10,000 Matching Annotations
  1. Last 7 days
    1. On 2022-09-05 18:03:38, user Michael L. wrote:

      Appreciate the close look at mechanism and the robust set of readouts. Overall an excellent study that will set a new benchmark for characterization of humoral responses to vaccination.

      Am curious about the group defined as having an interval between prior infection and booster of <180 days. These were 6 out of the 11 prior-infected patients. Would it be possible to show all intervals so we can see if the 180-day cutoff makes sense, and also see the distribution of intervals within this group? For example, there may be different implications if 5 of 6 patients were infected within 30 days before boost, vs. 5 of 6 patients infected more than 170 days ago.

      Thank you for the nice work.

    1. On 2022-09-13 12:47:02, user Yonatan Oster wrote:

      The article was published in a peer-reviewed journal:

      Cohen MJ, Oster Y, Moses AE, Spitzer A, Benenson S; Israeli-Hospitals 4th Vaccine Working Group. Association of Receiving a Fourth Dose of the BNT162b Vaccine With SARS-CoV-2 Infection Among Health Care Workers in Israel. JAMA Netw Open. 2022;5(8):e2224657. Published 2022 Aug 1. doi:10.1001/jamanetworkopen.2022.24657

    1. On 2022-09-23 18:40:11, user Andre Caldwell wrote:

      This is an interesting paper, with an innovative study design which includes individuals with specific mutation and risk variants for Alzheimer's disease. <br /> I really wanted to like this paper, but after ready it in depth, just the study design is worth.<br /> 1) this study generated data in more than 1 million nuclei. After QC only 300K pass QC, meaning that more than 70% of the data was removed. when a study remove 70% of the data, it is not clear if what is left is reliable. This is very concerning indicating a large problem in nuclei extraction, batch effect or data generation.<br /> 2) the most common cell type on this study was oligodendrocytes which is totally unexpected. None of the other published studies using the technology has this finding. In fact, normally neurons is the most common cell type. This support that there is a large problem with this data.<br /> 3) the authors forgot to include a very basic comparison which is the major cell proportion vs. status. This is striking as the authors have a nice previous papers in which they do the same with deconvoluted bulk-RNA seq and single nuclei RNA-seq. No presenting this data is suspicious, as is it one the basic analyses and a good positive control.

      Besides that, the paper is difficult to follow, tries to cover many things, but fails to go in any in detail or provide any interesting results, making the study very descriptive without providing clues about disease pathogenesis.

      this paper have been as a preprint more than one year, suggesting that the authors are having problems to published these findings. May be the reviewers had several concerns.

    1. On 2020-04-23 04:46:38, user Dennis Maeder wrote:

      Although flawed, this emphasizes the need for good representative sampling and antibody testing and the strong possibility that current case counts are wildly underestimated.

    2. On 2020-04-20 08:50:19, user dixon pinfold wrote:

      A great many commenters assert that people worried that they'd been exposed to the virus would be over-represented in the study. This seems speculative up to a point, but certainly plausible, and I do not wish to debate it.

      Some then go on to assert that anyone else would be too afraid to leave the house. Here I think they are on much less solid ground.

      For one thing, not knowing what was in the recruitment ad, we don't know if they were aware that they would remain in their cars, windows rolled up till finger-prick time.

      For another, it places a decisively higher estimation on fear (of infection resulting from the single excursion to the testing site) than on curiosity motivated by the desire to be rid of such fear once and for all. This must be true for some people, but for some, surely, it was the other way around.

      Then there is the matter of age. Here I freely admit to the speculative element, but it has been for me very easy when out in public in recent weeks to tell by their behaviour how much less fearful younger people are, if they're fearful at all. Who could fail to notice?

    3. On 2020-04-17 21:03:35, user John Ryan wrote:

      The researchers identified that 50 out of 3,300 participants tested positive for CV-19 antibodies. Spinning this as 50 to 80 times greater than current prevalence rates as determined through testing is disingenuous. The posted study does not account for the significant upward adjustment from 1.5% of participants to a 2.4% to 4.2% in the general population given the study participants were a skewed convenience sample drawn from Facebook participants, many who believed they had been exposed to CV-19 and had had previously experienced symptoms consistent with CV-19.

    4. On 2020-04-17 21:28:07, user Daniel Shanklin wrote:

      This study abstract should be rewritten as follow: "A study of Facebook users who thought they might have COVID-19 resulted in a roughly 2.49% to 4.16% positive-test rate"

      The fact that you've extrapolated this to an entire population is confounding.

    5. 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 2020-04-23 12:44:36, user dirk van renterghem wrote:

      The problem is the absence of randomisation. Were patients given HC or HC+Azitro at admission, or because they were deteriorating? If so (in some) we cannot compare the deteriorating with the non-deteriorating population... In the HC group 17% had creatinine>5mg/dl, much worse than the no-drug group... , also more anemia an lymphopenia.

    2. On 2020-04-21 20:33:30, user Roleigh Martin wrote:

      Why was not Zinc added to the dosage, many clinical reports have been made about how critical Zinc level monitoring and Zinc supplementation is to successful use of this Rx.

    3. On 2020-04-22 02:06:38, user David B Joyce wrote:

      19 patient shifted fromNo HC to HC(7) or HC+AZ(12) after ventilation. Ventilation is obviously a sign of increasing severity and greater risk of death. If all of these ventilations resulted in death, then the pre ventilation treatment fatality statistics might look like 22%(HC), 13% (HC+Az) and 21% No HC. Need the data on individual outcomes. Also not impressed with the cohorts.

      SPo2 >95: 63%(HC) 57.5%(HC+Az) 73.4%(No HC)<br /> BP> 159: 19.6% 9.7% 9.5%<br /> creatinine>5 17.5% 11.5% 7.6%

    4. On 2020-04-22 17:28:38, user Gooney wrote:

      You can’t expect prospective randomized placebo controlled conclusions from a retrospective study. You can conclude that the manner in which the drugs were use led in a VA setting showed no benefit and demonstrated harm. Further detailed studies with significant power would be needed for more elaborate conclusions. Why are we using the drug? Based off a study that had 30 patients and reported outcomes that were not likely to occur given the number of patients included in the study. You need 100 patients for one death. Over 70 patients in the same 100 will recover without incident. Yet people are prescribing a drug that potentially could do harm.

