6,062 Matching Annotations
  1. May 2026
    1. On 2020-08-11 11:14:29, user One bird one cup wrote:

      Limited evidence to support effectiveness of quarantine? <br /> SARS: 8,098 cases worldwide. About 5300 in China. "Most included trials had poor design, reporting and sparse events." No difference between N95 and surgical masks? <br /> I'm not buying this.

    1. On 2020-08-11 14:13:04, user Randy Von Fistenburg wrote:

      Has this type of study not already been performed in other countries before this? It was my understanding that results of such studies from countries whose initial wave hit earlier than UK, concluded no increased risk for those with HIV infection (on ARV treatment). It would seem that government health officials, NHS patient advice and statements from HIV organisations and charities were entirely wrong when, at the start of the lockdown period, they assured public the complete opposite was the case: As long as those infected with HIV were taking ARV medication then they did not have increased mortality risk compared to rest of population. I remember a small study done in Barcelona and a larger one in China both seemed to indicate no increased risk, but I find it highly irresponsible for advice from official sources that was then used to make policy on what was considered high risk groups and organisation of shielding and other provisions and protections , not be backed up by research such as this study to be absurd - Its outrageous for these for these statements and advice to have been offered in the first place!

    1. On 2020-08-13 08:17:50, user Blanket Box wrote:

      This paper fails to define what constitutes a Covid "case" and so the statistics are essentially meaningless. There are multiple problems with national "case" data, including multiple swabs from one person being counted as multiple unique "cases", and serology (antibody) tests being counted as "cases" . However the major problem with "case" counts is that PCR testing creates cases. PCR does not verify presence of viable virus. The virus is not isolated. PCR amplifies viral RNA. However, people recovered from Covid shed inactive viral fragments for around 3 months. These are detectable by PCR and create false positive results - which are counted as "cases". The test is quite literally creating the cases. The number of PCR amplification cycles selected by the operator will determine the number of positive tests. More cycles will manufacturer more RNA and result in more positive results and therefore more cases. There is no peer reviewed methodology for determining how many cycles because the PCR test is not a diagnostic test and should not be used as such. One of the foundational principles of diagnosis is that the usefulness of a lab test is measured by how frequently the test results confirm the clinical diagnosis of symptoms by a doctor. Most of these so called “cases” do not represent people diagnosed with any disease or presenting any symptoms. They are positive PCR tests and nothing more. It should not be inferred or implied that a positive PCR test represents a unique individual with an active infection because that is simply not the case.

      Most of the links about PCR test including shedding of inactive virus by recovered people can be found in this article https://www.conservativerev...

      Other useful links are<br /> https://vimeo.com/443416775<br /> https://twitter.com/ussuric...<br /> https://medium.com/@vernunf...

    1. On 2020-07-08 21:52:08, user F Philibert wrote:

      Faulty Data sources were used in this study.

      I question the use of the GVA data, which was generated by an organization with its own agenda, rather than FBI data, which is more accurate but lags behind.

      As well, NICS checks do not represent a one-to-one count against firearms purchases; In most states, <br /> 1. Multiple guns can be purchased on a single NICS background check,<br /> 2. Holders of Carry Permits may not need NICS Checks, and <br /> 3. NICS checks are also performed for other reasons, such as Purchase or Carry Permit issuance or renewal. <br /> To get a proper number for gun purchases, consult data from the National Shooting Sports Foundation.

      The cause and effect are likely backwards here. Coinciding with the pandemic were riots and civil disturbance, which increased violence, and likely caused a surge in firearms purchases for self protection. Also, with the 2016 election cycle comes the threat of increased Gun Control, and perceived restriction on ability to purchase firearms in the future. Nothing increases a population's desire for an object more than perceived future scarcity. E.g., Toilet Paper at the outset of the pandemic.

      Note also that there was a surge in firearms sales in 2013, with a corresponding DECREASE in crime.

      I find the conclusions of this study to be questionable at best.

    1. On 2020-07-09 05:04:08, user Hesham wrote:

      Based on your validation data (p1 of the supplemental material), you had better sensitivity/LOD for E, N1, and N2 than you did for IP2/IP4. Therefore if you were able to detect IP2/IP4 in the March 12, 2019 samples (Fig 2A in your results), you should have been able to detect E, N1 and N2. But you didn't ! This is not consistent with the presence of SARS-Cov-2 and would never qualify as a positive result.

      I would question the wisdom of publishing such tentative data, especially in the current environment. There are people such as Tom Jefferson of Oxford who are citing your work as "proof" to support outlandish claims about the origins of this virus. I fear this article is causing more harm than good.

    1. On 2020-08-14 09:13:14, user Alexandre Júlio wrote:

      Louis Pasteur taught us the importance of Pasteurization. Against air-borne epidemics, we are needing a safe indoor place to drink & eat. Up-down HEPA laminar flow is a speciality that I knew only in semiconductor clean rooms. Against Covid-19, my faith is going to UHT treated air, cooled to lower than 50ºC by heat-exchange with aspirated air. Further cooling may be provided by humidification with sterilized water and/or heat pump. What are UHT-air parameters used in Japan?

    2. On 2020-08-13 12:21:29, user Justin Cotney wrote:

      These Cq values are at the very unreliable end of the instrument's detection range. Most biologists and in my own lab do not trust Cq values greater than 35. The instrument will usually report a number even in negative controls as was seen in their table. Performing a melt curve analysis after the PCR reveals if it is the product you were expecting or spurious amplification. Please show qpcr traces and melt curves.

    1. On 2020-08-14 16:20:29, user Paul Gordon wrote:

      Very interesting, thanks for posting. The paper described 649 genomes, but only 253 appear to be in GISAID. Do you know if the remaining genomes will be released? Thanks!

    1. On 2020-07-10 16:14:28, user Copernicus wrote:

      Hosting lectures with many students in an indoor environment, based on recent scientific guidance on small particles, will not be easy and the solution seems to be mostly online. virtual and tutorials. The questions then arises why should students pay high fees. best to delay until next year and let students take a gap year!

    1. On 2020-08-22 13:26:22, user Euan Arnott wrote:

      Very valuable paper! I second the previous enquiry about crew age data, since I suspect that they might be younger than the population average in such a physically demanding job? Ditto the enquiry about WHEN the key Abbott-positive trio were actively sick. Would it be possible to screen the three who were Abbott-positive but neutralising-negative to see if they show specific antibodies to endemic coronaviruses OC43, 299E, NL63, or HKU-1? This might help to understand if a recent non-COVID coronavirus infection reduces the Positive Predictive value (PPV) of the Abbott test (via anti-Nucleoprotein antibody cross-reactivity). Even just a question to the whole crew as to who had ANY cold-type symptoms within the month before sailing might be useful data. Again, a great paper.

    2. On 2020-08-20 15:31:30, user Matt Price wrote:

      6 people had antibodies to SARS CoV2 prior to departure, 3 of whom had neutralizing antibodies (i.e., much more potent). Of the 3 who didn't have neutralizing antibodies, all developed symptoms and became PCR+ during the trip. I have a few comments for the authors, that I think would be helpful to address (unless I missed it):

      1. Did those 3 without neutralizing abs later develop neutralizing antibodies?
      2. Were they (as someone below suggests) the carriers who might have brought the virus on board, since PCR does have a high rate of false negatives (i.e., failing to detect virus when in fact it is there)? This might be difficult to test, as you don't have samples during the trip...
      3. How many of the 104 with positive PCR and later seroconverted developed neutralizing antibodies (i.e., is it common that everyone develops potential immunity?)

      Very nice work.

    3. On 2020-08-21 13:41:13, user CodeJ wrote:

      While it is great that we have some concrete evidence that being infected/testing positive for antibodies gives you protection, how long does protection last? Is it 3 months? Is it 1 year? Is it lifelong? I want to know when these three Ab+ individuals were actually exposed to the virus, though I acknowledge that this information could be difficult to obtain. Based on what we know about SARS and common cold causing coronavirus strains, this protection may be short-lived. These questions needs to be answered before the pandemic can truly be over and an effective vaccination strategy can be developed, but we obviously need more time to answer these questions, as well.

      Also, while the studies of the neutralizing antibodies are promising, there is no evidence that the neutralizing antibodies they detect actually protect people from getting reinfected, as T cell response also seems to be important, which is highlighted by other studies. Additionally, are these antibodies present in serum getting to the mucosal sites of infection they need to be in order to protect? Importantly, this study does underscore the need to test the therapeutic and prophylactic potential of monoclonal Abs directed against the virus (i.e. the NP protein or S) that can perhaps be derived from these neutralizing Abs present in convalescent individuals.

    1. On 2021-05-16 08:22:03, user Kohsuke Imai wrote:

      Yang Y, Shen C, Li J, Yuan J, Wei J, Huang F, Wang F, Li G, Li Y, Xing L, Peng L, Yang M, Cao M, Zheng H, Wu W, Zou R, Li D, Xu Z, Wang H, Zhang M, Zhang Z, Gao GF, Jiang C, Liu L, Liu Y. Plasma IP-10 and MCP-3 levels are highly associated with disease severity and predict the progression of COVID-19. J Allergy Clin Immunol. 2020 Jul;146(1):119-127.e4. doi: 10.1016/j.jaci.2020.04.027. Epub 2020 Apr 29. PMID: 32360286; PMCID: PMC7189843.

    1. On 2021-05-17 17:12:31, user Cathy Crowe wrote:

      Thank you for this. In Toronto, Canada we've now had over 120 shelter outbreaks with over 1500 people infected. In fact we had to take the city to court to ensure at least 2 metre (6 feet) physical distancing would be ordered. Congregate shelters continue to have outbreaks, some are on their 2nd and 3rd. Post COVID the new model of shelter delivery must be one person per room, one couple per room, one family per room while they wait for housing and the housing has to be fast tracked.

    1. On 2021-05-21 20:59:55, user Harold Thimbleby wrote:

      From harold@thimbleby.net

      I mailed the author for correspondence constructively two weeks ago but I have had no reply.

      I am a professor of computer science. The Excel spreadsheet is, sadly, appalling and needs a lot of professional work to be believable. There is no useful documentation about how it is intended to work. It is obscure and impossible to check. I doubt it is correct, unless evidence can be provided. In short, the results described in this paper cannot be relied on or used for any public health purposes.

      Have any of the authors carefully reviewed the spreadsheet? Any independent parties? If so I think the paper should say so.

      Best wishes, though, with this important work.

      -Harold

    1. On 2021-05-25 20:24:16, user Green Ranger wrote:

      The results and conclusions of this study are wrong. The authors mistook the ivermectin and control arms of one of the RCTs that they included. Look at figure 2. The results from Niaee 2020 are dramatically misreported. The actual results for that study are as follows:

      Control groups: 11 deaths out of 60 patients.<br /> Ivermectin groups: 4 deaths out of 90 patients.

      When this is corrected, the results of this meta-analysis confirm what other meta-analyses have found. Ivermectin use is associated with approximately 66% reduction in Covid fatalities. And this result is statistically significant.

