1. Last 7 days
    1. On 2022-02-07 21:44:51, user Isaac Tian wrote:

      Hello, we're the authors of citation #20. We had a few suggestions after reading your work.

      1. A practical deployment of the network would ideally use some other silhouette imaging method such as a CT scan or an RGB photo like you suggested in the Study Limitations section. The sentences that referenced our work didn't mention our attempt to estimate total and regional body fat using a 2D RGB camera image.<br /> Our study data, composed of 2D coronal and sagittal images coupled with 2-fold DXA composition measurements, may be relevant to validating your method on non-MRI inputs. Additionally, I believe our parallel effort in estimating body composition from 2D silhouettes should be cited and compared against. We also did estimate compartmental body fat as arm, leg, and visceral fat. Our initial model was not very flexible in pose due to the smaller training set available at the time, but we have since corrected for this.

      2. I recomputed our errors as MAEs to directly compare against your results, and assuming an adipose tissue density of 900 g / L, this came out to 121 g and 151 g for males and females, respectively. This is about 3-4x less than the magnitude of error reported in your draft. An analysis on the RMSE may be appropriate as large scale data may inflate R2.

      A collaboration may be appropriate once this draft has passed peer review in which your network is used as the pre-trained initialization to fine-tune on silhouettes segmented from another imaging source, such as our Shape Up! dataset which was stratified by age and BMI. This also addresses the bias concern you mentioned as your MRI dataset has an average age of 65.

      Thanks for sharing your work!

    1. On 2020-08-02 11:49:02, user Rosemary TATE wrote:

      Excellent paper. Thank-you so much for uploading the appropriate checklist. This seems to be almost always ignored!

    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 2021-09-13 15:48:07, user Bennie Schut wrote:

      In a followup it might be interesting to compare myocarditis requiring hospitalizations in both vaccine and covid groups. Not all myocarditis requires hospitalization and being infected now seems more of a when than an if. We already know covid causes myocarditis, so for risk assessment we would need to understand if one is better than the other. This study doesn't show this yet. But very interesting nevertheless.

    1. On 2020-04-20 17:09:11, user Michele Faucci Giannelli wrote:

      Could you add the fraction of asymptomatic in Table 2. I.e. provide it broken down by age? This can really help in modelling the infection beyond Vo'. Thanks!

    1. On 2024-08-21 16:23:52, user DUPA- Preprint Review wrote:

      Overall, this is a well-designed and conducted analysis that provides valuable insights into comorbidity patterns among early COVID-19 deaths in the United States. The manuscript presents important findings on the morbidity patterns associated with COVID-19 mortality and offers valuable insights for public health strategies. The latent class analysis (LCA) is a widely utilized clustering method for investigating comorbidities, which effectively addresses the issue of collinearity among comorbidities in high-risk populations. It could help identify disease patterns and understand disease relationships. The findings give researchers and health departments detailed knowledge to quickly identify vulnerable populations and provide protection in these public health emergencies. However, addressing the suggestions outlined above will enhance the clarity, transparency, and impact of the study. Therefore, we recommend the manuscript for publication with minor and major revisions.

      Major Comments:

      In Materials and Methods section, line 6 of the second paragraph, it is noted that cardiovascular disease (CVD) includes a variety of diseases/conditions with different prevalence and severity. For example, hypertension may have a significantly higher prevalence compared to other diseases within the CVD group, potentially leading to a disproportionate representation. Is it possible to list the prevalence of individual diseases in the supplementary material? Additionally, It would be beneficial to separate the diseases that have more than 60%(or other value)prevalence as the sensitivity analysis. This approach could enhance the stability of the study by avoiding amplifyfication of the effects from individual diseases with high prevalence. On the other hand, it also provides more details and discussion for the formation of the present results.

      Minor Comments:

      1. In the Abstract, Results section line 3: the phrase “A low frequency of comorbidities” is not precise. Use several words to express “where the prevalence of each comorbidity group was less than that of the entire sample” could be clear.

      2. In the Introduction, paragraph 1: <br /> The study effectively reaffirms the importance of cardiovascular disease and diabetes. Including a comparison with other studies conducted during the same period would provide valuable context.

      3. In the Discussion section, paragraph 2, line 3-6:<br /> Cardiovascular disease was present at 23%, even in the "minimal prevalence" category, which includes cardiovascular disease and diabetes, prominent cardiovascular disease without diabetes, and "minimal prevalence." Is there a difference in the distribution of each disease? Could this same/different distribution further explain the large proportion of "minimal prevalence" in people over 85 years old?

      4. In the Discussion section, paragraph 2, line 7-11:<br /> What are the mechanisms behind the high rankings for kidney disease and chronic lung disease.

      5. In the Discussion section, paragraph 2, line 1:<br /> In addition, please briefly state the underlying mechanisms behind cardiovascular disease and diabetes, such as mechanisms of interaction between cardiovascular disease and diabetes.

      6. In the Discussion Section, paragraph 4, line 2:<br /> The discussion effectively interprets the findings, particularly identifying the "minimal prevalence" class. But besides the eldest group, the proportions of this class still lead in other age groups. Is there any other explanation for why the "minimal prevalence" class still experienced significant mortality? It would also be helpful to provide more details based on citations 28,29(or other literature) to explain the reasonableness of proportions. This additional detail could offer deeper insights into the underlying factors contributing to their outcomes.

    1. On 2024-02-26 17:15:50, user Ciarán McInerney wrote:

      Please, justify the<br /> decision to use a random dates for control patients because it doesn’t make<br /> sense to me. Either you are trying to distinguish cases from controls (across<br /> patient groups), or you are trying to distinguish diagnosis dates from<br /> non-diagnosis dates (within the cases). The control group, by definition, have<br /> never had a diagnosis, so any features that your feature-selection protocol<br /> suggest cannot and should not be interpreted as features indicating a diagnosis<br /> date. Please, explain what you think your feature-selection is actually<br /> comparing. Later on you say that you use the odds ratio of PC onset within the<br /> three-year follow-up window; Why don’t you just say outcome = No occurrence for<br /> all controls?

    1. On 2020-11-18 21:50:14, user Hamid Merchant wrote:

      Very interesting findings. Can you post the Ct values of all individual patients at different time points in a table as a supplementary data file please?

    1. On 2025-11-30 14:34:14, user Jeff Lubell wrote:

      This article has now been published in a peer-reviewed journal. Please use that version. Thank you. Here is the citation: Torok RA, Lubell J, Rudy RM, Eccles J, Quadt L. Variant connective tissue as a risk factor for long COVID: a case-control study of data from a retrospective online survey of adults in the USA and UK. BMJ Public Health. 2025 Sep 17;3(2):e002949. doi: 10.1136/bmjph-2025-002949. PMID: 41001233; PMCID: PMC12458677.

    1. On 2022-02-03 08:04:13, user dgatwood wrote:

      Any chance a future update to this article could include the VE data against hospitalization *prior* to the third dose of mRNA-1273 (for comparison purposes)? Even a citation would help.

    1. On 2024-07-22 18:26:39, user Harmen Draisma wrote:

      Figure 1A "WES", "10,463,945 (NC[, Non-coding presumably])" seems to be at variance with page 4 "WES ... 10,463,945 were in coding regions"?

    1. On 2021-09-14 21:28:12, user Alberto wrote:

      23 vaccinated individuals, samples collected 5.2 weeks (average) after the second dose of the vaccine. No information about age, health, etc... compared to 10 individuals infected one year prior to taking the blood samples and 7 infected less than 2 months prior to taking the blood samples. Again no information about age, health, etc...

      Conclusion: "Hence, immune responses after vaccination are stronger compared to those<br /> after naturally occurring infection, pointing out the need of the vaccine to overcome the pandemic".

      Isn't that conclusion going well over the possibilities of this study? When in real world studies with cohorts of > 25.000 individuals it has been proven that the immunity acquired from infection is vastly superior to that from vaccination, how should we take these results?

    1. On 2020-04-05 13:03:21, user Rosemary TATE wrote:

      Authors can you please upload the supplementary material. All I could find under supplementary materials are the figures that already appear at the end of the document. It would be very useful to see the list of your sources of data, and also details of the model used.

    1. On 2025-03-07 06:35:55, user H Soori wrote:

      The manuscript presents a critical examination of science-related populism and its impact on public health during the COVID-19 pandemic in Iran. While the authors aim to illuminate the detrimental effects of political decisions on health outcomes, the framing of Iranian scientists and health workers raises several ethical and factual concerns. First and foremost, the manuscript appears to overlook the immense efforts made by Iranian scientists and healthcare professionals during one of the most challenging public health crises in recent history. Despite facing significant barriers, including sanctions and limited access to resources, Iranian scientists worked diligently to combat the pandemic. Accusing them of contributing to the crisis undermines their hard work and sacrifices, particularly when approximately 400 health staff lost their lives while serving their communities. The analysis seems to simplify a complex situation by attributing adverse health outcomes solely to political resistance and delays in vaccination. It is crucial to consider the broader context, including international dynamics, supply chain disruptions, and the unprecedented nature of the pandemic. Such factors played a vital role in vaccination delays and should not be overlooked in the pursuit of a singular narrative. While the manuscript discusses the dangers of science-related populism, it inadvertently engages in a form of populism itself by painting a one-dimensional picture of Iranian public health responses. This approach risks alienating those who worked tirelessly on the front lines, suggesting that the authors may not fully appreciate the nuances of scientific work in politically charged environments. The findings advocating for a global commitment to uphold scientific integrity are undoubtedly important; however, this message would benefit from a more nuanced discussion that recognizes and honors the contributions of Iranian scientists and health workers. Instead of casting blame, the narrative should focus on collaborative efforts and the need for solidarity in the face of global health challenges. In conclusion, while the manuscript raises valid concerns about the implications of political actions on public health, it fails to adequately recognize the contributions of Iranian scientists and healthcare workers. A more balanced approach that acknowledges their dedication and sacrifices would enhance the manuscript's credibility and foster a more constructive dialogue on public health policy and scientific integrity.

      Hamid Soori<br /> Professor of Epidemiology

    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 2020-04-30 19:12:43, user Sinai Immunol Review Project wrote:

      Main findings<br /> This report describes the use of systemic tissue plasminogen activator (tPA) to treat venous thromboembolism (VTE) seen in four critically ill COVID-19 patients with respiratory failure. These patients all exhibited gas exchange abnormalities, including shunt and dead-space ventilation, despite well-preserved lung mechanics. A pulmonary vascular etiology was suspected.

      All four patients had elevated D-dimers and significant dead-space ventilation. All patients were also obese, and 3/4 patients were diabetic.

      Not all patients exhibited an improvement in gas exchange or hemodynamics during the infusion, but some did demonstrate improvements in oxygenation after treatment. Two patients no longer required vasopressors or could be weaned off them, while one patient became hypoxemic and hypotensive and subsequently expired due to a cardiac arrest. Echocardiogram showed large biventricular thrombi.

      Limitations<br /> In addition to the small sample size, all patients presented with chronic conditions that are conducive to an inflammatory state. It is unclear how this would have impacted the tPA therapy, but it is likely not representative of all patients who present with COVID-19-induced pneumonia. Moreover, each patient had received a different course of therapy prior to receiving the tPA infusion. One patient received hydroxychloroquine and ceftriaxone prior to tPA infusion, two patients required external ventilator support, and another patient received concurrent convalescent plasma therapy as part of a clinical trial. Each patient received an infusion of tPA at 2 mg/hour but for variable durations of time. One patient received an initial 50 mg infusion of tPA over two hours. 3/4 patients were also given norepinephrine to manage persistent, hypotensive shock. Of note, each patient was at a different stage of the disease; One patient showed cardiac abnormalities and no clots in transit on an echocardiogram, prior to tPA infusion.

      Significance<br /> The study describes emphasizes the importance of coagulopathies in COVID-19 and describes clinical outcomes for four severe, COVID-19 patients, who received tPA infusions to manage poor gas exchange. While the sample size is very limited and mixed benefits were observed, thrombolysis seems to warrant further investigation as a therapeutic for COVID-19-associated pneumonia that is characterized by D-dimer elevation and dead-space ventilation. All four patients had normal platelet levels, which may suggest that extrinsic triggers of the coagulation cascade are involved.

      The authors suspect that endothelial dysfunction and injury contribute to the formation of pulmonary microthrombi, and these impair gas exchange. Pulmonary thrombus formation has also been reported by other groups; post-mortem analyses of 38 COVID-19 patients' lungs showed diffuse alveolar disease and platelet-fibrin thrombi (Carsana et al., 2020). Inflammatory infiltrates were macrophages in the alveolar lumen and lymphocytes in the interstitial space (Carsana et al., 2020). Endothelial damage in COVID-19 patients has also been directly described, noting the presence of viral elements in the endothelium and inflammatory infiltrates within the intima (Varga et al., 2020). One hypothesis may be that the combination of circulating inflammatory monocytes (previously described to be enriched among PBMCs derived from COVID-19 patients) that express tissue factor, damaged endothelium, and complement elements that are also chemotactic for inflammatory cells may contribute to the overall pro-coagulative state described in COVID-19 patients.

      References<br /> Carsana, L., Sonzogni, A., Nasr, A., Rossi, R.S., Pellegrinelli, A., Zerbi, P., Rech, R., Colombo, R., Antinori, S., Corbellino, M., et al. (2020) Pulmonary post-mortem findings in a large series of COVID-19 cases from Northern Itality. medRxiv. 2020.04.19.20054262.

      Varga, Z., Flammer, A.J., Steiger, P., Haberecker, M., Andermatt, R., Zinkernagal, A.S., Mehra, M.R., Schuepbach, R.A., Ruschitzka, F., Moch, H. (2020) Endothelial cell infection and endotheliitis in COVID-19. Lancet. 10.1016/S0140-6736(20)30937-5.

      The study described in this review was conducted by physicians of the Divisions of Pulmonary, Critical Care, and Sleep Medicine, Cardiology, Nephrology, Surgery, and Neurosurgery and Neurology at the Icahn School of Medicine at Mount Sinai.

      Reviewed 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.

    1. On 2020-11-06 03:35:38, user AliD wrote:

      The final version of the article has been published on the journal of Aging Clinical and Experimental Research in Sep 2020. Please use the following information to cite the article.

      Daneshkhah, Ali, Vasundhara Agrawal, Adam Eshein, Hariharan Subramanian, Hemant Kumar Roy, and Vadim Backman. "Evidence for possible association of vitamin D status with cytokine storm and unregulated inflammation in COVID-19 patients." Aging Clinical and Experimental Research 32, no. 10 (2020): 2141-2158.

    1. On 2020-02-03 16:29:21, user Sarah wrote:

      Hi, I'm not sure why you use the study 3 (Read et al.2020) estimate at 3.8. Their estimate is 3.11 (95%CI, 2.39-4.13). Is it an error?

    1. On 2021-12-16 04:37:21, user Jordan Atchison wrote:

      A little concerned about the comparison to the NNT for ASA of 333. That value of 333 is calculated over a span of 6.6 years, but it's unclear over what time period the author's NNE applies to. Is it 1 prevented transmission per day, 1 prevented transmission per average length of incubation period, or some other time period?

