertension seems to be strongly associated with this risk. It is important to remember that the decline in testosterone secretion in humans can be explained by 4 factors: age, obesity, associated comorbidities, and smoking [3]. Strangely, the ACE2 protein is expressed in many tissues, including the testicle [4]. These avenues could be explored to better identify the influence of sex hormones on the ability to resist viral disease;

· a cytokine storm is reported during the respiratory distress phase in 20% of Covid-19 + patients with multi-organ failure and hypotension refractory to standard treatment [5]. How does the adrenal cortex function react in this critical situation? Is there an analogy with what has been well described in septic shock? [6]. We already know that corticosteroids are not useful in the treatment of pulmonary lesions associated with severe respiratory distress, and are indeed deleterious by delaying elimination of the virus. Is there any form of resistance to glucocorticoids?

· the Covid-19 epidemic has served as an opportunity to adopt teleconsultation to respond to the urgent need for continuity of care. This is bound to lead to reimagining a definitive shift to telemedicine in the management of chronic diseases, which is liable to disrupt our practice and teaching and also the entire economic system of health-care.

In this issue of the Annals, a current update on the relationships of diabetes, but also obesity, with the risk of contracting Covid-19 or developing a severe form is presented. This didactic article by Laura Orioli et al. [8], documented by a literature in full effervescence would be very useful for the informed reader or the general practitioner and will enable him to follow the future recommendations to treat the Covid+ diabetic patients.

Endocrinologists and diabetologists, like many other specialists, must prepare for this very immediate deadline.

The reader will find the answers to the questions posed by aging, which is the center of attention of the whole medical community, in the management of thyroid diseases. This consensus statement, coordinated by Philippe Caron, is remarkable, practical and exhaustive. It is based on the extensive clinical experience of its authors.

Pugeat M, Chabre O, Van Tyghem M-C. Covid-19: The challenges facing endocrinology. Annales d'Endocrinologie 2020;81:61-2. Covid-19: The challenges facing endocrinology - ScienceDirect
 


Even in non-pandemic years, influenza and other etiologies of pneumonia represent the eighth leading cause of death in the United States, and respiratory viruses are the most commonly identified pathogens among hospitalized patients with community-acquired pneumonia (1).

Epidemics of seasonal influenza occur on an annual basis. In the United States, the 2019-2020 seasonal influenza epidemic resulted in tens of millions of cases—the majority of which occurred before the coronavirus disease 2019 (COVID-19) pandemic surged.

Now, COVID-19, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is an ongoing pandemic that has strained and, in some locales, overwhelmed healthcare systems.

What can we expect as the COVID-19 pandemic evolves and seasonal influenza comes again?

How can the epidemiology and biology of these infections inform our preparation strategies?

The last influenza pandemic, caused by the then-novel H1N1pdm09 virus, began in the spring of 2009 and caused an estimated 61 million cases, 274,000 hospitalizations, and 12,500 deaths in the United States over the following year (2). Despite its inclusion in the influenza vaccine since 2010, H1N1pdm09 circulates annually in the community and was the predominant influenza A virus strain during the 2019-2020 influenza epidemic.

In contrast, the last human coronavirus epidemic, SARS (caused by SARS-CoV), abated because of aggressive containment procedures before a vaccine could be deployed; community transmission of SARS-CoV has not occurred since 2004. Based on the course of the COVID-19 pandemic to date and anticipated vaccine development timelines, it is clear that SARS-CoV-2 will not follow the abruptly terminating trajectory of SARS-CoV.

Rather, it is likely that community transmission of SARS-CoV-2 will continue as we enter the next influenza epidemic. Several factors, at least in part, will determine the overall severity of the upcoming respiratory virus season and can inform how we prepare:



Humans have suffered from influenza for millennia, and we can expect that the new reality of COVID-19 will only complicate the next influenza season. Measures to reduce the overall burden of respiratory viral infection—including social distancing, increased vaccination rates, availability of diagnostics, and addressing healthcare disparities—are paramount in planning for the months ahead. Moreover, careful evaluation and modification of these factors will enhance preparedness ahead of viral pandemics yet to come.