      A source for this.

    2. On 2021-05-26 03:59:44, user Steve Kirsch wrote:

      Why hasn't this paper been retracted yet?

      They reversed the numbers for the Niaee study which was pivotal to their conclusion. See this tweet from CovidAnalysis for details on the switch. There is also a video from Niaee himself attesting to the fact ivermectin works.

      When you use the correct data, it shows ivermectin works. No surprise.

    3. On 2021-07-01 02:18:40, user akcita wrote:

      I was hoping that there would be obvious conflicts of Interest. Alas, it seems the Authors barely reviewed their own study and left it to a technical editor, and the viewing public to fix their bad science...

    1. On 2021-05-26 14:43:55, user Donepudi Raviteja wrote:

      Sorry Sir, but this article need so much more rigorous Multivariate statistics like PCS, MANOVA etc.,. The statistics are basic and also misleading to some extant. In correlation matrix (Figure 3) the correlation between deaths per million and sanitation parameters looks identical to correlation between age >65 years and sanitation parameters. This show that the confiding factor is age distribution. If a proper multivariate analysis is done this would have been easily identified and avoided as discussion point. A simple age adjusted death-rate correlation with sanitation parameters would also be sufficient.

    1. On 2021-05-27 14:27:10, user Michael W. Perry wrote:

      This study reinforces an earlier Danish one published in the Annals of Internal Medicine which found that the result of mask wearing had so little statistical significance it could be "compatible with a 46% reduction to a 23% increase in infection."

      Results:<br /> A total of 3030 participants were randomly assigned to the recommendation to wear masks, and 2994 were assigned to control; 4862 completed the study. Infection with SARS-CoV-2 occurred in 42 participants recommended masks (1.8%) and 53 control participants (2.1%). The between-group difference was –0.3 percentage point (95% CI, –1.2 to 0.4 percentage point; P = 0.38) (odds ratio, 0.82 [CI, 0.54 to 1.23]; P = 0.33). Multiple imputation accounting for loss to follow-up yielded similar results. Although the difference observed was not statistically significant, the 95% CIs are compatible with a 46% reduction to a 23% increase in infection.<br /> https://www.acpjournals.org...

    1. On 2021-05-29 01:46:20, user David Steadson wrote:

      Why were respiratory issues etc not part of the symptoms studied? They are typically listed as frequent long covid symptoms. Ref 10 for example says -

      "Insomnia (18.6%), respiratory symptoms (including pain and chest tightness) (14.7%), nasal congestion (12.4%), fatigue (10.8%), muscle (10.1%) and joint pain (6.9%), and concentration difficulties (10.1%) were the most frequently reported symptoms."

    1. On 2021-05-30 06:25:34, user Allan Saul wrote:

      I was struck by the difference in the efficacy estimates in this paper and the estimates from Israel for efficacy against the B.1.117 variant e.g., https://www.medrxiv.org/con...<br /> It would be useful if the authors could make some comment on the apparent differences in results.<br /> Also, I am a bit perplexed at the time frame for estimating efficacy following first vaccination with BNT162b2 vaccine. Paper says that the efficacy was measured "21 days or more after the first dose up to the day before the second dose" . Recommended time for the second dose IS on day 21 so how come there are ANY cases? Presumably, second doses were delayed. In view of earlier data that suggests that the BNT162b2 is substantially more effective in the 4th week following a single dose (in absence of a second dose) than in the third week, it would be useful if the authors can be more explicit about the observation windows.

    1. On 2021-06-01 22:05:39, user st_publichealth wrote:

      The article is interesting. A few questions to the authors. Did you pre-specify the definition of negative PCR?<br /> Did you compare changes in viral loads from the baseline? Since the median viral load was higher in the placebo arm, this might have affected the likelihood of viral clearance at day 6 and it should be accounted for.

    1. On 2021-06-07 12:30:38, user UNG wrote:

      Covishield vaccine is essentially spike protein, while Covaxin was whole virus. I don't understand why the antibody titre was measured against only spike protein? also one should used multiple brand kit (at least two) to get the fair idea of the antibody titre.

    1. On 2021-06-12 09:02:36, user Daksya Siddhi wrote:

      One bit of information that I did not find is the data on the age of the Vitamin D measurements. Since these measurements can span from 2 weeks to 2 years prior to hospital admission, their predictive value for Vitamin D levels at time of infection can't be judged, or at very least, won't be consistent. Can this data be provided?

      Additionally, it is mentioned that the most recent Vitamin D measurement is used. For those patients for whom multiple measurements are available, what is the trend - stable, increasing or decreasing? That could affect their imputed Vitamin D level at time of infection.

    1. On 2021-06-13 17:13:57, user artpatronforever wrote:

      Quote "No drug for prevention or treatment in earlier stages of COVID-19 are yet found;" In an alternate reality certainly that could be true. In that same alternate reality likewise it could be true that a dosage of a vaccine is properly the same for a 100 pound woman as for a 300 pound man. I choose not to place confidence in wisdom offered from that alternate reality where originates such lame disinformation. Truth has no agenda but disinformation certainly does have an agenda.

    1. On 2021-06-14 19:15:42, user Alhaji Abubakari Sadiq wrote:

      Can i please get the vaccine acceptance scale for my study. I will validate it anyway. Maybe provide some information about the it for me

    1. On 2021-03-20 03:55:01, user Jean Tyan wrote:

      Very inspiring and socially relevant work! Regarding your DAG, social determinants of health appear to be confounders on both the pathways between biological aging and healthspan and between biological aging and biological aging* due to the directionality of the arrows. I’m not sure I quite understand the correct analysis approach in this situation when evaluating the potential relationship between biological aging and healthspan—should regression models adjust for social determinants, even though they are conceptualized as an upstream cause? In addition, do you have any thoughts on how social determinants and weathering may be linked differently to aging, depending on the type of health outcome measured? A recent systematic review (Forde et al., 2019) reviewed studies on weathering examining a range of different health outcomes (e.g., allostatic load, mortality, telomere length, etc.) and found conflicting results—I would be interested to hear what you think of how these outcomes may relate to biological aging. Many of these variables are also available in the HRS data and could definitely be interesting to explore using the mediation analysis methods you describe here!

    1. On 2021-03-22 19:00:50, user Trash Trashisfree wrote:

      57 patients in the placebo arm, yet using 54/58 surviving in the placebo arm. Something is wrong in the math it's either 57 patients in Placebo or 58 patients in placebo.

    2. On 2021-03-26 21:03:47, user odevinyak wrote:

      The authors should use Fisher's exact test on mortality data. This leads to p-value of 0.119. The overall mortality difference is non-significant.

    1. On 2021-03-26 17:47:12, user ayman alqunneh wrote:

      • This article represents one of the most robust, well-organized studies I have ever read and reviewed.
      • Its large sample size gives the article a high level of reliability and trust.
      • Although the results of this study did not significantly differ from other studies published in this field, its focuses on Arabic-speaking communities gives its uniqueness and makes it special.
      • Elements assessed by the researcher and his colleagues were inclusive and well selected.
      • Inclusion and exclusion criteria for individuals selected to be included in the analysis make research unbiased.
    1. On 2021-03-27 21:56:08, user Jesse Knight wrote:

      Please note the following correction to the posted article (including numbers in the abstract):

      In the previous version of this work, the parameters theta = [alpha, beta] were calculated incorrectly because the Kullback-Leibler divergence was defined in the wrong direction. The impact on generation time parameters and statistics is as follows (original -> fixed): shape (alpha): 1.813 -> 1.633, scale (beta): 2.199 -> 2.498, mean: 3.99 -> 4.08, SD: 2.96 -> 3.19. The qualitative interpretation of results is unchanged, and the corrected version should appear soon on the Infectious Disease Modelling journal site. We are unable to edit the version posted here. We sincerely apologize for this error.

      The error correction is shown here: https://github.com/mishra-l...

    1. On 2021-03-28 05:46:23, user Kareem Choucair wrote:

      This article really shows what it is like to be a medical student and the crucial role that partaking in research has in their training. I greatly believe that the implementation of an evidence-based approach in exploring this topic has been used excellently and it has really compounded how research participation is one of the most crucial parts of generating an outstanding physician. Hopefully compulsory research modules become more prevalent as a result within medical schools globally. Well done altogether.

    1. On 2021-04-06 18:30:59, user John Simeral wrote:

      A version of this manuscript has now been peer reviewed and accepted at IEEE Transactions on Biomedical Engineering. This medRxiv page will shortly link to that version, which is also indexed at PubMed:<br /> IEEE doi: 10.1109/TBME.2021.3069119. Online ahead of print.

    1. On 2021-04-07 03:09:47, user Jesse Baker wrote:

      I think Table 1 should list, for each age group and month, the actual number of cases and the number of people who were tested for Covid, as these quantities are needed to interpret the case fatality rates (CFR) given there. It is well known that the CFR generally decreases as more people are tested for the virus; the tests discover mild infections otherwise overlooked. If younger people were becoming less likely to seek testing while older people maintained their previous testing habits, this might explain at least part of the observed increase in the CFR and the bias toward younger ages.

      I’m not an expert in such matters, and concern over the new strains P.1, B.1.351 and especially B.1.1.7 extends to the USA as they begin to circulate here. The April 6 New York Times noted an increase in hospitalization among Americans under age 50 during March, but it has yet to be reflected in case fatality rates for that group.

    1. On 2021-04-07 23:31:13, user Risham S wrote:

      What about therapies like entyvio? Can anyone shed some light on that? Many thanks for the study , a great help for CID patients like me. Appreciate it.

    2. On 2021-04-27 20:11:38, user BenSahn wrote:

      I'm one of those people. I had Rituximab infusions in November for IgG4-RD. In March I got the J&J COVID vaccine while on a low dose of prednisone. Last week, after a few weeks off prednisone, blood test showed I had no COVID anti-bodies.

    1. On 2021-04-13 23:06:29, user disqus_pagO5NCOKq wrote:

      From the abstract above: "After the second vaccination, 31.3 % of the elderly had no detectable neutralizing antibodies"... does that mean the vaccination offers NO benefit to 1/3 of the "elderly"?

    1. On 2021-04-15 16:36:59, user AYUSH YADAV wrote:

      I want to ask about the validity of Data on Spectacle Wear, which you obtained from reference no. 20 of your article {Sheeladevi et. al.}, the analysis of Spectacle use was not done in that research paper; it was based on refractive errors, and also the predominant region covered by the reference 20 's study {Sheeladevi et. al.} was of Southern India, while your study takes into consideration a North Indian population, as I shall quote from the study, "Fifteen studies were included from South India, one each from Western and Central India, and one study covered 15 states across India" , I think you need a much better method to assess the Spectacle use in general population.