    1. On 2020-04-23 13:10:03, user ABO FAN wrote:

      The overwhelming majority of Japanese people who are positive for COVID-19 are seniors in their 60s or older (easily infected). On the other hand, many foreigners are in their 20s to 40s (not easily infected). Cruise ship passengers are mainly senior Japanese and foreign families. When you correct for age, the number of Japanese positives is overwhelmingly low.<br /> Now it is statistically clear that BCG is effective.<br /> Since the original data from the Japanese Ministry of Health, Labour and Welfare provide only the number of positive individuals, the age structure of all passengers, including non-infected ones, is unknown. I suspect that an opponent wrote this paper in bad faith even if he knows the truth. https://uploads.disquscdn.c...

    1. On 2020-04-24 05:31:54, user Rajendra Kings Rayudoo wrote:

      To <br /> Yang Yu, Yu-Ren Liu, Fan-Ming Luo, Wei-Wei Tu, De-Chuan Zhan, Guo Yu, Zhi-Hua Zhou

      I read the paper want to know how this accurately measures the presymptomatic and asymptomatic people in populated countries like India <br /> And can you please tell how this actually works and give results to calculate<br /> And I also want to know how much percentage there will be the sucess ratio.

      By my opinion the 1st case to the recent one the areas which are located the surrounding people should be Quarantine and time and tested and also tells the people who they contacted in the period of time

    1. On 2020-04-28 14:00:55, user Sinai Immunol Review Project wrote:

      Main Findings<br /> This preprint sought to compare the daily deaths in countries using CQ/HCQ as a treatment from the beginning of the COVID-19 pandemic to those that did not. From a list of 60 countries in descending order by number of confirmed cases, 16 countries were selected for inclusion into either the high CQ/HCQ production or use group, versus not. Countries were included if they met the criteria for having data from the day of the 3rd death in the entire country and the daily deaths for the 10 days immediately following, until both groups were populated with a list of 16 (Figure 1: Table with the CQ/HCQ group list; Figure 2: Table with the “control” group list). For each group of countries, the average daily deaths were determined, and the curves projected to illustrate trajectories. In Figure 3, the author suggests that the deaths in the countries belonging to the control group follow an exponential curve, while the progression of average daily deaths in the countries with greater use of CQ/HCQ follow a polynomial curve.

      The author then applies Auto Regressive Integrated Moving Average (ARIMA), a modeling tool used for time-series forecasting (i.e., predicting the future trajectory of data over time using the data from previous time points as predictors in a linear regression). The Auto Regressive component refers to each difference between two previous time points that make the model “stationary” (current – previous); the Moving Average is the number of forecast errors from calculating these differences that should go in the model. The author uses ARIMA to predict the next 10 days of mean deaths for the CQ/HCQ list (Figure 6) and the control countries (Figure 8). In figures 9 and 10, autocorrelations of residuals are performed to determine internal validity of the model, here defined as no significant autocorrelations.<br /> In conjunction, the author argues that these findings support major differences in death rates between countries that use/mass produce CQ/HCQ versus those that do not.

      Limitations<br /> The title of this study refers to itself as an ecological study, an observational study in which the data are defined at the population level, rather than individual. Although this study design allows for rapid hypothesis testing in large datasets, a robust ecological study should account for as many known risk-modifying factors or confounders as possible. Subsequently, any results should be reviewed under strict criteria for causality, since there is high probability of the outcomes falling under the definition of ecological fallacy, which occurs when inferences about individuals are determined from inferences about a group to which they belong.

      This study conflated the use and mass production of CQ/HCQ at the start of the COVID-19 pandemic in each respective country, with that country’s direct pandemic response. It is never explained whether use or production is the key output for any given country, which are vastly different metrics. The author fails to consider other reasons for having existing infrastructure for the mass production of drugs like hydroxychloroquine, whether the country was a global supplier of the medication (India), or is a region where malaria is endemic (India, Pakistan, Indonesia, Malaysia, South Korea), which may correlate to both chloroquine production and use. Notably, the countries from which studies of HCQ in the treatment of COVID-19 have been predominantly performed (China, France, USA), are all in the control list of countries. Additionally, the data for cases and deaths were collected from reports accessed from https://www.worldometers.in... data were not selected from the top countries using a methodological approach, but rather skipping certain countries to use only the most complete death data for the timeframe of interest, allowing for bias introduced by the reporting of each individual country.

      With regards to the statistical methods applied, namely ARIMA, they are non-standard practices for interpreting the results of an ecological study. The first problem with this, in my opinion, is that the message will be difficult to interpret and criticize for many scientists, as ARIMA will be unfamiliar to most in the biological sciences. Further, the models applied (Table 4) do not take into account any confounders, which is a requirement for robust analysis of an ecological study. There are only 3 variables in this type of model: p, the autoregressive coefficient, q, the moving average coefficient, and d, the difference between points in the time-series. Any flaws or bias inherent to the input data are then upheld and propagated by the model, which does not allow for any other variable that would contribute to the risk of death.

      Significance<br /> The faults of the stratification of countries into the groups proposed in this study, together with the unorthodox application of ARIMA modeling, make it challenging to accept the conclusion that the author draws in this study. The apparent decrease in death rate in countries with a high production/use/either/or of CQ/HCQ could be due to any number of other factors for which this study did not account. The top 5 countries in both confirmed cases and reported deaths are all in the control list, which has no relationship to the amount of CQ/HCQ production within those countries yet skews the data to make the dynamics of death rate appear more dramatic.

      Reviewed by Rachel Levantovsky as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn School of Medicine at Mount Sinai.

    1. On 2020-05-05 13:21:34, user Franko Ku wrote:

      Hope this is right about the mechanism and she gives some insight on HCQP <br /> https://m-jpost-com.cdn.amp...<br /> excerpt<br /> The Italian Medicines Agency (AIFA), the national authority responsible for drug regulation in Italy, has an approved trial of hydroxychloroquine on 2,500 patients, which will start in early July and focus on the use of hydroxychloroquine in prophylaxis, Chiusolo said. The study, for which preliminary data would be ready within 16 weeks, will look at whether the preventive intake of the drug decreases the probability of contracting COVID-19 when one comes directly into contact with a positive patient.<br /> THE ROLE of hydroxychloroquine in the prevention and fight against coronavirus was also the subject of a study published in The International Journal of Antimicrobial Agents, which describes how a healthcare worker infected with the novel coronavirus traveled freely within a hospital before being diagnosed with the virus.<br /> “It was not possible to quarantine everyone who had come into contact with the healthcare worker,” Chiusolo said. So, they treated 211 healthcare professionals and patients with hydroxychloroquine. After 10 days, nobody tested positive for the coronavirus.<br /> Furthermore, Chiusolo told the Post, the Italian Society of Rheumatology interviewed 1,200 rheumatologists throughout Italy to collect statistics on contagions. Out of an audience of 65,000 chronic lupus and rheumatoid arthritis patients who systematically take hydroxychloroquine, only 20 patients tested positive for the virus.