Singer BD. COVID-19 and the next influenza season. Science Advances 2020:eabd0086. COVID-19 and the next influenza season
 
Why is trump taking HCQ if he doesn't
have coronavirus, and it doesn't prevent it?
Don't believe for one minute that he has EVER taken even one small dose of ANY drug. This is a jackass who is even afraid to take Tylenol. Here's his strategy. He wants everyone to think he took a drug that every expert has stated would not only be useless with the coronavirus, it is extremely dangerous because of side effects that could cause heart and other issues. Him and his defiant macho attitude. He wants everyone to think he's tough and invincible. What he doesn't want anyone to dwell on is that in fact in a recent NEW YORK TIMES commentary, he does own a piece of one of the manufacturers of Hydroxichlouriquin. Gee what a surprise!

So the other day he stated that he had been on this drug for a couple of weeks and now he's off it. He said SEE, I TOOK IT AND I'M OK. SO IF YOU CAN GET THEN TAKE IT BECAUSE IT WORKS. This guy will do or say anything. But the bottom line however is that all of this horseshit, is nothing more than deflection from the pandemic and the devastating daily news that he doesn't want to talk about.

All he knows how to do is LIE LIE LIE. Pick a subject and he'll concoct some bullshit story about it. This country is a mess medically and financially and it's becoming painfully obvious that this mental pigmy has absolutely no idea how to right the ship. He still has NO FEDERAL PLAN for this pandemic nor any plan for restoring the economy. He has never had any managerial skills even dating back to his business. He operated as a dictator would. He never was capable of taking advice. No business he has ever been affiliated with, has ever been successful. Six (6) Bankruptcies should paint the real picture of this con artist whose only tool is HOW GOOD CAN HE LIE! ( from Quora)
HCQ may help PREVENT the disease.
Google the Indian study where they are giving it to tens of thousands of cops to see if it works as a preventive measure.

Also, Trump proved that you don't die or get sick from taking it for a short period of time.
Don't ever take it nonstop, though.

I know that Chloroquine, which is very closely related to HCQ is very safe as I got it prescribed at least once, if not twice in Costa Rica.
The first time it was meant to prevent myself from getting malaria from mosquito bites.
The second time if I'm not mistaken, CQ was prescribed to me for Dengue fever. It was an off label use but it seemed to work.


[OA] Covid-19: The challenges facing endocrinology.

The Covid-19 pandemic has hit the planet like a tidal wave, imperiling the lives of thousands and threatening health systems with collapse. In this issue of the Annals of Endocrinology, Alexandre et al. [1] remind us that the gateway to Sars-CoV-2 is the angiotensin II converting enzyme (ACE2), physiological regulator of the renin-angiotensin system (RAS).

Angiotensin II stimulates the secretion of aldosterone via the AT1 receptor of the adrenal gland (glomerulated zone) and has its own vasoconstrictive, pro-fibrosing, pro-inflammatory activity. ACE2 converts angiotensin II-[1–8] to angiotensin-[1–7], which has properties opposite to those of angiotensin II, and is therefore a negative regulator of the RAS.

The legitimate question raised by the authors is whether the prescription of converting enzyme inhibitor [1–10] (ACEi) and angiotensin receptor type 1 blockers (ARAII), very widely used in hypertension treatment, may increase the risk of developing severe acute respiratory syndrome in Covid-19-infected patients.

It is convincingly explained why, on the basis of the available evidence, scientific societies do not recommend discontinuation of hypertension treatment by ACEi and ARAIIs in Covid-19+ patients. Therapeutic prospects and the first trials of the use of the soluble form of ACE2 as a virus trap are underway.

Covid-19 challenges the endocrinologist in many ways. Three in particular are worth raising here:

· the relative protection of children, presumed to be healthy carriers, and the lower incidence of death in women (1/3) suggest that the hormonal environment and genetic aspects are factors for surviving Covid-19. We know for example that the TLR7 gene present on the X chromosome is a receptor which influences antiviral response [2]. Paradoxically, as immune response is stronger in women, contributing to greater susceptibility to autoimmune disease, this flaw becomes an advantage over viral infection. In men, who make up more than two-thirds of deaths from Covid-19, risk is higher after 50 years and even more after 70 years. But age is not the only factor; a context of metabolic syndrome with overweight, diabetes and hypertension seems to be strongly associated with this risk. It is important to remember that the decline in testosterone secretion in humans can be explained by 4 factors: age, obesity, associated comorbidities, and smoking [3]. Strangely, the ACE2 protein is expressed in many tissues, including the testicle [4]. These avenues could be explored to better identify the influence of sex hormones on the ability to resist viral disease;