    1. On 2024-10-22 02:44:40, user CDSL_JHSPH wrote:

      Thank you for sharing your preprint paper, which I found to be a substantial contribution to the field of clinical trial design, especially in optimizing treatment duration for TB. Your adaptation of model-based methods, such as MCP-Mod and FP, to duration-ranging trials demonstrates their superiority over traditional qualitative methods in detecting duration-response relationships and estimating the MED, particularly in small sample Phase II trials. I appreciate your acknowledgment of the risk of underestimating the MED in some model-based approaches, especially at smaller sample sizes, and your suggestion to use a more conservative threshold like the lower confidence bound is a crucial safeguard. Expanding on how trial design parameters, such as spacing between durations and sample size imbalances, might influence the accuracy of these methods could provide even greater insights. Overall, this paper provides a great framework for enhancing trial efficiency, and I look forward to seeing how your research evolves in the future.

    1. On 2020-04-08 15:02:17, user Dr. Noc wrote:

      I think that we have to be careful to not interpret these results the wrong way. We know that older patients are at higher risk of mortality. By selecting for patients who have recovered from disease, the patient group may be biased toward those who had stronger production of nAbs (especially in the most at-risk group).

      That is to say that, although it may appear that higher titers of nAbs are correlated with the groups that tend to have more severe disease outcomes, that doesn't necessarily mean that nAbs are contributing to the severity of outcomes, but rather that they may reflect a "survivorship" type of bias.

    1. On 2020-05-03 01:22:06, user tom wrote:

      Very fine work here addressing the pressing need for credible validation of a high-quality antibody test. One question that I have is whether the 2018-19 sera were confirmed to have a representative prevalence of common cold coronavirus antibodies. It would also be nice to see a serosurvey that follows up on its indicated positives with a good ELISA or even neutralization assay.

      Since the authors did not go into much interpretation, here are some back of envelope thoughts:

      Boise has a 228k population * 1.79% seroprevalence = 4080 estimated exposures.

      Ada County (in which Boise lies) has a 392k population, has had 663 recorded cases to date = 0.17% cumulative incidence, and has 17 recorded deaths = 2.6% CFR.

      As the rest of Ada County's incidence should lag Boise metro a good bit due to the ex-metro's lower population density and thus lower average Rt, Boise should account for more than its pro rata share of the county's covid burden. Let's say Boise accounts for 100 more than its 386 pro rata share of the county's 663 cases, and 3 more than its 10 pro rata share of the county's 17 deaths. 13 deaths out of Boise's 4080 serologically estimated exposures = 0.32% IFR. (That's about 8x lower than Ada County's CFR, which is roughly in line with the 10x differential between the cumulative reported case incidence and the detected seroprevalence). This is about half the estimated IFR using NYC's reported deaths and the recent serological survey there.

      Any IFR estimate presently inferrable from these data is provisional and likely to increase though, because while Idaho's new cases have been squelched long enough for essentially all past and current infections to have developed antibodies, it's quite likely that more deaths will occur among the currently active cases. I'd guess >25% more based on the histogram of reported case dates, so IFR likely >0.40%.

      Of course with only 13 deaths, any such IFR estimates are subject to a wide confidence bracket, and very sensitive to the accuracy in counting of deaths.

    1. On 2020-07-24 16:23:32, user David Gagnon wrote:

      Was any data collected on the numbers for the ages of the people in the same household?This section was badly written, is missing something, or I just don't understand something in the language. 15.5% is the lowest of those numbers and that seems odd, since the I would guess the majority of 2 person households to be couples without kids, both young and old, and in the latter case the secondary infection should have been notably high, right?<br /> There are also three number in the section that correspond to three groups:<br /> "The secondary infection risk for study participants living in the same household increased from 15.5% to 43.6%, to 35.5% and to 18.3% for households with two, three or four people respectively (p<0.001). "<br /> Is the 18.3% for households with more than 4 people? Is it then 18% per person?

    1. On 2020-04-10 07:15:55, user Chris Romo wrote:

      Wow, what a tough crowd this is.

      First, thank you for this intuitive tool! In less than an hour, I am better informed now, when compared to the collective several weeks of endless barrage of media getting the message out.

      To the tough crowd: <br /> I get it folks, you want to see different information. Might I recommend a "suggestion" over harsh criticism? When offering feedback, footnote the source from which you are referring to? Keep in mind, there is a great deal of underlying data that informs this tool. Imagine what that meaning had, how that probably had to be massaged to meet the abstract's intent.

    2. On 2020-04-06 23:24:28, user Mastah Plannah wrote:

      It is ridiculous that the model still says that Massachusetts has NOT implemented a Stay At Home order. Therefore the model is useless for Massachusetts.

      Massachusetts did implement stay-at-home. They did it on the early side on March 23.

    1. On 2020-04-02 00:26:45, user Rick wrote:

      This must have been translated from Chinese, because some sentences make no sense, and probably have placed the wrong words in places of importance, ie. Besides, a larger proportion of patients with improved pneumonia in the <br /> HCQ treatment group (80.6%, 25 of 32) compared with the control group <br /> (54.8%, 17 of 32). Notably, all 4 patients progressed to severe illness <br /> that occurred in the control group." Flip the words, improved and pneumonia, and the whole meaning changes. Did patients "improved with pneumonia", or what?

      Also, what the hell does absorption of pneumonia mean? Did they get better or worse? It's very hard to tell from this translation.

    1. On 2024-04-11 17:53:00, user eysen wrote:

      JMIR Publications and PREreview are pleased to announce our next Preprint Live Review on Friday, April 19 at 9am PT / 12pm ET / 4pm UTC which discusses this preprint

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      The Live Review is hosted by two facilitators from the PREreview team with experience in moderating virtual collaborative review discussions. They will guide participants through a constructive discussion of the following preprint: Assessing the Incidence of Postoperative Diabetes in Gastric Cancer Patients: A Comparative Study of Roux-en-Y Gastrectomy and Other Surgical Reconstruction Techniques - by Tatsuki Onishi

      Live Review Details:

      WHEN: Friday, April 19 at 9am PT / 12pm ET / 4pm UTC

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      WHAT: The participants will be guided through a constructive discussion of the following preprint: Assessing the Incidence of Postoperative Diabetes in Gastric Cancer Patients: A Comparative Study of Roux-en-Y Gastrectomy and Other Surgical Reconstruction Techniques - by Tatsuki Onishi medRxiv: https://doi.org/10.1101/202...

      A review will be then written and published on PREreview.org within the following 2 weeks. Participants will have the chance to help compose the final review and be recognized as reviewing authors.

      HOW: To participate, please complete the following registration form. You will receive an email from PREReview with a link to a Zoom room and a passcode.

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    2. On 2024-04-11 17:36:56, user JMIR Publications wrote:

      Join JMIR Publications & PREreview for a Live Review of this preprint: Assessing the Incidence of Postoperative Diabetes in Gastric Cancer Patients: A Comparative Study of Roux-en-Y Gastrectomy and Other Surgical Reconstruction Techniques - by Tatsuki Onishi medRxiv: https://hubs.la/Q02stzCL0

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    1. On 2020-04-15 03:25:26, user Realist50 wrote:

      On top of ideas for society - i.e., that most places should follow a path more like Sweden than full lockdowns - doesn't this strongly argue for Human Challenge trials among lower-risk groups to speed vaccine development?

      As some background, my understanding is that Human Challenge Trials speed tests of the efficacy of vaccines by intentionally exposing vaccinated individuals to the virus. Otherwise, people are vaccinated and essentially told to go on with life, with vaccine efficacy only observed by comparing rates of infection to a control group over time.

      The idea has already been proposed for COVID-19, but AFAIK it hasn't yet been implemented anywhere. Human Challenge Trials aren't a new idea: they've historically been used for diseases where the risk from infection is viewed as manageable. This analysis therefore supports the idea that Human Challenge Trials are ethical for those who are relatively young without obvious risk factors.

    1. On 2022-03-23 02:12:03, user Guest wrote:

      Hello authors,<br /> Thank you for submitting a preprint of this interesting study on the virome to a public domain. I have a few questions regarding your methods and materials.<br /> First, the detailed description of sample collection was great, but I could not find any internal standards for the PCR steps, DNA extraction, or isolation of VLP. These might have been stated, somewhere else perhaps, but I could not identify them. However, for sample collection, how did you determine the location and type of wounds that would be tested? Was there a specific location or depth for chosen wounds or just all types stated that were within the frames of the criteria?<br /> Secondly, the methods for sample processing and DNA extraction are excellent, but I cannot seem to find any information regarding the primers used or the number of cycles performed while analyzing 16S rRNA. I could not find the total number of sequences obtained per sample, however, the quality reading for the viral reads was in-depth and well covered. I did not find any profile or 16S normalization or a total quantification of bacterial or bacterial numbers (like qPCR).<br /> Thirdly, I did not find anything about OTU abundance corrected for variance in copy numbers or variance in genome size. I also could not find any method details regarding coverage of communities measured or if there was any comparison to the dominate to rare. One last question, what do you define as ‘deep sequencing’ regarding this study?<br /> Overall, I found this article very interesting and a good read. Thank you for providing such excellent work with the virome. I have not seen many studies regarding the effects of the virome on human healing, host interactions, or composition until recent years, but this article provides a great starting point for these types of studies.

      SHSU5394

    1. On 2020-04-15 14:12:18, user Ed Fisher wrote:

      This regimen looks to be substantially different from those being used in the US. E.g., approximately double the HCQ dosage, no Azithromycin and in some US uses, no zinc. How does that impact the comparison?

    1. On 2022-01-12 16:00:26, user Robert Nelson wrote:

      Regarding the matching based on vaccination status. The percentage of the matched delta having any vaccine was 64% vs 69% of matched Omicron cohort. (no vaccine = 36% and 31% respectively). The percentage of delta (matched) with 2 doses = 54% vs 58% for Omicron. So we're looking at about a 7 to 8% advantage to omicron cohort if we assume less severity or decreased chance of death. But when you apply that differential to the HR it doesn't change the outcome very much.

    1. On 2020-04-19 16:32:58, user Robert S. wrote:

      What is the false positive rate of the test used? What is the cross-reactivity of the test with other coronaviruses that share sequence homology with the spike protein of nCoV-2?

    2. On 2020-04-20 17:17:34, user Andy wrote:

      On the self-selection, non-random bias, participants were asked about "prior clinical symptoms".

      But even that is not enough to correct the bias. People are more likely to participate if they think they have been exposed, not just because they had symptoms.

      So the result is still going to be wrong after accounting for "prior clinical symptoms", because participants were self-selected for exposure.

    3. On 2020-04-17 20:43:16, user Drew Middlesworth wrote:

      I was estimating the true infected numbers were 10-20x higher than the reported numbers based off the hospitalization rates, I wasn't expecting it to be this high. Although folding these numbers into NY infected counts would mean that over 100% were infected which can't be right. My estimate would show about 25-50% infected currently.

      Although the other thing that would skew this, by using Facebook ads and not doing a random population pick, you would skew the results higher as people who were sick in Jan-Feb would be more likely to respond to the ad to get tested. They could easly be 2-3x too high which would be more inline with the numbers I was estimating based off hospitalization rates.

    4. On 2020-04-19 00:34:15, user SonoranSeeker wrote:

      Considering that this virus is extremely contagious, two or three times that of the flu, and considering that this extremely contagious virus was circulating unabated for a relatively long time, this study is probably pretty accurate. It is also in line with the study in Germany and modelling of virus spread based on previous corona virus characteristics. <br /> This could be why there were so many deaths in such a short time. Let's hope it burned hot, but will flare out just as fast.

    5. On 2020-04-20 21:52:38, user charles young wrote:

      Doesn't specificity of 99.5% mean 0.5% false positive? Similarly, 98.3% (one side of 95CI range for specificity) implies 1.7% false positive. If all 3330 subjects were actually not infected, we would still expect 56 (false) positives, which is more than raw actually observed positives of 50. So the test results are consistent with a true rate of zero.

      Other concerns have been raised by many people, including but not limited to sampling bias. They tend to enlarge the confidence level of specificity, and increase the number of false positives expected. The result that has caught so much attention of 50-85-fold more cases is not supported by the data here.

    6. On 2020-04-20 22:26:21, user Andy wrote:

      Preliminary results of USC-LA County are out. Unfortunately, that study also suffers from self-selection bias. We need to know how many people were contacted initially; should we count those who declined to participate as presumed negatives?

      In the Santa Clara study, people were contacted initially through Facebook. We need to know how many people saw the ad, and should we also count those who declined to participate as presumed negatives? (Surely the authors know how many people saw the Facebook ad.)

      Edit to add: Wait a minute, I just saw comment by Anon who participated with a link but without Facebook. So the study is even more flawed.

    1. On 2021-03-22 13:21:54, user Stephen B. Strum wrote:

      The Gorial et al. study in my opinion is a weakly positive study re ivermectin. The IVM group had 25% of patients with co-morbidities vs 45% in the non-IVM group. Gorial's reference 14 is a retracted paper (Patel). Positive findings re IVM were shorter times ot – PCR with 7 days for IVM vs 12 for non-IVM. Mean hospital days 42% less in IVM arm. I wish Gorial would have detailed the 2 fatalities in the non-IVM arm. Someone should have proofed this paper; it is very sloppily written. In contrast, the paper by Krolewiecki et al. is very impressive re IVM & the importance of pharmacokinetics.

    1. On 2021-10-24 07:24:16, user Otmar S wrote:

      Dysguesia is the leading indicator which can also be seen for children regarding other studies (for example CLOCK). I can´t find the question/incidence of Dysgeusia for children in this study. I wonder why. No data?

    1. On 2020-10-16 12:16:12, user Torbjørn Wisløff wrote:

      I would seriously consider revisiting the analyses. In Figure 2c, the RR of 1.00 seems not to correspond with the somewhat diverging curves. In Figure 2a, on the other hand, the RR is 0.95, but the curves follow each other very closely.

    2. On 2020-11-21 23:33:56, user VirusWar wrote:

      Dr Soumya Swaminathan, Scientific chief of WHO explained on ECCVID conference that in Solidarity trial, hydroxychloroquine (HCQ) was widely used in Standard of Care group, despite rules said it should not. She said they had to do some "adjustment" but this doc don't talk about this issue or any adjustment.

      Dosage of Hydroxychloroquine is also far too high and patients in that group are worse at entry than the one in supposed "control" group.<br /> There is a big issue in mortality graph over time in Figure 2a for remdesivir : death rate at 28 days is supposed to be 11% but graph shows it at 13%

      It is odd to compare HCQ against HCQ

    1. On 2021-09-23 15:49:33, user kdrl nakle wrote:

      What is needed more is the distance between the shot and data collection. We need longer duration period for VE evaluation. Your time period is too short.