      Then we have a questionable prevention trial for prevention with HCQP funded by Gates Foundation at Univ of Washington where the placebo is high dose Vitamin C instead of inert pill. Why? So the results aren't as different. They should also give same amount of Vitamin C to the HCQP arm.<br /> https://clinicaltrials.gov/...<br /> excerpt<br /> This is a randomized, multi-center, placebo-equivalent (ascorbic acid) controlled, blinded study of Hydroxychloroquine (HCQ) post-exposure prophylaxis (PEP) for the prevention of SARS-CoV-2 infection in adults exposed to the virus<br /> also see for others joing<br /> https://www.clinicaltrials....<br /> In fact here's one of the studies using Vitamin C and zinc and Vit. D with HCQ<br /> https://www.clinicaltrials....

      There need to be many many more trials and studies including zinc.<br /> Here is one:<br /> https://www.clinicaltrials....

      Some good news about Gilead's remdesisvir but if accurate as Dr. Fauci said will need an anti-inflammatory cohort. We have one in HCQP AND zinc.<br /> https://www.insiderbaseball...

    1. On 2025-09-29 22:21:03, user A.O. Akinrinade wrote:

      Hello,

      In Figure 2 (page 8), I believe it would be helpful to have a color legend showing these archetypes you've inferred. I think at least having the archetype number annotated would make it easier to connect the figure to the text.

      Best,<br /> Ayomikun

    1. On 2025-11-30 07:05:45, user Ali Rahimi wrote:

      Dear authors,

      I have read your interesting article. I think the following revisions would strengthen the article:

      Abstract<br /> Clarify that the 72.4% and 38.2% figures come from patients reporting barriers, not from the full sample, so the denominator is clear.<br /> Keep wording aligned with the design: change “barriers limit uptake of cataract surgery in Bangladesh” to “barriers were commonly reported among patients undergoing cataract surgery in Bangladesh.”<br /> Make the main statistical result consistent with the Results: state that education, income and prior surgery were associated with the number of barriers (Adj R² = 0.138).

      Introduction<br /> A few sentences are long and repetitive around “accessibility” and “health inequities”. Tighten these into one concise paragraph without changing meaning.<br /> Where you describe evidence as “scarce”, add 1 sentence that positions your study among Bangladeshi work (rural children, Rohingya, etc) and makes clear that prior studies were population specific.

      Methods<br /> In “Participants and data collection” clarify in one sentence that 595 patients consented, but analyses of barriers use 583 due to item non-response.<br /> Briefly describe how the “fear score (0–5)” and “barrier count” were constructed (number of items, response scale, direction).<br /> You model a count outcome with linear regression. Add one line acknowledging that barrier counts were approximately normal and that this approach was chosen for simplicity; alternatively mention that Poisson or negative binomial regression would give similar interpretation.

      Results<br /> Ensure mean age is reported consistently (Abstract uses 62 years, Table 1 has 61.3). Choose one rounding rule and use it everywhere.<br /> Replace approximate p notation “p ? 0.003” and “p ? 0.221” with standard “p = 0.003” and “p = 0.221”.<br /> Table 3: the p value shown as “1” for “Afraid of surgery” under gender should be reported as “1.000” or the exact test result.<br /> Table 4: the p values for “Number of reported barriers” currently read “> 0.001”; this should be “< 0.001”.<br /> In the text for section 3.3, “The geographical barrier of transportation is predominant in our study” is misleading because cost is clearly highest. Rephrase to “an important barrier” rather than “predominant”.

      Discussion<br /> Soften causal phrasing. Examples:<br /> “Patients who delay seeing an eye doctor are more likely to postpone surgery and show up with advanced cataracts” could be “Patients reporting delays in seeing an eye doctor often present with more advanced cataracts.”<br /> Any sentences that link barriers directly to “prolonging the waiting period” or “contributing to disability” should be framed as association, not cause.<br /> When you describe gender norms and decision making, keep language neutral and clearly signpost what comes from your data versus from cited literature.<br /> Consider one short sentence acknowledging that your barrier profile reflects people who ultimately accessed surgery and may under-represent those who never reach services.

      Limitations<br /> Add explicit mention that the cross-sectional design and the hospital-based sample (only patients scheduled for surgery) limit causal inference and generalisability to all people with cataract in Bangladesh.<br /> You already mention possible social desirability bias; make that sentence more direct and link it to self-reported barriers.

      Conclusion<br /> Tone down strength of generalisation: instead of “The study's strength lies in its inclusion of a diverse population, thereby increasing its generalizability” use “The inclusion of patients from hospital clinics and outreach camps provides some diversity, although findings still reflect one service network.”<br /> Rephrase recommendations as suggestions: “could help improve access” or “may help bridge the knowledge gap” rather than “can facilitate” or “will improve”.<br /> Keep the ending sentence tightly tied to your data: emphasis on cost, transport, time, fear, and gendered escort constraints.

      Tables and Figures<br /> Check that the labels in Figure 1 and Figure 2 match exactly the barrier wording used in the questionnaire and in the text (for example “hospital too far / no transportation”).<br /> Consider adding “multiple responses allowed” to the figure legends for barriers.

    1. On 2025-11-30 17:00:32, user Cyril Burke wrote:

      RESPONSE TO REVIEWER #2<br /> June 27, 2022<br /> Reviewer #2: Thank-you for the opportunity to review this work which highlights the importance of monitoring serum creatinine over time and how this can be a useful tool in detecting possible CKD. This is an important topic as the use of sCr on its own is certainly under-utilized and changes are often missed because they don’t fall into a predefined category.<br /> Thank you for considering our manuscript and for your detailed comments.

      MAJOR CONCERNS

      A. “Choi- rates of ESRD in Black and White Veterans” doesn’t fit with the rest of the paper including the title; the introduction and conclusion also don’t adequately address this portion of the paper. It feels disjointed from the main point of discussion which is the use of sCr in screening “pre-CKD”. This section and discussion should be removed and possibly considered for another type of publication.<br /> We have attempted to clarify this inclusion. This manuscript could be divided into three or four short papers, increasing the likelihood that any one of them would be read. However, different groups tend to read papers about screening for kidney impairment, racial disparities, cofactors in modeling physiologic parameters, or policy proposals to encourage best practices. Despite the appeal of perhaps three or four publications, we decided to tell a complete story in a single paper, but we are open to suggestions.

