On 2020-12-07 04:14:29, user Luis Ricardo Illescas wrote:
I think it would be important to separate the group that died in the street from the rest of the group that includes dying in houses, accommodations, shelters. They reflect a different level of tragedy
On 2023-06-01 13:18:49, user Ning Zhang wrote:
Please link this to the journal version. This manuscript has been accepted by the Global Health Journal (https://doi.org/10.1016/j.g... "https://doi.org/10.1016/j.glohj.2023.05.001)"). https://www.sciencedirect.c...
On 2020-07-24 04:38:59, user Dr Prachi Sinkar wrote:
How are you sure it was not against COVID? if you are negative when you are tested for COVID but exposed to it before or after - still Ab against COVID possible?
On 2021-12-16 16:22:57, user itellu3times wrote:
While I understand the place for these calculations given the social and government actions around the world, even the necessity for someone to do it, and it comes out on the correct side of things, I must point out that it is also socially deranged and mathematically extremely vague. "The unvaccinated" do not even exist as such in US, EU, UK, and other places where the pandemic has run now for two years, almost all will now have contracted and recovered from COVID, have natural immunity, and be no more at risk of getting or giving COVID than any of "the vaccinated". I would like to see studies of just where these "unvaccinated" patients today are even coming from - are they all immunocompromised, or vitamin D compromised, or are the figures cooked by authorities who use biased procedures "for reasons of public health", to bias the results? We know "the vaccinated" transmit the virus too, is that supposed to comprise the "base rate" here? How about reversing this, what if the vaccinated are excluded, what's the NNT then? But, whatever the calculation here, forward or reverse, the odds calculated are for one event, and when there are N such events even small odds are enough to propagate. Now, perhaps this factor is already comprised in this "base rate", I guess it is, but then the real odds for a single event may be much lower. You are then talking about socially exclusionary processes that even the article states are really for reasons of coercion, for event numbers that are truly tiny. Is this rational? Oh, and the SAR numbers must be considered plus or minus 80%, instances of any type event may be vastly better, or worse. Very hard to use such things to base any serious decisions on at all. Though, in science, I guess someone has to give it a look, as seems to have been done reasonably here.
On 2020-12-24 10:34:39, user Aroop Mohanty wrote:
The review is one of the first of its kind at a national and international level. It is good to see that mobile health intervention found effective in improving maternal health outcomes. The review and meta-analysis did very well and need of hours for developing country including India. the methodology and search strategy used very clear and crisp and elaborated in detail. I am impressed that the use of Mhealth intervention improved maternal outcomes. <br /> The use of the PICO approach and exclusion of research done in developed countries have a direct implication of the work in low and middle-income countries like India.<br /> The research question is clear and concise<br /> I am highly recommending such kind of work to improve maternal and child health indicators in developing countries.
On 2021-09-16 08:25:05, user Dr Siona Bastable wrote:
Overlap with effects of ADHD symptomology is striking....
On 2020-07-27 06:46:38, user OxImmuno Literature Initiative wrote:
On 2020-07-27 13:58:22, user Rosemary TATE wrote:
Excellent and interesting paper. However, although you say you adhered to the relevant EQUATOR (TRIPOD) guidelines I note that you have not uploaded the checklist. Very few people seem to do this although they tick the box that they have. I'm wondering why? Can you enlighten me?
On 2020-12-30 22:01:49, user Henry wrote:
" translated to a rise of 21.1 nmol/L of 25OHD in the UK Biobank population, a rise that is comparable to what can be achieved with vitamin D supplementation, especially in short courses[38]."
A 21nmol/liter serum raise is not much. That is what you get when you supplement too little vitamin D (400 iu / day for short courses).
Did you compare 150 nmol / L and higer to 30 nmol / L? I would say someone has optimal vitamin d at 150 nmol / L.
On 2021-09-19 05:15:21, user Les Smith wrote:
The background rates between 2017 and 2019 are not a valid basis for comparison. The rates of GBS, Bell's Palsy, Neuralgic Amyotrophy, and other such disorders have been significantly suppressed during the pandemic by efforts such as masking and isolation.
On 2020-08-08 00:52:19, user Cyraxote wrote:
The covidestim site shows 12 rows of 4 states. That's 48 states. Maryland is one of the missing ones, but I don't know the other.
On 2021-01-20 15:30:41, user Zuzana Kollarova wrote:
This statement is NOT TRUE and the citizens of Slovakia have no idea they are a part of some medical research:<br /> "All necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived - Yes"
We have been all forced to this by a number of restrictions and consequences presented by the prime minister and government prior the testing and they let the "choice" to us. If we wouldn´t take part on that testing we couldn´t go to work, to any store, bank, post office etc.. Only basic needs could by fulfilled like grocery shopping, pharmacy etc. Healthy people who refused to take part on this had to stay at home in quarantine like they were infected and could go outside without the risk of getting a fine, if a police would control them randomly on the streets. This lasted 14 days.
They used army, our president found out just from the papers and not officially. She has been called a traitor by the prime minister just one day before the mass operation should start, when she asked for a really voluntary participation for the citizens.
The testing has been done by anonymous, also not always professional medical staff, without knowing their names and place of work.
Those blue papers (test result confirmation) do not contain the necessary legal requirements to be called a "certificate" officially by the law.
And now, we are in the middle of 2nd mass "screening" now, since Jan 18 2021 during the winter, even though the scientist didn´t recommend it at all in current situation.
And again- no one is collecting our written and signed consent. From Jan 27 2021 there will be again 2 groups of people - the "blue" ones and the rest of us. The country will be then split into two half by the results and the worse half of the country has to undergo this procedure 1-2 times again until the Feb 07 2021 and until our prime minister will be satisfied with the results...
On 2021-01-23 12:27:23, user Martin wrote:
Testing was forced and not voluntary. No ethical guidelines were followed. Slovak citizens were forced to go on testing sites to get tested otherwise they would get fine and can not go to job. Even prime minister Igor Matovic (who made people go to testing by force) said few weeks after testing in national TV, that testing was not voluntary.
There is a lot of sources online, even on Youtube (in Slovak language).
In these days, another forced testing is in progress with more severe penalties for people who not attend. For example - who did not attend this testing, from 27th January cant even go out to the nature alone (with no people around). Violation = 1000 eur fine (averege monthly salary in our country).
This goverment totally ignores rule of law and basic principles of law state.
On 2021-08-21 22:44:12, user Ands Hofs wrote:
Can we please introduce more calibrated PCR that measures the mucosa DNA count and gives out<br /> Viral Load = viral units / mucosa DNA units?<br /> Only then the force and technique of swabbing is not changing the resulting viral load wildly.
Even RTLAMP.org is able to do this, open science test, might be liked by some in the comments here, done in a parallel test, and Boston Children's Hospital did a very good job showing children sometimes have 10x higher calibrated viral loads, which has to be treated early with determination in nasopharynx and mouth, like with xylitol + Grape Seed Extract nasal spray, puff and breathe in a bit to protect vocal chords, upper trachea, whole nasopharynx. Vulnerables: add azelastine as pre-spray dito. Report on CARVIN (11.8.2021) shows excellent efficacy.
If you want "life" reproduction rate, you have to train a dog, see scent dog identification of samples .. covid. Work of TiHo, small animals university Hannover. Built a training device they call scent learning box, like a game for the dog. In one week it is on 95% congruency of PCR, but better: 4 days before infectiousness, and quasi live. It doesn't over-diagnose and does diagnose viral replication. <br /> There is a group that built a speech interface for a dog. This would enable to train the dog on many illnesses, differentiate flu from covid, and even predict severe case, as it can smell susceptibility to autoantibodies (or in another picture: prevalence of MCAS, see Prof. Afrin on Covid. Having deep implications on therapy and prevention. The tricky part is to diagnose MCAS with its 200 mostly congruent symptoms to Post-Covid. So obviously related except scarred tissue of course.)
Even better: build an electronic nose as sensitive as a dog's nose on some marker molecules for covid and a tensor flow neural network in a mobile phone to read it out. The do progress with mice conk cell detecting proteins they use as film on a chip based electronic nose.
On 2021-08-24 01:52:14, user Raihan Farhad wrote:
Please answer the following, in the interest of academic integrity: <br /> 1. What is the effectiveness of masks used in your model? What number did you use? What type of mask? Worn in what way. I can only assume, given the absence of any experimental data regarding un-regulated masks stopping Covid aerosols, you either assumed the effectiveness of a mask or used someone else's assumption. Please divulge.
What is the assumption you made about % of kids having been exposed already? Covid has been around for a while now. If you assumed 0 previous exposure, that is unrealistic, but please state so clearly. If you assumed any other number, please explain how you came to that number and state that number.
What is the duration of infectiousness assumed in your model. According to science, someone infected is infectious for about 5 days. After that, even if he dies, he is not infectious. Please explain the temporal nature of infectiousness assumed in your model.
Please make your entire model / simulation software (all code) and all parameters, assumptions public.
On 2020-08-18 17:33:47, user Rodolfo Rothlin MD wrote:
Dear Dr. Turgeon,<br /> Thank you for your commentary and your interest in our manuscript. Please, find my answers below.