· a cytokine storm is reported during the respiratory distress phase in 20% of Covid-19 + patients with multi-organ failure and hypotension refractory to standard treatment [5]. How does the adrenal cortex function react in this critical situation? Is there an analogy with what has been well described in septic shock? [6]. We already know that corticosteroids are not useful in the treatment of pulmonary lesions associated with severe respiratory distress, and are indeed deleterious by delaying elimination of the virus. Is there any form of resistance to glucocorticoids?

· the Covid-19 epidemic has served as an opportunity to adopt teleconsultation to respond to the urgent need for continuity of care. This is bound to lead to reimagining a definitive shift to telemedicine in the management of chronic diseases, which is liable to disrupt our practice and teaching and also the entire economic system of health-care.

In this issue of the Annals, a current update on the relationships of diabetes, but also obesity, with the risk of contracting Covid-19 or developing a severe form is presented. This didactic article by Laura Orioli et al. [8], documented by a literature in full effervescence would be very useful for the informed reader or the general practitioner and will enable him to follow the future recommendations to treat the Covid+ diabetic patients.

Endocrinologists and diabetologists, like many other specialists, must prepare for this very immediate deadline.

The reader will find the answers to the questions posed by aging, which is the center of attention of the whole medical community, in the management of thyroid diseases. This consensus statement, coordinated by Philippe Caron, is remarkable, practical and exhaustive. It is based on the extensive clinical experience of its authors.

Pugeat M, Chabre O, Van Tyghem M-C. Covid-19: The challenges facing endocrinology. Annales d'Endocrinologie 2020;81:61-2. Covid-19: The challenges facing endocrinology - ScienceDirect
SARS-CoV-2 can get into the cells trough many other receptors other than ACE-2, so you at this point all doctors are missing the mark here.



On that I agree
Anyone who attends public parties right now is a total idiot.
 


If you’re following at all the search for COVID-19 treatments, and possibly even if not, you will have seen the flurry of media coverage for the observational study in The Lancet ‘Hydroxychloroquine or chloroquine with or without a macrolide for treatment of COVID-19: a multinational registry analysis. It made the news not least because hydroxychloroquine is the drug President Trump says he is taking in the belief that it will reduce his chance of catching COVID-19. This view is not backed up evidence until some randomised trials come in. Getting in before the trials, the Lancet study used propensity score matching to try to control for the non-random treatment. It found that taking hydroxychloroquine and chloroquine were associated with an increased risk of heart problems.

I am highly skeptical of the powers of hydroxychloroquine with relation to COVID-19 (‘skeptical’ in the sense that I have suspended judgement for now - there simply isn’t evidence either way). But I want the test of its properties to be done properly, with random controlled trials. And if we are to use observational studies (which I do not object to, they just aren’t as useful as an experiment where you can manipulate the treatment), they have to use real data.

The data in that study, and in at least https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3580524., were provided by an Illinois firm called Surgisphere. Allegedly the data represents the treatment and health outcomes of 96,032 patients from 671 hospitals in six continents. However, there is simply no plausible way I can think of that the data are real.

I’ll say that again - I believe with very high probability the data behind that high profile, high consequence Lancet study are completely fabricated.

If Surgisphere can name the 671 participating hospitals or otherwise prove that the data is real I will retract that statement, delete this post or write whatever humbling apology they desire. But I think there’s nearly zero chance of that happening.

...
 

Soon we'll see lots of very cheap weights for sale on Craigslist.


Opening bars and restaurants or going to them is just stupid.

You'll need to take out your mask to be able to eat or drink.
And yes, I'm a conservative and I proudly wear masks as I'm not stupid and I'm aware how masks can help prevent you from getting the virus, while being cheap and widely available. Not so much for the N95s though.




If you’re following at all the search for COVID-19 treatments, and possibly even if not, you will have seen the flurry of media coverage for the observational study in The Lancet ‘Hydroxychloroquine or chloroquine with or without a macrolide for treatment of COVID-19: a multinational registry analysis. It made the news not least because hydroxychloroquine is the drug President Trump says he is taking in the belief that it will reduce his chance of catching COVID-19. This view is not backed up evidence until some randomised trials come in. Getting in before the trials, the Lancet study used propensity score matching to try to control for the non-random treatment. It found that taking hydroxychloroquine and chloroquine were associated with an increased risk of heart problems.