      Black Americans suffer three times the kidney failure of White Americans. Other minority groups also have excessive rates of kidney disease. However, analysis of Veterans Administration interventions can bring that ratio close to one, similar interventions might also reduce to parity the risk for Hispanic, Asian, Native Americans, and others. Within-individual referencing should allow better monitoring of all patients and help to reveal the circumstances and novel kidney toxins that lead to progressive kidney decline. The ability to identify a healthy elderly cohort with essentially normal kidneys would help to calibrate expectations for all. Better modeling of GFR should help everyone, too.

      Over eight decades, anthropologists have had little scholarly success in diminishing the inappropriate use of ‘race’. Keeping these parts together may be no more successful, but we feel compelled to try.

      B. Cases 1 - 3, (lines 93 – 122): where are these cases from? There is no mention of ethics to publish these patient results, which appears to be a clear ethics violation. If so, these cases should be removed and patient consent and ethical approval obtained to publish them.<br /> The authors describe the reasons for not obtaining an ethics waiver for this secondary data analysis. Despite this, the relative ease of obtaining an ethics waiver for secondary data analysis usually means that this is done regardless.<br /> We take patient privacy seriously and have completely de-identified the Case data, as required by Privacy Act regulations. We understand that no authorization or waiver was necessary. We discussed the issues with an IRB representative, reviewed the relevant regulations, and confirmed no need for formal review of a secondary analysis of already publicly available IRB-approved data or of completely de-identified clinical data collected in the course of a treating relationship.

      IRBs have a critical role to play, but many (including ours) are overworked. We understand the impulse authors feel to gain IRB approval even when the regulations clearly do not required it. As we discuss in the revision, there is a more significant matter that IRBs could help to resolve if they have the resources to do so. For all of these reasons, and even though we, too, felt the urge to obtain IRB approval, we resisted adding “just a little more” to their work.

      C. The message of the article and data representation is unclear: do the authors wish to show that sCr is superior to eGFR in this “pre-CKD” stage, should both be used together? Do the authors wish to convey that a “creatinine blind range” does not exist? Or is the aim to demonstrate that continuous variables should not be interpreted in a categorical manner?<br /> Our interest is detection and prevention of progression of early kidney injury at GFRs above 60 mL/min – a range in which eGFR is especially unreliable. We have advanced the best argument we can to detect changes in sCr while kidney injury is still limited and perhaps reversible. If experience reveals that some avoidable exposure(s) begins the decline, then clinicians might alert patients and thereby reduce kidney disease. How best to use longitudinal sCr remains to be determined from experience. However, our message is that early changes in sCr can provide early warning of a decline in glomerular filtration. We are confident that clinicians can learn to separate other factors that may alter sCr, as we do for many other tests.

      MINOR CONCERNS<br /> ABSTRACT<br /> A. Vague. Doesn’t give a clear picture of the study<br /> We have tried to clarify the title and abstract and are open to further suggestions.

      INTRODUCTION<br /> B. 51 – 57: needs to state that these stats are from e.g. the US. The authors should consider adding international statistics to complement those from the US.<br /> We have updated the statistics on death rates from kidney disease to include US and global data.

      C. 68: reference KDIGO guidelines, state year<br /> We now reference the KDIGO 2012 guidelines.

      D. 75 – 77: is this reference of the New York Times the most appropriate?<br /> We have expanded this section with peer-reviewed, scholarly references. However, we found Hodge’s summary of the issue succinct and hence potentially more persuasive for some than decades of scholarly references that have had limited or no effect in the clinic.

      E. 82: within-individual variation not changes (this is repetition of the point made in lines 425 – 427, but should match the language)<br /> We have matched the language.

      F. 82 – 84: reference? If this is a question it should be presented as such<br /> We have attempted to clarify this statement.

      G. 84: “normal GFR above 60” = guidelines (including KDIGO) do not refer to 60 as normal GFR, 60 – 89 is mildly decreased. (see line 126)<br /> We agree and have corrected the language.

      H. 93: avoid the use of emotive words such as apparently (also in line 428)<br /> We wanted to emphasize appearance without proof and have made these changes.

      I. 94: “Not meeting KDIGO guidelines”: KDIGO 2.1.3 includes a drop in category (including those with GFR >90). This would appear to include some of the cases listed. Additionally, albuminuria should have been measured for case 2 and 3.<br /> We have clarified that cases may or may not fit KDIGO categories, though that question will frequently arise in evaluating sCr changes. Where available, we have added urine protein and/or albumin results to the Cases.

      J. 97: “progressive loss of nephrons equivalent to one kidney”: this is based on a single creatinine measurement.<br /> Since the original submission, we discovered for this Case (now Patient 3) early serum creatinine results and notes indicating a six-month period off thiazide diuretic. This data clarified the baseline and showed a remarkable effect of thiazide diuretic on sCr. We have added follow-up sCr results and details of thiazide use to the ASC chart.

      K. 93 – 122: Could any of these shifts be explained by changes in creatinine methodology or standardization of assays, especially over 15 – 20 years (major differences between assays existed before standardization and arguably still exist with certain methods).<br /> It would be useful to see a comparison between serial sCr and eGFR measurements on the same figure. There appears to be significant (possibly more pronounced) changes when eGFR is used. As line 87 mentions changes in eGFR may be as useful (and in some situations more useful) than changes in sCr alone.

      It would be helpful to have a chronology from each local laboratory with the date of every change in creatinine assay or standardization. However, any single shift draws attention but does not necessarily indicate significant change in glomerular filtration. After one or several incremental increases, over at least three months, the sCr pattern may meet the reference change value (RCV) that signals significant change. In the future, from age 20 or so, a patient’s medical record should retain the full range of the longitudinal sCr for true baseline comparison.

      As noted in the revised manuscript, Rule et al showed that there is measurable nephrosclerosis even in the youngest kidney donors, suggesting that some injuries (perhaps exposure to dietary toxins) may begin in childhood and that early preventive counseling may be worthwhile. Experience will show whether this can slow progression to CKD. As we note, quoting Delanaye, sCr accounts for virtually 100% of the variability in eGFR equations based on sCr (eGFRcr), and these equations add their own uncertainties, so no, we do not believe that eGFR is more useful than sCr when GFR is above 60 mL/min and possibly much lower as well.

      We have added eGFR results to the ASC charts (in blue), though availability was somewhat limited.

      L. 127 – 142: should there be separate charts for males and females, the differences in creatinine between males and females needs to be discussed somewhere in the paper.