    1. On 2021-04-16 16:18:49, user S Wood wrote:

      Since we first posted this a couple of results from direct statistical measurements have come out that are broadly in agreement with the paper's results on incidence and its timing relative to lockdown. Figure 1 of this REACT-2 report shows the reconstructed time course of symptom onset, which lags infection by 5 to 6 days. Reported ONS incidence reconstructions from statistical infection survey data tell a similar story. This paper, now published in Biometrics, also produces similar results on incidence and R, by a different approach.

    1. On 2020-05-18 08:51:23, user Joanna Treasure wrote:

      People are citing this study as indicating that chidren do not bring the infection home, but the study only identifies the first person showing symptoms and sign, which may be less apparen in children. Circular argument.

    2. On 2020-08-17 14:30:16, user Ciron Soauv wrote:

      This study was cited in a nice powerpoint (link below) made by the Dr.<br /> Wanderson Oliveira from Brazil Ministry of Health, titled "scientific<br /> evidence of pandemic impact". It is being circulated on WhatsUp, together<br /> with videos from Dr. Ioannidis from Stanford, who suggests mortality rates are<br /> around 0.1%. Unfortunately, many people in that country, where more than 100,000<br /> people died of COVID, minimises the pandemic impact justifying it with those<br /> pre-prints. Noted, no fault on the authors – they are the ones that need to get<br /> “immune” to misrepresentation.

      https://www.sinprolondrina....

    1. On 2021-04-22 07:09:12, user Dimitar Kolev wrote:

      Can somebody please explain how they give results of 18-64 years already, but generally Sweden counties still not even call (or just started to call 60+ years old only). Or those are only risk groups, doctors, law enforcement and army? Or what?

    1. On 2021-04-24 23:50:51, user Chucky2017 wrote:

      I'm not sure where to post for an expert opinion, but I have been searching and still can't find an answer. Maybe someone here could be kind enough to direct me.

      If you delay the Phizer second dose for 3 months (or even 2 months) we see a fall off in antibodies. When you get your second shot what happens? Does it become less effective than if you had it in the 21 days? So basically is there a study that has someone who had it in 21 days, take their blood and compare them to a person that got it 3 months later and see what level of antibodies they have compared to the person with 21 days.

      Canada is delaying the phizer shot by 4 months, would a person be better off not getting the second shot and redue the schedule again.

    1. On 2021-04-25 15:46:55, user Annette Toledano wrote:

      Congratulations on advancing the understanding of the range of symptoms in hospitalized COVID-19 patients. I am surprised that pain was not a common symptom in the population you examined. I found elsewhere (Persistent neurologic symptoms and cognitive dysfunction in non-hospitalized Covid-19 “long haulers.” E. Graham, March 2021, Annals of Clinical and Translational Neurology), pain afflicted 43% of "long haulers." <br /> Are you aware of a review paper on the clinical manifestations of non-hospitalized COVIS-19 patients? <br /> It appears the Cov-Sars-2 virus affinity to target organs varies in different populations. In some people, the innate immune system's initial response in endothelial cells can lead to lung or vascular symptoms. In others, infected nerve cells can lead to pain.

    1. On 2021-04-25 20:26:35, user Steven Wouters wrote:

      Since this study group consisted of health care workers, it is likely that natural immunity was acquired in these individuals. That immunity may also have been acquired asymptomatically without ever testing pcr positive.(1)

      It is possible to find out whether there is naturally acquired immunity by using biomarkers. There is a difference between the antibodies elicited by natural infection compared to that from the vaccine. Since the vaccine does not have other parts besides the S-protein in contrast to wild virus.

      Zhongfang Wang, Xiaoyun Yang, Jiaying Zhong, Yumin Zhou, Zhiqiang Tang, Haibo Zhou, Jun He, Xinyue Mei, Yonghong Tang, Bijia Lin, Zhenjun Chen, James McCluskey, Ji Yang, Alexandra J. Corbett & Pixin Ran https://www.nature.com/arti...

    1. On 2021-04-26 16:44:55, user Stuart Weisberg wrote:

      This article has now been published with a revised title "Distinct antibody responses to SARS-CoV-2 in children and adults across the COVID-19 clinical spectrum". The PMID is 33154590

    1. On 2021-04-27 06:36:03, user Miguel Pedrera Jiménez wrote:

      Hi, I'm Miguel Pedrera, from Hospital Universitario 12 de Octubre in Madrid, Spain. Great job, very interesting manuscript. We have recently published an article about a methodology to obtain useful data for clinical research from EHRs, applied to COVID-19. I am sending you the link in case it is of your interest: https://www.sciencedirect.c...

    1. On 2021-04-29 12:05:31, user Anders Julton wrote:

      Correct me if I'm wrong, but the actual air rate change efficiency of the HVAC alone in the hospital room seems quite low. My calculations yielded about 30% using eq. 2.1.6 in a book (linked below, linking is weird) on air rate change measurements. The control room had roughly 100% efficiency.

      I used C(t = 10)/C(0) ~ 0.5 for the hospital room and C(t=40)/C(0) ~ 0.2 for the control room.

      https://www.aivc.org/sites/...

    1. On 2021-04-29 19:23:16, user ohminus wrote:

      No reference to the national testing strategy? The assumption that asymptomatic people are mainly treated unter OuS is questionable, given how many are tested under the national testing strategy.

      The notion that 50% is a low predictive value is likewise questionable. If anything, given the low prevalence in an asymptomatic population tested without any reason to suspect COVID infection, 80% is a questionably high positive predictive value.

    1. On 2021-05-06 20:18:47, user Murray Stein wrote:

      Important, well-conducted study. Results are puzzling. Antidepressant effects of IV ketamine are nicely replicated. Anti-PTSD effects are not. PTSD symptoms were reduced substantially after first infusion in all 3 groups (albeit statistically significantly more in the standard-dose ketamine group), and then stayed low and drifted a bit lower over the remainder of the study. Response rates were high and non-significantly different between all 3 groups (~60% for each of the ketamine groups, ~ 50% for the placebo group). This high a placebo response would not have been anticipated -- particularly given the selection of participants to have failed at least one adequate SSRI trial (although one wonders if this qualifies them as "antidepressant-resistant"). Will require some rethinking about future PTSD trial designs, including possibility that we should be measuring PTSD outcomes differently (i.e., doing something other than asking repeatedly about the 20 symptoms in DSM-5). I would be interested in hearing what others think, particularly with regard to clinical implications.

    1. On 2021-05-13 22:21:36, user Jason wrote:

      This paper should be removed for the lack of data, incorrect use of equipment as stated earlier, and improper testing conditions. Information such as flow rates, particle size concentration, and thermal conditions should have been presented, however are left out. As stated above, every other study conducted on this matter (which was done with correct equipment) shows very different results. This paper further spreads misinformation about mask efficiency and lacks any supporting scientific evidence or results to support the claims made.

    1. On 2021-09-17 19:08:20, user 4qmmt wrote:

      Seems that the higher antibody titers in previously infected persons can be easily explained by the fact that their immune system was already primed. The broader response to VOC would also reflect that condition. The more important question which this study does not address is whether the higher antibody titers reflect any benefit to the subject. Unfortunately, the study concludes that they do, but lacks any follow-up and provides no actual evidence for such a claim.

    1. On 2021-09-20 16:46:59, user Inga Andersdotter wrote:

      This is exactly what Dr. Scott Gottleib predicted would happen (a subvariant of Delta with mutations taking over next,) so it will be very interesting to keep track of this one. There hasn't been much traction in the general media yet.

    1. On 2021-09-21 11:26:35, user 4qmmt wrote:

      Anti-spike, anti-RBD and neutralization levels dropped more than 84% over 6 months’ time in all groups irrespective of prior SARS-CoV-2 infection. At 6 months post-vaccine, 70% of the infection-naive NH residents had neutralization titers at or below the lower limit of detection compared to 16% at 2 weeks after full vaccination. These data demonstrate a significant reduction in levels of antibody in all groups.

      The decrease reported here for previously infected seems opposite many findings in other papers and suggests that those infected and recovered who then receive the shot lost immunity that they had. That is quite troubling.

      Compare for example:<br /> https://doi.org/10.1038/s43...<br /> https://doi.org/10.1126/sci...<br /> https://doi.org/10.1016/S26...<br /> https://doi.org/10.3201/eid...

    1. On 2021-09-22 12:36:03, user Jakefromstatefarm wrote:

      So if the myocarditis rate is 1/1000 and nearly all of those that developed it were men, isn't the real number for men more around 1/500?

    2. On 2021-09-23 11:48:38, user Arturo Tozzi cns wrote:

      This is the problem with Preprints. <br /> This manuscript lacks the true denominator for the number of vaccinations, therefore it is useless. In order to get published, it requires huge improvements. <br /> However, it will the same go through the press worldwide and will become a must for No-Vaxes.

    3. On 2021-09-24 14:10:59, user Kelly Ellis wrote:

      They haven't compared any unvaccinated people in this study, yet the anti-vaxers are already claiming it proves the mRNA vaccine causes this.

    1. On 2021-09-23 16:12:53, user kdrl nakle wrote:

      Surprisingly high and in discord with most known researches so the real question here is how good is the data collection on infections.

    1. On 2021-09-26 08:50:51, user Robert Clark wrote:

      Ironically, their estimate of 1/1,000 might be right specifically for young men, in Canada, and after 2nd dose.<br /> Firstly, Israel has estimated it in young men as 1/3,000 to 1/5,000, not 1/25,000. Then oddly, by U.S. standards, according to the article, most got Moderna for 2nd dose in Canada, and Moderna the more injurious one, and with more cardiac side effects.

      Robert Clark

    1. On 2021-09-27 10:13:38, user Clemens Hlauschek wrote:

      If Covid-19 deaths have such an impact on a newborn's life expectancy today, you are computing the wrong metric.

      The mortality data above 60 can be used to show that previously calculated life expectancy estimates for them have been overly optimistic, but for not much more. Does that mean we can not remain optimistic about the life expectancy of children born today? From what we know today, children very likely won't die in significant numbers from Covid-19 when they are over 60.

    1. On 2021-09-29 05:55:21, user Maria Schilling wrote:

      "Overall, our study demonstrates the potential of mRNA vaccines to induce, maintain, and shape T cell memory through vaccination and revaccination." ????

    1. On 2021-09-30 10:12:58, user Alberto wrote:

      There seems to be something wrong with the numbers. Among the vaccinated, there are 82 infections, but 168 hospitalizations. Many undetected infections? False negatives? In contrast, among those with natural infection there are 28 infections and 19 hospitalizations.

      Leaving the infections aside, among the vaccinated, the rate of hospitalizations was 0.45%, while among those with natural infection it was 0.34%. That's an overall better protection against hospitalization from natural infection than from vaccination, something completely missing in the abstract. It's true that among those above 65 of age, hospitalizations are a bit higher in the natural infection group (0.52% vs. 0.43%), a less significant difference especially given the low numbers (13 hospitalized in the 65+ natural infection group).