The rationale for selecting July 31st was made for several reasons: First, we assumed that by that date we would have between 50 and 100 patients. Although our estimated sample size was 390 (which we rounded to 400), it is worth noticing that this number accounts for a scale factor on both the mean and the variability estimations; without these factors, the estimated sample size was 52 patients total, and with only a variability factor of 2 the total estimated number was 100. Therefore, we evaluated that July 31st was an appropriate time to make the first interim analysis. Second, as you may know, Argentina was expected to be peaking around that time. And it actually seems that it may be doing it right now. So, a second reason for that date was our prediction that if the results were valuable it could be a useful information for our health authorities. The trial is still ongoing and a second interim analysis will be carried out at 140 patients.<br /> 2. In version 1 of the article on this site, the Methods section had a sentence that stated "No concealment mechanism was implemented". This was subsequently removed in version 2 yesterday. Please clarify what is meant by this. Did the authors mean to imply that allocation concealment was not performed, or was this an erroneous statement intended to describe the unblinded nature of the study? Please also describe the process for treatment allocation and how allocation concealment was maintained.
The sentence you refer to was removed because it was inaccurate. The problem emanated from the fact that our protocol did not foresaw a concealment mechanism. However, during the conduct of the trial, although no mechanism like closed envelopes with randomization was used, on site enrollment was made by an investigator and randomization was made by a second investigator who was unaware of the clinical characteristics of the participant. We are confident that no bias towards the control group was present as reflected by data on table 1 of our manuscript.<br /> 3. The authors describe a change in the primary outcome in terms of timing of CRP measurements. However, I note that the clinicaltrials.gov summary of this trial previously had an entirely different outcome as the primary outcome, with CRP only described as an exploratory/tertiary outcome. The authors should describe the timing and rationale for switching the outcome from a clinical one (need for supplemental oxygen in the first 15 days post-randomization) to the inflammatory biomarker CRP.
As you might have read in the methods section of our manuscript, data from our trial was uploaded by a third party. Unfortunately, endpoints from a working version of the protocol were submitted. This was corrected as soon as we noticed it.<br /> 4. Despite changing the timing of CRP measurements, data on this modified primary outcome of CRP was missing in a large proportion of patients at day 5, and in the majority of patients at day 8. Further details should be provided regarding the reason for missing data, how this was handled in their analyses, and how this should temper conclusions.
Data missing from days 5 and 8 were related to several factors. Some patients were discharged before day 5 and before day 8. Others were lost at day 5 for logistical reasons. <br /> No imputations were done to account for these values.<br /> 5. Finally, performing an interim analysis and disseminating their results in the midst of an open-label trial with subjective endpoints can pose challenges to maintaining impartiality. The authors should describe how they will mitigate potential allocation, performance, and detection and attrition bias during the remainder of the trial.
We disagree with CPR measurements being subjective<br /> Again, thank you for helping us clarify these points.<br /> All the best,<br /> Rodolfo Rothlin
On 2021-01-30 21:28:00, user Sharif Ismail wrote:
This article has now been published in PLoS ONE.
It can be found here: https://journals.plos.org/p...
On 2021-02-03 00:57:08, user kdrl nakle wrote:
Internationa Univerlsity?<br /> C'mon, nobody proofreading the paper?
On 2021-10-01 18:41:38, user Paul Tupper wrote:
Thanks for this very valuable study. Do you have plans to do a similar one for younger age groups?
On 2020-08-24 11:06:25, user Atif Habib wrote:
An excellent paper which provided the importance of short birth intervals and the associated factors in the context of Pakistan. The results indicate that lack of contraception and illiteracy significantly contribute to the problem however it is pretty evident that priority should be given to modern contraception which is comparatively a low hanging fruit in comparison to averting illiteracy.
On 2021-06-25 00:23:11, user Otheus wrote:
While I would like to believe the results of this study, the details and the presentation of their numbers leaves much to be desired for the numerically astute/obsessed. A CI of "0 to infinity" means someone has not really done the statistics right at all. In the online preprint of the article, which may be an older version, the article cites -- somewhat deceptively -- provides the percentages in terms of the number of infections in one group with respect to the number of infections in another group. So, 99.3% of the infections were from people not previously infected and not vaccinated and 0.7% of infections were from vaccinated group. The problem with doing it that way is that you have a much larger population of people not infected and not vaccinated than the other sub-populations.
Imagine you have two drawers of socks, and in each drawer, there is the same ratio of white socks to red socks -- let's say 1 red sock for every 9 white socks, ie, 10% red. You then pull out 10 socks from each drawer. From the first drawer, you pull 5 red socks and 5 white socks, and from the second drawer, you pull 1 red sock. It would seem the first drawer had a greater percentage of red socks. In fact, the first drawer had 500 socks and therefore 50 red socks, while the second drawer had exactly 10 socks and only 1 red sock. The probability of this happening in each case is about the same. The number of red socks to socks drawn from the first drawer is 50%, but for the second drawer, it is 10%. But if you look carefully, the first drawer has 5x the number of red socks as the second. The ratio of red socks drawn to total *red* socks in that drawer is 10% in both cases.
At any rate, from the math given, I calculate that the rate of those got sick among those who were not vaccinated and did not have previous infection was about 10%, while the rate of those who got sick among those who either had been vaccinated or had a previous infection was about 1.2%. Since 0 people with a previous infection reported getting sick, we get 0%. What's significant here is that the population of those unvaccinated and not infected was 10x higher than that last group.
An important sentence from the paper sticks out: "Not one of the 2579 previously infected subjects had a SARS-CoV-2 infection, including 1359 who remained unvaccinated throughout the duration of the study." Those numbers appear high enough with respect to the lower bound of the infection rate (1.2%) to have enough statistical power. You'd expect to find at least 31 cases for the null hypothesis. It seems quite improbable to get 0 results unless previous infections provide very strong protection.
On 2020-08-26 13:53:31, user Melimelo wrote:
This is amazing. Well done! Can you share pictures of the equipment you made?
On 2020-05-03 17:48:53, user Sinai Immunol Review Project wrote:
SUCCESSFUL MANUFACTURING OF CLINICAL-GRADE SARS-COV-2 SPECIFIC T CELLS FOR ADOPTIVE CELL THERAPY
Leung Wing et al.; medRxiv 2020.04.24.20077487; https://doi.org/10.1101/202.... 20077487
Keywords
• SARS-CoV-2 specific T cells
• Adoptive T cell transfer
• COVID-19
Main findings
In this preprint, Leung et al. report the isolation of SARS-CoV-2-specific T cells from two convalescent COVID-19 donors (n=1 mild, n=1 severe; both Chinese Singapore residents), using Miltenyi Biotec’s fully automated CliniMACS Cytokine Capture System: convalescent donor PBMCs were stimulated with MHC class I and class II peptide pools, covering immunodominant sequences of the SARS-CoV-2 S protein as well as the complete N and M proteins; next, PBMCs were labeled with a bi-specific antibody against human CD45, a common leukocyte marker expressed on white blood cells, as well as against human IFN-?, capturing T cell-secreted IFN-? in response to stimulation with SARS-CoV-2 peptides. Post stimulation, IFN-?+ CD45+ cells were identified by a mouse anti-human IFN-? antibody, coupled to ferromagnetic dextrane microbeads, and magnetically labeled cells were subsequently isolated by positive immunomagnetic cell separation. Enriched IFN-?+ CD45+ cells were mostly T cells (58%-71%; CD4>CD8), followed by smaller fractions of B (25-38%) and NK cells (4%). Up to 74% of T cells were found to be IFN-?+, and 17-22% of T cells expressed the cytotoxic effector marker CD56. Very limited phenotyping based on CD62L and CD45RO expression identified the majority of enriched CD4 and CD8 T subsets as effector memory T cells. TCR spectratyping of enriched T cells further revealed an oligoclonal TCR ß distribution (vs. a polyclonal distribution pre-enrichment), with increased representation of Vß3, Vß16 and Vß17. Based on limited assumptions about HLA phenotype frequencies as well as estimated haplotype sharing among Chinese Singaporeans, the authors suggest that these enriched virus-specific T cells could be used for adoptive cell therapy in severe COVID-19 patients.
Limitations
This preprint reports the technical adaptation of a previously described approach to isolate virus-specific T cells for targeted therapy in hematopoietic stem cell transplant recipients (reviewed by Houghtelin A et al.: https://www.ncbi.nlm.nih.go... "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5641550/pdf/fimmu-08-01272.pdf)") to PBMCs obtained from two convalescent COVID-19 patients. However, not only is the title of this preprint misleading - no adoptive cell transfer was performed -, but this study also lacks relevant information - among others - on technical details such as the respective S epitopes studied, on the precise identification of immune cell subsets (e.g. NK cells: CD56+ CD3-?), data pertaining to technical stimulation controls (positive/negative controls used for assay validation and potentially gating strategies), as well as on the percentage of live enriched IFN-?+ CD45+ cells. Generally, a more stringent phenotypical and functional characterization (including coexpression data of CD56 and IFN-? as well as activation, effector, proliferation and other markers) would be advisable. Similarly, in its current context, the TCR spectratyping performed here remains of limited relevance. Most importantly, though, as noted by the authors themselves, this study is substantially impaired based on the inclusion of only two convalescent donors from a relatively homogenous genetic population as well as by the lack of any potential recipient data. In related terms, clinical criteria, implications and potential perils of partially HLA-matched cell transfers are generally not adequately addressed by this study and even less so in the novel COVID-19 context.
Significance
Adoptive cell therapy with virus-specific T cells from partially HLA-matched third-party donors into immunocompromised recipients post hematopoietic stem cell transplantation has been successfully performed in the past (cf. https://www.ncbi.nlm.nih.go... https://www.jci.org/article... "https://www.jci.org/articles/view/121127)"). However, whether this approach might be clinically feasible for COVID-19 therapy remains unknown. Therefore, larger, more extensive studies including heterogeneous patient populations are needed to assess and balance potential risks vs. outcome in the new context of COVID-19.