      We do not think there should be separate charts for men and women based on size. The role of sex in eGFR equations is mainly based on the presumption that the average woman has less muscle mass than the average man. Clinicians care for individuals, not averages, and this sweeping generalization that increases agreement of the average of a population introduces unacceptable inaccuracy to individual care. Within-individual comparison eliminates the need for assumptions on relative size or muscle mass. Major changes in an individual’s muscle mass will usually be evident to the clinician who can adjust for them.

      However, reports suggest significant influence of sex hormones on renal function, including effects of estrogen and estrogen receptors, such as reducing kidney fibrosis, increasing lupus nephritis, and increasing CKD after bilateral oophorectomy. The mechanism of these effects and how they might be incorporated into eGFR estimating equations is unclear, but the effort may benefit from a more individualized approach with focus on a measurand rather than matching population-based averages of a quantity value (calculated from measurands).

      M. Similarly, is this suitable for all ages?<br /> We think so. Another sweeping generalization based on age merely introduces another inaccuracy which complicates the task of clinicians caring for individuals. Older persons have varying health, athleticism, muscle mass, dietary preferences, etc. Rule et al reported that biopsies of about 10% of older kidney donors had no nephrosclerosis. Within-individual comparison eliminates the need for assumptions on relative muscle mass or inevitable senescent decline in nephron number. We substitute the assumption that any change in an individual’s muscle mass will be evident and can be accounted for. A seemingly ubiquitous risk factor, or factors, starts injuring kidneys at a young age, which we may yet identify.

      N. 162 – 163: rephrase<br /> Done.

      METHODS<br /> O. 185 – 193: aim belongs in the introduction, can be adjusted to complement paragraph 178 – 182.<br /> Reorganized and rewritten.

      P. 196 – 205: reference sources

      References provided.

      Q. 224 – 247: not in keeping with the rest of the article or title and conclusion

      We have revised and restructured this section.

      RESULTS<br /> R. If eGFR is treated as a continuous variable does inverted sCr still have higher accuracy?<br /> We believe so. Serum creatinine is a measurand and reflects the total sum of physiologic processes, known and unknown. In contrast, eGFR equations yield a quantity value, calculated from a measurand and dependent on the assumptions and approximations incorporated by their authors. The eGFR equations are thus necessarily less accurate than the measurands they are derived from, in this case, sCr. In a hyperbolic relationship, as the independent variable drops below one and approaches zero, the effect is to amplify the inaccuracy of the independent variable in the dependent variable. By avoiding the mathematical inverting, the data suggest that direct use of sCr is far more practical for pre-CKD.

      S. As mentioned, the section on ESRD in black and white veterans doesn’t fit in with the rest of the article.<br /> We have revised, reorganized, and rewritten. We also outlined our rationale above.

      DISCUSSION<br /> T. As mentioned, section 4.1 doesn’t fit in with the rest of the article. As the authors note the correlation between illiteracy and CKD is likely not causal.<br /> See above.

      U. 387: erroneous creatinine blind range. The data presented does not show this is erroneous there is still a relative blind range. A distinction must be made between a population level “blind range” and an individual patient’s serial results. The data and figure 4 in particular demonstrate the lack of predictive ability of sCr above 40ml/min compared to below 40ml/min at a population level. For an individual patient this “blind range” is more relative, and a change in sCr even within the normal range may be predictive. (Note: the terminology “blind range” is problematic).<br /> We agree. On reading closer, Shemesh et al call attention to “subtle changes” in serum creatinine even though they had access only to the uncompensated Jaffe assay, so their recommendation to monitor sCr is even more forceful, today, due to more accurate and standardized creatinine assays. We have attempted to clarify this in the manuscript.

      V. 399 – 400: “rose slowly at first and then more rapidly as mGFR decreased below 60” this refers to a relative blind range. Whether these slow initial changes can be distinguished from analytical and intra-individual variation is the question that needs to be answered before we can say a “blind-range” doesn’t exist for an individual patient.

      We appreciate this observation. We believe longitudinal sCr is worth adopting to gain insights into individual sCr patterns, which may reveal early changes in GFR, among other influences on sCr. This is a low-cost, potentially high-impact population health measure, and there seems little risk in trying it because many clinicians already use components of the process.

      W. 425 - 432: sCr is indeed very useful when baseline measurements are available. eGFR remains useful when baseline sCr is not available or when large intervals between measurements are found.<br /> As Delanaye et al noted, virtually 100% of the variability in longitudinal eGFR is due to sCr, so we understand that the errors in eGFR can be (and usually are) greater than but cannot be less than those in sCr.

      X. 425: low analytical variation- if enzymatic methods are used<br /> Lee et al suggest that even the compensated Jaffe method provides some accuracy and reproducibility, which may allow longitudinal tracking of sCr even where more modern assays are as yet unavailable.

      Y. 428: avoid the use of “apparently”<br /> Done.

      Z. 430: reference 56 compares sCr and sCysC with creatinine clearance NOT with mGFR, this does not prove that mGFR has greater physiologic variability. Creatinine clearance is known to be highly variable (partially due to two sources of variability in the measurements of creatinine: serum and urine).<br /> The creatinine clearance is another form of mGFR, and our understanding of it begins with the units: if the clearance or removal of creatinine were being measured, the units should be umoles/minute, but they are mL/min. “Clearance” is an old concept coined by physiologists to describe many substances, such as urea, glucose, amino acids, and other metabolites. Since creatinine is mostly not reabsorbed and is only slightly secreted in the tubules, the “creatinine clearance” became a measure of GFR. The ratio of urine Creatinine to serum Creatinine is simply a factor for how much the original glomerular filtrate then gets concentrated (typically about 100-fold) by the kidney. Since the assumption is that the timed urine was once the rate of glomerular filtrate production, the creatinine clearance is a measure of the GFR.

      Creatinine clearance has some inaccuracies based on tubular secretion, but also has some advantages: blood concentrations are essentially constant during urine collection, no need for exogenous administration, and reliable measurements in serum and urine. The methods that we often call mGFR also have problems, including unverifiable assumptions about distributions, dilutional effects, and others we cite in the text. None of these are direct measures of GFR. Due to changes in remaining nephrons, even true GFR itself is not strictly proportional to the lost number of functional nephrons, which seems the ultimate measure of CKD that Rule et al estimated from biopsy material.