      As for deaths, the numbers are too low in all groups to draw any conclusions. The total deaths in each group are 2 (0.036%) in the natural infection group and 8 (0.021%) in the vaccinated group. Among the 65+ groups, is 2 in the natural infection group (0.08%) vs. 5 in the vaccinated group (0.03%). But then in the <65 group it's 0 deaths in the natural infection group (0%) vs 3 deaths in the vaccinated group (0.02%).

      The numbers and conclusions shown in the abstract are completely at odds with these real numbers shown in the paper itself. Not to mention the strange pattern shown in the numbers where most infections/hospitalizations in the natural infection group happened in June (with very low numbers in July and August), while in the vaccinated group most infections/hospitalizations happened in July and August, with very low numbers in June. So an analysis of June alone would agree with the abstract, but an analysis of July and August alone would be the complete opposite.

    2. On 2021-10-05 13:49:34, user helene banoun wrote:

      This study does not take into account infections between dose 1 and dose 2. Indeed, the vaccinated did not produce enough antibodies during this period and are therefore not considered as vaccinated; but as the vaccination takes place during an epidemic period, we cannot afford to write off the infections taking place during this crucial period.<br /> Indeed, ADE seems to cause post-vaccination outbreaks according to other studies (e.g., https://www.medrxiv.org/con... "https://www.medrxiv.org/content/10.1101/2021.05.27.21257583v1)")

    1. On 2021-09-30 19:29:51, user Jakob Heitz wrote:

      Did you account for the previous infected who died or never recovered, because of long covid?

      This reminds me of a study the navy did of war planes in world war 2. They found the majority of bullet holes in returned planes were in the wing tips and central body. Therefore, they decided to reinforce those parts. What they forgot was that the planes that got shot in the engines never returned to base.

    2. On 2021-10-16 15:36:50, user Alex wrote:

      Clearly there are some very logical arguments here and whilst I think it’s absolutely logical that having had COVID is the best defence against COVID and as the virus is in the environment so we are likely to encounter it again can someone tell me why vaccines are effectively being forced on people and recommended for children even though a large number have had the virus and to date is very low risk?

    1. On 2021-10-02 22:04:46, user Eve Wurtele wrote:

      What do the following abbreviations mean? (They are labels for SRA experimental description. I can't figure this out from reading the preprint. Thanks!!<br /> HCW_0184_FUP4<br /> HCW_0184_FUP3<br /> HCW_0184_FUP2<br /> HCW_0184_FUP14<br /> HCW_0184_FUP1<br /> HCW_0184_BL<br /> HCW_0180_BL<br /> HCW_0175_FUP4<br /> HCW_0175_FUP3<br /> HCW_0036_FUP14<br /> HCW_0017_FUP1<br /> HCW_0017_BL

    1. On 2021-10-03 09:39:18, user kdrl nakle wrote:

      Associated is the key word. It really means nothing. It is like claiming that people not washing their teeth are more susceptible to COVID, which is probably true as they are likely the ones to be with poorer overall health.

    1. On 2021-10-04 17:19:09, user Bearwallow wrote:

      Thank you for this interesting study. Well done! Has it yet been peer reviewed yet? or are your conclusions too easy and cost effective to implement? The world medical industry seems to prefer complicated expensive patented experimental "solutions". I so hope your study receives the attention it deserves. <br /> The dose of honey seems quite large. 1gm/kg/day- just asking- just making sure, is this correct? I saw one other study used 0.5 gm/kg/day. Thank you and keep making your useful discoveries.

    1. On 2021-10-09 23:18:22, user kdrl nakle wrote:

      On the contrary, this research has no practical value whatsoever as we surely won't be seeking polio vaccination against SARS-CoV-2. However it may have a theoretical value in the way to explain why the spread of one virus can inhibit the spread of another.

    1. On 2021-10-12 07:42:23, user Ralph Feltens wrote:

      One conclusion that can not be drawn from this study is that vaccination (with a mRNA-based Covid-19 Vaccine) provides stronger immunity than a SARS-CoV-2 infection.<br /> In contrast to an infection with the virus, with the mRNA-based vaccine only antibodies against the spike protein are produced.

      And T- and B-cell-based immunity is another topic altogether ...

    1. On 2021-10-21 21:51:01, user CDSL JHSPH wrote:

      Thank you for sharing your clinical study! I greatly enjoyed reading your experimental design and wanted to compliment the impeccable organizational flow of this manuscript. I also appreciated the information discussed in the introduction, since I wasn't fully aware of the details regarding BA metabolism and the link it had to the microbiome. I noticed in the section of the results discussing "age related changes in bile acid and microbiome profiles" figure 2D was mentioned twice, if I am not mistaken I believe figure 2C shows an increasing trend with age. I was also wondering whether you encountered any outliers in the P2Ab group, that may have been omitted due to an insignificant contribution, that did not show a significant decrease in conjugated bile acids over time? If there were any, could this be due to confounding lifestyle factors? Once again, this was a very interesting experiment and i'm hoping to see larger studies conducted in the future!

    2. On 2021-10-26 03:27:22, user Rahi Brahmbhatt wrote:

      Dear authors,

      Firstly, thank you to the authors for sharing this commendable work. The manuscript is well written and signifies an important contribution to the field. Furthering research on the effects of the gut microbiome on bile acid metabolism is groundbreaking for the understanding of many metabolic and immune disorders. The introduction and discussion sections were the absolute powerhouses of this manuscript. They both displayed tactics that will help reach a broad audience, such as detailed background information and the connection of bile acid regulation to several high profile metabolic disorders. Furthermore, the specialization of the gut microbiome effects on bile acid regulation on type one diabetes offers great hope in further understanding the pathogenesis of T1D. Both the introduction and discussion sections were clear and easy to follow, and I greatly appreciated the acknowledgement of limitations and areas to improve in future studies.

      However, a few minor points to consider in the methods, figures, and results section. In the experimental design conducted, is there any standardization done to account for the disproportionate sample sizes? Could the inclusion of more subjects that progressed to single or multiple autoantibodies impact the findings for the P2Ab group? In the comparisons between the P2Ab group and the controls, how this gap in sample size (nearly double the amount of CTR subjects) accounted for? Furthermore, a combination of the clinical study setting of the methods section and first section of the results may lead to a clearly understanding of the experimental design as a whole. Currently, the first result seems to repeat the initial study set up than indicate a result from the set up. Also, there is a section in the results that seems to have incorrectly identified 2C as 2D in the written section. Lastly, if possible a condensification and simplification of figures 4 and 5 may allow for a clearer understanding of how bile acid profiles change the regulation of bile acid metabolism in progression to islet immunity. Perhaps a figure correlating the changes in the profile and it's direct change in the metabolism pathways as displayed in figure 3 would help in this understanding.

      Finally, this manuscript opens up many pathways for further gut-microbiome-bile acid regulation studies. The suggestion of incorporating lifestyle factors such as diet and environmental factors that impact the gut microbiome allows for a coherent and logical flow of how research in this field may progress. Once again the paper was an excellent concept and more studies should be done to further our understanding of the gut microbiome's contribution to islet autoimmunity. I look forward to seeing this paper post publication and thank you for your contribution to science!

    1. On 2021-10-23 19:26:47, user kdrl nakle wrote:

      Not going into formulas used but the premise is good and last paragraph of conclusion in regard to boosters is also very good argument.

    1. On 2020-05-25 21:46:44, user ben marafino wrote:

      Interesting finding. However, the study, as designed currently, does not exclude the possibility that the drop in mortality rate in April was principally driven by increased testing picking up more out-of-hospital, and thus less severe, cases. What proportion of the sample was hospitalized in April versus March?

    1. On 2020-05-26 09:04:49, user Plonit Almonit wrote:

      When comparing CFR rates of different countries, the differing testing regimes need to be taken in account (minimally by including the highly differing positive rates per test in the calculation in some way.) A raw data comparison doesn't make much sense.

    1. On 2020-05-27 05:29:08, user Mark van Loosdrecht wrote:

      Nice work congratulations. Measuring in thickened sludge would have the disadvantage of a certain time delay, primary sludge is more direct related to the load of the day of sampling and likely therefore more suitable? Could you establish if there was viral RNA decay between primary sludge and thickened sludge? Any indication if virus was infective?

    1. On 2020-05-30 18:13:16, user Sam Wheeler wrote:

      What's the result for different types of masks? Surgical mask, FFP3 mask, FFP2 = KN95 = N95 mask? The most well known brands like 3M, vs. unknown brands?

    1. On 2020-06-02 14:41:57, user Matthew Healy wrote:

      If at least some of the institutions participating in a seroprevalence study have access to stored blood samples collected before December 2019, those could also be used as negative controls.

    1. On 2020-06-02 15:13:39, user Sinai Immunol Review Project wrote:

      Title <br /> Serum protein profiling reveals a landscape of inflammation and immune signaling in early-stage COVID-19 infection

      Keywords<br /> • Serum Profiling<br /> • Cytokines<br /> • Protein array<br /> • CCL2<br /> • CXCL10

      Main Findings<br /> In this preprint Hou et al., analyze serological immune mediators and other proteins from individuals with early COVID-19 symptoms using an antibody microarray that detects 532 target proteins. Patients were classified as COVID-19 (n=13) or influenza (n=15) based on positive RT PCR test for SARS-CoV-2 RNA (COVID-19) or FluA, FluB, RSV RNA (all classified as influenza group).<br /> 88 up-regulated and 37 down-regulated proteins were identified by comparing COVID-19 and influenza patient groups (p-value < 0.05). Some of those up-regulated ytyl34proteins were reported before, such as IFN-????, IL-6, CXCL8, CCL2, CXCL10 and some that were not previously associated with COVID-19, such as IL-20, CCL27 and IL-21. Complement proteins C1R and C7, as well as PLG were found to be reduced in COVID-19 patients.

      After performing a correlation analysis of the differentially upregulated proteins and clinical data, the authors found a positive correlation between expression of several proteins in the CCL2 and CXCL10 signaling pathways and clinical parameters typically related to liver and renal function, myocardial injury, inflammation and infection, as well as neutrophils counts. Conversely, most of these same proteins show a negative correlation with lymphocyte counts.

      Limitations<br /> The control “influenza group” had patients negative for influenza virus but positive for RSV, and thus the nomenclature should be revised. As noted by the authors, a larger cohort should be used to validate findings. There is no multivariate analysis, and identification of independent or confounding variables. Even though several proteins were differentially expressed between the patient groups, there was significant overlap between the groups, which may preclude the use of any single protein as a biomarker. Data on clinical variables should have been included in main figure. It is unclear why the authors annotated serum proteins in cellular components. Proteins in CCL2 and CXCL10 interaction network are largely overlapping, but the authors do not emphasize it. <br /> Authors didn’t show lymphocyte and neutrophil counts. Since it is known that severe COVID-19 patients can present lymphopenia and neutrophilia, it would be important to have this information in their cohort as they are correlating protein levels with neutrophils and lymphocytes.<br /> Authors claim that CCL2 can act as an autocrine factor that promotes viral replication in infected macrophages, and cite one paper with HIV, but authors should discuss that this chemokine recruits monocytes to the site of infection and then could contribute to the increased inflammatory response related to COVID-19.