This review was undertaken by V. van der Heide as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn school of medicine, Mount Sinai.
On 2020-05-05 03:43:04, user Sinai Immunol Review Project wrote:
A possible role of immunopathogenesis in COVID-19 progression
Anft M., Paniskaki K, Blazquez-Navarro A t al.; medRxiv 2020.04.28.20083089; https://doi.org/10.1101/202...
Keywords
• SARS-CoV-2 spike protein-specific T cells
• COVID-19
• adaptive immunity
Main findings
In this preprint, 53 hospitalized COVID-19 patients, enrolled in a prospective study at a tertiary care center in Germany, were assigned to moderate (n=21; light pneumonia), severe (n=18; fever or respiratory tract infection with respiratory rate >30/min, severe dyspnea, or resting SpO2 <90%), and critical subgroups (n=14; ARDS, sepsis, or septic shock) according to clinical disease. Moderately and severely ill patients with a PCR-confirmed diagnosis were recruited within four days of clinical onset, whereas critically ill patients were enrolled on average within 14 days of diagnosis on admission to ICU. To account for the overall longer hospital stay in ICU cases prior to inclusion, repeated blood samples were obtained from moderately and severely ill donors within eight days post recruitment. For 10 out of 14 ICU patients, no follow up blood samples were collected. At recruitment as well as on follow-up, circulating lymphocyte counts were below reference range in the majority of enrolled COVID-19 patients. Relative frequencies were significantly reduced in critically vs. moderately, but not vs. severely ill individuals, with substantially lower NK as well as CD8 T cells counts, and a concomitant increase of the CD4:CD8 T cell ratio in ICU patients. Basic phenotypic and immune cell subset analysis by flow cytometry detected lower frequencies of central memory CD4 T cells as well as reduced terminally differentiated CD8 Temra cells in critical COVID-19. Moreover, a decrease in activated HLA-DR+ CD4 and CD8 T cells as well as in cytolytic CD57+ CD8 T cells was observed in critical vs. severe/moderate disease. Similarly, frequencies of CD11a+ CD4 and CD8 T cells as well as CD28+ CD4 T cells were lower in critically ill donors, indicating a general loss of activated bulk T cells in this subgroup. In addition, a reduction of both marginal and transitional CD19+ B cells was seen in patients with severe and critical symptoms. Of note, on follow-up, recovering severe COVID-19 patients showed an increase in bulk T cell numbers with an activated phenotype. Importantly, SARS-CoV-2 spike (S)-protein-specific CD4 and CD8 T cells, identified following stimulation of PBMCs with 15-mer overlapping S protein peptide pools by flow-cytometric detection of intracellular CD154 and CD137, respectively, were found in the majority of patients in all COVID-19 subgroups at the time of recruitment and further increased in most subjects by the time of follow-up (antiviral CD4 >> CD8 T cells). Most notably, frequencies of both antiviral CD4 and CD8 T cells were substantially higher in critically ill patients, and virus specific CD4 and CD8 T cells in both critically and severely ill subgroups were shown to produce more pro-inflammatory Th1 cytokines (TNFa, IFNg, IL-2) and the effector molecule GzmB, respectively, suggesting an overall increased magnitude of virus-specific T cell inflammation in the context of more severe disease courses. Furthermore, frequencies of antiviral CD4 T cells correlated moderately with anti-S-protein IgG levels across all patient groups.
Limitations
In general, this is a well executed study and most of the observations reported here pertaining to overall reduced bulk T cell frequencies (along with lower NK and other immune cell counts) as well as diminished numbers of T cells with an activated phenotype in ICU vs. non ICU COVID-19 corroborate findings in several previous publications and preprints (cf. https://www.jci.org/article... https://academic.oup.com/ji... https://www.nature.com/arti... https://www.medrxiv.org/con... https://www.medrxiv.org/con... "https://www.medrxiv.org/content/10.1101/2020.04.17.20061440v1.full.pdf)"). Notably, in contrast to many previous reports, the prospective study by Anft et al. enrolled a relatively larger number of COVID-19 patients of variable clinical disease (with the exception of mild cases). However, there are a few weaknesses that should be addressed. Most importantly, the choice of statistical tests applied should be carefully revised: e.g. comparison of more than two groups, as seems to be the case for most of the figures, requires ANOVA testing, which should ideally be followed by post-hoc testing (despite the somewhat confusing statement that this was conceived as an exploratory study). Given the overall limited case numbers per clinical subgroup, trends even though they might not reach statistical significance are equally important. Similarly, some statements are overgeneralized and should be adjusted based on the actual data shown (e.g. the authors continue to refer to gradual reductions of activated T cell subset numbers in moderately vs. severely vs. critically ill patients, but for the majority of data shown substantial differences are apparent only in ICU vs. non-ICU patients). Moreover, it would be helpful to include representative FACS plots in addition to explanatory gating strategies provided in the supplemental document. There are also several inconsistencies regarding the order of data presented here (e.g. in the main manuscript, Fig S5 is chronological referred to before Fig S4) as well as pertaining to relevant technical details (according to both the main manuscript and the gating strategy in Figure S5, virus-specific CD4 T cells were identified by CD154 expression; however, in figure legend S5 virus-specific CD4 T cells are defined as CD4+ CD154+ CD137+). Additionally, from a technical point of view, it is somewhat intriguing that the percentages of virus-specific T cells identified by expression of CD154 and CD137, respectively, following peptide simulation seem to differ substantially from frequencies of CD154+ or CD137+ INFg+ virus-specific T cells. Assuming a somewhat lower extent of cellular exhaustion in the moderate COVID-19 group, one would expect these cell subsets to mostly overlap/match in frequencies, therefore suggesting slight overestimation of actual virus-specific T cell numbers. In this context, inclusion of positive controls, such as CMV pp65 peptide stimulation of PBMCs from CMV seropositive donors, in addition to the already included negative controls would also be helpful. Moreover, in view of the observation that virus-specific T cells were found to be increased in critically ill ICU over non-ICU patients, a more stringent characterization of these patients as well as assessment of potential associations with clinical characteristics such as mechanical ventilation or death would add further impact to the findings described here. Finally, this study is limited to anti-S protein specific T cells. However, evaluation of N and also M-protein specific T cell responses are likely of great interest as well based on current knowledge about persistent M-protein specific memory CD8 T cells following SARS-CoV-1 infection (cf. https://www.microbiologyres... "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.82839-0)").
Significance
In addition to reduced frequencies of activated bulk T cell numbers, the authors report an enhanced virus-specific T cell response against S protein epitopes in critically ill COVID-19 patients compared to severely and moderately ill individuals, which correlated with anti-S protein antibody titers (also cf. Ni et al.: https://doi.org/10.1016/j.i... "https://doi.org/10.1016/j.immuni.2020.04.023)"). This is an important observation that mirrors previous data about SARS-CoV-1 (cf. Ka-fai Li C et al.: https://www.jimmunol.org/co... "https://www.jimmunol.org/content/jimmunol/181/8/5490.full.pdf)"). Furthermore, in accordance with a recent preprint by Weiskopf et al. (https://www.medrxiv.org/con... "https://www.medrxiv.org/content/10.1101/2020.04.11.20062349v1.full.pdf)"), virus-specific CD4 T cells were found to increase in most patients over time regardless of clinical disease, whereas antiviral CD8 T cell kinetics seemed slightly less pronounced. Moreover, in the majority of moderately and severely ill cases, virus-specific T cells against the S protein could be detected early on - on average within 4 days of symptom onset. Longitudinal studies including larger numbers of COVID-19 patients across all clinical subgroups are therefore needed to further evaluate the potential impact of this observation, in particular in the context of previously described pre-existing memory T cells cross-reactive against human endemic coronaviruses (cf. https://www.medrxiv.org/con... https://journals.sagepub.co... "https://journals.sagepub.com/doi/pdf/10.1177/039463200501800312)").
This review was undertaken by V. van der Heide as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn school of medicine, Mount Sinai.
On 2021-02-19 21:51:45, user Michael Verstraeten wrote:
Did you consider to imply Flaxman e.a., Estimating the effects of non-pharmaceutical interventions on Covid-19 in Europe, Nature, 584, 257 - 261 in your study, or didn't it meet the inclusion criteria?
On 2021-07-08 05:59:35, user Dr.G.R.Soni wrote:
Comments on preprint medRxiv publication entitled "Efficacy, safety and lot to lot immunogenicity of an inactivated SARS-CoV-2 vaccine (BBV152) : A double blind, randomised, controlled phase 3 trials" reg.
This is regarding indigenously developed inactivated SARS-CoV-2 vaccine by M/s Bharat Biotech, Hyderabad by using vaccine strain NIV-2020-770 containing D614G mutation. The conventional vaccine consists of 0.5 ml volume having 0.6 ug of virus antigen and results of phase 3 clinical trial available on preprint of medRxiv publisher suggest that the vaccine is of good quality if not best//excellent and the vaccine in my opinion can be used by many under developed and developing countries. However, following are the further comments:
Results claimed for vaccine efficacy against severe symptomatic, asymptomatic and delta variant like 93.4%(95% confidence interval CI 57.1-99.8), 63.35( CI 29.0-82.4) and 65.2% (CI 33.1-83.0) respectively are statistically highly insignificant because of lesser precision and wide confidence interval. Even over all vaccine efficacy reported to be 77.8% (CI 65.2- 86.4) is not highly significant. This may be due to known and unknown variations as well as lesser number of participants involved in clinical trials. Of course the study was designed to obtain a two sided 95% CI for vaccine efficacy with lower limit greater or equal to 30% but it is only applicable when vaccines of high efficacy are not available. Whereas now fact is that the efficacy of Moderna, Pfizer, Johnson & Johnson, Sputnik etc. vaccines has been reported to be more than 90.0% with better precisions.