      AA. The limitations of sCr for screening should also be discussed: differences in performance and acceptability between enzymatic and Jaffe methods (still widely used in certain parts of the world), the effect of standardizing creatinine assays (an important initiative but one that could also produce shifts in results around the time of standardization- see cases), low InIx means that once-off values are exceedingly difficult to interpret, is a single raised creatinine value predictive (or should there be evidence of chronicity): similarly are there effects from protein rich meals, etc (The influence of a cooked-meat meal on estimated glomerular filtration rate. Annals of Clinical Biochemistry. 2007;44(1):35-42. doi:10.1258/000456307779595995)<br /> We have added discussion of additional references on reproducibility of sCr assays and discuss dietary meat and, in Part Three, possible dietary kidney toxins.

      CONCLUSION<br /> BB. The discussion recommends using SCr above eGFR while the conclusion recommends the NKF-ASN eGFR for use in pre-CKD and ASC charts. While the use of both together in a complementary fashion is understandable- this needs to be congruent with the discussion, aims and results.<br /> We have rewritten this section. We would welcome any further recommendations.

      Cyril O. Burke III, MD, FACP

    1. On 2020-04-21 09:07:53, user Maria wrote:

      At last, bravi! In Italy now they cannot say more that " coronavirus in the air" is a fake news. They ignore that humidity surrounding the membrane of the virus preserves its dimensional stability and integrity, as elementar chemistry teaches. Now I suggest to test the infectivity of Sars.CoV2 under different conditions of relative humidity of air. Since a low relative humidity favours the evaporation of water from the virus surface, I predict that the persistence of the virus decreases.

    1. On 2020-04-22 12:29:26, user rupesh chaturvedi wrote:

      Well immunity is outcome of humoral immune response. In these model authors assume that all the subjects infected with virus would generate a sustainable and durable IgG response. Where is data? Do we have data to show after infection how much immunity is generated? <br /> Please see a recent study from China. If 30% do not have antibody response then the at best case we will reach below 70%. I do not not if that will be really a Herd Immunity.<br /> Biological phenomena based models need to adjust the dynamics for the variables of biological process. A linear models should not be used to make policy decision unless backed up by understanding of biological events.<br /> Rupesh

    1. On 2020-04-22 14:52:42, user Philippe BROUQUI wrote:

      This unpublished paper raises serious doubts about the scientific value of research

      Missing data <br /> This is a retrospective study on medical records carried out on 12 health care centers in the Ile de France. There is no missing data on the 19 basic variables out of the 181 patients followed in these centers which is remarkable when known that the main drawback of retrospective studies is precisely the loss of information. This is important because it can skew the reported balance in both groups. For example, it seems unlikely that the "Child B liver cirrhosis or more yes/no" data was found in retrospect in all computerized medical records in this study. It probably lacks the "I don't know." This casts doubt on the reality of the retrospective nature of the data collection.

      Inclusion criteria O2 to 2l<br /> This criterion is in line with the HCSP's recommendation and included in Decree No. 2020-337. However we see oxygen was at 2l/mn in 50% of patients with extremes of 2 to 4L/mn which appears to be more of a criterion of inclusion adapted to the law than clinical reality.

      Excluding patients who received HCQ 48 hours after inclusion.<br /> But above all, we have been be surprised by the fact that among the control group there are in fact 8 patients out of 97 who received hydroxychloroquine but after 48 hours. In the final analysis they are removed from this control group. This is a scientific misconduct because these patients should have been included in the treaties and not in the controls.

      This likely changes the results and may even be the balance of groups in terms of comorbidity

    1. On 2020-06-25 15:16:45, user dottore b wrote:

      "Dexamethasone reduced deaths by one-third in patients receiving invasive

      mechanical ventilation (29.0% vs. 40.7%, RR 0.65 [95% CI 0.51 to 0.82];

      p<0.001)" is misleading as this is an 11% decrease in the death rate. It's like saying the death rate went from 2% to 1% and trumpeting a "50% reduction in the rate of death".

      For those interested in a very good discussion of this trial from Dr Dan Griffin an intensivist at Columbia, this is a great link and every practitioner should be a TWIV listener

      https://www.microbe.tv/twiv...

    1. On 2023-11-12 16:14:24, user Julian Gough wrote:

      We have noted that in a small number of cases this work is being cited in the literature as a positive GWAS association for the ERAP2 gene, however we would like to be clear that we are making no such claim, and urge authors to take care in citing this work. We are pleased that for the majority of citations authors have not misrepresented the findings.

      Analysis of subsequent genetic datasets for COVID-19 mortality [not yet published] could suggest that risk factors (reported here and elsewhere) are different at different points in time, as the virus itself has mutated, medical care has evolved, vaccination has been introduced and population vulnerability and exposure has changed. Therefore we also ask readers to take note that the conditions under which the (very early) data collected by UKbiobank during the first wave of the pandemic -- analysed in this work -- may be very different from present, future or past conditions during other waves of infection.

    2. On 2020-07-07 14:02:12, user David Curtis wrote:

      I have some concerns about rs150892504.

      According to ExAC it is rare in Europeans but has an allele frequency of 0.04 in Ashkenazi Jews. <br /> https://gnomad.broadinstitu...<br /> https://gnomad.broadinstitu...

      Likewise, it has an allele frequency of 0.03 or 0.04 in the IBD exomes:<br /> https://ibd.broadinstitute....

      This raises the possibility that the results you obtain may be due to some kind of population stratifcation which has not been adequately corrected for.

    1. On 2020-07-06 15:38:39, user Alexander Pearlman wrote:

      why is placebo sterile saline soln.--and not formulated with lipids as the mRNA-LNP (scrambled) drug product? is this a safety concern? or expect immunog. sig. from a scrambled construct?

    1. On 2020-07-08 18:28:20, user Paul Gordon wrote:

      Hi, thanks for posting. Have the new Italian genomes described been posted to a public repository? A quick search of the paper and both GenBank/GISAID didn't reveal these identifiers or entries matching the metadata provided in Table S1. Thanks!

    1. On 2024-06-16 14:15:45, user Praba wrote:

      Dear Authors, this paper is interesting. Congratulations to all authors. Could you please give complete details about the FnCas9 purification (How much vol of culture was used to purify the proteins that was shown in Suppl Fig 9 and what was the yield obtained at the end. These information are not trivial and they are important for the researchers who follow the paper. Hope you will append the details.

    1. On 2020-07-12 18:19:53, user Doug Vaughan wrote:

      Very interesting study. PAI-1 provides a site of convergence for risk (age, obesity, diabetes) and mechanisms driving thrombosis (inflammation, activated renin-angiotensin system, endothelial dysfunction) in patients with COVID-19. Failure of the endogenous clot-dissolving system is most likely a key contributor to morbidity and mortality as demonstrated here. Just last week, we secured an IND from the FDA to begin testing of a novel orally-active inhibitor of PAI-1 (TM5614) in high-risk patients with COVID-19. This Phase 2 study will enable the first use of this drug in USA.