    1. On 2025-07-06 08:41:23, user xu-sheng zhang wrote:

      Dear medRxiv staff

      I just want to inform you that our article has been [published in The Lancet Regional Health - Europe 2025; https://doi.org/10. 1016/j.lanepe.2025. 101364<br /> with a title: "Cost-effectiveness of vaccination strategies to control future mpox outbreaks in England: a modelling study". could you please help signpost to it.<br /> Best wishes<br /> Xu-Sheng Zhang

    1. On 2021-11-28 23:39:37, user Silje Nes wrote:

      The study compares a group of PCR positive individuals to a group of PCR negative individuals, in order to find out what impact Covid infections have had on the use of healthcare services. The underlying assumption is that the PCR negative group is a representative selection of the general population that have not had Covid. This fails to acknowledge some important characteristics of the PCR negative group.

      To distinguish between individuals who had Covid or not, the authors look at all positive and negative tests within a given time frame. As mentioned in the paper, there was limited testing capacity in Norway during the first 3 months of the pandemic. Only a minority (typically healthcare workers and close contacts of confirmed cases) had access to PCR testing at the time of their first symptoms. The study concludes that the limited testing «affects the groups with COVID-19 and no COVID-19 to an equal extent». This is not entirely correct. Individuals without access to testing in the early months who were to develop persistent symptoms, would typically be tested several weeks or even months after first symptoms. Most individuals with Long Covid from the first months would therefore have only a negative PCR test result, and consequently end up as part of the comparison group. According to FHI’s own numbers, 220 had been admitted to intensive care by 10 May 2020, and 471 by 1 Feb 2021, implying almost half of the Covid infections took place before testing was available to the general population.

      Since we don’t know from the start what proportion of Covid infected people needed access to healthcare over an extended period of time, it is difficult to assert to what extent the outcome of the study is affected by these falsely negative individuals being part of the comparison group.

      The consequences of having persistent Covid symptoms without a formal diagnosis, in regards to use of healthcare services, is not clear. Doctors could choose to thoroughly examine the patient in order to rule out other morbidity, or tell the patient that it would pass by itself, and to wait it out, with no further examination.

      In addition to this, an unknown number of individuals will have had false negative PCR test results, and therefore be part of the «No Covid» comparison group despite having had Covid. <br /> Also significantly, the study fails to take into account the fact that many individuals would get tested because they were showing symptoms of Covid, and that this implies illness that could affect their use of healthcare services, regardless of cause. The selection in the comparison group is therefore skewed towards a part of the population who were sick.

      Thus, in actuality the groups that are compared look like this: <br /> - PCR positive – Covid infected<br /> - PCR negative – Three subcategories (unknown ratio): <br /> –– No symptoms (close contacts, general population)<br /> –– Symptoms (other disease)<br /> –– (Long) Covid infected, tested while no virus present

    1. On 2020-10-26 17:59:08, user Meng-Ju Wu wrote:

      Hi! It is interesting to read the paper in discussion for EVs to differentiate ALS from healthy and diseased groups. And I want to share my thought on the study.

      I think the main contribution of the study includes the purification of EVs with the nickel-based isolation compared to the conventional methods that makes the analysis of specific EV parameters highly sensitive and reliable. If the EVs are reliably differentiate ALS patients from healthy and diseased group, clinical assessment with the blood test will significantly shorten the diagnosis time for ALS and that the treatment may be started as early as possible. In addition, if biomarkers are available to detect ALS patients, it means that we can develop the treatment specific to ALS using their unique properties. Patients can avoid costly and lengthy process of ALS diagnosis.

      I have two questions considering the methods. First, why was the supernatant from human plasma diluted in filtered PBS once but the serum from mice required 10 times for dilution? Second, what was the temperature and humidity condition for the incubation of activated charged agarose beads in NBI? I think the time to use the obtained serum would be the limitation of this approach. The content of the EVs might be changed if the centrifuged plasma samples are not immediately used. Such compositional change may be subject to the storage condition and the degradation rate of each specific proteins. It may also vary among species. Therefore, a specific time period to analyze the plasma should be strictly regulated.

      In general, I think there are no major grammatic or spelling errors. However, the content may be modified in order to make it more logical and convincing to read. In the introduction part, I think it is important to summarize how is ALS diagnosed clinically. If the readers are informed that electrophysiologic diagnosis takes longer time and effort and make the diagnosis, they would appreciate the value of blood test to detect suspected ALS patient in prodromal state. In the last paragraph of the introduction, it is not reasonable to mention that the study results suggesting EVs are food biomarkers. It should be mention in the discussion or conclusion section. In the material section, the time of patient inclusion was missing. In the animal model, the paper should mention why only female mice with SOD1G93A and male mice with TDP-43Q331K were studied. Also, the timing to study the two different genes as well as the number of the mice were concerning to interpret the results. I want to suggest making a visual diagram on the machine learning technique. You did a great job in comparing the difference between ultracentrifugation and NBI using EV-like liposomes. As such, I want to suggest applying the same comparison onto the animal model to test the reliability of the using the NBI method alone in the paper. The results and the discussion are well-written and consistent with the tables and figures provided

    1. On 2021-11-05 05:54:24, user Zakir Husain wrote:

      A revised version of the paper (National Lockdown and COVID-19 <br /> Containment in India) was published in Economic & <br /> Political Weekly, Vol 56, Issue 39 on 25 September 2021. the paper may <br /> be accessed from: <br /> https://www.epw.in/journal/...

    1. On 2022-10-28 07:00:48, user Sujoy Ghosh wrote:

      This manuscript has now been published as follows: <br /> Ghosh, S., Roy, S.S. Global-scale modeling of early factors and <br /> country-specific trajectories of COVID-19 incidence: a cross-sectional <br /> study of the first 6 months of the pandemic.<br /> BMC Public Health 22, 1919 (2022). https://doi.org/10.1186/s12...

      Kindly update the link in medrxiv. Regards, Sujoy Ghosh

    1. On 2021-09-12 10:37:13, user 4qmmt wrote:

      The level of protection and durability of immunity derived from an immune response to natural infection versus that derived from an immune response to a narrow target like the Spike protein seems perfectly understandable and expected.

      Both are natural immune system responses. The only difference is the target. There is no "magic" to the vaccine. Thus, I would be very interested if someone could explain how an person's immune response to a single element of the virus can possibly be better than an immune response in that same person to the whole virus which includes the same single target.

    2. On 2021-08-26 18:20:25, user thestreetlawyer1 wrote:

      Love to see this peer reviewed. Been really trying to determine what is the best move for me. Hard to put all the dogma and peer pressure aside (from both sides). I'm curious how this data reckons with u.s data on hospitalizations, seems most of our hosp cases are unvaccinated.

    3. On 2021-08-27 16:48:32, user Edward wrote:

      This study adds important previously unreported information comparing natural post-infection immunity to immunity after vaccination. Unfortunately, the study risks giving the false impression that it is better to go ahead and seek natural immunity over vaccine immunity. The study, for example, does not take into account covid-attributable excess deaths. Thus, by default, those with natural post-infection immunity considered in the study are covid survivors. Hence, they can be expected to have stronger immunity than those who died because of covid. While the basic premise that natural immunity is stronger than vaccine immunity in the abstract, I suspect it is better to get a milder case of breakthrough covid than to risk death in search of natural immunity. We need a much larger study, ideally prospective, and will have to measure the frequency of "long haul covid" cases between the vaccinated and unvaccinated.

    1. On 2020-04-21 08:34:15, user Maria wrote:

      Don't you think that lung capacity differences are instead the key to explain the lower incidence and severity of the disease in women and children? Thank you.

    1. On 2020-05-01 19:31:01, user Randy Jackson wrote:

      Thank you for this contribution. I found it very useful for understanding the tradeoffs between deaths from the virus and duration of the epidemic with alternative social distancing scenarios. But, you don't discuss or address the immunity bit. With R0=2.75, ~100% immunity is achieved, but very low percentages of population with lower R0. So, my question: What happens when such a large part of those still alive aren't immune? Rebound?

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

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

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

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

    1. On 2021-01-07 14:02:12, user Meerwind7 wrote:

      Household size (number of siblings) was not taken into account?<br /> If I understand correctly, the multi-variant analysis showed that population density has negligible, insignificant effect on its own, and what was perceived to be a density effect in the separate statistics for each veriable was just the result of positive correlation between social deprivation and density?<br /> It might be meaningful to perform multi-variable statistical tests once again for local prevalence, social deprivation and each of the other influences as third (possibly) independent variable.

      Population density was just used as a digital property (less or above 500 /km2) in the multi-variable modeling, not the exact figure? <br /> As the density in built-up areas almost always exceeds 500 /km2 by far, it would appear to be more meaningful to distinguish at a higher cut-off level, for example >5000 /km2, which is more representative for multi-story housing. That will aso be representative for more extensive use of public transportation in the area other than for ways to school. It could also be plausible that quite low density leads to higher risk (due to longer distances to school spent in busses), and also high density, but medium density is associated with lower risks.<br /> The regional incidence seems to be taken into account with a logarithmic relation; I wonder if results would look different for a linear analysis.

    1. On 2021-06-20 12:02:21, user ThaomasH wrote:

      1. I wish the results were translated into unites that would permit estimation of the benefits of mask-wearing in terms of days of sickness and death.
      2. I wish the results spoke to the issue of benefits to the wearer vs benefits to others.
      3. I do understand the conclusion that mandates had zero effect on mask wearing.
    1. On 2020-06-24 10:51:55, user Alev Kiziltas wrote:

      Artificial intelligence has an important potential in healthcare. Not only the Dermatologist, all healthcare professionals can use TzancNet with less margin of error in the cytology of erosive-vesiculobullous diseases

    1. On 2023-11-29 10:44:02, user Theo Sanderson wrote:

      Thank you for posting this preprint.

      Sequencing data can be found via Sequence Read Archive (SRA) accession PRJNA1043164.

      I have not been able to locate these data on the SRA - could you provide a link? Many thanks.

    1. On 2021-01-15 21:12:09, user Florian wrote:

      Hello, I can only tell it from an UK perspective, I think your hard date on Lockdown measures and that they only did apply on the date you mentioned is false. I recall in the week you are mentioning Social Distancing, I was cutting the business trip short to travel back home and from that point forward many people including me worked from home. Our client even sent everyone into the home office one week prior. Think this illustrates quite well that the policy wasn't in place the behaviour lol had to adapt a couple of weeks later was adapted by many at that point in time. So your interpretation of the data at least for parts of the UK where I can speak for is flawed.

    1. On 2020-05-11 18:13:35, user Dianelos Georgoudis wrote:

      The IFR is very sensitive to the age distribution of a country, so the same model can produce an IFR varying from 0.3% for Pakistan to 1.4% for Italy (and 0.6% for the world). So I don't understand what the 0.75% value in this paper even means.

    1. On 2020-12-06 20:15:11, user Murilo Perrone wrote:

      It appears to me that the 8 patients on the treatment group who did not make it where exactly the ones who failed to reach adequate levels of 25OHD (above 30 ng/mL). The chart indicates that 5 patients from the treatment group failed even to reach 20 ng/ml. Unfortunately, the study gives no clue about this possible correlation, but that's my best guess.

      I noticed that ventilation machine requirement was reduced by more than 50% in treatment group, but all 8 patients from treatment group who required it didn't survive. There is an indication that their outcome was predictable. IMHO, their specific data should be analyzed.

    1. On 2025-02-25 16:04:51, user Peter C Gøtzsche wrote:

      You estimate that from 1.4 to 4.0 million lives were saved with the covid vaccines.

      I do not remember having seen a paper with so many assumptions before. You do sensitivity analyses but I wonder what the reliability of this study is.

      You assume, for example, that absent vaccination, the whole world would have got infected with the Omicron variant, and that vaccines reduce mortality by 75%.

      Since the virus mutates all the time, and since there were too sparse data on mortality in the randomised trials to tell us if the vaccines reduce mortality, I am sceptical towards any estimation of what a possible effect on mortality would be, and I would expect this to be a rapidly moving target, too. We have seen how rapidly the protective effect against infection dropped after the trials were done, down to about 50%. Most people I have talked to, including myself and my wife, got covid despite being fully vaccinated, but of course, we might have died if we had not been vaccinated.

      On p29, you write: Vaccine effectiveness for death: We assumed VE=75% during the pre-Omicron period and 50% during the Omicron period.

      Where did these estimates come from? I wonder if it is possible to say anything about an effect on mortality.

    1. On 2023-12-19 12:39:03, user Christos Proukakis wrote:

      Response to: “Is Gauchian genotyping of GBA1 variants reliable?”

      Marco Toffoli1,2, Anthony HV Schapira1,2, Fritz J Sedlazeck2,3,4, Christos Proukakis1,2 *

      1. Department of Clinical and Movement Neurosciences, Queen Square Institute of Neurology, University College London, UK
      2. Aligning Science Across Parkinson’s (ASAP) Collaborative Research Network, Chevy Chase, MD 20815, USA
      3. Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX, USA
      4. Department of Molecular and Human Genetics, Baylor College of Medicine, TX, USA

      * To whom correspondence should be addressed: c.proukakis@ucl.ac.uk

      We recently described two methods for GBA1 analysis, which is hampered by the adjacent highly homologous pseudogene: Gauchian, a novel algorithm for analysis of short-read WGS, and targeted long-read sequencing 1. Tayebi et al have applied the former to WGS from 95 individuals, and compared it to Sanger sequencing 2. They report concordant genotypes in 85, while 11 had discrepant calls (we note that this leads to a total of 96). In addition, they report 28 false Gauchian calls in 1000 Genomes Project (1kGP) samples. Gauchian was developed because the homology of the GBA region requires a short read variant caller that does not rely solely on read alignments, and can identify specific variants known to be pathogenic. To understand the cause of these discrepancies, we reviewed their data, and conclude that they are mis-interpreting Gauchian results in 8 of the 11 discrepant samples, and incorrectly using Gauchian to analyze low-coverage 1kGP samples.

      Among the 11 (11.5%) samples with inconsistent calls with Sanger (Table 1), four (Pat_08, Pat_26, Pat_28 and Pat_58) were not called as the variants are not on Gauchian’s target list, which includes all ClinVar variants in December 2021. These variants, and any others, can be easily added (see Supplementary Information). Three other samples (Pat_75, Pat_76 and Pat_79) had low data quality resulting in large variation in sequencing depth across the genome, as shown by the median absolute deviation (MAD) of genome coverage: 0.269, 0.128 and 0.127 (three highest values among all samples). Gauchian recommends trusting calls in samples with MAD values <0.11, and produces a warning message if this is exceeded. In all three samples, the GBA1+GBAP1 copy number was a no-call (marked as “None” in the output file), indicating that Gauchian could not determine the copy number due to high coverage variation. Variants were not called because no further analysis was done beyond copy number calling. These should not be viewed as false negatives, as the warning message and the report of no-calls should prompt the user to obtain higher quality data or consider alternative sequencing. Among the remaining 4 samples with inconsistent results: Pat_03 had a Gauchian call of heterozygosity for p.Asn409Ser, while Sanger reports this as homozygous. Review of the IGV trace (Tayebi et al. Supp Figure 1) shows that at least 10 reads (around a fifth of the total) have the reference base, and therefore it is hard to conclude this is homozygous. Review of the Sanger trace (not provided) could determine whether there is a low peak representing the reference allele. We cannot provide a conclusion, and additional analysis is recommended. Mosaicism could be a plausible explanation, and this has been reported in GBA1 3,4, albeit not at this position. Pat_47 had a false negative p.Leu483Pro call. Pat_16 was indeed wrongly genotyped as homozygous for p.Asn409Ser, related to the adjacent c.1263del+RecTL deletion. Pat_92 had all expected variants called, but the heterozygous p.Asp448His was mis-genotyped as homozygous. In summary, there is one false negative and two wrongly genotyped variants (heterozygous variants called homozygous). Gauchian’s precision is therefore 98.9% (175 out of 177 calls are correct). Its allele-level recall/sensitivity is 99.4% after excluding alleles not on Gauchian’s target list, and samples which could not be analyzed due to high coverage variation. Alternatively, it can be calculated as 97.2% if only samples with high coverage variation are excluded, 96.2% if only alleles not on the target list are excluded, and 94.1% if all these samples are considered .