Again vaccine efficacy reported for elderly patients viz. 67.8% (CI 8.0- 90.0) shows very poor precision and widest CI means high uncertainty and least confidence in data.
No vaccine efficacy data submitted after first dose of vaccine administration and reason furnished by the sponsor is because of low number of Covid-19 cases reported and this is not very convincing. Comparison of vaccine efficacy between two doses is important to know the progress of efficacy.
GMT was reported to be higher i.e.194.3 ( CI 134.4-280.9) in vaccinees who were seropositive for SARS-CoV-2 IgG at base line than in those who were seronegative 118.0 (104.0-134.0). The difference is not even two fold whereas in other studies including Pfizer more than 4-6 fold increase in immune response has been reported even after single dose of vaccine under such conditions. This may be due to killed nature of present vaccine which is in general less immunogenic than live vector and m-RNA based Covid-19 vaccines.
The immune response of three vaccine lots of vaccine in terms of GMT 50 is 130, 121.2 and 125.4 Vs 13.7 in placebo which seems to be optimum but much higher immune response has been reported in other internationally approved vaccines.Why the IgG GMT titre after two doses of vaccine studied by ELISA has not been reported separately for each lot of vaccine rather overall titre against S1 protein, N protein and RBD has been reported i.e. 9742 EU/ml, 4161 EU/ml and 4124 EU/ml respectively? Since RBD is part of S1 protein therefore S1 titre includes RBD titre also. It means ELISA IgG antibody titre of these viral proteins are roughly equal hence this needs clarification. Anyway unless the titre of these neutralizing and ELISA IgG antibodies are compared with sera of asymptomatic, symptomatic and severely recovered covid-19 patients or immune sera of WHO, US, EU approved vaccines available in market it is very difficult to say whether the immunogenicity of present vaccine is at par or not with these standards?
The lesser efficacy of present vaccine than other approved vaccines by the US, WHO and EU may also be due to lack of T cell mediated cytotoxicity response; this is why this response is not measured in the present study.
When Covid-19 disease is known to affect men and women differently so separate clinical trial data are required to be submitted by the sponsors. However in the present study no marked difference in GMT,s for neutralizing antibodies at day 56 was found when assessed based on age and gender. This is very surprising and difficult to believe because age definitely and gender also are known to affect the immune response of any viral vaccine.
Reasons for contracting Covid-19 disease by some vaccinees are to be given specially when immune-compromised and immunosuppressed etc. patients have already been excluded from the study.
As per WHO requirement the minimum level of protecting antibodies should be there up to six months therefore sponsors have to continue the study and then can claim the actual efficacy of vaccine.
Indigenous development of SARS-CoV-2 killed vaccine by conventional method using Indian isolate in the country is an excellent attempt for controlling the Covid 19 disease. The vaccine so far seems to be good based on the results of controlled clinical trials and its effectiveness will be further come to know over the time after its massive use in vaccination program. It is nice that the said vaccine has been exported to many other countries. Let us hope for its early approval by WHO for emergency use.
Dr.G.R.Soni
On 2020-09-10 21:35:51, user Nadav Rakocz wrote:
This paper was presented as part of the KDD'20 AI for COVID-19 workshop.<br /> A short talk can be found here: https://insights.kensci.com...
Or here:
On 2021-07-11 12:09:52, user Radical Rooster wrote:
The article fails the first test of objectivity: SELF COLLECTED SAMPLES. Scientific research must be rigorous, procedures cannot vary from one person to another. Sampling must be done by only a select group of samplers. In this paper, there were 3,975 samplers.
On 2021-07-17 14:17:15, user killshot wrote:
Unless "efficacy" and "positivity" are more clearly defined, this is meaningless. Eg, using PCR amplification of 35 or greater for diagnosis then using an amplification of 24 for "transmission" would greatly favor vaccine-related prevention of transmission but would be faux data. Also, unless there is randomization for vitamin D levels -- shown to impair virulence if > 36 ng/mL -- the data is also meaningless.
On 2020-09-29 04:18:22, user Melvin Joe wrote:
Its good sign ! ! By wearing the masks we could flatten the curve of affected persons. I am strictly using HY Supplies Inc masks to reduce the infection !!
On 2021-09-01 16:05:27, user 4qmmt wrote:
The phrase "previously infected" is not accurate. According to the study, they were previously positive per PCR test, even though they had info on symptoms.
(2) unvaccinated previously infected individuals, namely MHS members who had a positive SARS-CoV-2 PCR test recorded by February 28, 2021 and who had not been vaccinated by the end of the study period;
Per MoH reports, Israel runs PCR at Ct up to 40. The level of false positives must therefore be taken into account. Since they are unknown, the best estimation, and the only one which makes any sense, is previously positive and symptomatic. Maccabi knows this data. This is even stated in the study:
information about COVID-19-related symptoms was extracted from EMRs, where they were recorded by the primary care physician or a certified nurse who conducted in-person or phone visits with each infected individual.
But the study says
unvaccinated previously infected individuals, namely MHS members who had a positive SARS-CoV-2 PCR test
The fact that they did not take that into account in the study tells you that the numbers of previously PCR + and symptomatic is lower than just positive PCR. In fact, the tell you that of 19 previously PCR+ in the recovered cohort, only 8 were symptomatic.
So, of those 8, Maccabi knows who was symptomatic before, but the paper does not discuss that. Why? Look at the Cleveland Clinic study which found 0 reinfections in their > 1300 previously PCR positive and symptomatic unvaccinated workers.
From page 7 of that study
"The health system never had a requirement for asymptomatic employee test screening. Most of the positive tests, therefore, would have been tests done to evaluate suspicious symptoms."<br /> What this means is that this Maccabi data study is actually setting the lower limit for the multiple of protection of natural immunity over vaccinated, i.e., at least 27X better, and likely orders of magnitude greater than that.
On 2021-09-09 09:59:21, user Patricia wrote:
This is one of a many studies that confirm what we already know, and that the CDC has confirmed, with >50% infected not knowing they are infected and being asymptomatic. Of those with symptoms, 80% are mild with cold-like symptoms and 80% of deaths are elderly. The US has a 1.6% death rate with SARS2, far below Peru's 9.2% or Mexico's 7.8% or Sudan/Syria 's 7.4% - out of 200 countries, the USA ranks #85/86 in the world. That is most likely due to the CDC refusing to support any safe COVID treatments successfully used around the world, the Media and Politicians condemning and smearing safe treatments (even banning use in multiple states), and the DO NOTHING APPROACH of : if you are really sick and need medical attention, quarantine and do nothing until you are on death's doorstep and need an ambulance & ventilator. Physicians that defied the nonsense & political hatred, by saving lives and treating COVID with very safe FDA approved drugs - with the common practice of off label use to treat the symptoms - show extremely low deaths rates. Excluding the CDC's push to use the very expensive Gilead's Remdesivir intravenously in Emergency settings that has a 2/3 success rate and ZERO STUDIES or Vanderbilt's monoclonal antibodies - There are over 1,000 studies with over 35 easily accessible drugs, that ALL PROVE INCREASED IMPROVEMENT. So why did the CDC and Doctors discourage any treatment and push the DO NOTHING UNTIL YOU ARE ALMOST DEAD PROTOCOL? In 21 months, since the first death in January 2020, 12% of the US Citizens have tested positive. >80% have mild to moderate symptoms. We have no idea how many had SARS2 because we have no idea how many more were asymptomatic. However, the CDC estimates 114.7M Americans have had SARS2 and have natural immunity. According to far left Media sites, the worst states to manage COVID are those with >200 cases per million, NY 349, NJ 284, SC 273, NV 237, DE 221, DC 209, MA 207 per million population. The most heavily populated states were the first states to be afflicted with COVID - 39M CA & 30M TX hovered around 97 per million, despite having highly criticized opposite approaches of CA Strict Lockdowns versus Texas Open with common sense guidelines. Since that revelation, COVID tracking was suspended by many or dates cherry picked when it became popular to smear successful states to deflect from the fact that the vaccine do not work and hence - are not a vaccine. They never said it would stop the disease, just somehow promised people wouldn't have as severe symptoms. Like treating flu with medicine to ease the symptoms for recovery. The US dismisses the chaos around the world, MSM refuses to inform us on major protests around the world that have been occurring for months. Why isn't the Oxford Director of Vaccines statement on every paper and news segment? He confirmed the vaccine isn't stopping SARS2 and herd immunity with it is "unachievable" and "mythical". What we do factually know today - is very detailed tracking in Iceland and Israel, who were also very PRO-VACCINE. Vaccinating ~90% of their populations, only to see a far worse spike of cases in SARS2 outbreaks that appeared in July August 2021. The inventor of the new mRNA vaccine publicized problems with using the vaccine, warning of manipulating antibodies that would results in weaker SARS2 variants become more virulent and slipping past the VAX'd immune system, creating a huge rebound of illness. And this summer, we are witnessing his expert analysis come to fruition.
On 2021-08-26 23:02:47, user Klaskow wrote:
So when is the Peer review going to be scheduled?