I am highly skeptical of the powers of hydroxychloroquine with relation to COVID-19 (‘skeptical’ in the sense that I have suspended judgement for now - there simply isn’t evidence either way). But I want the test of its properties to be done properly, with random controlled trials. And if we are to use observational studies (which I do not object to, they just aren’t as useful as an experiment where you can manipulate the treatment), they have to use real data.

The data in that study, and in at least https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3580524., were provided by an Illinois firm called Surgisphere. Allegedly the data represents the treatment and health outcomes of 96,032 patients from 671 hospitals in six continents. However, there is simply no plausible way I can think of that the data are real.

I’ll say that again - I believe with very high probability the data behind that high profile, high consequence Lancet study are completely fabricated.

If Surgisphere can name the 671 participating hospitals or otherwise prove that the data is real I will retract that statement, delete this post or write whatever humbling apology they desire. But I think there’s nearly zero chance of that happening.

...

That "data" is all made up
this video explains why in an easy to understand way
 
Unmasking History: Who Was Behind the Anti-Mask League Protests During the 1918 Influenza Epidemic in San Francisco?

On April 17, 2020, San Francisco Mayor London Breed did something that had not been done for 101 years. She issued an order that face masks be worn in public as a measure to help prevent the spread of infectious disease in the midst of a pandemic.

This act promptly raised questions about how things were handled a century ago. The media soon picked up on the antics of an “Anti-Mask League” that was formed in San Francisco to protest this inconvenience, noting some historical parallels with public complaint about government overreach.

This essay dives deeper into the historical context of the anti-mask league to uncover more information about the identity and possible motivations of those who organized these protests. In particular it shines light on the fascinating presence of the leading woman in the campaign—lawyer, suffragette, and civil rights activist, Mrs. E.C. Harrington.

Dolan, B. (2020). Unmasking History: Who Was Behind the Anti-Mask League Protests During the 1918 Influenza Epidemic in San Francisco? UC Berkeley: UC Medical Humanities Consortium. Retrieved from https://escholarship.org/uc/item/5q91q53r
 
Unmasking History: Who Was Behind the Anti-Mask League Protests During the 1918 Influenza Epidemic in San Francisco?

On April 17, 2020, San Francisco Mayor London Breed did something that had not been done for 101 years. She issued an order that face masks be worn in public as a measure to help prevent the spread of infectious disease in the midst of a pandemic.

This act promptly raised questions about how things were handled a century ago. The media soon picked up on the antics of an “Anti-Mask League” that was formed in San Francisco to protest this inconvenience, noting some historical parallels with public complaint about government overreach.

This essay dives deeper into the historical context of the anti-mask league to uncover more information about the identity and possible motivations of those who organized these protests. In particular it shines light on the fascinating presence of the leading woman in the campaign—lawyer, suffragette, and civil rights activist, Mrs. E.C. Harrington.

Dolan, B. (2020). Unmasking History: Who Was Behind the Anti-Mask League Protests During the 1918 Influenza Epidemic in San Francisco? UC Berkeley: UC Medical Humanities Consortium. Retrieved from https://escholarship.org/uc/item/5q91q53r

When Mask-Wearing Rules in the 1918 Pandemic Faced Resistance
https://www.history.com/news/1918-spanish-flu-mask-wearing-resistance

The influenza pandemic of 1918 and 1919 was the most deadly flu outbreak in history, killing up to 50 million people worldwide. In the United States, where it ultimately killed around 675,000 people, local governments rolled out initiatives to try to stop its spread. These varied by region, and included closing schools and places of public amusement, enforcing “no-spitting” ordinances, encouraging people to use handkerchiefs or disposable tissues and requiring people to wear masks in public.

 
[Video] ICYMI: A French designer has created a cylinder of transparent plastic that hangs from the ceiling which allows diners to enjoy their meal.
 


Stuck inside? Yeah, I know you are. Me too. With the Covid-19 pandemic raging, it hasn't been easy to maintain almost any normal routines, and that includes weight lifting. But if you don't maintain, you lose your gains.