      Significance<br /> This study shows the potential use protein array to simultaneously identify many different proteins in serum of COVID-19 patients.<br /> The authors identify several differentially expressed proteins (potential biomarkers) and correlate them with clinical indices that give insights on possible therapy targets in COVID-19.

      Credit<br /> Reviewed by Alessandra Soares-Schanoski as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn School of Medicine, Mount Sinai.

    1. On 2020-06-07 14:24:04, user kenneth katz wrote:

      ABO epitopes are post-translational modifications (diifferent patterns of glycosylation). The S protein is highly glycosylated around the region of receptor binding. Could it be the association of severity correlating with glycosylation variation be because the same glycosylation variation is applied to the S sites and affects S function?

    1. On 2020-05-06 00:34:42, user mvandemar wrote:

      It doesn't state in the study, but wouldn't people willing to venture out to be tested possibly be more likely to be ones who were ignoring social distancing orders, and if so a higher risk population? If that were the case would that skew their extrapolations to the community as a whole?

    1. On 2020-05-06 00:54:07, user Alessandro_Machi wrote:

      We had a U.S. Senior flu epidemic in 2017-2018 that probably killed 100,000 seniors even though only 61,000 were reported. Flu and pneumonia deaths were being renamed among Seniors as death by Natural Causes, Respiratory Failure, Heart Attack on their death certificates. I have multiple links to stories about how badly the flu epidemic was during the 2017-2018 Senior flu epidemic. The problem was no numbers were being reported during the epidemic, thus allowing Emergency response to pretend there was no senior flu epidemic.

    1. On 2020-05-06 06:16:09, user JL Segovia wrote:

      Mike Bray, Craig Rayner, François Noël, David Jans, Kylie Wagstaff,<br /> Ivermectin and COVID-19: a report in Antiviral Research, widespread interest, an <br /> FDA warning, two letters to the editor and the authors' responses, Antiviral Research, 2020, http://www.sciencedirect.co...

      "Ivermectin’s key direct target in mammalian cells <br /> is a not a viral component, but a host protein important in <br /> intracellular transport (Yang et al., 2020);<br /> the fact that it is a host-directed agent (HDA) is almost certainly the<br /> basis of its broad-spectrum activity against a number of different RNA <br /> viruses in vitro (Tay et al., 2013; Yang et al., 2020).<br /> The way a HDA can reduce viral load is by inhibiting a key cellular <br /> process that the virus hijacks to enhance infection by suppressing the <br /> host antiviral response. Reducing viral load by even a modest amount by <br /> using a HDA at low dose early in infection can be the key to enabling <br /> the body’s immune system to begin to mount the full antiviral response <br /> before the infection takes control."

    1. On 2020-05-06 23:30:49, user Bárbara Souto wrote:

      Patients of the non-chloroquine group started to be monitored six days before the chloroquine group. Consequently, it is clear that the chloroquine group participants would have an early clearance of virus RNA. The median of day difference between start of symptoms and start treatment (monitoring) was 6 days. Exactly the same difference between the medians of viral RNA clearance day between the groups, as show in the KM curve. In fact, the results from this study strongly suggest that there is no effect of chloroquine on viral clearance.

    1. On 2020-05-07 22:07:31, user Dan T.A. Eisenberg wrote:

      Have you done any tests to see how stable the samples are for longer periods of time than in this paper? Also, can you clarify which Norgen RNA purification kits you used (Cell-Free or Total RNA kits)? Thank you. Trying to get this ramped up in my lab.

    2. On 2020-09-28 14:47:49, user Screamin_Jay wrote:

      If saliva testing accuracy has been demonstrated to be equal to the nasal swab method, why subject patients to the uncomfortable nasal swab? Why is, then, all testing not saliva-based?

    1. On 2020-05-10 00:42:01, user cm wrote:

      "Assuming a molecular clock rate of 8 x 10- 4 with a standard deviation of 5 x 10- 4 substitutions per site per year, we used TreeTime to estimate the dates of branching events in the phylogeny and re-rooted the phylogeny to maximize the correlation coefficient of the root-to-tip plot. The command-line options for treetime were --reroot least-squares --clock-filter 3 --tip-slack 3 --confidence --clock-rate 0.0008 --clock-std-dev 0.0005. The resulting time trees are provided in Supplementary Data 1."

      Why is the molecular clock assumed without any citation justifying it with empirical evidence?

    1. On 2020-05-11 17:35:00, user DickRuble wrote:

      s-CRP has been shown to correlate with BMI and waist circumference. We know that Covid patients with obesity fare much worse than other patients. It's been shown by others that low vitamin D also correlates (though causality is not established) with high s-CRP. I fail to see the novelty of the finding to justify publishing this paper. A majority of elderly patients show "vitamin D deficiency". They also fare poorly when infected with Covid-19. They also have loss of hair. Should we make them wear wigs, because loss of hair correlates with severity of symptoms?

    2. On 2020-05-19 06:40:04, user Mike Stevens wrote:

      You’ve resubmitted this, but it isn’t any better.<br /> You haven’t even shown a correlative relationship, let alone a causative one.

    1. On 2020-05-15 13:29:32, user Atsushi NARABAYASHI wrote:

      Dr. Wyllie,

      Please tell me saliva collection were before nasopharyngeal collection or after, on each collection.<br /> If saliva collection is after nasopharyngeal collection, saliva may contain sputum from lower respiratory systems.

    1. On 2020-05-15 10:17:49, user Jean-Michel Boiron wrote:

      Hi,<br /> I think you may consider writing "Compared with the control group, HCQ with or without azithromycin (AZI) showed no benefit in viral clearance of SARS-CoV-2 (odds ratio (OR) 1.95, <br /> 95% CI 0.19-19.73) or reduction in progression rate (OR 0.89, 95% CI0.58-1.37)" instead of "Compared with the control group, HCQ with or without azithromycin (AZI) <br /> showed benefits in viral clearance of SARS-CoV-2 (odds ratio (OR) 1.95, <br /> 95% CI 0.19-19.73) and a reduction in progression rate (OR 0.89, 95% CI <br /> 0.58-1.37), but without demonstrating any statistical significance.", which is misleading.

    1. On 2020-05-15 12:51:54, user Marjukka Mäkelä wrote:

      Dear Sir

      Summaryx Ltd, a company preparing systematic reviews (SRs) and health technology assessment reports, is currently finalizing an SR on the effectiveness of using masks in public for preventing the spread of influenza-like illness (ILI). Our literature search produced 6 primary studies and 6 SRs as material, and one of the SRs was a preprint of “Facemasks and similar barriers to prevent respiratory illness such as COVID-19: A rapid systematic review” by Brainard et al. We believe there is a mistake in their GRADE tabulation (Table 1) that seriously distorts the results. For the first outcome “Primary prevention, well wear masks – RCT data – outcome ILI”, they report the risk without masks to be 108 and with masks 102 ILIs per thousand. This is a difference of six per thousand, or six per mil, not per cent, as the abstract tells. When looking at original data, it may be that the numbers ought to be 105 and 102, which gives an even lower effect.

      We suggest Brainard et al. should change their conclusion, as formulated in the Abstract: ”In 3 RCTs, wearing a facemask may very slightly reduce the odds of developing ILI/respiratory symptoms, by around 6% (OR 0.94, 95% CI 0.75 to 1.19, I2 29%, low certainty evidence).” should be corrected to ”In 3 RCTs, wearing a facemask may very slightly reduce the odds of developing ILI/respiratory symptoms, by around 0,6% (OR 0.94, 95% CI 0.75 to 1.19, I2 29%, low certainty evidence).” There are several other places in the paper that need correction regarding this apparent mistake.

      On behalf of Summaryx ltd., <br /> Yours sincerely, <br /> Marjukka Mäkelä, MD, PhD,M.Sc.(ClinEpi)<br /> Professor emerita

    1. On 2020-05-15 14:20:03, user Boonton wrote:

      Has someone read the larger study? How do they verify so few outdoor cases? Given 14 days is a lot to remember for people who haven't been locked down, it doesn't seem clear to me how you know someone didn't get it from outdoors or an outdoor person didn't get it indoors?

    1. On 2020-05-15 22:43:37, user Milesy Mathis wrote:

      Seems like the takeaway is include zinc and start the HCQ/AZM early, not after they become acute and are getting put on ventilators (itself questionable since the standard ARDS vent protocols don't seem well matched to the peculiar oxygen deprivation symptoms without pneumonia that COVID seems to present with). That Univ. of Albany study that CNN was touting has NO MENTION of zinc, another retrospective in the same State - hard to believe that level of ignorance of past research into coronavirus or RNA virus therapy exists among some of these providers.

    2. On 2020-05-19 11:46:53, user James Eridon wrote:

      Very practical, reasonable approach to the issue. Seems to indicate about a 50% reduction in poor outcomes. Not a silver bullet, but certainly a big deal, especially considering the low cost and ease of treatment. Tired of complaints about how it’s not double blind and randomized - that doesn’t make it invalid. It’s the sort of argument made by someone trying to advance an agenda, rather than knowledge. <br /> One minor point. I believe the OR and p-value on Intubation in Table 3 are off. The actual values are somewhat better than those shown.

    1. On 2020-05-17 16:22:51, user Sinai Immunol Review Project wrote:

      Main findings<br /> The impact of SARS-CoV-2 infection and subsequent COVID-19 disease in pregnant women at different trimesters is not well described. The precise influence of a potentially dysregulated antiviral response to this pathogen during pregnancy is unclear, so a better understanding would guide management for pregnant women, who may be more susceptible to infection. Here, Hosier et al. profile a case of a woman with COVID-19 in the second trimester of pregnancy with severe hypertension, elevated liver enzymes, and coagulopathy. These symptoms led to a diagnosis of severe preeclampsia.

      The patient initially presented with a high fever, non-productive cough, nausea, diarrhea, diffuse myalgias, anorexia, and malaise. A RT-PCR test for SARS-CoV-2 RNA in a nasopharyngeal swab of the patient was positive. Upon admission, the patient was treated for hypertension, disseminated intravascular coagulopathy, and she eventually elected to terminate via dilation and evacuation. During surgical management and recovery, the patient developed lymphopenia, though she was able to be extubated and weaned to room air on post-operative day 1. The patient was given hydroxychloroquine. Two days later, her coagulation markers improved, and she was discharged.

      RT-PCR and sequencing and phylogenetic analyses showed that the placenta and umbilical cord were positive for SARS-CoV-2 RNA, but no other major fetal tissues tested positive. Saliva and urine, collected from the patient, also tested positive, although the oral and nasal swabs did not. Whole genome sequencing of the viral genome isolated from the placenta was phylogenetically similar to those isolated from local cases of SARS-CoV-2 infection and those identified in Europe and Australia.