On 2021-08-30 00:23:58, user Bob Robertson wrote:
The conclusions in the results section regarding relative efficacies of convalescent immunity and vaccine-induced immunity are incorrect because they are based on improper comparisons.
Using the same improper comparisons, one would conclude that a 98%-off coupon saves the purchaser twice as much as is saved by a 96%-coupon.
What should instead be compared are the magnitudes of the reductions in symptomatic infections relative to naive immunity, and reductions in hospitalizations relative to naive immunity, as well as deaths, and maybe total infections too (though this one's a bit tougher).
If you have access to Israel-based numbers, all the better, but, for now, I'll assume that the percentage of symptomatic infections in Israel is comparable to that in the US... where 85% of pre-vaccinated, first infections are symptomatic, where 5% of infections lead to hospitalizations, and where 0.64% of infections lead to death. https://www.cdc.gov/coronav...
As a rough estimate, about 540 unvaccinated people who'd not previously been infected would've gotten infected out of a group of 16,214 (based on an assumption that 20% of people get infected per year... divided by 6 to represent those likely to be infected in a two-month span).
So, to compare the efficacies of convalescent and vaccine-induced immunity at staving off all infections, we'd have to look at their reductions in infections relative to those with naive immune systems.
540-19 gives us 521 infections avoided via convalescent immunity.<br /> 540-238 gives us 302 infections avoided via vaccine-induced immunity.<br /> From there, <br /> (521-302)/302 = 0.73, <br /> so, convalescent immunity against all infections could be said to be 73% better than vaccine-induced immunity, or 1.73 times better.
Of the 540 estimated infections expected from 16,214 naively immune, 85% would've been expected to experience symptomatic infections; so that's 457 estimated symptomatic infections.
457-8 gives us 449 symptomatic infections avoided via convalescent immunity.<br /> 457-191 gives us 266 symptomatic infections avoided via vaccine-induced immunity.<br /> From there,<br /> (449-266)/266 = 0.69,<br /> so convalescent immunity against symptomatic infections could be said to be 69% better than vaccine-induced immunity, or 1.69 times better.
Of the 540 estimated infections expected from 16,214 naively immune, 5.16% would be expected to end up in the hospital; that's 28 hospitalizations.
28-1 gives us 27 hospitalizations avoided via convalescent immunity.<br /> 28-8 gives us 20 hospitalizations avoided via vaccine-induced immunity.<br /> From there,<br /> (27-20)/20 = 0.35,<br /> so convalescent immunity against hospitalization could be said to be 35% better than vaccine-induced immunity, or 1.35 times better.
Deaths were the same, so, they each seem to be 100% effective against death (compared to the 4 deaths that would've been expected in the naively immune.
Given that 20% more of the vaccinated group had comorbidities than did the previously infected group, and that there were more than 2.5 times the number of immunocompromised and more than double the number of individuals with cancer, all results should be weighted by reasonable estimates related to comorbidities' impacts on outcomes. I find it quite surprising that comorbidities would've proven to have no impact on your results, and assume there's some mistake there too.
<edit><br /> I've since been informed that the metric about which I'm whining is called relative risk, that relative risk is totally a standard metric, and that I should separate my concerns about public misunderstanding from expert publication... it'd still be cool if y'all chose to add additional metrics for plebs like myself.<br /> </edit>
On 2022-05-02 23:00:41, user Brian Mowrey wrote:
The authors evince no apparent regard for the importance of the interval between PCR+ and serum sample (PDV), especially given the small number of presumed infections among the mRNA-1273-vaccinated in the main analysis, simply remarking
Anti-N seropositivity at the PDV was similar when stratified by median days from illness
Not for the vaccinated, it wasn't (50% vs 32% when stratified, Table 1). Did the authors merely lump both groups together to get around investigating why N-seropositivity was 18% lower in the -5-53 day vaccinated set?
In fact, the same stratification should have been expected to produce different N-positivity rates in the placebo group, had infections been evenly spaced in the -5-53 day interval. Since the authors find only 74% Day 29 N-positivity for placebo participants who are PCR+ on Day 1, and 60% on Day 57 for placebo who are PCR+ on Day 29, it's clear the placebo group isn't defying standard expectations about seroconversion not being instantaneous (bearing in mind a higher false positive rate on Day 1/29 due to screening, obviously) - until the main analysis, when suddenly there is no apparent penalty for near-PDV infections. So maybe there were almost no near-PDV infections in the placebo group (as in, infections skewed toward February due to seasonal patterns) while in the vaccine group the opposite was true (infections skewed to March due to the waning of infection efficacy)?
Thus, both the values for the placebo group and Covid-vaccine group suggest uneven time between PCR+ and PDV. The authors make no comment on this problem and *do not present* a plot of to-PDV-intervals for either group, even though they obviously had full access to that data. This is a glaring oversight at best.
It's not the only one. Have the authors never heard of false positives / base rate fallacy? I doubt it. So why isn't this taken into account, when comparing a group with a frequent outcome to a rare outcome? Among 14.5k participants in both arms, a mere 25 false PCR+ in both groups would be enough to render the main results way off the mark (Placebo: (100% x (1-((.066x648 - 25)/(648-25)) = 97.1% mRNA-1273: 100% x (1-((.593x52 - 25)/(52-25)) = 77.8%). Yet no consideration of the problem is made. The word "false" is not even in the text.
On 2021-04-13 23:43:54, user greenorange041 wrote:
I think it is quite important to differentiate between simple cloth masks and medical / FFP2 masks that were adopted relatively recently and were shown to be more effective in preventing possible contagion. Accounting for this could potentially make a big difference and lead to smaller estimated effects for some measures given that visitors wear more efficient masks.
Another aspect to consider is that some activities banned as a result of the NPIs can be performed both indoors and outdoors. You seem to be aware of this difference, but apparently you are unable to consistently account for it in your analysis. Hence you cannot differentiate between the effect of closing indoor gastronomy and closing only outdoor gastronomy (and hence reopening it) with all necessary hygienic measures in place, which will presumably be far less significant.
The NPIs on your list are also defined quite broadly. In particular you don't consider closing sport facilities and banning even outdoor sports to be a separate NPI. Banning hotel stays for touristic purposes is also not on your list.
Finally, you don't seem to account for season or weather in your analysis. In winter when people tend to have weaker immunity, some measures can indeed make a difference. But in summer the situation can be quite different and some measures could add little no value.
A very sad and disappointing consequence of this study is that it motivates governments to keep in place the same already known plain and undifferentiated measures even though 1) their effect may be largely overestimated in the current situation (by that I first of all mean wide adoption of masks and FFP2 masks in particular as well as limits on the number of visitors / clients that are already in place) and 2) their effect can be different under different conditions (indoor / outdoor activities), however this difference is not analysed.
Another disappointing consequence is that not listing and not analysing certain more detailed measures (closing sport facilities and banning tourist stays in hotels) will most certainly lead to keeping them in place even though the study doesn't provide any explicit evidence in favour of such measures.
To put in in another way: can someone get an answer to the following questions from your study: what is the possible negative (if any) effect of opening retail given that everyone wears an FFP2 mask and there is a limit on the number of clients, what is the possible effect of allowing outdoor sports, of allowing outdoor gastronomy with sufficient hygienic precautions in place (though without express testing), what is the possible effect of opening hotels? And (what is more important), what is the effect of all this given warm temperatures and more daylight? As far as I understand, it is not possible to answer these questions based on your study, but governments may still be tempted to interpret the conclusions as a justification not to relax any measure in a meaningful way.
Of course, correct me if I am wrong.
On 2021-04-29 12:24:41, user Ric wrote:
I think that this estimation strategy is seriously flawed.
The underlying assumption is that Rt is on averge constant over time, unless some measures are taken by the government. This is obviously false, since all epidemic sooner or later ends even without any intervention. Moreover, government actions are obviously taken when the number of cases is already high and Rt could have started to decline on its onw, so you are basically confusing a correlation with causation.
This is seriously concerning. I have already seen articles by general press pushing for more interventions based on this completly unreliable estimations. Please revised your methodology completly or be clear that this is a correlation that does not estimate any effect
On 2020-10-27 16:47:39, user Kamran Kadkhoda wrote:
Low prevalence....low PPV....meaning serology is not reliable.
On 2021-11-12 10:44:25, user Ken wrote:
The next step could be linking the TeKWP to the hospitalization rate in the ICU so to have a real time indicator on the stress that the structure can withstand in relation to the new cases
On 2021-09-08 22:00:39, user Cheeseman wrote:
The authors' statements regarding the effectiveness of universal masking must be in concordance with a systematic review from December 2020 titled "Physical interventions to interrupt or reduce the spread of respiratory viruses" (https://dx.doi.org/10.1002/... "https://dx.doi.org/10.1002/14651858.CD006207.pub5)").
The key discussion element is: "The pooled estimates of effect from RCTs and cluster-RCTs for wearing medical/surgical masks compared to no masks suggests little or no difference in interrupting the spread of ILI (RR 0.99, 95% CI 0.82 to 1.18; low-certainty evidence) or laboratory-confirmed influenza (RR 0.91, 95% CI 0.66 to 1.26; moderate-certainty evidence) in the combined analysis of all populations from the included trials."
This review stands in stark contrast to the authors' position that face masks are effective at mitigating viral transmission. To maintain scientific legitimacy, the authors must decrease the strength of their claims on mask effectiveness in light of this review article.
On 2021-08-05 18:32:18, user Anette Stahel wrote:
Dear moderator,
I've now reviewed, edited and updated my earlier comment to the present study [1]. I hope this will allow for it to be posted.