    1. On 2020-07-17 11:16:47, user ADisquietingSuggestion wrote:

      This paper puts the global burden of COVID-19 at 4.3 million YLL. The WHO tables on disease burden put this in context: all of the top 20 diseases by YLL are above 25 million. How would you characterize this comparison?

    1. On 2020-07-17 15:36:12, user Mathieu Perrin wrote:

      Dear authors,

      thank you for raising awareness that a low FPR does not per se translate into a high significance of a positive result. Hopefully, this will encourage labs to make an EQA for SARS-CoV-2.

      1) Is it possible that the FPR actually depends on the prevalence rate? For instance, if the prevalence is high, there is a greater risk to contaminate a negative sample.<br /> 2) Should the FPR be lower if two tests are conducted on the same person? I expect this to be the case unless a negative patient always give positive results for some reason. If so, the practice of double testing should be generalized. I understand you have trouble determining precisely how each country defines a positive result, whether it is on a sample basis or if samples are pooled or if an individual gets tested several times.

      Regards,<br /> Mathieu

    1. On 2020-07-18 00:08:26, user dottore b wrote:

      As an emergency physician turned co-voligist (not my choice!), this paper is one of the single most important papers of the year. Period. We need to get governments, academic institutions, payer providers and even venture capital in public-private partnerships deploying this system today

    1. On 2020-07-19 05:03:49, user HarryDeedra Hodges wrote:

      The tweet storm is quite odd. Seems like a mini-army, particularly in Spanish moving the story along. Others seems quite happy to spread the negative results. The patients seem evenly matched, but nearly all needed O2 supports implying quite ill, more HCQ patients were > 70 than the control. Dosage was 1600mg loading, 400 mg daily for 9 days, no mention of zinc. No adverse effects noted. The dosage is only slightly higher than the evolving standard which includes zinc. The study shows HCQ without zinc not useful in critically ill patients.

    2. 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 2020-07-19 22:45:26, user George wrote:

      " Lettuce consumption increased COVID-19 mortality."<br /> If you lack the commonsense to see how ridiculous that is, at least put it in non-causal language next time.

    1. On 2020-07-20 15:23:57, user Gerald Williams wrote:

      I have followed your work since April NBC story.

      You said you followed the Zelenko protocol (HCQ+Zn+Azithromycin) and just added Ivermectin in order to get the great results.

      In a prior version of your article I recall reading that you had HCQ & Azithromycin in a large % of the Ivermectin group as well as in some of the "usual care" group. You never mention critical Zinc in your article. If I was reviewing, I would want to know the details even if they may make the study more "messy". Your results are already very significant in that adding Ivermectin to the Zelenko cocktail extends efficacy to many days later.

      There is no need at this time to kill placebo group by having a DB RCT.<br /> What is needed is to repeat protocol where the the control group exactly follows the Zelenko protocol (now in preprint or via Yale's Dr. Risch review in Am. J. Epidemiology) vs the Zelenko protocol + Ivermectin. You should reference.

      It is not just you, but every article on treatment should document # of days since first symptoms and # of days since hospitalization (if former isn't known).

      The current hypothesis is that Zelenko protocol works great up to 5 days of symptoms and sometimes up to 7 days. Your addition of Ivermectin extends that window into many days after hospital admission, It is no coincidence that in the less severe group you did not find significance because the Zelenko protocol was adequate (except some patients didn't receive full Zelenko protocol.

      Your protocol makes Remdesivir obsolete, dangerous and too expensive.

      You can follow me and others on Twitter to continue discussion,.<br /> It is shameful that Big Pharma is suppressing this very important finding.

      Ideally the Zelenko protocol should be followed at first signs of symptoms and if fails, around day 6, can add Ivermectin to cocktail and repeat (in outpatient or hospital setting).<br /> As you know, Doxycycline (doesn't interact w/HCQ) can be substituted for Azithromycin, so no need for outpatient cardiac monitoring. Perhaps even use the 4 drug cocktail in outpatient setting from start, if continues to prove safe.

    1. On 2020-07-20 17:17:47, user JayTe wrote:

      In the Annals of Internal Medicine, the authors demonstrated in the research article, Cloth Masks and Surgical Masks Ineffective in filtering SARS-COV-2 in COVID-19 Patients, Oberg and Brousseau demonstrated that surgical masks did not exhibit adequate filter performance performance against aerosols measuring 0.9, 2.0 and 3.1 um in diameter. As well Lee and his colleges showed that particles 0.04 to 0.2 um particles can penetrate surgical masks. If we assume that the SARS-COV2 particle has a similar size to the SARS-COV1 particle even surgical masks are unlikely to effective filter the virus. In this study the primary means of the spread was via coughing. Now the author of this article claims that it is primarily via contact or droplets!?! If a person has respiratory issues due to covid-19, would it not make sense that they would be coughing? If you have persons that are not ill or asymptomatic then given the existing evidence, there is little to no chance of an individual becoming ill by the transmission of the SARS-COV2 virus. Doing a meta-study where one chooses studies that conform to their particular perspective and avoids the probability of transmission via coughing doesn't help the debate on the value of masks.

      It also excludes the negative effect of wearing masks which in a 2015 study in the BMJ: “A cluster randomised trial of cloth masks compared with medical masks in healthcare workers“ highlighted that not only are these masks 100% ineffective at reducing the spread of COVID-19, but they can actually harm you since the moisture retention, reuse of cloth masks and poor filtration may result in increased risk of infection.

    2. 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 2020-07-22 03:42:29, user Steven Hall wrote:

      I would love to know was there any determination as to the best wearable. <br /> I run a Circulation Clinic and We have all of our Clients use wearable to help us get the best results. You feed back would be very helpful. Blessings Steven Hall Director of the Fountain of Youth Circulation Clinics 425-770-9466 https://happyheartclinic.com/

    1. On 2020-06-22 23:00:16, user Marcus Quintilian wrote:

      Some iportant words are missing: "Our machine learning analysis also showed that the two groups were linearly separable. .....incubation of COVID-19 along with previous statistical analysis. "

    1. On 2020-07-23 15:48:06, user Joseph Psotka wrote:

      a couple of factors you did not take into account: 1. Florida's population is much smaller than the official one because about a third of all "residents" leave in April and May, when it gets seriously hot. 2.) Maryland and Virginia suffer from contagion from New York which increased their Re in the peak months, so your model probably underestimated as New York declined.