      Serologic testing for patients' antibodies revealed high titers of anti-SARS-CoV-2 IgG and IgM antibodies. These levels were reportedly the highest of the 56 COVID-19 patients admitted to the Yale New Haven Hospital, suggesting that the patient was not unsuccessful in eliciting a humoral response.

      Gross pathological examination revealed a marginally adherent blood clot, presenting as a focal placental infarct, while histological analyses using CD3 and CD68 as markers revealed an infiltration of T cells and macrophages, which suggests that fibrin-dense intervillositis may have contributed to the coagulopathy observed in the patient. No necrotic tissue was seen. Immunohistochemistry staining for the SARS-CoV-2 spike protein and in situ hybridization for the SARS-CoV-2 RNA revealed that the infection of fetal tissue was localized preferentially to the syncytiotrophoblasts of the placenta.

      Electron microscopy confirmed the presence of viral particles (75-100 nm in diameter) in the cytosol of placental cells.

      Limitations<br /> Technical<br /> This report profiles a single patient to describe the impact of COVID-19 in pregnant women. Without a larger sample size, it is difficult to assess, however, how infection or peak disease at a given trimester differentially influence prognosis and clinical outcome. It is also important to note that this patient was diagnosed with an underlying autoimmune disease, psoriasis. It will also be important for future studies to consider the stage of pregnancy and whether COVID infection leads to other pregnancy-related disorders, such as recurring miscarriage, fetal growth restriction and possibly even increase in size of fetus creating challenges for delivery.

      Biological<br /> Finally, it is unclear whether these placental cells express the ACE2 receptor. Though electron microscopy, among other methods, identified viral particles in placental cells and indicated SARS-CoV-2 infection of the placenta, the authors did not demonstrate that the syncytiotrophoblasts expressed the ACE2 receptor, which has been shown to be the target of SARS-CoV-2 viral entry into host cells.

      Additional considerations<br /> The immunology of pregnancy is not static - the myeloid and T cell repertoire of the placental micro-environment is dynamic throughout the different trimesters. For instance, during the first trimester, trophoblastic cells secrete cytokines and chemokines that promote the recruitment and infiltration of circulating monocytes, neutrophils, NK cells, and T cells (1,2). This trafficking is essential, and disruption of any elements of this signaling axis results in poor pregnancy outcomes (1). Notably, NK cells and monocyte-derived macrophages are responsible for decidual vascular and tissue remodeling (1,2).

      The second trimester, however, is described as an anti-inflammatory stage, characterized by the induction of regulatory T cells by decidual CD56brightCD16- NK cells and monocyte-derived macrophages. Interestingly, a population of TH17 cells are also present and expand during the second trimester (1). The third trimester is then marked by a return to an inflammatory phenotype (1). It is unclear how these differential states are influenced by an antiviral response to SARS-CoV-2 infection. The authors reported the presence of macrophages and T cells, but a lack of more specific stains and analyses make it difficult to precisely characterize the immunological anomalies of the placental micro-environment in pregnant women with COVID-19. The role of decidual NK cells is likely to be especially important, given their role in trophoblast-mediated immune modulation during the different trimesters of pregnancy and their role in the antiviral response to viral infections.

      Significance<br /> Hypertensive disorders, like preeclampsia, in pregnant women increase the likelihood for complicated pregnancies, and recent studies of the field suggest that dysregulated immune activity may partially be responsible for these outcomes. The trimesters of pregnancy exhibit different immune landscapes, so the presence of certain microbes, including viral pathogens, is likely to perturb homeostatic immune processes that are required for a normal pregnancy. The impact of SARS-CoV-2 infection, therefore, warrants its own investigation, as the health outcomes of COVID-19 are especially poor. The authors report direct infection of the syncytiotrophoblast by SARS-CoV-2. These cells are derived from trophoblasts, which play an important immuno-modulatory role in all three trimesters of pregnancy. So, collectively, given the role of the ACE2 receptor as the target of SARS-CoV-2 viral entry and the involvement of ACE2 in the physiology of preeclampsia, the two pathologies likely share altered immune states and a dysfunctional renin-angiotensin-aldosterone system (RAAS) as etiologies.

      This review was undertaken by Matthew D. Park as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn school of medicine, Mount Sinai.

      References<br /> 1 Mor, G., Aldo, P., & Alvero, A.B. The unique immunological and microbial aspects of <br /> pregnancy. Nat. Rev. Immunol. 17, 469-482 (2020).<br /> 2 Yockey, L.J., Lucas, C., & Iwasaki, A. Contributions of maternal and fetal antiviral <br /> immunity in congenital disease. Science. 368, 608-612 (2020).

    1. On 2020-05-18 08:41:42, user Anton De Spiegeleer wrote:

      @jkoenin, what do you mean by 'questionably executed' from a scientific viewpoint? We agree it is a small study with limitations (also clearly mentioned in the study), however we believe it is well-conducted and valuable. We would be happy to hear concrete possible improvements of the study or current alternatives to save lives of older COVID-19 residents from you.

    1. On 2020-05-18 23:55:59, user BannedbyN4stickingup4Marjolein wrote:

      I find the conclusions of this paper seem to have been presented in a quite mis-leading way. I say this because of the many Twitter comments above which appear to have come from people who have been thus mis-led: their inference is that contracting Covid-19 is no more dangerous for an under-65 year-old than driving a car.

      This is clearly not what the paper calculates - it looks at the combined probability of both contracting COVID-19 AND death from it during the first wave of the epidemic. An epidemic of this nature spreads in a series of multiple outbreaks each with its own start date and peak. Country totals for a specific date range do not necessarily capture the intensity of a "wave".

      The actual risk of dying from Covid-19 is larger, since we must consider not just the risk of dying in this short period, but over the next 18 months or so (presuming successful implementation of yet to be proven immunisation strategies). This additional risk could possibly dwarf that experienced so far in any location where the government cannot get itself in control of the transmission rate.

      Also, "comorbidities" and "underlying diseases" are referred to, but given no clear definition. What for example is "hypertension"? Does it involve having been prescribed medication for this condition? Having abnormal blood pressure recorded at any one time? Without careful examination of the data and these definitions, it could just be that most of the dead have ended up being lumped under the comorbidity/underlying diseases heading, with a resulting bias to the study's conclusions.

    1. On 2020-05-19 03:07:59, user rferrisx wrote:

      Hoping to find these two segregated: "Prior COPD or asthma". Trying to figure out why the 25M who have asthma in the US don't show up much at all in Covid-19 comorbidities.

    1. On 2020-05-19 09:44:20, user Ivan Berlin wrote:

      This is a unique sample. Why not to compare the COVID-19 + sample to a matched COVID-19 - sample? We lack case-control studies in this field.

    2. On 2020-09-14 23:14:12, user arkancide_is_real wrote:

      When are we going to see the data associated with this project? Source code merely shows how to generate output.

      The data should be openly available, given the supervising author's history.

    1. On 2020-05-22 01:22:41, user Dee Bee wrote:

      So one wonders how the model does in predicting the pandemic path as controls are relaxed. From a couple of statements, at the end of the abstract indicates, seems like not so much.

    1. On 2020-05-25 09:06:03, user Paul Ananth Tambyah wrote:

      Would be good to know the breakdown within the bigger groups of healthcare professionals and healthcare associate professionals - in particular how many had direct patient contact

    1. On 2020-08-02 18:17:55, user iVX Engineering wrote:

      Why on earth they used such dangerously high dosing (800mg per day is the daily max according to FDA, with most other studies using 400) 2400mg dose in the first day? This is a toxic dose. What is these doctors trying to do, intentionally poison patients? Who reviewed the ethics of doing this and why was this allowed? And why are there no comments in the paper justifying this extremely high dosing? In addition to this there needs to be a portion of the discussion addressing how potential toxicity from high doses may have influenced the results.

    1. On 2020-07-30 17:31:33, user Wayne Saslow wrote:

      Aerosol-sized droplets have been studied by physicists since at least 1897, when J. J. Thomson used them in determining the properties of electrons. In a chamber with no air current, he observed the fall of a water droplet; from its terminal velocity v he estimated the droplet radius R -- at terminal velocity the force of gravity downward is balanced by the (Stokes) drag force upward. The gravity force varies as the droplet volume (proportional to the cube of R) but the Stokes drag force is proportional to vR, so at terminal velocity v is proportional to the square of R: doubling R makes v four times larger.

      Therefore the larger droplets in an aerosol fall out quickly, but the smaller droplets (but not too small to include a virus particle) remain much longer. So it should not be surprising that aerosols are important for coronavirus transmission; they stay in the air much longer than larger droplets.

      To finish the story, knowing the droplet radius R helped Thomson in the following way: he was able to obtain the gravitational force on the droplet. He then put a sheet of negative charge below the aerosol, and found that some of the droplets floated, so the electric force due to electrons on the aerosol cancelled the gravitational force. This permitted an estimate of the charge on the electron. A few years later Millikan used less-quickly evaporating oil drops to make a more accurate measurement of the electron charge.

      Why care? Without electrons, no atoms; without atoms, no molecules; without molecules, no DNA; without DNA, no biology.

    1. On 2020-08-02 00:11:16, user Michael Verstraeten wrote:

      I would like to make also a suggestion. <br /> 1. Calculate the amount of people infected in the whole population on the highest result of your research, by age category. (That's a simplification since there are also other relevant factors then age, like comorbidity factors but ok). <br /> 2. Add to this amount the results from the positive PCR-tests in the hospitals until that moment (Also a problem since there is a % of false negative results, but ok) <br /> 3. Estimate the amount of patients whit a general problem who were refused to get a blood test due to a suspicion of Covid - 19 and were not admitted to the hospital (if possible). And add them to the grand total. <br /> 4. From there on you can make an estimate based on the weighted average evolution of the deaths from de date corresponding to the testdate pn (a few days later then the test dates). It seems to be a relatively good assumption to consider that de evolution of the infections will be relatively equal to the evolution of the deaths / age category. <br /> 5. There is one problem however: we are not sure about the exact amount of deaths due to Covid. 73 % of people deceased in the care homes were not diagnosed and the tests have a big error margin. And diagnoses are maybe wrong due to extended diagnose protocols. Maybe it would be a good idea to calculate an average on the evolution of deaths and hospital admissions. Even if the latter depends on the admission policy.

      Even with the uncertainties and the quite big error margin, maybe it will be possible to come with such an exercise closer to the real number of the infected population.

    1. On 2020-08-05 12:20:29, user Per Sjögren-Gulve wrote:

      Have the authors tested whether the sample of incubation days is normally distributed or not? If not, it is more appropriate to present the range of the observed values than to report 95% CIs. The latter requires that the parameter is normally distributed (the arithmetric mean is equal to the median).

    1. On 2020-08-05 17:49:59, user Dieter Mergel wrote:

      Note from the author:<br /> Error in Figure 4 and Figure 5.