I'm sorry, but this study is not correct. That is, the pool of people used as denominator when calculating the percentage of COVID-19 infected people who developed CVT and PVT is greatly inadequate. I'll explain what I mean.
In the abstract of the study, it's stated:
"COVID-19 increases the risk of CVT and PVT compared to patients diagnosed with influenza, and to people who have received a COVID-19 mRNA vaccine."
However, when comparing the risk of developing condition X from disease Y with the risk of developing condition X from something else, eg vaccine Z, you first and foremost need to make a correct assessment of how how large the pool of people with disease X is. And to do that, you need to make an estimate. Merely counting the number of people who've sought out primary or secondary care for their symptoms won't do. Not even if you include all the people who were asymptomatic but sought out the care center anyway in order to take a test to see if they were infected (simply because they wanted to know) and then tested positive.
No, you need to include all infected persons in the total pool of people belonging to the health care facility/facilities in question, including the ones who don't go test themselves because of being asymptomatic, or of not having the energy to do it due to their symptoms, or of being into alternative medicine, or of lacking interest/knowledge about the infection et c. There may be many of different reasons. This means you need do make an estimate, otherwise the denominator in the calculation of the percentage who develop condition X from infection Y becomes incorrect.
A study measuring the risk of developing condition X from infection Y using a smaller denominator than one including everyone infected may be useful at times, but it can not be used for comparison with a correctly calculated vaccine risk.
I will use the study Estimation of the Lethality for COVID-19 in Stockholm County published by the Swedish Public Health Agency [2] as an example of a correctly calculated risk, based on an adequately defined denominator. The fact that this is a calculation of the lethality percentage from COVID-19 and not the CVT and PVT percentage is irrelevant, the point is that the same mathematics used in this study should've been applied in the present Oxford University study. From page 13 in the Swedish study, in translation:
"Recruitment was based on a stratified random sample of the population 0-85 years. In the survey we use, the survey for Stockholm County was supplemented with a self-sampling kit to measure ongoing SARS-CoV-2-infection by PCR test. The sampling took place from March 26 until April 2 and 18 of a total of 707 samples were positive. The proportion of the population in Stockholm County which would test positive was thus estimated at 2.5%, with 95% confidence range 1.4-4.2%."
For a complex reason, which I won't go into but is described in detail in the study text, one needs to use a slightly higher percentage when multiplying it with the total number of people in the pool, but that's of minor importance. Anyway, in this study they had to use the figure 3,1169% and when they multiplied it with the number of people in Stockholm County, 2 377 000, they got 74 089. This estimate was then the correct denominator to use when calculating the percentage of people who died from COVID-19 in Stockholm County during this time period.
The numerator was the number of people who died in Stockholm County with a strong suspicion of COVID-19 as a cause, which was 432, no incorrectness there either - as long as a suspected cause number, not a diagnosed cause number, is also used as the numerator when calculating the lethality from the COVID-19 vaccine when the infection lethality and vaccine lethality rates are compared.
So, what they found was that the lethality from COVID-19 in Stockholm County was 0,58%. This is a correct figure, as long as we keep in mind the fact that some of the suspected COVID-19 deaths may later become diagnosed as unrelated to the infection.
The above is thus how the authors of the present Oxford study should've carried out their calculations but they didn't. From their text:
"Design: Retrospective cohort study based on an electronic health records network. Setting: Linked records between primary and secondary care centres within 59 healthcare organisations, primarily in the USA. Participants: All patients with a confirmed diagnosis of COVID-19 between January 20, 2020 and March 25, 2021 were included."
This excludes a considerable amount of infected persons in the total pool of people belonging to all of these primary and secondary care centers, who didn't go test themselves because of a number of reasons (being asymptomatic, being alternative medical, not having the energy or interest for it, et c).
If they'd used the adequate figure in the denominator, the percentage of people established to've developed CVT and PVT from COVID-19 would've gotten vastly lower. However, the percentage of people determined to've developed CVT and PVT from the mRNA COVID-19 vaccines was fully correctly carried out since there are no unregistered vaccinated cases and therefore the registered figure is to be used.
Via the Oxford study's Figure 2 and Table S2 [3], I calculated the following figures: First time CVT cases diagnosed after administration of the mRNA COVID vaccines amounted to 6.6 per million and first time PVT cases after same vaccines amounted to 12.5 per million.
Now, there's a study titled Estimation of US SARS-CoV-2 Infections, Symptomatic Infections, Hospitalizations and Deaths Using Seroprevalence Surveys published by the American Medical Association [4], which has estimated the percentage of infected people in the US looking at roughly the same time period as the Oxford study. From the paper:
"An estimated 14.3% (IQR, 11.6%-18.5%) of the US population were infected by SARS-CoV-2 as of mid-November 2020."
With an infection rate around 14.3%, the estimated number of infected people of the 81 million patients in the healthcare database referred to in the study would've amounted to 11 583 000. This number gives us a hint as for the size of the denominator which should've been used in the calculation instead of the figure of 537 913 confirmed diagnoses.
However, since the Oxford study not only looked at CVT and PVT arising from people having the infection around mid-November 2020 but looked at a much longer time period, from January 20, 2020 to to March 25, 2021, a number far greater than 11 583 000 should be applied. What we need is to estimate how many of the 81 million patients which were infected at least once during these 14 months in question. For the calculation to be really accurate, we need the total, accumulated number of infected people. But since that number isn't found without a very comprehensive and time consuming investigation, we instead have to use the signs ">" ("greater than") and "<" ("less than") here. So, the correct denominator, which should've been used instead of the 537 913 figure, is >11 583 000.
Further, the study says that first time CVT was found in 19 of the patients following COVID-19 diagnosis and first time PVT in 94. This actually means that the rates of CVT and PVT elicited by COVID-19 were much lower than the rates of CVT and PVT elicited by the vaccines. COVID-19 elicited PVT cases, correctly calculated, amounted to <8.1 per million - only about two thirds of the 12.5 per million for the vaccines - and the CVT cases amounted to <1.6 per million - a mere fourth of the vaccines' 6.6.
Interestingly, with their work including this method error, these authors have provided scientific validation of the growing suspicion that the COVID-19 vaccines give rise to thrombocytic complications to a much greater extent than does COVID-19 (which is the opposite of what's stated in the study), because even if the 537 913 figure is inadequate, the other figures in the study are most likely not.
It should also be said that the disclaimer inserted towards the end of the Oxford study by no means can be referred to in order to justify this method error. From the disclaimer:
"However, the study also has several limitations and results should be interpreted with caution. (--) Third, some cases of COVID-19, especially those early in the pandemic, are undiagnosed, and we cannot generalise our risk estimates to this population."
The reason why this passage cannot be referred to, is that 11 000 000 or so omitted cases impossibly can be defined as "some", when the number of denominator cases determined in the study merely constitutes a small fraction (5%) of that figure.
Finally, I'd like to suggest a reading through of the English translation of the Swedish COVID-19 lethality study that I took up in the beginning of my text as a correct, comparative example [5]. This is the main paper that the Swedish equivalent to CDC, the Public Health Agency (Folkhälsomyndigheten), refers to when talking about the COVID-19 lethality here and it's put up on one of the major information pages of their website. I really recommend reading all of it, because it explains so well and in such detail how come this model of denominator calculation without exception must be used in studies like these, which aim to investigate the rate of injuries/complications arising from an infectious illness.
Anette Stahel <br /> MSc in Biomedicine <br /> Sweden
References
On 2020-04-02 20:13:43, user Sinai Immunol Review Project wrote:
Main findings: The authors analyzed 4000 test results from 28 COVID-19 patients of which 8 were confirmed severe COVID-19 cases and 20 were confirmed cases of mild COVID-19 infection. They found that the overall level of serum CRP increased in all cases irrespective of the disease severity. They observed that serum cystatin C (CysC), creatinine (CREA), and urea, biochemical markers of renal function, were significantly elevated in severe COVID-19 patients compared to mild patients.
Critical Analyses: <br /> 1. Figure duplication in panels G and H of Figure 2 <br /> 2. Survey area is limited to one center.<br /> 3. Small number of participants in the survey.<br /> 4. Elderly people in severe groups and relatively younger people in the milder group. The baseline parameters may differ in both groups, considering the age difference.<br /> 5. Although not clearly stated, this is a cross sectional study and interpretation of results is difficult. The markers that were found to be significantly different between groups are very non-specific. Renal failure and high LDH are not surprising findings in critically ill patients. <br /> 6. There is a very minimal description of the patient's baseline characteristics. It would be important to know for example what were the symptoms at presentation, how long patients had symptoms for before inclusion in the study, duration of hospitalization before inclusion. This would help interpret whether results reflect difference in severity of disease or simply a longer course of disease/hospitalization. <br /> 7. It is unclear what the authors mean in the discussion when they mention “which may be the result of prophylactic use of drug by doctor” (Discussion section, line 6). Type of the drug used is not specified.
Relevance: This study offers insights on some laboratory markers of mild vs severe cases of COVID-19 infection. Glomerular cells highly express ACE2 which is the cellular receptor for SARS-CoV-2, and impaired kidney function might represent a marker of virus-induced end organ damage.
Reviewed by Divya Jha/Francesca Cossarini as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn school of medicine, Mount Sinai.