      Tayebi et al. concluded that Gauchian is not able to call recombinant variants without providing orthogonal evidence. In Pat_95, Pat_71 and Pat_16, they examined alignments in IGV and reported absence of supporting reads for Gauchian calls, but all recombinant alleles called by Gauchian were consistent with Sanger. This highlights that read mapping in this region is unreliable (variant supporting reads may align to the pseudogene), making interpretation of alignments in IGV very challenging. Gauchian is designed to untangle ambiguous alignments, locally phase haplotypes and make correct calls. Particularly, in Pat_95, they claimed that Gauchian called the expected RecNciI variant but got the mechanism of the recombinant allele wrong (gene conversion vs. gene fusion). This claim appears to be based on incorrect interpretation of IGV alignments, i.e. seeing 3’ UTR mismatches associated with GBAP1 does not necessarily indicate gene fusion, as they can be misalignments, or even part of the gene conversion. The RecNciI in Pat_95 is a gene conversion, as indicated by the normal copy number between GBAP1 and GBA1. Tayebi et al. claimed that this is a gene fusion without orthogonal evidence. In addition, they claimed that Gauchian misreported copy numbers in Pat_92, Pat_42 and Pat_72, again without orthogonal evidence. We validated Gauchian copy number gains by digital PCR in four cases 1. While particular recombinants could be prone to erroneous copy number calling, we do not know what “other techniques'' identified a different copy number in Pat_92. Orthogonal validation using digital PCR would resolve this. Finally, it is true that Gauchian does not have all possible recombinants on its target list, as it is designed to focus on recombinant variants in exons 9-11, because others are rare and detectable with standard callers.

      Tayebi et al. reported 4 samples where Gauchian missed variants in GRCh38 compared to GRCh37. Among these, two (Pat_35, Pat_75) were due to incorrect alignment settings that resulted in abnormally low mapping quality throughout the region. It is likely that ALT-aware alignment was on for all samples except these two. The remaining two (Pat_16, Pat_78) reflected an area of improvement for Gauchian to better call p.Asn409Ser, which is not a GBAP1-like variant, and can thus be called well by standard callers.

      We reported Gauchian calls of 1000 Genomes Project (1kGP) samples, validating some by targeted long reads 1. Gauchian called zero samples with biallelic variant in exons 9-11. However, Tayebi et al. reported a completely different set of Gauchian calls in the same samples (in their Table 4). This was caused by incorrect use of Gauchian on old low coverage WGS (median coverage <10X, https://ftp.1000genomes.ebi... "https://ftp.1000genomes.ebi.ac.uk/vol1/ftp/phase3/data/)"), rather than 30X (https://ftp-trace.ncbi.nlm.... "https://ftp-trace.ncbi.nlm.nih.gov/1000genomes/ftp/1000G_2504_high_coverage/data/)").

      We are grateful to Tayebi et al for assessing Gauchian analysis of this very challenging gene 2, but note that most discrepancies were due to incorrect use or misinterpretation of results. “No call” samples due to inadequate data quality cannot be considered false negative, as no calls are provided, and warnings of noisy coverage are given where applicable. Samples with inadequate coverage should obviously be avoided, as Gauchian is expected to perform at coverage >30X. Gauchian does not call variants not on its target list, which can be expanded. We provide updated recall (99.4%) and precision (98.9%) values. We have not seen any evidence of the alleged inability of Gauchian to call recombinant variants, and would welcome orthogonal copy number assessment of discrepancies. We show that Gauchian can be used for GBA1 assessment when coverage and data quality are adequate. We do note a limitation in genotyping p.Asn409Ser, a non-recombinant variant that can be called by standard variant callers, which we recommend running together with Gauchian for a complete call set. Finally, in clinical cases where absolute certainty is required, Sanger sequencing could be considered, with targeted long read sequencing another option 1,5–7.

      Table 1. Details on the 11 samples where Gauchian and Sanger are inconsistent.

      Gauchian calls Sanger Assessment,Tayebi et al. Our assessmentSample Copy Number of GBA1 and GBAP1 GBAP1-like variant in exons 9-11 Other unphased variants Genotype Prediction

      Pat_08 4 None p.Asn409Ser p.Asn409Ser/p.Gln389Ter False Negative Missed variant is not on Gauchian's target list

      Pat_28 4 None p.Arg535His p.Arg535His/Cys381Tyr False Negative Missed variant is not on Gauchian's target list

      Pat_58 4 None p.Asn409Ser, p.Arg296Ter p.Asn409Ser, p.Arg296Ter, c.203delC False Negative Missed variant is not on Gauchian's target list

      Pat_26 4 None p.Asn409Ser p.Asn409Ser/p.Arg502Cys False Negative Missed variant is not on Gauchian's target list.

      Tayebi et al.’s Supplementary Figure 1 shows no variant at p.Arg502Cys (c.1504C>T), but a different variant at the neighboring position, p.Arg502His (c.1505G>A), which is not on Gauchian's target list.

      Pat_75 None (No Call) NA NA p.Arg502Cys/p.Arg159Trp Missed Copy number is a no-calldue to high variation in depth so no further variant calling was performed. Coverage MAD 0.269

      Pat_76 None (No Call) NA NA p.Asn409Ser/p.Asn409Ser Missed Copy number is a no-call due to high variation in depth so no further variant calling was performed. Coverage MAD 0.128

      Pat_79 None (No Call) NA NA p.Leu483Pro/p.Arg502Cys Missed Copy number is a no-call due to high variation in depth so no further variant calling was performed. Coverage MAD 0.127

      Pat_03 4 None p.Asn409Ser p.Asn409Ser/p.Asn409Ser False Negative Gauchian call is supported by reads, see Tayebi et al.’s Supplementary Figure 1.

      Pat_47 4 None p.Asn409Ser p.Asn409Ser/p.Leu483Pro False Negative True false negative

      Pat_16 3 c.1263del+RecTL/ p.Asn409Ser, p.Asn409Ser p.Asn409Ser, c.1263del+RecTL False Positive Heterozygous p.Asn409Ser misgenotyped as homozygous as Gauchian did not know the exact breakpoint of the c.1263del+RecTL deletion, which is very close to p.Asn409Ser.

      Pat_92 7 p.Asp448His/p.Leu483Pro,p.Asp448His p.Asp448His/ p.Leu483Pro+Rec7 False Negative There is no false negative. Rec7 is reflected in the copy number call (copy number gain). This GBAP1 duplication does not have any functional impact on GBA, so Gauchian does not report it as a GBA variant. Heterozygous p.Asp448His misgenotyped as homozygous.

      Acknowledgements

      We are grateful to Xiao Chen and Michael Eberle for helpful comments. They are former employees of Illumina and current employees of Pacific Biosciences. This research was funded in in part by Aligning Science Across Parkinson's [Grant numbers 000430 and 000420] through the Michael J. Fox Foundation for Parkinson's Research (MJFF).

      Competing interests

      FJS receives research support from PacBio and Oxford Nanopore. AHVS has received consulting fees from AvroBio, Auxilius, Coave, Destin, Enterin, Escape Bio, Genilac, and Sanofi and speaking fees from Prada Foundation.

      Supplementary Information

      Add new variants to Gauchian’s config file

      The four new variants can be added to Gauchian’s config file as follows.

      For hg38, add the following lines to gauchian/data/GBA_target_variant_38.txt

      chr1 155236304 A GBAP G c.1165C>T(p.Gln389Ter)<br /> chr1 155236327 T GBAP C c.1142G>A(p.Cys381Tyr)<br /> chr1 155239989 CGGGGGT GBAP CGGGGGGT c.203delC(p.Thr69fs)

      Add the following line to gauchian/data/GBA_target_variant_homology_region_38.txt<br /> chr1 155235195 T 155214568 C c.1505G>A(p.Arg502His)

      For GRCh37, add the following lines to gauchian/data/GBA_target_variant_37.txt<br /> 1 155206095 A GBAP G c.1165C>T(p.Gln389Ter)<br /> 1 155206118 T GBAP C c.1142G>A(p.Cys381Tyr)<br /> 1 155209780 CGGGGGT GBAP CGGGGGGT c.203delC(p.Thr69fs)

      Add the following line to gauchian/data/GBA_target_variant_homology_region_37.txt<br /> 1 155204986 T 155184359 C c.1505G>A(p.Arg502His)

      Bibliography

      1. Toffoli, M. et al. Comprehensive short and long read sequencing analysis for the Gaucher and Parkinson’s disease-associated GBA gene. Commun. Biol. 5, 670 (2022).

      2. Tayebi, N., Lichtenberg, J., Hertz, E. & Sidransky, E. Is Gauchian genotyping of GBA1 variants reliable? medRxiv (2023) doi:10.1101/2023.10.26.23297627.

      3. Filocamo, M. et al. Somatic mosaicism in a patient with Gaucher disease type 2: implication for genetic counseling and therapeutic decision-making. Blood Cells Mol. Dis. 26, 611–612 (2000).

      4. Hagege, E. et al. Type 2 Gaucher disease in an infant despite a normal maternal glucocerebrosidase gene. Am. J. Med. Genet. A 173, 3211–3215 (2017).

      5. Pachchek, S. et al. Accurate long-read sequencing identified GBA1 as major risk factor in the Luxembourgish Parkinson’s study. npj Parkinsons Disease 9, 156 (2023).

      6. Graham, O. E. E. et al. Nanopore sequencing of the glucocerebrosidase (GBA) gene in a New Zealand Parkinson’s disease cohort. Parkinsonism Relat. Disord. 70, 36–41 (2020).

      7. Leija-Salazar, M. et al. Evaluation of the detection of GBA missense mutations and other variants using the Oxford Nanopore MinION. Mol. Genet. Genomic Med. 7, e564 (2019)

    1. On 2020-06-05 07:12:39, user Matthias Hübenthal wrote:

      Thanks to Ellinghaus et al. for sharing these interesting results. The authors utilized rs8176747, rs41302905 and rs8176719 to predict ABO blood types. Combinations of the inferred blood types then have been used to predict case/control status employing logistic regression. Alternatively, one could base the prediction on a genetic risk score incorporating the ABO SNPs. Boxplots of the risk scores could then be used to illustrate group-wise differences. However, for completeness association results for the ABO SNPs should be reported and discussed.

    1. On 2025-04-08 13:30:55, user Malin wrote:

      Interesting study! The method description is quite limited, what was the size and material of the funnel? What was the airflow through the funnel and the residence time for aerosol particles from exhalation to detection?

    1. On 2020-04-03 02:55:33, user Gideon Mordecai wrote:

      Thank you for this work, I think it is an important contribution. Can you please add more information in the methods for the network/ cluster analysis. Also, is it possible to use the genomic/ network data to quantify which group contributes more to transmission; asymptomatic (/mild symptoms) vs more severe symptoms?

    1. On 2020-07-13 18:19:24, user Dana C. wrote:

      This study simply takes the estimated number of firearms in America and the annual firearm death rate then assigns a ratio. They apply this ratio to new firearm purchases with little or no adjustment for rioting, calls to defund police departments etc. The source of much of the data used is from The Gun Violence Archive which does not allow open access to it's data, it's criteria in forming and gathering it's data and is an openly anti gun organization.The results of this study have not been peer reviewed or subjected to any critical scrutiny. The results of this study are misleading at best and political biased and fraudulent at worst. It's no secret that a study can be manipulated to produce the desired end result which is clearly the result here. I have one question for those who prop up their ideologies with pseudo science, why are the 400,000 homicides (this is the most conservative estimate) that are prevented by legal/lawful gun owners annually never included in studies such as this?

    1. On 2021-12-16 12:03:32, user J W wrote:

      The result are interesting, however the discussion is biased due to scientifically irrelevant political concerns. The impossibility of comparing the effectiveness of specific vaccines among themselves and with respect to reinfections can be solved by age stratification for which data is available. The other discussed concerns are of minor impact, are to be treated within statistical uncertainty and last not least they apply for the study od waning immunity itself. The people vaccinated early are in no way statistically the same ones as the one with the delay.

    1. On 2022-02-09 01:07:23, user Avi Bitterman wrote:

      This paper dichotomizes a continuous variable to get a barely statistically significant result (P=0.044). But this is just dichotomania. Time to treatment is a continuous variable, not a binary variable. The appropriate test for this continuous variable is a regression along the continuous variable. Not a dichotomized sub-group analysis.

      Using the same numbers this author uses from Table 1, we ran a regression which failed to show a significant effect of treatment delay on outcome P=0.13

      Aside from being the appropriate test, another advantage of a regression here is it avoids the possibility selective dichotomization along the proposed moderator variable to get the desired result (a barely significant P value the authors just so happen to have found).

      I would also be happy to have a discussion with the authors to elaborate on the above as well as discuss numerous other critical errors with this analysis as well.

    1. On 2025-06-04 17:34:59, user Sarah Jorgensen wrote:

      Questions for the authors: <br /> From the results, 11 children started GAHT within 12 months of GnRHa initiation and another 20 within 12-24 months (total 31, 31/94 (33%)), yet in the discussion, "more than half of the participants had initiated gender-affirming hormones over the 24-month follow up period." Could the authors resolve this apparent discrepancy?

      59 patients were assessed at 24 months. If 31 were not assessed because they started GAHT, there still appears to be 4 children unaccounted for. Were they lost to follow-up? What was their status at last assessment?

      Details on psychiatric medications at baseline and initiated during follow-up would be of interest and could be considered for inclusion as time-varying covariates in models.

      Given that 4-9 years have elapsed since GnRHa initiation, why was this analysis limited to 24 months follow-up? At the very least it would be of interest to know vital status and how many ultimately went on to receive GAHT versus desisted.

    1. On 2021-09-05 16:07:08, user JimmyJoe6000 wrote:

      Someone posted an inception to date chart using daily deaths for the two groups of countries. I can't see to find in in any of the articles like this. It mentioned John Hopkins along with this link. <br /> Anyone have the link to the chart?

    1. On 2020-06-26 22:10:08, user kpfleger wrote:

      On what date did the VDD protocol (table 1) commence? Is it possible to analyze COVID-19 outcomes (fatality, ventilator need, ITU admission, etc.) by baseline 25OHD on admission for before vs. after the VDD protocol started, as they did in the Singapore study: https://www.medrxiv.org/con... (which perhaps you should also cite BTW)? Or was 25OHD status not assessed for COVID-19 patients before the VDD protocol began?