      Fatality rates leT2000 in Figure 4 and lT18 in Figure 5 have to be shifted by 18 days to earlier dates. Fatality rate lT20 has to be shifted by 20 days to earlier dates.

      Updated version will be available shortly.

    1. On 2020-08-17 14:11:29, user Aaron J. Courtney wrote:

      Is the mask modeling based upon a surgical mask? Have you rerun the model assuming everyone wore N95s? Any eye protection to guard against conjunctiva infection? What factor did aerosol transmission, particularly fecal and urine aerosolization in community rest rooms, account for infectivity calculus? (recall Hong Kong high rise apartment building SARS-CoV-1 outbreak caused by faulty plumbing)

    1. On 2020-08-21 09:47:26, user David Simons wrote:

      Hi,

      It looks like this may already be formatted for submission but you may want to revisit the inclusion of Qi (reference 16) in particular.

      The relevant pre-print has only dichotomised smoking into current and non-current smokers. The authors do not make clear that non-current smokers are never smokers. I've found this difficult to mannage in our own work so we do not include them in meta-analysis if there is no explicit never smoker category. It is unclear from your manuscript how you manage this.

      Kind regards,

      David

    1. On 2020-08-23 18:52:01, user Michael Shodell wrote:

      Greatly enjoyed this paper as the logic, assumptions, and<br /> analyses are very-well described and readily followed. This also enables good critical assessments<br /> of the range of confidence to place in the numbers at which the author<br /> arrives. HOWEVER – by ignoring<br /> everything other than the sedentary in-flight, non-perambulating and generally<br /> observant passengers (see excerpts below), the author may have missed the<br /> greatest risk areas of flying.

      For instance, when disembarking at the destination, the more<br /> crowded the plane (eg. a plane with middle seats occupied), the riskier this<br /> part of travel. I can tell you from recent<br /> experience that for up to 10 minutes passengers crowd the aisles awaiting disembarking<br /> and, being the flight conclusion, often with masks at half-staff or barely<br /> covering the face at all.

      Probably similar consideration for use of toilets and aisle<br /> movement during the flight.

      106 We focus on a particular passenger who is traveling<br /> alone, and assume that the primary

      107 infection risk for this passenger arises from other<br /> passengers in the same row. We further

      108 assume that additional risk arises from passengers in<br /> the row ahead and row behind. For two

      109 reasons, we treat the risk posed by other passengers as<br /> negligible …

      … we treat the risks associated with boarding

      119 the aircraft, leaving the aircraft, visiting the<br /> lavatory, and touching surfaces in

      120 the passenger cabin, as second-order effects.

    1. On 2020-08-24 17:34:34, user Muhammad Shoaib Akhtar wrote:

      Seems good work. However, biochemical analysis of remedesivir inside body is an important aspect and must be focused as well.

    1. On 2020-08-25 17:13:15, user Benjamin Kirkup wrote:

      Despite some discussion and speculation about the diversity of the strains in a single patient at the start of one local outbreak, I don't see any data or analysis reflecting on the measured viral diversity of SARS-CoV-2 within any of the clinical samples; nor an analysis of whether that can be used to tie individuals together via the minor populations, for example [https://www.biorxiv.org/con...]. Instead, each sample is reduced, mapping to reference, to a consensus genome or partially covered consensus genome. Is there a way you could address the potential for minor populations in the samples; and leverage that for greater resolution in the transmission analysis?

    1. On 2020-08-25 19:43:48, user Allan H. SMITH wrote:

      Some readers may be misled by the title and abstract of this paper into thinking the Covid-19 epidemic is under control.

      Dr. Bhatia acknowledged that I was a reviewer, and I have been reviewing drafts of the paper and providing comments along the way. It is good to see work on epidemiological data concerning Covid-19. More is needed if we are to learn from the tragic mistakes which have been made in responding to the outbreak.

      My reason for writing this comment is that I fear it may appear to some that this paper indicates that the epidemic has been under control since early March. The confusion may arise from misunderstanding the term “epidemic growth rate”. If there were a sequence of 1,2,4,8,16,27 one could state that the epidemic growth rates has declined in the last period because the last number is 27, and not 32 which would be expected with a continuing doubling of rates. In fact, the greatest increase in this sequence is in last period, going from 16 to 27, an increase of 11 compared to the previous largest increase of 8. So, stating that the epidemic growth rate is declining does not mean the epidemic is under control.

      In fact, the epidemic in the United States charges on and is out of control. You can see evidence for this in Figure 1a in Dr. Bhatia’s paper. Hospital admission rates are mostly much higher than in early March, and many places have evidence of a resurgence in July.<br /> Mortality data give clear evidence of the catastrophe being experienced in some countries, especially the United States, Brazil, Peru, and India. The Johns Hopkins Coronavirus website gives excellent tracking graphs. https://coronavirus.jhu.edu/data/cumulative-cases You can get the death numbers by clicking in the dropdown box on the left. The top line in the graph is for the United Sates. You can see the curve seemed to start to flatten, but it has taken off again. I think this can reasonably be termed a public health catastrophe. Mortality rates like these have not occurred in any other developed nation, and they could have largely been avoided.

      To conclude, I thank Dr. Bhatia for his paper and extensive work analyzing the data, and for sharing it with me.

    1. On 2020-08-26 12:22:50, user Keir Philip wrote:

      A typo has been noted in table 3, which currently reads "No risk of cross infection", but should read "potential risk of cross infection"

    1. On 2020-08-29 05:11:06, user Daniel Connelly wrote:

      The practitioners at our office in NJ have been prescribing HCQ +zinc + azithromycin or doxycycline to newly diagnosed symptomatic Covid-19 patients since March. Our sample size is small and includes nursing home patients. To date, all patients improved rapidly, usually within 24 hours. The were zero hospitalizations, zero deaths and no reported side effects.<br /> The import number from the study is only 7.6% of outpatients were prescribed the drug. This could be because they were asymptomatic at the time and did not need it or it could be because of the oppressive political climate that suppressed the use of this life saving drug in New Jersey.

    1. On 2020-08-30 22:20:50, user JimboKatana wrote:

      Is the virus truly decreasing in virulence or is it following the phenomenon of decreased severity that occurs with viruses in the summer?

    1. On 2020-09-06 08:30:14, user Aporia wrote:

      No matter how you criticize the data- every argument still places these estimates FAR lower then what the media has been pushing . Add to that Dr Ioanidis's talks - we did this by being pushed into a panic- the total years of life lost this season due to Covid is on par wt a flu, but the lockdown will cause REAL LIVES LOST - via deaths of despair (suicides, crime, od etc)

    2. On 2020-09-08 19:17:49, user Jacques des Anges wrote:

      Some general data:<br /> in the US for the age group of 45-64 (82million people) there are about 30,000 deaths involved COVID-19, or about 1 in 2667. And about 1 in 2000 for the age group of 55-64. And over 6 million total confirmed cases in the US by sep 5th, or about 1 in 54 people?

      While the ensemble level infection and fatality probabilities for individual person to person contact calculated in the study might be useful for epidemiologists, they are not helpful for individuals to do a risk assessment in any way. Even if the results were accurate and the conclusions valid, which is what peer review helps to establish.

      The paper give a false sense that the risk is really low when the actual fatality numbers paint a different picture on individual interaction infection probability and overall outcomes. It will cause people to underestimate the probabilities, as is very common; see also: birthday problem. (https://en.m.wikipedia.org/... "https://en.m.wikipedia.org/wiki/Birthday_problem)").

      Numbers from CDC as of sep 5 2020. <br /> https://www.cdc.gov/nchs/nv...

    1. On 2020-09-06 14:23:35, user Knut Wittkowski wrote:

      The hypothesis of two strains in my manuscript, starting in the March 31 version, was confirmed in a July 2 paper in Cell. Korber (2020) identified two strains, D614 and G614, of which G614 is more virulent and arrived in Europe first in Italy.<br /> https://doi.org/10.1016/j.c...

    1. On 2020-09-07 11:18:03, user Maria Elena Flacco wrote:

      There are at least two major issues in the present pre-print manuscript:<br /> 1. <br /> The authors report that only one meta-analysis, published on MedRxiv, is currently available on the association between ACEi/ARBs use and severe/lethal COVID-19. However, at least two meta-analyses have been published on the topic in Medline-indexed journals (see for example Flacco et al Heart 2020 Jul 1:heartjnl-2020-317336 - doi: 10.1136/heartjnl-2020-317336);<br /> 2. <br /> All the included data seemingly came from observational, retrospective studies. The authors meta-analyze them computing RRs (and 95% CIs) using raw data, as if the studies were randomized controlled trials. This approach is not correct, as it is based upon unadjusted (and non-randomized) estimates: to account for the observational nature of the included data, a generic inverse-variance approach should have been used.

    1. On 2020-09-07 18:33:30, user Sunil Bhopal wrote:

      I have read the methods section several times and can't find any description of the tool or administration method for asking about these symptoms. Was this retrospectively done? At what time point? What was the recall period? Who asked the questions? Were they free-answers or multiple choice and so on. My apologies if this is already written up but I can't see it. Best wishes, Sunil Bhopal

    1. On 2020-09-11 04:45:37, user Guest wrote:

      Very insightful! As described in method section, you included variable with p < 0.2 for your model C, but as I can see from table 3, the variable "Age at first marriage" has p value > 0.2 in model B yet this variable was included in model C. I'm curious to know what assumptions were made to retain this variable for the final model despite it clearly could not pass the p<0.2 criterion?

    1. On 2020-09-13 16:40:32, user kdrl nakle wrote:

      One more non-randomized study where the selection of patients was obviously done with respect to their conditions. You can see that from age distributions of two groups. This repeats the same errors of previous non-randomized studies with roughly the same erroneous conclusions.

    1. On 2020-09-16 11:31:32, user Robert Eibl wrote:

      I remember the online meeting with a young virologist / university physician with patients; he claimed that, surprisingly, the co-infection of SARS-CoV-2 and influenza appeared to be lower than expected, but this was probably just the end of the flu season in Germany, when COVID-19 just gained speed.

    1. On 2020-09-16 12:25:37, user Paulo Portinho wrote:

      Hello, I could not understand how the estimated standardized cumulative death rates are 0.23% for HCQ group and 0.22% for NONHCQ group.<br /> Deaths NONHCQ 477, sample 164.068 = 0,29%.<br /> Deaths HCQ 70, sample 30.569 = 0,228%.<br /> I know it is standardized, but shouldn't it be around the average number?

    1. On 2020-09-18 17:21:48, user kdrl nakle wrote:

      Dysfunctional response of T cells (not just elderly) has already been reported in papers before but the reasons were unclear.

    1. On 2020-09-22 13:49:24, user Calvint33 wrote:

      Useful data. But if a ~30% reduction is not significant, then study was underpowered, no? Because 30% would be enough to act upon. Evidently the infection rate in Manitoba was too low for a good test even with this very sizable sample.