On 2021-08-09 17:23:34, user vaxpro wrote:
author indicated "The sample size of our trial design meets the minimum safety requirement of 3,000 study participants for the vaccine group, as recommended by the FDA, and WHO guidance". Neither FDA nor WHO recommends sample size for an individual study. sample sizes of the individual studies are driven by the objectives. sample size for approval is a different matter. In fact, what FDA says in the referenced document is that "FDA does not expect to be able to make a favorable benefit-risk determination that would support an EUA without Phase 3 data that include the following, which will help the Agency to assess the safety of the vaccine:...ii. All safety data collected up to the point at which the database is locked to prepare the submission of the EUA request, including a high proportion of enrolled subjects (numbering well over 3,000 vaccine recipients) followed for serious adverse events (SAEs) and adverse events of special interest for at least one month after completion of the full vaccination regimen". also "FDA does not consider availability of a COVID-19 vaccine under EUA, in and of itself, as grounds for stopping blinded follow-up in an ongoing clinical trial". WHO guidance is for general vaccine development with major caveats highlighted in the guidance document. the selective and mis- interpretation of the FDA and WHO guidance is regrettable.<br /> immunogenicity is the primary objective of the study. it's curious why author chose to report full set of IgG data at all visits but NT data only at selected visits.post injection pain was reported in ~20% placebo (saline) subjects, which far exceeded any historic rates in this type of population. although no impact on the interpretation of safety for the active arm within this double blinded trial, the observation should be investigated for potential trial conduct issues and discussed.<br /> author stated "MVC-COV1901 has recently been granted EUA in Taiwan". however this is not a scientific issue for this trial, should not be included in trial report in a peer reviewed journal.
On 2020-11-23 11:57:37, user Martin Kral wrote:
Will this method effect any of the antibodies that the immune may have developed. In other words, after the infection has subsided, will the natural immune system develop the necessary antibodies or will a vaccine still be necessary?
On 2020-12-01 22:15:47, user Pedro Emmanuel Alvarenga Ameri wrote:
Hello all, I just had a chance to read the preprint. The work is pretty cool. Im conducting an investigation to validate a few risk scores and Im interested to validate this one too at a Rio de Janeiro population. However, in order to do so, it would be necessary to have the model intercept in addition to the coefficients available at table 1. Additionally, it would be also necessary to have the predictors units not available in table 1, and the range of each predictor, to perform the same normalization informed at the methods section. Is it possible to inform these missing information? At last, the web calculator mentioned at the paper is an excellent way to show and use the results, however its web address is not informed in the manuscript. Where can I find this web calculator? Looking forward to see the final version of the manuscript. May the force be with you all.
On 2020-12-09 07:14:02, user JANAKI RAMANATHAN wrote:
this is interesting and is reinforcing the fact that the pandemic lockdown have created spaces for intervention of yoga therapy on digital spaces too. this is inevitable and may still continue even post covid i guess in different forms. pain is a corolllary in different spatial and socio economic and medical contexts.hope something substantial emerges
On 2020-12-09 14:33:35, user Elke Devocht wrote:
After completing formal peer review, this article was recently published by Plos one: <br /> https://journals.plos.org/p...
On 2020-12-11 00:19:16, user lbaustin wrote:
Please provide a better reference for Otros, T. O. et al. (2020) ‘Nutrición Hospitalaria’, pp. 0–3 I was unable to find this article. Which volume and issue number? Could you be referring to <br /> Macaya F, Espejo Paeres C, Valls A, Fernández-Ortiz A, González del Castillo J, Martín-Sánchez J, et al. Interaction between age and vitamin D deficiency in severe COVID-19 infection. Nutr Hosp [Internet]. 2020 [cited 2020 Oct 25]; Available from: https://www.nutricionhospit...
On 2020-12-12 04:13:41, user Hartmut Ziche wrote:
I am waiting impatiently for the publication of your second (late September/early October) seroprevalence study in French Guiana. I hope it confirms your model and possibly improves it's predictive capacity.
On 2020-12-14 15:13:45, user GH wrote:
The authors note that "The initial decrease in suicide rates during 1913-1918, with the lowest rate of 9.97 per 100 000 in 1918, was followed by an increase with the highest peak of 22.15 per 100 000 reached in 1970". Interestingly 1918 is the year before the spanish flu pandemic, and even more interestingly one of the mentioned peaks occurs in 1922 (15/100 000) (at the end of the pandemic). This is a 50% increase in 4 years, probably the biggest increase in the entire dataset. Doesn't this suggest a post/during-pandemic-effect at least for the spanish flu?
On 2020-12-17 23:14:59, user Rakshit Sidd wrote:
Hey Peter, Can you please let me know that which dataset you referred in to? I need the source.
On 2020-12-18 11:30:03, user Wendy Olsen wrote:
The paper is very useful.
It is informative about a free data source for India known as the covid19india website.
Since reading the paper, I explored this website. It has an API for data scientists to use the data. This paper by Vandana Tamraka, Ankita Srivastava, Mukesh C. Parmar, Sudheer Kumar Shukla, Shewli Shabnam, Bandita Boro, Apala Saha, Benjamin Debbarma, and Nandita Saikia is very useful in giving a summary of the age-sex-specific individual records in the database at a specific date in mid 2020. Since then, I believe the website Covid19india has now arranged to provide only District summaries which omits age-sex details.
The paper is also very useful in providing an analysis of cumulative cases, over time, from March to July 2020, with a spatial autocorrelation correction. This is impressive and helpful. On the other hand, the spatial autocorrelation variables are not causal mechanisms, and they can reduce the apparent impact of other variables that do represent background causes or events. Even so, apparently the social-group variables at the District level did have some correlation with the cases (ie with cumulative contagion) in the time-series model, even after the spatial correction.
I enjoyed the smoothly written conclusions of the paper.
Regards - Wendy Olsen - - @Sandhyamma is my Twitter name, or meet me alternatively using Facebook.
On 2020-12-20 22:03:54, user Sam Smith wrote:
Congratulations for publishing the research.<br /> Would any of the modern anti-allergy antihistamines probably work equally well? For example bilastine tablets? Then there is Azelastine nasal spray. So one could use both oral antihistamine and nasal antihistamine at the same time.<br /> And take it with famotidine = Pepcid of course.
On 2020-12-21 00:56:39, user RP Rannan-Eliya wrote:
These systematic review findings are largely consistent with the findings from our global ecological analysis of 172 territories just released in Health Affairs that controls for multiple interventions and factors during the first COVID-19 pandemic wave. The mask finding is buried in the paper, but when using daily mask usage as the intervention measure, we detected only a small beneficial impact of mask wearing, but it was not statistically significant.
RP Rannan-Eliya, N Wijemunige et al. 2021. Increased Intensity Of PCR Testing Reduced COVID-19 Transmission Within Countries During The First Pandemic Wave. Health Affairs.<br /> https://www.healthaffairs.org/doi/full/10.1377/hlthaff.2020.01409
It seems very difficult to detect statistically significant benefits from mask wearing for COVID-19 in global analyses that adequately control for other interventions, suggesting that the benefit is likely to be small at population level. One possible reason is that this is because mask wearing in most contexts is only mandated outside the home, whilst most SARS-CoV-2 transmission occurs inside the home in most countries. Another could be that the transmission blocking is weak in practice owing to problems in how people wear masks, compliance, etc.
On 2020-12-27 18:54:51, user Travis Cesarone wrote:
This is odd, PN Medical has suggested cloth masks cause hyperventilation. <br /> This drastically lowers CO2, constricting blood vessels in the brain, leading to severe anxiety. N95s and surgical masks are associated with hypercapnia which can cause confusion and disorientation.
This should be interesting in peer-review.
https://www.pnmedical.com/b...
Individuals have a false sense of security that masks are protecting them. This 'security' has not been quantified in any study, so it is false. Therefore, there is a false increase in mental health due to a severe fear of the virus.
On 2020-12-28 08:48:28, user Disqus wrote:
The study design is somewhat confusing, a cross-sectional and prospective study that appears somewhat more similar to an ecological one than others. The authors crossed<br /> data from multiple sources including some known for their unreliability. Most surprising the authors states that they were unable to find a correlation between the opening of schools and the increase in Rt (par. "School closures did not alter the rate of Rt decline in Lombardy and Campania"), a statement that appears in stark contrast to the trend of Rt<br /> in Fig.6A and 6C showing a net increase after the opening of schools from an<br /> initial pre-opening value of approximately 1 for Lombardy and 1.5 for Campania,<br /> to a peak value of approximately 2.6 (Lombardy) and 1.9 (Campania).<br /> Curiously, the authors comment only on the descending part of the two curves but avoid<br /> commenting on the ascending phase following the opening of the schools.<br /> Finally, in spite of the medRxiv warning, one wonders why the authors decided to disseminate their unverified and not and not yest reviewed results, through the italian media (see for example the facebook pages of the authors for the links), suggesting the idea of a) somewhat solid and well establisehd general conclusions and b) the review process is a purely formal matter and not of substance.
On 2020-12-29 18:14:28, user Pablo Pablo wrote:
Students and young people are the same set , so this research shows that young people are safer than population.
By converse, teachers and people with age to work are not the same set, so this research shows that teachers are less safer than population.
On 2020-12-28 18:07:37, user Rogerio Atem wrote:
The 3 preprints of this series on COVID-19 epidemic cycles were <br /> condensed into a single article that summarizes our findings using the <br /> analytical framework we developed. The framework provides cycle pattern <br /> analysis, associated to the prediction of the number of cases, and <br /> calculation of the Rt (Effective Reproduction Number). In addition, it <br /> provides an analysis of the sub-notification impact estimates, a method <br /> for calculating the most likely Incubation Period, and a method for <br /> estimating the actual onset of the epidemic cycles.