    1. On 2020-06-24 02:12:28, user Nobuhiro Sho wrote:

      Non-pharmcological intervention such as wearing mask is the key strategy for novel cotagious respiratory disease. Because drug’s efficacy is not adequately proven yet. This article shows the importance of masks for preventing the transmission of covid-19.<br /> Every contagious disease is multiplicative.<br /> As everyone is wearing mask, it reduces the huge amount of infection.

    1. On 2020-06-24 12:15:40, user Ayse Balat wrote:

      I would like to congratulate the authors introducing such a beneficial model for the diagnosis of erosive-vesiculobullous diseases. I am sure it would be one of the great methods for clinicians. Professor Ayse Balat

    2. On 2020-07-04 10:35:54, user Vincent Fokker wrote:

      I was reading your publication and I had some questions: (1) how does individual predicted probability work? is this based on certainty that it is this type of cell (as with resnet ?) and what thresholds are used? are different thresholds used for different cells it detects? and how did you define your final metrics?

      Definitely seems like an awesome solution to bridging the gap of knowledge and interpretation of medical personnel in assisting them to practice their job more informed and efficient. Keep up the good work!

    1. On 2020-07-24 23:05:36, user Guest wrote:

      IFR is a good thing to measure. I’d rather concentrate on Excess Deaths.

      Total Deaths from any cause are way up. There is a second spike forming (first was mostly NY city)

      Click: “Weekly Number of Deaths by Age,” then “Update Dashboard”

      Select a Jurisdiction or Age group if you wish to change the chart

      See the Weekly Deaths by jurisdiction and age group over the previous 5 years (gray) & this year (red)

      Title: <br /> Excess Deaths Associated with COVID-19

      https://www.cdc.gov/nchs/nv...

    1. On 2020-07-26 11:16:28, user Rosemary TATE wrote:

      This is a very interesting paper. However, I'm not convinced of the conclusions that the lower rate of test and hospitalisation are due to gender bias. It could be just that females have milder symptoms. And indeed the analysis shows that their symptom profile is different. Have the authors considered carrying out a multivariable analysis to adjust for some of these?<br /> I would suggest changing the title and moderating the conclusions. Incidentally, this is a cross-sectional study, and this should be mentioned somewhere. I would suggest replacing the term "big data" in the title with something more meaningful - as suggested in the StROBE guidelines. where is the checklist, could you please upload.

    1. On 2020-07-26 13:57:22, user catcarouser wrote:

      I’ve read the comments criticizing the study. Since Norway adopted the study standards and opened gyms, the infection rate there — well, look it up yourselves. This has been a success.

    1. On 2020-06-30 11:48:25, user J. M. Groh wrote:

      Hello, thanks for your important paper. May I suggest clarifying in the abstract the numerical effects that you saw, esp. reductions in the death rate in the treated group vs. controls (page 4, 5% mortality in the treated group vs. 45% in the control group, for groups of ~20 and ~50 patients). That is an impressive effect size. Thank you!

    1. On 2020-07-01 00:05:45, user ??? wrote:

      Dear Colleagues

      I'm Jaehun Jung, the corresponding author of the manuscript.

      Our manuscript was published after peer-review as follows.

      'Ji W, Huh K, Kang M, Hong J, Bae GH, Lee R, Na Y, Choi H, Gong SY, Choi YH, Ko KP, Im JS, Jung J. Effect of Underlying Comorbidities on the Infection and Severity of COVID-19 in Korea: a Nationwide Case-Control Study. J Korean Med Sci. 2020 Jun;35(25):e237. https://doi.org/10.3346/jkm...

      Our published version have the following changes, please refer to the newly published paper.

      1) Database changes<br /> -HIRA combines epidemiological investigations data from Korea's Centers for Disease Control and Prevention and extends the database until May 15. Our published version are based on this recent database. Therefore, the results of the pre-print version and the printed version are quite different.

      2) Case definition and comorbidity identification

      The pre-print version was able to check past history of more than 5 years. However, due to the expansion of the DB, only the past history can be confirmed within the past three years, and there has been a methodological adjustment.

    1. On 2020-08-03 13:49:53, user Michael wrote:

      You may be interested in our research at the optimized boarding of passenger groups in times of COVID-19. We find that the consideration of groups in a pandemic scenario will significantly contribute to a faster boarding (reduction of time by about 60%) and less transmission risk (reduced by 85%), which reaches the level of boarding times in pre-pandemic scenarios.

      The preprint publication “Analytical approach to solve the problem of aircraft passenger boarding during the coronavirus pandemic” is available here:<br /> https://www.researchgate.ne....

      Additional information about common passenger boarding in times of COVID-19 are available here:<br /> Evaluation of Aircraft Boarding Scenarios Considering Reduced Transmissions Risks (https://www.mdpi.com/2071-1... "https://www.mdpi.com/2071-1050/12/13/5329)").

    2. 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 2020-07-03 20:49:23, user Brooke wrote:

      "Asian" and "Other" are not appropriate ethnic categories. People of Chinese heritage are considered Asian. If you do not include Chinese people as Asians, then this ethnic category should be renamed "South Asian" (which includes people from India, Pakistan, Bangladesh, etc.). As for applying the term "other" to an ethnic group, this term literally "others" them. It may require more words to describe, but the more appropriate category for these participants would be "participants if more than one ethnicity or an ethnicity not listed in the survey." Although this tweet thread is about gender, the same gist applies here about ethnicity: https://twitter.com/theorig...

    1. On 2020-07-05 17:14:25, user Research Explained wrote:

      Unfortunately this study includes a great deal of speculation and very little evidence to back up the claims. The sample sizes were far too small and the primary outcome measure lacks statistical significance. The study also does not address the obvious confounding factor of the large health disparities between African Americans and other groups in the United States.

      Check out our general public friendly explanation of this study:<br /> https://www.researchexplain...

    1. On 2020-07-05 17:53:43, user Babak Navi wrote:

      The final version of this study was published in JAMA Neurology on July 2, 2020 and can be found at doi:10.1001/jamaneurol.2020.2730.

    1. On 2020-07-05 18:52:28, user Kamran Kadkhoda wrote:

      Neigher Abbott nor the authors used well pedigreed serum samples from patients recently infected with common coronaviruses . this means the specificity arm of the study is very well biased and essentially hundred percent is neither mathematically nor statistically possible.

    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 2021-04-07 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 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 2020-06-02 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 00:54:07, 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.

    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?

    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 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 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.

    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 2020-07-30 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 2020-08-25 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 2020-08-29 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