    1. On 2020-10-05 16:41:55, user Michael Sibelius wrote:

      Nice work! Now that epidemics have progressed quite a bit further in many of the countries mentioned in the paper, is there some evidence that this heard immunity due to variation in susceptibility, as discussed in this paper? I think I have seen it mentioned with regards to some individual geographic pockets in Italy and the US, but would be great to hear from the authors of this work.

    1. On 2020-10-14 16:27:56, user Darren Brown; HIV Physiotherap wrote:

      1) It would be beneficial to reference the long-term consequences (or sequelae) of COVID-19 as the patient preferred term of 'Long COVID". https://blogs.bmj.com/bmj/2....

      2) This manuscript has been poorly constructed. The structure should be introduction, methods, results, discussion, conclusion. This requires major revision.

      3) Because of the poor construction of this manuscript it is unclear to the reader what statistical hypothesis testing has been performed. It is not suitable to put statistical methodology in brackets in the results section.

      I would reject this submission, requiring major revisions.

    1. On 2020-10-27 04:44:07, user Crispus wrote:

      Did not control for vitamin D levels, zinc, viral load or obesity, nor was that data collected. Since these were not controlled, from what I gather, then it's possible that one group may have had more vitamin D, zinc or Greater BMI than the other groups. This means that if I tested for correlation between the mentioned factors and treatment, the correlation between the two would not be zero...An example of this would be if the group with higher obesity is more likely to be of the HCQ group. Hence a serious concern of potential omitted variable bias. Now just because bias is present doesn't mean the findings are useless. It depends on the direction of the bias. But many health practitioners recommend supplementing vitamin D and zinc, and it's known that obesity and viral load have an impact on mortality.

    1. On 2020-11-15 21:13:34, user Atomsk's Sanakan wrote:

      Some flaws in this study that render it's IFR estimate unreliable:

      1) He uses many studies that over-estimate the number of people that were infected [and thus under-estimate IFR], since these studies were not meant to be representative of the general population Ioannidis applies them to. He doesn't even follow PRISMA guidelines for assessing studies for risk of bias in a study's research design. "Bias" here does not refer to the motivations of the study's authors, but instead that the design of their study would likely cause their results to not be representative of the general population.<br /> 2) He exploited collinearity by sampling the same region multiple times, in a way that skews his results towards a lower IFR. He conveniently tends to avoid sampling an area multiple times when that area has a higher IFR.<br /> 3) He adjusts IFR downwards for reasons not supported by the analysis he cites for that adjustment.<br /> 4) He takes at face-value areas that likely under-estimate COVID-19 deaths, such as Iran, causing him to under-estimate IFR further.<br /> 5) He uses inconsistent reasoning to evade government studies that show higher IFR, even though governments are doing much of the testing needed to determine IFR. That includes Ioannidis ignoring large studies from Italy and Portugal that are more representative of the general population they sampled.<br /> 6) His IFR from a study in Brazil contradicts the study's own IFR, and his explanation for that makes no sense. This conveniently allows him to cut the study's IFR by about a 1/3.<br /> 7) His use of blood donor studies does not make sense, even if one sets aside the fact that blood donor studies would over-estimate population-wide seroprevalence. For example, he uses a Danish blood donor study that leaves out deaths from people 70 and older, to claim an IFR of 0.27% for adults. When those researchers performed a subsequent study in which they included people 70 and older, they got an IFR for adults that's 3 times larger than Ioannidis claims [0.81% vs. 0.27%].

      And so on.

      The sources below provide further context on this:

      https://rapidreviewscovid19...<br /> https://rapidreviewscovid19...<br /> https://rapidreviewscovid19...

      https://twitter.com/GidMK/s...<br /> https://twitter.com/GidMK/s... [ https://threadreaderapp.com... ]<br /> https://www.medscape.com/vi... { http://archive.is/O3vGs , https://threadreaderapp.com... }<br /> https://hildabastian.net/in...<br /> https://twitter.com/AVG_Jos...<br /> https://twitter.com/Atomsks...<br /> https://twitter.com/Atomsks...<br /> https://twitter.com/Atomsks...

      "Estimation without representation: Early SARS-CoV-2 seroprevalence studies and the path forward"<br /> Not-yet-peer-reviewed: "Assessing the age specificity of infection fatality rates for COVID-19: Meta-analysis & public policy implications" (comments on "selection criteria")

    1. On 2021-08-11 09:40:50, user Joao Martins wrote:

      Incredible! Violation of the underlying assumptions of the test used in this article!

      From its ref (10), Tajima's original proposal of D' test:<br /> "Assumption: In this paper we consider a random mating population of N diploid individuals and assume that there is no selection and no recombination between DNA sequences."

      Tajima's D' applies to "random mating populations of diploid individuals": do RNA-viruses fit in this description?

    1. On 2021-08-12 12:38:42, user Peter Colin wrote:

      Has there been any analysis of vaccine effectiveness in (1) persons who tested positive for Covid prior to vaccination, versus (2) persons who did not test positive prior to vaccination (negative and/or untested)?

    1. On 2021-08-18 15:39:23, user Lincoln Sheets wrote:

      This analysis seems to present a paradoxical finding, that there is an inverse relationship between early deaths from cancer and early deaths from CVD. If high animal-source diets lead to more early deaths from cancer, does that make it impossible for those same persons to die early from CVD? This is a detailed big-data study that deserves reivew, publication, and expansion by additional researchers.

    1. On 2021-08-23 04:17:45, user Anon wrote:

      How about selection bias? Vaccinated people take covid more seriously which would lead to less infections.Not to mention this study was before Delta took over so the results are irrelevant

    1. On 2021-08-26 11:13:46, user Fran Braga wrote:

      There's an English mistake in the interpretation section "Interpretation". The sentence "Coronavac vaccinees above 55 years" is repeated

    1. On 2021-07-11 12:03:24, user Charles L. wrote:

      At least in Fig.1, colors are interchanged (blue, and not green, seems to be the susceptible group).<br /> Also, wouldn't be more realistic to model when 70-80% of population is fully vaccinated? As a 100% vaccination campaign will never be achieved and official govt. states that 70-80% vaccination is the goal in several countries.

    1. On 2021-07-12 02:43:41, user Jennifer McDonald wrote:

      Dr Conly et al, I read your pre-print with interest. I have a few clarifying questions.

      First, given the demonstrated viral stability on hospital equipment/PPE, I am curious why there was no attempt to collect virus directly from used PPE. Does the pre-publication contain the full list of objects/equipment sampled, including those with negative results?

      Second, can you elaborate on the sampling method used to obtain the positive cultures off hands? Were these samples collected at random or immediately following a cough into the hands? Regarding the hand transfer experiment, were the hands washed in culture medium immediately following the transfer? Was this experiment attempted with a longer duration between cough-handshake and handshake-culture?

      Thank you for clarifying,<br /> Jennifer McDonald, MD, Ottawa

    1. On 2021-07-13 02:15:24, user ?0 wrote:

      Will note that absolute risk reduction between vaccinated and unvaccinated is 0.32%. The authors’ claims that the vaccines prevented death are not supported by the evidence provided, which is correlated in nature, not causative.

      A good paper on this issue: https://www.ncbi.nlm.nih.go...

    1. On 2021-07-14 20:26:08, user bruno ursino wrote:

      I came by this article now, so sorry for posting a comment at this time but it seems to me that no one pointed this out: the formula for the evaluation of Rt is completely wrong, indeed this can be shown just by applying this same technique to a simple SIR model.

      I think it's impossible to send here my plots, but I ask you to execute the following code using octave or matlab:<br /> `tf = 300;<br /> dt = 0.01;<br /> t = 0:dt:tf;

      mu = 1.7/100;

      T = 17;<br /> alfa = 1/T;

      R0 = 4;

      bN = R0*alfa;

      S = zeros(1,numel(t));<br /> I = zeros(1,numel(t));<br /> R = zeros(1,numel(t));<br /> d = zeros(1,numel(t));

      S(1) = 0.99999999;<br /> I(1) = 1 - S(1);

      for k = 2:1:numel(t)

      S(k) = S(k-1) + dt(- bNS(k-1)I(k-1));<br /> I(k) = I(k-1) + dt(bNS(k-1)I(k-1) - alfaI(k-1));<br /> R(k) = R(k-1) + dt(alfaI(k-1));<br /> d(k) = mu(R(k) - R(k-1));

      end

      T_steps = T/dt;

      Ri = zeros(1,numel(t));

      for k = (T_steps+1):1:(numel(t) - T_steps)

      aux = dt(sum(d((k):1:(k+T_steps))) - musum(d((k-T_steps):1:(k))));<br /> Ri(k) = d(k+T_steps)/aux;

      end

      R_t = zeros(1,numel(t));

      for k = (T_steps+1):1:(numel(t) - 2*T_steps)

      R_t(k) = dt*(sum(Ri(k:1:(k+T_steps))));

      end

      figure, plot(t((T_steps+1):1:(numel(t) - 3T_steps)), R_t((T_steps+1):1:(numel(t) - 3T_steps)))<br /> grid minor<br /> hold on<br /> plot(t((T_steps+1):1:(numel(t) - 3T_steps)), R0.(1-R((T_steps+1):1:(numel(t) - 3*T_steps))))`

      the blue line will be the Rt evaluated using your formula, while the red one will be the true Rt value. It's not only a matter of the exact values, but most importantly the issue is about the fact that your formula antedates the day in which Rt starts to decrease of a full month, thus it's not possible to use it to actually prove that the measures did or did not have an effect on the Rt value.

    1. On 2021-07-15 07:57:35, user John Lambiase wrote:

      What's truly interesting is that no one is talking about Fructose and refined sugar activating long term NLRP3 inflammasome in the Monocyte which reprograms the monocyte on a path of inflammation and upregulation of Reactive oxygen species which lowers nitric oxide in Endothelium. Sars CoV-2 seems to have a knack of exploiting and exacerbating this chronic inflammation in patients leading to an acute medical malody.

      What deactivates NLRP3 inflammasome? Olive Oil, Melatonin, Vitamin D Fish Oil, Resveritrol, Quercetin etal. Been taking doses of Oleic Acid for months because of all the research I was finding. Cashews high in Oleic Acid. If this all comes down to Anti Oxidants vs Oxidants then medicine is going to have serious explaining to do. Unfortunately that would never get out.

    1. On 2021-07-15 13:36:08, user Merlin Khoo wrote:

      This laboratory study seems to indicate the need for a booster 3rd jab based on the latest variant as the virus mutates further and further from the original wild type

    1. On 2021-07-16 09:27:55, user ??? wrote:

      There's recently published article presenting the application of brain temperature rhythm in outcome prediction after traumatic brain injury. This paper should be cited.<br /> "Kuo, L.-T.; Lu, H.-Y.; Huang, A.P.-H. Prognostic Value of Circadian Rhythm of Brain Temperature in Traumatic Brain Injury. J. Pers. Med. 2021, 11, 620. https://doi.org/10.3390/jpm..."