We're all trying our best to work out from home, but many people rely on the gym—and many are still closed. Running won't have the same effect as lifting weights—and bodyweight exercises, in which you use only your own weight for resistance, can't substitute for the barbells, dumbbells, and kettlebells you're used to.

My solution: I wear a 65-pound weighted vest (here's a good, similar one). I discovered it years ago when I was training for mountain climbs. At the time, I had to simulate the weight of walking up a mountain with a heavy pack on my back, and I wasn't able to take other climbers' advice and hike a nearby hill with a backpack full of sandbags because, well, I live in New York City. It just isn't feasible. So I picked up my gym's only weighted vest and hit the stair-climbing machine. It didn't take long to realize this thing would be great with other exercises, especially ones that focus on working the body's core, such as planks.

Weighted vests are covered in pockets on the outside and come with a bunch of small, brick-shaped weights that fit in them. The total weight varies based on the vest you buy, but most are 40 to 80 pounds. Say you buy a 60-pound weighted vest. It might have 20 pockets with 20 three-pound weights. Add or remove bricks to dial in the weight you want. Nothing is going to substitute for a squat rack at home, unless you lose your mind and weld a bar to a couple of kitchen appliances.

 
[OA] Physical Distancing, Face Masks, and Eye Protection to Prevent Person-To-Person Transmission of SARS-CoV-2 and COVID-19

Background - Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19 and is spread person-to-person through close contact. We aimed to investigate the effects of physical distance, face masks, and eye protection on virus transmission in health-care and non-health-care (eg, community) settings.

Methods - We did a systematic review and meta-analysis to investigate the optimum distance for avoiding person-to-person virus transmission and to assess the use of face masks and eye protection to prevent transmission of viruses. We obtained data for SARS-CoV-2 and the betacoronaviruses that cause severe acute respiratory syndrome, and Middle East respiratory syndrome from 21 standard WHO-specific and COVID-19-specific sources.

We searched these data sources from database inception to May 3, 2020, with no restriction by language, for comparative studies and for contextual factors of acceptability, feasibility, resource use, and equity. We screened records, extracted data, and assessed risk of bias in duplicate. We did frequentist and Bayesian meta-analyses and random-effects meta-regressions. We rated the certainty of evidence according to Cochrane methods and the GRADE approach. This study is registered with PROSPERO, CRD42020177047.

Findings - Our search identified 172 observational studies across 16 countries and six continents, with no randomised controlled trials and 44 relevant comparative studies in health-care and non-health-care settings (n=25 697 patients).

Transmission of viruses was lower with physical distancing of 1 m or more, compared with a distance of less than 1 m (n=10 736, pooled adjusted odds ratio [aOR] 0·18, 95% CI 0·09 to 0·38; risk difference [RD] −10·2%, 95% CI −11·5 to −7·5; moderate certainty); protection was increased as distance was lengthened (change in relative risk [RR] 2·02 per m; pinteraction=0·041; moderate certainty).

Face mask use could result in a large reduction in risk of infection (n=2647; aOR 0·15, 95% CI 0·07 to 0·34, RD −14·3%, −15·9 to −10·7; low certainty), with stronger associations with N95 or similar respirators compared with disposable surgical masks or similar (eg, reusable 12–16-layer cotton masks; pinteraction=0·090; posterior probability >95%, low certainty).

Eye protection also was associated with less infection (n=3713; aOR 0·22, 95% CI 0·12 to 0·39, RD −10·6%, 95% CI −12·5 to −7·7; low certainty). Unadjusted studies and subgroup and sensitivity analyses showed similar findings.

Interpretation - The findings of this systematic review and meta-analysis support physical distancing of 1 m or more and provide quantitative estimates for models and contact tracing to inform policy. Optimum use of face masks, respirators, and eye protection in public and health-care settings should be informed by these findings and contextual factors. Robust randomised trials are needed to better inform the evidence for these interventions, but this systematic appraisal of currently best available evidence might inform interim guidance.

Chu DK, Akl EA, Duda S, et al. Physical distancing, face masks, and eye protection to prevent person-to-person transmission of SARS-CoV-2 and COVID-19: a systematic review and meta-analysis. The Lancet. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31142-9/fulltext

 
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