    1. On 2021-12-07 11:30:00, user kdrl nakle wrote:

      This paper is not worth much as the authors failed to collect any real world data. It is not easy but that is something that needs to be done instead of replacing it with hypothesizing this or that.

    1. On 2021-07-30 14:06:06, user Luiz wrote:

      Even though, the vaccine protects the people from the very dangerous infection of covid -19, 15 people died in the vaccinated group and 14 died in th unvaccinated group?

    2. On 2021-08-02 22:47:42, user drwambier wrote:

      Please revise: "No new serious adverse events assessed as related by investigators were reported after data cut-off for the previous report."

      Previously reported: 2 deaths (BNT162b2) vs 4 (placebo), with zero deaths related to COVID19 in each arm. Death (any cause) is the main SERIOUS ADVERSE EVENT (SAE), and a higher number was reported, please revise accordingly.

      "During the blinded, controlled period, 15 BNT162b2 and 14 placebo recipients died; during the open-label period, 3 BNT162b2 and 2 original placebo recipients who received BNT162b2 after unblinding died. None of these deaths were considered related to BNT162b2 by investigators. Causes of death were balanced between BNT162b2 and placebo groups (Table S4).”

      Since you are reporting the 6 months data, please consider rephrasing to the full numbers: "18 deaths on BNT162b2 versus 16 deaths on the placebo (including the 2 deaths after receiving BNT162b2)." It is also important to specify the denominator for each group. It is unclear what is the total number of patients were followed-up for full 6 months, and how many were lost to follow-up (survivor bias?).

      "Cumulative safety follow-up was available up to 6 months post-dose 2 from combined blinded and open-label periods for 12,006 participants originally randomized to BNT162b2. The longer follow-up for this report, including open-label observation of original BNT162b2 recipients and placebo recipients who received BNT162b2 after unblinding, revealed no new safety signals relative to the previous report”.

      If 3 deaths happened in the BNT162b2 group until 1 month after Dose 2 during the blinded period and 5 in the placebo group, the new deaths after that month were: 15 for BNT162b2 and 11 for placebo (including the 2 deaths after receiving BNT162b2). Please verify if this is correct, if it is, please state specifically as this might be considered a safety signal.

      200 HIV patients data is still not disclosed. I understand that this is per protocol. However, we ask to please disclose the current HIV+ data, since many are receiving the shots under EUA without data of their subgroup analysis.

      Plus, assuming that those are in the 22,166 patients of BNT162b2 and 22,320 of placebo:<br /> Considering the “scenario of all patients followed, without unknown outcomes”:<br /> RR for death is 1.1328 (.5778-2.2208). An increase by 13% of all cause mortality in 6 months of follow-up including the part of vaccinating the placebo arm.<br /> The ages and gender of deaths would be informative for safety since populations were balanced by randomization please add a table with such information.

      Current data suggests that within 6 months of follow-up, BNT162b2 does not reduce all-cause mortality. There is a signal that it might increase all-cause mortality. <br /> Assuming that it would be difficult for investigators to access if deaths were related to BNT162b2 since myocarditis or heart-related side effects were initially thought to be unrelated to BNT162b2, also no previous signals of thrombosis were reported.

      Causes of death were assumed to be “Cardiac Arrest” or other "unknown" descriptions. There is even a “death” as cause of death on the table… "dementia?" For future trials or third injection, an active screening for myocarditis (Serum Cardiac Troponin T and Creatine Kinase–MB), and thromboembolic events would be prudent, specially in the >65 y.o. population, which may be more vulnerable to momentary reduction of cardiac muscle function through inflammation.

      As this was a healthy population (not treatment of COVID-19, etc), and deaths were rare. <br /> It seems that all-cause mortality was indeed more common than deaths by COVID-19 in the current manuscript, thus, they cannot be left aside from the trial results discussion. Please discuss specifically about the comparison of COVID-19 deaths in the control group vs the relative increase of deaths detected in the BNT162b2 group and how putting those numbers in the balance.

      About COVID-19 related deaths, the score was expected: 2 deaths on placebo (“COVID-19”) and 1 death in Vaccine ("COVID-19 pneumonia”). <br /> With the current safety data, caution is warranted, since the number to harm in the best scenario points that approximately 100 deaths could be attributed to the vaccine for every 1M fully vaccinated, if the increase in all-cause deaths is not a noise of low numbers.

      "Safety monitoring will continue per protocol for 2 years post-dose 2 for participants who originally received BNT162b2 and for 18 months after the second BNT162b2 dose for placebo recipients who received BNT162b2 after unblinding.”

      Was all the control group crossed-over to BNT162b2 post-unblinding? If so, please state and give the reasons why it was decided to do so. If there is no placebo arm for a safety control comparison, this safety monitoring will only be important if extreme flags happen: such as unexpected high number of serious adverse events emerge.

    1. On 2020-07-26 14:06:30, user Gordon Erlebacher wrote:

      I started to read the paper, but all the equations are missing. <br /> Here is an additional question. The contact matrix Mij measures to the average number of contacts between one person in group I and all members of group j. But are these different contacts or contacts with repetition? The different possible choices affects the spread of the virus. Any insight is appreciated.

    1. On 2025-04-01 17:33:08, user Richard DiBenedetto wrote:

      A number of Havana Syndrome victims reported a sudden onset of symptoms resembling effects of a concussion. Impairment similarity with areas of the brain affected by pesticides does not conclude cause of sudden concussion. Sudden symptoms from my personal experience were more like radio frequency, EMP or radar type technology. There has been much research on microwave bioeffects which is worth further study for a cause of Havana Syndrome.

    1. On 2021-07-04 13:24:54, user Matthias Maiwald wrote:

      Our article has now appeared here: <br /> Wan WY, Thoon KC, Loo LH, Chan KS, Oon LLE, Ramasamy A, Maiwald M. Trends in Respiratory Virus Infections During the COVID-19 Pandemic in Singapore, 2020. JAMA Netw Open. 2021 Jun 1;4(6):e2115973. doi: 10.1001/jamanetworkopen.2021.15973. <br /> https://jamanetwork.com/jou...

    1. On 2020-05-05 21:56:48, user Un Kwon-Casado wrote:

      Hi Anne- Great and exciting work! Do you know if its primarily shedded viral particles versus infected cells in the saliva samples?

    2. On 2020-05-25 16:42:05, user Kirsi Liimatainen wrote:

      Great work!<br /> This article was answer to my question why not to use saliva as Covid-19 virus sample material. If looking for smaller sample vial and method to collect saliva, I just tested using Samco 691-1S Large Aperature Plastic Transfer Pipet for collection of saliva: thought about some delicious food and pushed saliva between my lip and gum to be drawn up from there with soft transfer pipet. Collecting about 300 ul of saliva was easy task. Smaller orifice pipettes do not collect as well. As collection vial I used Thermo Scientific 3422 0.5 ml Screw CapTube, non-sterile. Caps to these tubes are separate and available with multiple colours, I think I used 3471GS. Pipet tip does fit to 2D barcoded "biobank" tube (like Matrix 3744-BR) , but there foaming makes filling the tube difficult.

    1. On 2020-03-15 18:34:58, user tusitw wrote:

      Are you also going to study as a function of humidity?<br /> Below LOD, do we know it is still capable of infecting? a question in the same theme as Stefano Gaburro...

    1. On 2021-08-06 02:14:00, user Peat Floss BS MS MD wrote:

      Assuming the 60 million + people served by this healthcare system are roughly representative of the united states, roughly 5% of them would be expected to be between 12-17. That's roughly 3 million people. CDC estimated infection rate in that age group is about 36%. That's about 1 million covid infections in this cohort if its roughly representative. You can throw some pretty massive error bars on there to account for seeking outside care and the possibility of an unusually old or young sample and never get close to the numbers used in this paper

    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 2020-12-10 17:00:23, user Susan Bewley wrote:

      Thanks Russell & team. Would it be possible for you to share the following on #medRxiv too? (i) the research information leaflet you describe, (ii) the informed consent form, (iii) the statistical plan mentioned as S2. Best wishes

    1. On 2023-06-15 06:08:48, user Ashok Palaniappan wrote:

      A peer-reviewed version of the preprint has now been published:<br /> Muthamilselvan S and Palaniappan A (2023) BrcaDx: precise identification of breast cancer from expression data using a minimal set of features. Front. Bioinform. 3:1103493. doi: 10.3389/fbinf.2023.1103493

    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.

    1. On 2025-01-10 21:50:46, user Harold Bien wrote:

      Fascinating article. Given that each individual VOC in Fig 1 appears to have significant overlap between each group and wide distributions, it would be interesting to learn how the various machine learning algorithms used each VOC and the resulting model. Could the authors provide more information on the ML algorithms used, how it was trained, and how the ROCs were constructed?

    1. On 2021-12-24 17:48:21, user BernardP wrote:

      Looking at the graphs, I see both vaccines lose all effectiveness at 90 days, but worse, actually drop into strong negative effectiveness after that time.

      This would mean that these vaccines *increase* one's chances of infection after the initial 90 days "honeymoon" period.

      Am I getting this right?

      If so, why are governments pushing third doses as Omicron is becoming dominant?

    1. On 2021-02-24 02:58:40, user Eric O'Sogood wrote:

      1. The trial was stopped early and did not enroll enough subjects to meet its own initial power calculations. 2. Single dose ivermectin at this stage is not the recommended regimen. 3. Ivm arm had the highest d dimer (p 0.01) and I do not see any discussion of anticoagulant beyond thromboprophylaxis. 4. Absorbtion of ivm with food rises ~4 fold, was it given on an empty stomach or with food? 5. The authors write that this is the first trial of ivm vs placebo. There are already 5.
    1. On 2022-09-20 14:08:25, user JonJ wrote:

      A modified version of this manuscript has been published under a new title, "Use of smartphone mobility data to analyze city park visits during the COVID-19 pandemic." https://www.sciencedirect.c....

      Please note that the published manuscript employs an expanded sample of city parks, following an update to the SafeGraph dataset.

    1. On 2022-03-10 00:32:30, user Elena Schindler wrote:

      I read the article "Researcher finds stunning rate of COVID among deer..." on NPR.

      I wonder whether mosquitos or deer ticks could go on to transmit COVID from deer blood to humans, other deer, or other species. Perhaps examining the blood from live ticks on dead deer might be a place to start.

    1. On 2021-05-05 01:00:46, user Andre Boca Ribas Freitas wrote:

      Unfortunately, the drop of proportion of elderly people among total of deaths is due in large part to the increase in deaths among young people!<br /> This is due to the characteristics of variant P.1, which leads to more serious cases among young people.

    1. On 2020-06-01 12:41:21, user Ron Conte wrote:

      SARS-CoV-1 (causes SARS) is more similar to SARS-CoV-2 (causes Covid-19) than these cold coronaviruses used in the study. SARS antibodies last 2 to 3 years ("Duration of Antibody Responses after Severe Acute<br /> Respiratory Syndrome", Emerging Infections Diseases, 13:10, 2007), and "Memory T cell responses targeting the SARS coronavirus persist up to 11 years post-infection" (dx.doi.org/10.1016/j.vaccin... "dx.doi.org/10.1016/j.vaccine.2016.02.063)").

    1. On 2021-03-23 01:25:16, user Nneoma Nzeduru wrote:

      Great work on this article! This article does a wonderful job at analyzing data on the short term outcomes of the Lumbar Laminoplasty. I noticed that you mentioned a limitation of this study is that does not measure VAS score with activity. From personal research, I discovered that walking is an effective means of a supporting recovery, why did the study not include the relationship between VAS score and activities like walking and other low impact activities?

    1. On 2021-01-21 13:08:34, user John H Abeles wrote:

      This analysis is largely of hospitalised patients with more severe Covid19– when viral replication has already peaked and patients are suffering largely from hyperinflammation/hyperimmune effects

      Many studies of early, outpatient treatment ie within 5 days of onset of symptoms have shown benefit of combinations of hydroxychloroquine with zinc and either azithromycin or doxycycline

      Likewise, most viral diseases respond to antiviral drugs only in early stages eg influenza to oseltamivir or herpes to valacyclovir

    1. On 2022-06-22 21:00:15, user Tony Blighe wrote:

      The only mechanism discussed which would increase CO2 was the dead space in the mask, but I wonder if another mechanism may contribute.

      When breathing through the nose, air is expelled at high speed and moves away from the body. A mask has the effect of diffusing and slowing the expelled air so that it hangs around the face, which would result in more of the expelled air being inhaled on the next breath.

      I saw this diffusion effect very clearly myself when I asked my brother, who is a smoker, to inhale from a cigarette and breath out normally while wearing a surgical mask. Rather than blowing downwards from his nostrils and away from his face, the smoke formed a cloud around the mask.

    1. On 2022-05-22 17:15:49, user Teresa Moreno wrote:

      UPDATE MAY 2022: lessons for the monkeypox viral outbreak?

      According to the Johns Hopkins data repository (updated in Dong et al 2020), case numbers of COVID-19 in Spain rose steadily and rapidly after the early December 2021 holiday to an omicron-driven post-Christmas peak far higher than any other during the SARS-CoV-2 pandemic. On 8th December 26,412 new cases were recorded, whereas by 11th January 2022 this figure had risen an order of magnitude to 292,394. The entirely predictable threat of a countrywide viral superspreading event boosted by Christmas celebrations, many in poorly ventilated indoor environments, had become real, with deaths from the disease peaking in late February 2022.

      In May 2022 cases of monkeypox suddenly emerged in several countries worldwide. The pathogen responsible for this enzootic disease is belongs to the Orthopoxvirus genus which includes the virus causing smallpox. How is this global outbreak of monkeypox being transmitted? As in the early days of the emergence of COVID-19, initial public health statements are emphasising personal hygiene and avoidance of close physical contact with the saliva or lesions of infected individuals (ECDC 2022; Koslov 2022). The World Health Organisation states that "monkeypox virus is transmitted from one person to another by close contact with lesions, body fluids, respiratory droplets and contaminated materials such as bedding" (WHO 2022). This initial reaction to a new pattern of infectious disease is familiar (Moreno and Gibbons 2021). The spread of the now-eradicated smallpox virus was similarly considered to have been transmitted primarily by fomites and close contact, until the classic nosocomial outbreak in the German town of Meschede. Study of this event concluded that cases spread inside the hospital were infected by virus particles disseminated by air over a considerable distance (Wehrle et al., 1970, see also Gelfand and Posch 1971; Fenner et al., 1988; Tellier et al., 2019). Reviewing the history of this disease, Milton (2012) concluded that "the weight of evidence suggests that fine particle aerosols were the most frequent and effective mode of smallpox transmission". Given our precautionary recent experience and slow start with SARS-CoV-2, we argue that we should be treating this unexpected new zoonotic poxvirus outbreak as likely being driven at least in part by viraerosol transmission. It is another wakeup call for treating indoor air ventilation issues more seriously.

      References<br /> Dong E, Du H, Gardner L. An interactive web-based dashboard to track COVID-19 in real time. Lancet Infect Dis. 2020 May;20(5):533-534. doi: 10.1016/S1473-3099(20)30120-1. Epub 2020 Feb 19. Erratum in: Lancet Infect Dis. 2020 Sep;20(9):e215. PMID: 32087114; PMCID: PMC7159018.<br /> European Centre for Disease prevention and Control. Epidemiological update: Monkeypox outbreak. 20 May 2022. <br /> Fenner, F., D.A. Henderson, I. Arita, Z. Jezek, I.D. Ladnyi. Smallpox and its eradication. WHO, Geneva (1988), p. 1460p<br /> Gelfand, H.M., J. Posch. The recent outbreak of smallpox in Meschede. West Germany. Am. J. Epidemiol., 93 (4) (1971), pp. 234-340, 10.1093/oxfordjournals.aje.a121251<br /> Moreno, T., Gibbons, W. 2021. Aerosol transmission of human pathogens: From miasmata to modern viral pandemics and their preservation potential in the Anthropocene record. Geoscience Frontiers. DOI:10.1016/j.gsf.2021.101282<br /> Kozlov, M. 2022: https://www.nature.com/arti... "https://www.nature.com/articles/d41586-022-01421-8)")<br /> Milton, D.K.. What was the primary mode of smallpox transmission? Implications for biodefense. Front. Cell Infect. Microbiol, 2 (2012), p. 150, 10.3389/fcimb.2012.00150<br /> Tellier, R. Aerosol transmission of influenza A virus: a review of new studies. J. R. Soc. Interface, 6 (2009), pp. S783-S790, 10.1098/rsif.2009.0302.focus<br /> Wehrle, P.F., J. Posch, K.H. Richter, D.A. Henderson. An airborne outbreak of smallpox in a German hospital and its significance with respect to other recent outbreaks in Europe. Bull. World Health Organ., 43 (5) (1970), pp. 669-679<br /> World Health Organisation. Multi-country monkeypox outbreak in non-endemic countries. May 21 2022. https

    1. On 2022-04-05 16:53:48, user Anil wrote:

      Dear authors,

      Thanks for this piece work and sharing this in the form of a preprint! I can tell a great amount of thought and care went into this paper. As was already mentioned by others on social media, there is extra care warranted around the wording used in this paper, particularly around the phrasing of "remaining childless". Having children is not the default path in a person's life and being childfree shouldn't read like being a problem.

      I also have concerns on sib-disconcordance for socio-economic-environmental factors that may have confounded your analyses. For example, exposure to urbanicity. People who live in cities report higher rates of certain medical conditions, e.g. schizophrenia, and also are more likely to not have children. Can you also exclude economic/educational effects? An analysis were these factors have been taken into account would greatly help clarify.

      More on exposure to urbanicity: if you have zipcodes of individuals you could stratify your analyses by kilometer difference in living in/near a city between sibs. Or limit your analyses to sibs who live close to each other. (if you have longitudinal data on location, that would be even better of course!).

      There are other mechanisms that likely explain at least some of the effects you observe. For example, LGBTQ+ people are more likely to suffer from mental illnesses and are also more likely to not have children as well, which is not because they fall ill but due to socio-political-legal structures in society.

      In general, I think that people who deviate from cisheteropatriarchal norms (which has strong beliefs on reproduction) experience more hardship in their lives. LGBTQ people are an example of this but not the only group. Women who choose to live childfree will experience more hardship as well. My guess is that part of what you are measuring is how these people suffer in a heteropatriarchal society. The question then is by how much?

      Your definition of partnership is not inclusive to LGBTQ+ individuals. Same-sex partnership has only recently become legal in Finland and Sweden, so you are likely defining these people as "partnerless". Not sure how much this will impact your findings but it is good to mention this limitation.

      I felt it was important to share these thoughts and I hope they serve to be of use.

      All the best, Anil

    1. On 2021-06-11 18:53:43, user SemperCogitens wrote:

      A couple of things people really need to note here:<br /> 1) This is PRE-publication. It hasn't been peer-reviewed. Everything on this website is such. It cannot be regarded the same as something which has gone through the full process with a respected journal.<br /> 2) This is an observational study (retrospective cohort). It is NOT a randomized, placebo-controlled clinical trial. Only the RCT can prove causation. This is hypothesis-generating research only. It does not PROVE HCQ works, merely suggests that.

      3) If you dig in a bit, they define "treatment" to include only 37 of the advertised 250ish patients in the cohort, specifically those receiving >3,000mg HCQ and >1g azithromycin. Small sample sizes should always be viewed with extreme skepticism. Less than 30ish and your p-value is essentially meaningless.

      4) The overall mortality rate of the total group was ~80%! These people were old, unhealthy to begin with, admitted to the hospital after nearly a week of progressing symptoms, required ICU care, intubation, and mechanical ventilation. These were very sick patients.

      5) Clinically, we see a pattern for the treatment of ARDS and secondary pneumonia, not COVID. High dose corticosteroids work (we know this for ARDS), tocilizumab, a potent anti-inflammatory works (we have some data for this in ARDS as well). And azithromycin is a very common drug to treat bacterial pneumonias that often pop up secondary to lung disease like this.

      So, please avoid jumping to unsupported conclusions. If we want real answers, we have to keep our skepticism, and be very careful in our analysis. The key here is we need corroborating studies. An April 2020 study at the VA showed exactly the opposite effect of HCQ in a similar patient population (though the VA obviously serves more males).

    1. On 2020-04-10 22:02:12, user Todd Johnson wrote:

      Have any of the causal inference researchers at Harvard taken a look at this? Do we know enough to create a few candidate causal DAGs to know what to adjust for?

    1. On 2020-05-11 14:36:45, user Willyboy wrote:

      What about the age? and other factors which can impact the result?<br /> most of the countries with low death rate are also countries with young population.<br /> for example, Morocco has only 7% of 65+<br /> while a country like Germany has 22% of 65+ people !!!

      so the analysis must be executed by group of age, and also has to insure the way the people are counted (as this differs from 1 country to another)<br /> and the analysis must also exclude other factors which can impact the results.

      Russia has authorized all the drugs, and based on my finding they are not using the HCQ , they claim using other drugs with effective impact on the patients. (I dont have the name of these drugs, but its not HCQ)

    1. On 2020-08-08 05:01:13, user Callum J.C Parr wrote:

      So after the initial seed from China there was a second from Europe and “other countries” (whatever that means) and the slow move to control immigration allowed this. So what do you think about the current growth in cases seen in japan has pretty much blocked entry from any country?

    1. On 2020-04-16 21:55:50, user Sinai Immunol Review Project wrote:

      Title:<br /> Immunopathological characteristics of coronavirus disease 2019 cases in Guangzhou, China<br /> The main finding of the article: <br /> This study analyzed immune cell populations and multiple cytokines in 31 patients with mild/moderate COVID-19 (ave. 44.5 years) and 25 with severe COVID-19 (ave. 66 years). Samples from patients with fever and negative for the SARS-COV-2 test were used as control. At inpatient admission, total lymphocytes number was decreased in severe patients but not in mild patients, whereas neutrophils were increased in severe patients. CD4+ and CD8+ T cells were diminished in all COVID-19 patients. CD19+ B cells and NK cells were decreased in both mild and severe patients, however, severe patients showed a notable reduction. These data might suggest a profound deregulation of lymphocytes in COVID-19 patients. Further analysis showed significant increases of IL-2, IL-6, IL-10 and TNF? in blood of severe patients at the admission. Sequential samples revealed that IL-2 and IL-6 peaked on day 15-20 and declined thereafter. A moderate increase of IL-4 was seen in mild/moderate patients. Thus, elevation of IL-2, IL-6 can be indicators of severe COVID-19.<br /> Critical analysis of the study: <br /> There is no information on when the patients were assessed as severe or mild/moderate, at inpatient admission or later. The authors could have analyzed the correlation between immune cell population and cytokine levels to see, for example, if severe lymphopenia correlated to higher elevation of IL-2.<br /> The importance and implications for the current epidemics:<br /> While similar findings have already been shown, the data corroborates alterations in circulating adaptive and innate immune cell populations and cytokines, and its correlation to disease severity. The increase of IL-2 and IL-6 at the admission might an indicator to start intensive therapies (like convalescent serum) at an early time.

    1. On 2020-05-30 02:40:13, user M Del wrote:

      If you look at the data table from the study of NY Columbia university the mortality rate is higher for blood type O+ median age 54.8 was 12.4% of the infected and for blood type A+ median age 61.8 it was 12% of the infected , type O has less positive cases compared to the representation of percentage of population but mortality was a little higher even when they were younger.

    1. On 2021-06-13 01:37:36, user Fisher Wright wrote:

      The study shows that there is a negligible differential effect size of masks when not-very-large, different proportions of mask use (e.g. 65% vs. 75%) between populations occur. What the study doesn't show is there is no effect size from mask use. You would have to compare no use to use (e.g. 0% vs. 75%) between populations to do that.

      Secondly, I have some skepticism concerning the main result since it didn't seem like they controlled for confounders. States with greater mask use may share other differences (e.g. denser urban areas with crowded housing) compared to states with lesser mask use. Did they simply assume these confounders would cancel out?

    1. On 2020-06-23 16:30:13, user Sinai Immunol Review Project wrote:

      Systems-level immunomonitoring from acute to recovery phase of severe COVID-19<br /> Rodriguez et al. medRxiv [@doi:10.1101/2020.06.03.20121582]

      Keywords<br /> • COVID-19<br /> • cytokines<br /> • immunomonitoring

      Main Findings<br /> In this preprint, Rodriguez et al. performed longitudinal, systems-level immunomonitoring on blood from 39 COVID-19 patients using mass cytometry (CyTOF) and Olink to better understand the mechanisms behind hyperinflammation in severe COVID-19. 17 subjects were inpatient; 22 were recovered patients. CyTOF was used to track immune cell populations over time while Olink was used to measure 180 plasma biomarkers from the acute disease phase and recovery. Importantly, none of the 39 patients in this study received any immunomodulatory therapies and therefore the data reflect the natural course of COVID-19 disease.

      Several immune cell populations changed with COVID-19 disease progression. Neutrophils rose during the acute phase and decreased with recovery; in contrast, eosinophils, basophils, and all dendritic cell subsets all increased with recovery. Total CD4 and CD8 T-cells peaked at about 2 weeks into disease progression, with the largest increases seen in proportion of CD127+ CD4+ memory T-cells and CD57+ CD8+ memory T-cells. <br /> To further study the phenotype of the increased eosinophils seen with disease recovery, the authors used Partition-based graph abstraction to analyze changes in eosinophils on a single cell level. The authors report a transient expansion of CD62L+ eosinophils coinciding with IFN levels on days 2-6.

      To determine the immunological correlates with IgG response, the authors used a mixed effect model using immune cell proportions and levels of plasma protein biomarkers. IFNg, IL-6, CXCL10, CSF-1 and MCP-2 negatively correlated with IgG response while CXCL6, CD6, SPRY2, CD16- basophils and CD16+ basophils positively correlated with IgG response. <br /> Next, the authors built a multiomic trajectory of recovery using multiomics factor analysis. This analysis identified decreasing levels of IL-6, MCP-3, KRT19, CXCL10, AREG, and IFNg with recovery while classical monocytes, non-classical monocytes, CD56dim NK cells, eosinophils, and gD T-cells increased with recovery.

      Limitations<br /> Though the authors do a good job of balancing the sex ratio in their patient population, age ranges between symptomatic patients (40-77 yo) vs recovered patients (28-68 yo) may be contributing to immune phenotype. Median age of each group should be provided. While the authors state that the study captures longitudinal immune monitoring from acute to recovery phase, it is unclear which of the symptomatic patients, if any, were monitored through actual recovery. The authors’ claims would be better supported with paired analysis of symptomatic patients during their hospital course with the same patients after recovery, rather than a separate cohort of recovered patients.

      The changes in immune cell populations over time reported in Fig. 3 would benefit from statistical analysis to denote which changes are statistically significant. Indeed, several of the trends reported, such as total CD4+ T-cells, CD127+ memory CD4+ T-cells and CD57+ CD8+ T-cells seem to be driven only by a few patients.

      Previous work by Mesnil et al. 2016, as cited by the authors, report that CD62L+ lung resident eosinophils suppress excess Th2 inflammation after house dust mite (HDM) challenge in mice and have a more regulatory phenotype than CD62L- inflammatory eosinophils [1]. Here, Rodriguez et al. suggest that this increase in CD62L+ eosinophils may contribute to lung hyperinflammation in acute respiratory distress syndrome (ARDS) in COVID-19. While more studies are needed to address this potential contribution, one suggestion would be to see if there are differences in the number and phenotype of CD62L+ eosinophils between the ICU and non-ICU patients in Rodriguez et al.’s cohort. While it is possible the increased number of CD62L+ eosinophils may contribute to hyperinflammation, the more regulatory phenotype of CD62L+ eosinophils as reported by Mesnil et al. may instead point to a role for suppression rather than contribution to lung hyperinflammation.

      In all analyses conducted, further stratification by ICU vs non-ICU patients may also be informative.

      Significance<br /> This preprint provides system-wide longitudinal analysis of plasma biomarkers and immune cell populations from a cohort of inpatients with severe COVID-19. Because the patients were untreated with any immunomodulatory drugs, the authors are able to describe trends through the natural progression of COVID-19 in patients who ultimately recover.

      Specifically, CD62L+ eosinophils are found to be expanded in the blood corresponding to a period of lung hyperinflammation in severe disease. Additionally, a higher abundance of circulating basophils is correlated to increased anti-SARS-COV-2 IgG response. Both findings warrant further investigation into the previously undescribed role of both eosinophils and basophils in COVID-19.

      Furthermore, the authors show that biomarkers such as IFNg, CXCL10, and IL-6 negatively correlate with both humoral response and recovery. The negative correlation with IL-6 and IgG response is particularly surprising, given that IL-6 has been shown to promote antibody production in B-cells [2]. Moreover the authors cite Denzel et al. 2008, which shows that basophils with antigen bound to their surface enhance antibody production through IL-6, yet in this study basophils and IL-6 negatively correlate at recovery [3]. These findings further highlight the importance of studying the role of inflammatory cytokines in both the development of severe disease and recovery.

      References

      1. Mesnil C, Raulier S, Paulissen G, et al. Lung-resident eosinophils represent a distinct regulatory eosinophil subset. J Clin Invest. 2016;126(9):3279-3295.

      2. Dienz O, Eaton SM, Bond JP, et al. The induction of antibody production by IL-6 is indirectly mediated by IL-21 produced by CD4+ T cells. J Exp Med. 2009;206(1):69-78.

      3. Denzel A, Maus UA, Rodriguez Gomez M, et al. Basophils enhance immunological memory responses. Nat Immunol. 2008;9(7):733-742.

      Credit<br /> Reviewed by Steven T. Chen and Alexandra Tabachnikova as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn School of Medicine, Mount Sinai.

    1. On 2021-08-12 13:45:33, user Paul52 wrote:

      The broader numbers don't come from polling, they come from people who saw the survey and filled it out. <br /> That kind of self-selection will produce skewered results. If 35% of the people claiming to be PhDs said they're hesitant it means that of the people who chose to answer 35% of those claiming to be PhDs answered they're not going to take the vaccine.

      It doesn't mean they have PhDs.

      And it doesn't mean that 35% of PhDs are hesitant.

    1. On 2021-12-22 22:18:39, user Le Bon wrote:

      Interesting work.<br /> I suggest to the authors to add another analysis grouping all vaccinated patients 3 month after dose 2, including thoose having received the dose 3 and simulating an ITT analysis.

      There are several possibilities here.<br /> 1)The vaccine efficacy of 2 doses is really negative for Omicron 3 months after vaccine, and the third dose is really efficient against Omicron, at least during one month.<br /> 2)The negative efficacy is due to a temporal bias, or a selection bias (for example the more careful persons get vaccinated first) ins this case the 2 doses could be without a negative efficacy, but the efficacy of the third dose could be an artefact.

      Those 2 groups have to be merged, and analyzed in time.

      Typically, if the merged group has zero efficacy, an artefact is likely.<br /> If the merged group has globally a positive efficacy, a real effect of the the third dose is likely. (But no conclusions on the negative effect of 2 doses)

      If the merged group has globally a negative effect, it means a real negative effect of 2 doses after 3 months (but no conclusions on the positive effect of 3 doses)

    1. On 2020-05-13 10:08:28, user Benjamin Hartley wrote:

      Hi, Can you clarify the meaning of the theta "infection" parameter in equation 1 (years 2015-2019) which multiplies the death rate? Is this a typo, or set to 1?

    1. On 2020-07-10 23:56:52, user John Pearson wrote:

      IF the death rate is 0.04% = 0.0004 then 136592/.0004 = 341Million Americans who have already had the disease> Thus not only do we have herd immunity the entire country has already had the virus and we're all better!!! Yet we'll probably have 70,000 new cases today and the population of the US is 330 Million. In short this work is dangerously and clearly false.

    1. On 2020-12-03 15:34:00, user joetanic wrote:

      Quite interesting data. I'm wondering whether anyone knows why France does not perform these tests?

      Or the US? It seems a broad study, especially in France which seems to be bucking the trend, so to speak, would make clear what the future holds in many places.

    1. On 2023-01-26 06:31:51, user Yasir E A Elsanousi wrote:

      Splendid well structured article addressing an interesting and contemporary health issue. My comments towards improving this study:<br /> 1) The authors may wish to begin the methodology & data section with a paragraph that explicitly names the method type and clearly describes what was going to be done with data. The research problem should be stated here.<br /> 2) Although use of 'first-person' style of writing is not inappropriate, but there is overuse of first person pronoun ('we' .., and also 'our'). It is advisable to replace most of these instances with third person items (e. g 'the study focuses on..etc) or use of passive voice (dengue incidence was calculated..etc)<br /> 3) The ‘Conclusion’: authors may wish to present the most important outcomes of the study first. The sentence “The short period ... relationships." may be deferred to a later position in the section, or better still be duly recognized as one of the ‘Limitations’ of the study.<br /> Thank you: Yasir Elsanousi

    1. On 2025-08-08 09:31:31, user David Fournier wrote:

      Dear authors, commenting on the recent Nat. comm. release, did you actually studied the direct connection in the samples from encode ad brains you studied between histone modifications and actual expansions? i dont see a plot of histone modifications versus repeat expansions directly plotted from the same individual. Did you check that? Thanks.

    1. On 2021-04-12 14:22:11, user Okan Bulut wrote:

      Our study has been accepted for publication in the Journal of Mixed Methods Research. Please see the full citation, including the title change for our study below:

      Poth, C., Bulut, O., Aquilina, A., & Otto, S. (In press). Using data mining for rapid complex case study descriptions: Example of public health briefings during the onset of the COVID-19 pandemic. Journal of Mixed Methods Research.

    1. On 2020-04-14 07:12:46, user Ole 500 wrote:

      So they dosed the subjects at x2 and x3 the normal dosage of 400 mg/day. If I'm reading this right, they overdosed the patients and rediscovered known overdose side effects?

    1. On 2021-08-05 06:56:54, user Piet Streicher wrote:

      How do you account for "survivorship bias" in the case of the vaccine. If prevalence was high during the vaccination phase, then infection prior to the 14d after 1st dose or prior to 7d after 2nd dose would remove people from the pool, creating a bias towards those that made it past this point. They then appear to have a higher level of protection (say 86%) when in fact this group has been through a selection process already.

    1. On 2021-02-08 21:37:49, user Raymond Lam wrote:

      Note that another study on this topic, using the same database, was published recently: Rhee SJ, Lee H, Ahn YM. Serum Vitamin D Concentrations Are Associated With Depressive Symptoms in Men: The Sixth Korea National Health and Nutrition Examination Survey 2014. Front Psychiatry. 2020 Jul 30;11:756. PMID: 32848932

      Although our analysis methods were slightly different, we came to the same conclusions, so we will not be submitting this to a journal, but wanted to have it available to other researchers.

    1. On 2020-05-05 20:54:15, user japhetk wrote:

      This study has serious flaws and I will reject if I were a reviewer.

      First,<br /> this study doesn't have a control data such as the blood sample of a <br /> few years ago. Although, the kit maker advocates the specificity of <br /> 100%, various test kits including the innovita's one which championed <br /> 100% specificity were already shown to show the inferior data compared <br /> with the maker's advocates.

      Second, as pointed out,

      Tests<br /> were done for randomly selected preserved serum from patients who <br /> visited outpatient clinics of the hospital and received blood testing <br /> for any reason. Patients who visited the emergency department or the <br /> designated fever consultation service were excluded to avoid the <br /> overestimation of SARS-Cov-2 infection.

      SARS-COVID-19 is already <br /> known to cause atypical symptoms even in the "asymptomatic" (in terms of<br /> typical symptoms of infection) such as stroke, and various other <br /> thrombotic symptoms. So, this exclusion criteria is not enough <br /> apparently to avoid biased sampling and overestimation.

      In Japan, this apparently seriously flawed study without review is reported widely<br /> and people even some doctors now say the real fatality rate of <br /> SARS-COVID-19 is 0.05%! based on this study (they seemed to have <br /> forgotten Japanese patients in the diamond princess ship showed the <br /> higher mortality rate compared with age-matched patients of westerners <br /> in the same ship). This is a nightmare for the public health of Japan.

    1. 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 2022-01-13 14:50:32, user Erik Petersen wrote:

      One of the findings that is going to be predominantly taken from this study is that, "vaccinated individuals have significantly lower IVTs." However, upon looking at the data in Figure 4A specifically, we see just under 3 (2.9?) FFU/ml in unvaccinated individuals compared to ~2 FFU/ml in vaccinated individuals. Would you please explain how this constitutes a "significant" reduction?

    1. On 2021-12-14 17:22:40, user Ronnie wrote:

      they refuse to properly interpret the data ...?

      Reaching the unvaccinated with current vaccines remains a priority in order to reduce transmission levels and reduce the potential for severe disease in the immunologically naïve.

    1. On 2021-03-13 17:03:28, user peterjohn936 wrote:

      Improving the Immunity System should have been a standard of care response to COVID especially treatments that are already standard. I am type 2 diabetic, my doctor prescribed vitamin D for me years ago. GPs should be asking their diabetic patients to take extra care to watch their blood sugar levels, to exercise more, and to try to lose weight.

    1. On 2020-02-17 08:52:17, user Ellie_K wrote:

      Once this paper has been peer-reviewed, could someone post here in the comments where (i.e. in which scholarly journal) it is published? Thank you!

    1. On 2022-01-04 09:33:05, user Paolo Maccallini wrote:

      Dear all,

      I made an attempt at calculating the proportion of asymptomatic Omicron infections in function of the same parameter in the case of Delta infections, among unvaccinated individuals. I used the data presented in this paper, particularly the data relative to the subjects enrolled in the Ubunto trial (Omicron wave) and those of the population included in the Sisonke sub-study (Delta wave). The result is that, if we assume a prevalence of asymptomatic infections of 17% for the Delta variant, then we have that the prevalence of asymptomatic infections for the Omicron variant is about 60%, in unvaccinated subjects. The details of the calculation I performed can be found here: https://paolomaccallini.com...

    1. On 2025-07-12 21:55:39, user David C wrote:

      Amazing substantive and methodological contribution. Hats off to the authors.

      I'm wondering, if however, there might be selection bias in which high-mortality households are underrepresented in the sample. In the extreme, households in which all members have died would, by definition, not be represented in the sample (I think).

      If this type of selection bias holds, the counts could be significant underestimates of the true mortality counts. I'd love to hear the authors' and readers' thoughts on this matter.

    1. On 2020-12-11 00:01:06, user lbaustin wrote:

      Has this article been submitted to a journal yet? If not, please add to the conclusion the point that for people living in modern settings, dietary sources and sunlight rarely provide adequate amounts of vitamin D, which is why the authors of the papers reviewed here generally support universal supplementation with vitamin D3.

      Also, excluding RCTs is so unusual in a review of the evidence that this decision needs to be justified.

      And, Hastie, et al., did not have a true sample size of 348,598. Only 1474 of the individuals in the UK Biobank database had Covid-19 test results. Of these, 449 had at least one positive test, and the remaining 1025 had only negative results. Similar sample size adjustments should be made for the other studies (Merzon and Kaufman) using "big data."

    1. On 2021-08-08 14:35:35, user Yaakov Kranz wrote:

      Hi I'm curious was this study taking into acount the Delta variant?<br /> Did anything cahnge since then with regards to the Delta variant?<br /> Thanks!

    1. On 2020-06-27 15:28:25, user Tim Pollington wrote:

      I'm finding Fig.1 helpful. But to avoid confusion would be good to use different symbols for fwd/backward/intrinsic distribs e.g. currently \tau_{i1} for Fig.1A,B & C.

    1. On 2020-06-05 17:35:30, user wbgrant wrote:

      Dark-skinned people living in Spain are at an increased risk of COVID-19 due to lower vitamin D production from solar UVB. This effect probalby explains the finding for Sub-Saharan Africa and the Caribbean. Not sure about Latin America, where rates are very high in several countries. See:<br /> Grant WB, Lahore H, McDonnell SL, Baggerly CA, French CB, Aliano JA, Bhattoa HP. Evidence that vitamin D supplementation could reduce risk of influenza and COVID-19 infections and deaths. Nutrients 2020, 12, 988. https://www.mdpi.com/2072-6...<br /> and references thereto at scholar.google.com<br /> as well as this response<br /> Grant WB, Baggerly CA, Lahore H. Response to Comments Regarding “Evidence that Vitamin D Supplementation Could Reduce Risk of Influenza and COVID-19 Infections and Deaths”. Nutrients 2020, 12(6), 1620; https://doi.org/10.3390/nu1...

    1. On 2021-12-12 01:32:39, user Wild Bill, Jr. ????:????:?? wrote:

      When I first read this paper, a year ago, I was skeptical about it. The alarmists presented what seemed to be some strong arguments against it

      However, with the passing of time, infection-fatality rate statistics and deaths from all causes statistics support the Stanford team's hypothesis: The dreaded virus has turned out to be a lot less lethal than the alarmists claimed it was.

    1. On 2022-01-11 20:23:50, user Sam Smith wrote:

      What is the optimal RH = relative humidity for health? Too dry air increases covid risk because it is not healthy for your airways.

    1. On 2021-07-29 08:08:57, user Salvatore Chirumbolo wrote:

      The evidence that acetaminophen (paracetamol) worsened the rate of hospitalization in COVID-19 patients respect to NSAIDs such as indomethacin, is the major highlight of this contribution. The Italian Ministry of Health (Nov 30th 2020) recommended only paracetamol and a watchful attitude during the early onset of COVID-19, to simply dampen fever and related pain (see https://www.bmj.com/content... "https://www.bmj.com/content/368/bmj.m1086/rr-18)"). So, NSAIDs are not dangerous for early and mild COVID-19 as initially believed, whereas paracetamol is. In this perspective, in Italy a wide community of citizens, professionals, physicians, caregivers, practitioners, attorneys and so on, joined together to promote the best COVID-19 home therapy at the earliest (within first three days from positive swab or symptoms), to reduce hospitalization (and mortality), as paracetamol exacerbates COVID-19 immuno-thrombosis, probably leading even to death (see Pandolfi S, Simonetti V, Ricevuti G, Chirumbolo S. Paracetamol in the <br /> home treatment of early COVID-19 symptoms: A possible foe rather than a <br /> friend for elderly patients? J Med Virol. 2021 Jun 25. doi: <br /> 10.1002/jmv.27158). Hoping that politics may take into account the evidence reported by the current medical science.

    1. On 2020-05-15 15:29:20, user Irving Kushner wrote:

      Finding a low serum vitamin D concentration does not necessarily indicate vitamin D deficiency. There is now abundant evidence that vitamin D is a negative acute phase reactant – that is, its serum concentration falls during inflammatory states, as do albumin, transferrin, zinc and iron concentrations, in contrast to C reactive protein (CRP), which is a positive acute phase reactant.https://www.ncbi.nlm.nih.gov/pubmed....

      This conclusion is supported by several lines of evidence: vitamin D levels have been found to be decreased in a number of inflammatory states. https://www.ncbi.nlm.nih.go..., https://www.ncbi.nlm.nih.go...<br /> Vitamin D levels fall following a variety of inflammatory insults, such as surgical procedures. https://www.ncbi.nlm.nih.go..., https://www.ncbi.nlm.nih.go..., https://www.ncbi.nlm.nih.go...<br /> And, as the authors indicate, it is well recognized that serum CRP and vitamin D levels are inversely associated. https://www.ncbi.nlm.nih.go..., https://www.ncbi.nlm.nih.go...

      There is really nothing new in this study. The abstract states that they used CRP levels as a surrogate for vitamin D levels. So what they actually found was that higher CRP levels are associated with the risk of severe COVID-19. We knew that already.<br /> From Maria Antonelli and Irving Kushner, Case Western Reserve University

    1. On 2020-06-30 21:10:32, user Stephen Cherniske wrote:

      This is rather paradoxical, in that IL-13 is generally considered to be an anti-inflammatory cytokine, as in IBS. Even more surprising: the observed beneficial effect of DHEA treatment of murine IBS appears to result in part from increased IL-13 expression in colonic epithelial cells. REF: Immunobiology. 2016 Sep;221(9):934-43. doi: 10.1016/j.imbio.2016.05.013. <br /> Dehydroepiandrosterone (DHEA) Restrains Intestinal Inflammation by Rendering Leukocytes Hyporesponsive and Balancing Colitogenic Inflammatory Responses<br /> Vanessa Beatriz Freitas Alves , Paulo José Basso et al.

    1. On 2020-04-30 02:42:13, user Tyler Chen wrote:

      I appreciate the authors’ urgency in addressing SARS-CoV-2 decontamination for reuse of N95 filtering facepiece respirators (FFRs). In the spirit of that urgency and health impacts, I note two concerns with the current preprint that could accidentally cause confusion: (1) The paper claims N95 filtration is preserved after microwave-generated steam, whereas the test listed in the methods was a TSI quantitative fit test, which is primarily designed to test fit, not necessarily filtration. (2) The paper’s claim of a universally accessible N95 decontamination protocol may accidentally overstate the N95 models for which this protocol is verified. N95 models vary widely in their construction and resistance to steam heat, so any models other than the one used in this experiment will likely require thorough testing before this method is applied.

      I would suggest that the authors make the following changes:<br /> (1) Clarify whether or not filtration is verified at larger particle sizes and charge (e.g. 0.26 microns, uncharged). If filtration is not yet verified at larger particle sizes, this test may be important to verify N95 performance following microwave steam treatment.<br /> To provide some background: The TSI 8026 Particle Generator generates 0.04 micron particles [1] that are intended to be readily filtered by the N95, and are assumed to only enter the N95 through gaps in the face seal and not through the mask material itself [2]. It is possible for N95 FFRs to pass quantitative fit tests while still failing filtration tests at different particle sizes--one study “observed [protection factors] <100 even for subjects who passed fit testing (fit factor > 100)” [3]. Therefore, fit testing using the 8026 particle generator does not imply that N95 filtration is necessarily preserved at larger particle sizes which are most relevant for filtration effectiveness in the SARS-CoV-2 pandemic, especially given the fact that the decontamination treatment may shift what particle size is most penetrating for the N95. Recent non-peer-reviewed research shows N95 material suffering a decrease in filtration of 0.26 micron particles after 4-5 cycles of 10min stovetop steam treatment [4], though it is unclear from this manuscript if the MGS treatment did not reach this limit, or that the limit was not observed due to the different particle size used. Therefore, testing for quantitative fit should perhaps be supplemented by filtration tests at larger particle diameters (whether from this study or by citing others), especially when a decontamination process is involved such as steam heat that has an unknown effect on the most penetrating particle size for the N95. Given the potential for widespread implementation of this protocol it seems important that this point be clarified.

      (2) Secondly, it may be important to notify readers that the performance of the N95 model in this paper likely cannot be generalized to all N95 models without further testing. N95 models vary widely in construction and resistance to steam, and each model should be individually verified to maintain both fit and filtration by this protocol before use. This is supported by the fact that N95 models can vary widely with respect to the most penetrating particle size, and each country may only have access to certain N95 models [3,4,5]. Furthermore, there is literature evidence that the mask performance in response to steam and heat also varies across N95 models (see the table of results in Appendix B https://www.n95decon.org/fi... "https://www.n95decon.org/files/heat-humidity-technical-report)"). Therefore, it is important to clarify in the text that this method is not yet universally-validated -- N95 fit has only been verified for the 3M 1860 molded N95 in particular, and other models are likely to have significantly different behavior. Independent verification of both fit and filtration may be needed for other N95 models.

    1. On 2021-02-21 14:31:34, user DMac wrote:

      Good day. I've found this work immensely valuable as a reference for discussions in our office. With new variants developing and particularly the "UK" B.1.1.7 and "South African" or B.1.351 variant spreading, I wonder to what extent the changes they reflect would impact modeling results. I expect most variables are the same, but wonder if the added efficacy of transmission can be accounted for with the model. As an interim approach, might one adjust downwards the risk tolerance or other variable to approximate adjustment for the variants?

    1. On 2020-03-25 17:42:51, user Rudolf Brüggemann wrote:

      It is a bit irritating that version1 and version2 give different values for the half-lifes. Is there an error based on a factor ln10 somewhere? The half-lifes in Table 1 of the supplement of the published version are much smaller than those in Table 1 in the preprint version. E.g., half-life (median) for steel 13.1 hours in the preprint, median of 5.63 hours in Table 1 of the Supplement of the published version.

    1. On 2020-08-12 12:37:37, user Marc Imbert wrote:

      It is worth to not that this study has more cormobity and symptomes for the group treated with HCQ and AZT. All patient not treated has a mild desease while about only 63% in the group treated. Further one should use a healthy scientific scepticims regarding hasting conlusions based on studies at the late stage of the desease. In particular with the description of the evolution of the disease which is now known,

      .

    1. On 2020-05-14 14:35:10, user Hans Tinger wrote:

      3% after 1 Werk, 6%after 2 Weeks, 9% after 3 Weeks... I am curious for week 4-8. Will you publish preliminary results soon again?

    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 2020-04-22 23:36:03, user Omar Arellano-Aguilar wrote:

      I recommend you to review the work of Patricia Gundy (2008) in the Food Environ Virol 1:10-14 how analyzed coronaviruses in water and wastewater and she found that this kind of virus did not survive in wastewater.

    1. On 2021-06-21 01:41:23, user Downtown-Pete wrote:

      Just one question about this statement in your"Materials&Methods": .."between November 1, 2020 and March 5, 2020.." : I assume you mean March 2021? <br /> It would make a difference, if the statement as currently written (March 2020)<br /> is indeed correct.

    1. On 2021-02-06 06:55:29, user kdrl nakle wrote:

      Non-randomized comparison of apples to oranges (dosages, numerous differences in groups etc). Too small samples for so many variables.

    1. On 2020-04-24 02:17:08, user Neal R Monda wrote:

      Why isn’t doxycycline replacing azithromycin which should not be combined with hydroxychloroquine due to their compounded QT potential?

    1. On 2020-07-19 15:32:00, user Helene Banoun wrote:

      Prior infection by seasonal coronaviruses does not prevent SARS-CoV-2 infection and associated Multisystem Inflammatory Syndrome in children

      https://www.medrxiv.org/con...

      June 30, 2020

      This June 2020 study shows how difficult it is nowadays to admit that antibodies in viral infections are only a witness of the infection and do not mean much about the protection conferred.

      The authors acknowledge this in the text of this multi-disciplinary study, but it does not appear in the abstract, the conclusion or the title.

      Almost 800 children were tested.

      Only humoral immunity was tested.

      In children who tested positive for SARS-CoV-2 (there is no mention of Rt-PCR or other confirmatory tests), 55% had neutralizing antibodies (in vitro); in children with Multi Inflammatory Syndrome "Kawasaki like", 70% had "neutralizing" Ac. There is no correlation with traces of previous HcoV infection (detected by the presence of anti S and anti N Ac). The authors wonder whether the MIS could be explained by the presence of facilitator Ac (low or non-neutralizing Ac or cross-reactive to HcoV and SARS-Cov-2).

      Clinical aspect: 70% of the seropositives did not present a specific Covid syndrome (only headache, nasopharyngitis and shortness of breath). This percentage is comparable to that found in adults.

      This confirms the low rate of children with clinical Covid syndrome.

      The prevalence of seropositivity in children is comparable to that found in adults (between 10 and 15% of the population). All seropositives present neutralizing Ac but these appear with a delay of several weeks compared to the first antibodies. The "neutralizing" Ac appear earlier and at a high rate in patients with severe Covid.

      This confirms previous studies that correlate the level of Ac to the severity of the disease. Therefore, neutralizing Ac are not correlated with protection.

      The seroprevalence of HcoV infections is 100% in adults. Children are finally as much infected by Covid as adults, present an asymptomatic picture as often as adults and therefore there is no reason to explain a lower level of damage in children not a higher level of cross-immunity with HcoV.

      The authors admit that Ac are only a control for infection and are not correlated with protection against disease.

      They also admit that the relevance of neutralization tests performed with pseudoviruses can be questioned because they do not involve the ACE2 receptor.

      In addition, helper T lymphocytes reactive to SARS-CoV-2 epitopes detected in healthy subjects do not recognize the spike binding domain (SBD).

      In contrast to the results of cellular immunity studies, here antibodies against Hcov and cross-reactive to SARS-CoV-2 do not confer protection against Covid.

      Profiles of children with MIS show that this syndrome is due to a non-specific inflammatory response. The data collected do not imply that previous Hcov infections would facilitate SARS-CoV-2 (and MIS) infections by ADE

      Therefore, this study cannot conclude that there is no cross-immunity with HcoVs since it only measures humoral immunity (and for some antibodies only). The papers by Grifoni, Braun and Le Bert showed this cross-immunity at the cellular level.

      Braun et al., 2020-1, https://www.medrxiv.org/con...

      Grifoni et al., 2020 https://www.cell.com/cell/p...

      Le Bert et al;, 2020 https://www.biorxiv.org/con...

      All this reinforces my belief that antibodies (in viral infections) are only a witness and not a sign of protection. On the contrary, immunity is mainly cellular (innate in a primary infection and adaptive in a re-infection); innate humoral immunity also intervenes rapidly via non-specific factors (such as interferon1 for example). The role of antibodies in reinfections can be discussed: protection or facilitation?

    1. On 2021-02-02 12:13:10, user Miriam wrote:

      Nobody in Slovakia was informed about this research. And it was not voluntary as they signed. There was and there is still strictly prohibited to go at work and to the nature if we are not tested. The final result of this mass testing is, that numbers of covid positive strongly increase. That is all. I am really afraid about my human rights in future.

    1. On 2021-07-22 17:54:22, user John Aach wrote:

      I wonder if the authors of this interesting study might comment on two questions that come to mind: (1) There seems to be no information on whether / how many of the subjects in the 2021 delta cluster had been vaccinated or previously infected. It could be very valuable to know if viral load differed for subjects that were naive to SARS-Cov-2 vs. previously-infected / vaccinated. Was there a reason this wasn't done, or was this tried and found inconclusive? (2) This compares CT data derived from oropharyngeal swabs used and analyzed from the 2021 delta cluster vs. CT numbers derived from swabs used in the 2020 outbreak. Can it be assured that swabs, sample gathering, and analysis protocols used in the 2020 outbreak are sufficiently comparable to those used > 1 year later in the 2021 delta cluster, to ensure that CT numbers don't differ due to batch effects or differences in materials and protocols?

    1. On 2022-08-14 15:08:34, user Peter J. Yim wrote:

      The trial registration at ClinicalTrials.gov listed three primary endpoints:<br /> 1. Number of hospitalizations as measured by patient reports. [ Time Frame: Up to 14 days ]<br /> 2. Number of deaths as measured by patient reports [ Time Frame: Up to 14 days ]<br /> 3. Number of symptoms as measured by patient reports [ Time Frame: Up to 14 days ]

      The publication reports the outcomes for none of those endpoints. (the endpoints were changed after publication on ClinicalTrials.gov)

      1. The rate of hospitalization was reported at 28 days. That was registered as a secondary outcome.
      2. Mortality was reported at 28 days. That was registered as a secondary outcome.
      3. The number of symptoms was only reported at baseline.

      This article is close to irrelevance on the question of the efficacy of ivermectin in COVID-19.

    1. On 2021-12-21 20:45:47, user Martin Manuel Ledesma wrote:

      It is an essential paper, but sadly, the unvaccinated group is composed of people with higher rates of comorbidities and complications, so it is highly unfair compared to a vaccinated group with lower rates of comorbidities. Therefore, it is impossible to derive the conclusion that they intended to do, and the conclusion would be that immunocompromised leads to an evolution of SARS-CoV-2.

      What they found is similar to described in this paper:

      Recurrent deletions in the SARS-CoV-2 spike glycoprotein drive antibody escape. DOI: 10.1126/science.abf6950.

      The problem is in the immunocompromised rather than in the unvaccinated.

    1. On 2019-01-29 09:53:14, user DM wrote:

      This is an interesting study. I wonder about the complexity of the sequence that the mice would need to learn in order to maximize their rewards and whether it is actually possible for any species to either learn or reliably perform it at maximum efficiency.

      Has the same sequence been tested in, for example, humans (looking at locations on a screen rather than running around a maze)? Another way at getting at this would be to train mice in the sequence and let them perform it (this would remove the demands of learning the sequence, but still require them to perform it).

      My concern is that the interpretation that the mice adopted a strategy of increasing choice variability rather than learning the sequence changes depending on whether they would ever be able to learn the sequence or not.

    1. On 2023-07-14 07:11:33, user Kerwin W. wrote:

      This is an incredibly remarkable advancement in the field of neuroimaging. And the same time, I have one question about it. Does the signal of PDI is a <br /> manifestation of blood oxygen saturation of most vessels in brain ?

    1. On 2023-11-16 14:03:35, user Martin Carbó-Tano wrote:

      Final version published in: <br /> Carbo-Tano, M., Lapoix, M., et. al. The mesencephalic locomotor region recruits V2a reticulospinal neurons to drive forward locomotion in larval zebrafish. Nat Neurosci 26, 1775–1790 (2023). https://doi.org/10.1038/s41...

    1. On 2025-09-17 09:11:40, user Guest wrote:

      A very interesting and important paper but I have two main concerns.<br /> First, is a lack of an additional necessary control group (or maybe it’s just not explicitly stated?). The Cx3cr1-CreERT2 is a heterozygous KO of Cc3cr1. A control group with the Cre but no flox is necessary to determine that the results are related to the cross and not to the Cx3cr1 deficiency. Without that it’s not possible to attribute the results to the c1q KO alone.<br /> The second is that the wrong statistical test appears to have been employed throughout the paper. The authors are testing both c1q+/- and Arc+/- yet only perform one way ANOVA. This needs to be a two-way ANOVA and the overall ANOVA player should be reported on graph in addition to post-hoc values. If overall ANOVA p lacks significance the post-hoc results alone are misleading.

    1. On 2023-10-24 01:29:36, user Hironaka Igarashi wrote:

      Very nice work.<br /> There have been recent reports of immune cells invading the skull marrow during brain (broadly defined) inflammation, and if the bone marrow is a reservoir and transit point for immune cells, it would be very interesting to see the changes, since fortunately the skull marrow can be depicted on TSPO PET.

    1. On 2017-11-27 02:51:51, user Ira Trofimova wrote:

      Great paper. One more proof that lexical models (derived from verbal descriptors and not psycho-physiological experiments, like in temperament research) can only reflect socio-cultural, and not biological individ. differences. Well, personality is a socio-cultural concept but I wish FFM-ers stop claiming that they found human universals and biologically-based traits. First, such traits have specific name - temperament, and second - there is a century-long tradition of psycho-physiology of temperament traits that, magically, FFM-ers never notice. Yet, traditionally temperament had at least two dimensions related to energetic and emotionality aspects of behavioral regulation. Resemblance with the E and N, or even the fact that these two dimensions were known as temperament at least since Kant (1798) are never discussed by the FFM. And now, FFM-ers push biological sciences to fund biomarkers for their dimensions staying completely ignorant to history of science or to the flaws of their lexical approach, and don't even give credit to temperament research for E and N dimensions...

    1. On 2021-04-10 12:48:20, user Lavinia S wrote:

      Erratum: The following is the correct legend for Supplemental Fig. 4<br /> "Confocal images show damaged kinocilia following mechanical injury. Representative confocal images of hair cell kinocilia (acetylated tubulin immunolabel; magenta) and stereocilia (?actin-GFP; green) in control (A-A’’) and exposed (B-B’’) larval neuromast L4-6 immediately following sustained strong current stimulus. Kinocilia appear as intact bundles in the control neuromasts. Arrow indicated kinocilial swelling, arrowheads indicate split kinocilia in the exposed neuromasts. Scale bar: 5µm"

      Thank you Joaquin (@MadS100tist) for catching the error (and thouroughly reading our manuscript)!