We also offer an innovative model for estimating the "inventory" of infective people.
(Revised, not yet copy-edited)
On 2020-12-29 15:21:15, user Claus R wrote:
Please make sure you review the Nov 5 Frontiers in Medicine commentary on the Flaxman paper, https://www.frontiersin.org.... In it, Kuhbandner & Homburg argue (for the UK) that Flaxman et al. ignored that R was already very low at the time when NPIs could have taken effect, something you seem to be confirming with your more extensive analysis here.
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.
On 2021-01-01 08:15:38, user Forrest Weghorst wrote:
Figure 7 would be more informative if the graphs showed symptom trajectories of Positive Tests vs. No Positive Tests (which is what all the statistical tests are comparing in the corresponding paragraph), not Positive Tests vs. Everyone (including Positive Tests).
On 2021-01-06 17:08:20, user Jeff Boris wrote:
I would be careful with your definition of POTS--it is not as rigorous as it should be. For adults, it really should be a relatively persistent increase of HR of at least 30 bpm in the first 10 minutes of standing after supine position, with symptoms of orthostatic intolerance, and with a history of symptoms for at least 3 to 6 months (depending on the reference). I do find the sex, race/ethnicity, and symptom distribution to be very similar to that of both our demographics article (Boris JR Cardiol Young 2018) and the Dysautonomia International-sponsored article (Shaw BH J Intern Med 2019).
On 2021-01-20 21:42:40, user Cort Johnson wrote:
Such close similarity to ME/CFS with some expected differences - such as shortness of breath, early fever, loss of taste and smell.Unrefreshing sleep and IBS-like symptoms are very common in ME/CFS and it might be useful to track those in future studies. Low body temperature has been reported for ME/CFS and it would be interesting to see if that shows up over time.
Very early studies of the ME/CFS or rather ME outbreaks described a heterogenous melange of symptoms specific to each outbreak which resolved into a familiar pattern of fatigue, cognitive problems, etc. The groundbreaking Dubbo studies demonstrated that a wide variety of infectious triggers can produce the same long term symptom set. The results, then, are not surprising but it is still startling to see them.
Congratulations Body Politic for getting this and the other study together. We are in your debt.
On 2021-01-06 09:58:19, user Martin Reijns wrote:
Many new variants of SARS-CoV-2 are now in circulation, including variants that are thought to have higher rates of transmission, such as B.1.1.7 (VOC-202012/01) first detected in the UK and 501_V2 first detected in South Africa. Some of the nucleotide changes impact on viral RNA detection by qRT-PCR (depending on the variant and on the assay used), with S and N gene assays affected most commonly.
Our N1E-RP and N2E-RP multiplex assays still detect all of the main reported variants, including: B.1.1.7, 501_V2, 20A.EU1 and 20A.EU2.
I put together an updated SnapGene file with primers and probes of commonly used qRT-PCR assays on the genome sequence of the original Wuhan-Hu-1 isolate, with mutations that occur in common variants indicated. This file can be found here:
On 2021-01-06 18:15:01, user RT1C wrote:
minor correction: "moderate (100-101.9°F) and severe (<=102°F)." I think you meant severe to be greater than or equal to 102, not less than or equal to 102.
On 2021-01-06 18:36:37, user RT1C wrote:
In your discussion, I think you should distinguish between mechanisms proposed to work in vivo vs. those observed in vitro. For example, the high sugar concentration of honey may be antibacterial in in vitro tests/cultures, but when ingested, it will be diluted by other foods and liquids and irrelevant as a mechanism for antibacterial action. The same is true of the some the other suggested mechanisms.
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.
On 2021-01-08 21:27:37, user Marek J wrote:
What type of honey was used? Was the cumin milled before use?
On 2021-01-25 02:24:50, user Sohaib Ashraf wrote:
Kindly contact on twitter regarding this study for questions @SohaibAshrafMD<br /> Youtube Channel Dr Sohaib Ashraf, MD
Regards,<br /> Principal Investigator HNS-COVID-PK
On 2021-08-14 12:49:05, user Uncle George wrote:
Thank you for producing this research study. Its findings are very interesting and amazing. Due to the political correctness of society and pharma influences, this paper may never be peer reviewed. However, many people can benefit from it through this preprint article. Thank you again for your work!
On 2021-01-10 14:55:39, user Mmd wrote:
How Can I access the data?
On 2021-01-13 11:14:06, user Magnus Brink wrote:
Congratulations to a well conducted and highly interesting study. It seems out of doubt that IL-6 receptor inhibitors can save lives in covid-19. But what about time spent in the ICU? The headline in the prerelease by gov.uk reads: “NHS patients to receive life-saving COVID-19 treatments that could cut hospital time by 10 days”. I would say yes for saving lives but no for cutting time spent in ICU. Table 2 tell us that there are no differences in “Organ failure free days” (OSFD) in survivors; 14 days (IQR 7 to 17) for patients treated with tocilizumab compared to 13 days (IQR 4 to 17) for controls. The conclusion must be that tocilizumab will save lives but unfortunately not un-crowd our ICUs.
On 2021-01-15 10:11:06, user Martijn Weterings wrote:
This research shows an interesting significant difference between the groups. The contingency table <br /> 3, 2, 8, 1 <br /> 22, 23, 17, 24 <br /> is an indication for a significant dependency.
However this is likely caused by age differences (given the abundant information that indicates the relationship between age and risk of death). It is mostly the 3rd group with the highest number of deaths (8 deaths) and the highest estimated adjusted risk ratio (RR 2.18). This is also the group with the highest age.
It is very problematic that there is no clear dose response relationship.
Because this lack of a monotonic relationship between O3l and risk, it seems arbitrary to make a comparison between the 4th quartile and the first 3 quartiles. The observed effect is mainly due to the 3rd quartile having a high risk. One might just as well make a comparison between the 1st quartile and the last 3 quartiles and find a similar (though slightly less) significant result.
Besides other potential confounding variables it is the age distribution among the four quantiles which is remarkable and likely seems to be a strong influence on the statistical relationship. This means that the adjustment must be done with great care. I personally believe that currently the adjustment might be biased due to the binning of the continuous O3 levels into 4 quartiles and age might need to be included as a polynomial and not just a linear effect (it is actually unclear what sort of model has been used).
The problem with binning is that correlation between age and O3 levels might not be captured smoothly. The relationship is not linear (rather it is something exponential or logistic). For each increase 10 years increase in age there should be something like a 2 fold increase in risk of death (in this research the odds ratio is only 1.33 for a decade increase which is odd). This means that a group of 80 year olds and 60 year olds, with a mean of 70 years, are not comparable to a group of only 70 year olds. One might get peculiar results when the distribution of age in the different quartiles is not evenly distributed. (and possibly there could be some sort of Simpson's paradox due to the way that age is distributed within the 4 quartiles, if the 3rd quartile happens to have many people of 'very' old age then this might interact with the age effect, resulting in a reduced risk rate for the increase of age and an increased risk rate for the 3rd quartile)
I would suggest to provide a scatter plot of age versus O3l (along with some colour or markers for death vs no-death) which allows a more clear view of the structure in this data set and allows to see a more clear relationship with the O3l. It could also be interesting to see the output of a logistic model where O3l is treated as a continuous variable (potentially with some non-linear relationships like polynomials or interaction terms). Such a model would not have to treat the levels O3l levels as categorical, and would have less problems with non-homogeneous age distributions within the categories.
I would not be surprised to see some sort of clusters in the scatter plot of O3l versus age (and potentially deaths occur might occur more often in particular clusters). A more exploratory analysis of such structures might reveal more useful insights to generate hypotheses to be studied in future research.
On 2021-01-15 13:09:56, user disqus_5a4k87zf4B wrote:
Could you, as required by law, please declare your conflict of interest?
On 2021-01-18 20:12:59, user ad4 wrote:
The authors state that "only national lockdown brought the reproduction number below 1 consistently". This appears true for the first lockdown (23 Mar), but I'm not sure the same claim can be made about the second lockdown (beginning 05 November). I would strongly suspect that if Figure 1I showed data for December and January, we would see an increase in R above 1, despite tiered lockdowns at the time.
On 2021-01-19 14:48:37, user Laura Green wrote:
The authors' inability to control for potentially important cofounders renders this paper's conclusions unreliable.
On 2021-01-19 21:13:39, user Richard Brown wrote:
Did the clinical data record the NSAID (particularly Ibuprofen and Naproxen) taken early (later less relevant). In our veterinary field early NSAID therapy (meloxicam, Flunixin, ketofen) is regarded as highly relevant in these situations.
On 2021-01-20 08:54:27, user Mariluz Boquera Ferrer wrote:
Congratulation from your work. <br /> Would you send an e.mail address from the corresponding author to ask you some questions regarding this article?
On 2021-01-22 14:40:19, user Tim Meyer wrote:
It is understandable that the issue of the Covid-19 incidence in football (soccer) players is of general (and scientific) interest. Also, it makes sense to compare this incidence to the general population of that age. However, such comparisons have to be made in a scientifically sound manner. One of such principles - also on pre-print servers or possibly even more so on such platforms which are not peer-reviewed in advance - is the meticulous description of the methods being used. Unfortunately, crucial information about this is lacking for the article from Andersen et al. entitled „Incidence and relative risk of infection with SARS-CoV-2 virus (Covid-19) in European soccer players“.
It is not described how the infection numbers for the 5 leagues have been obtained (i. e. uncertainty about the numerator for the incidence calculation). Also, we do not get sufficient information about how the (estimated) incidence in the general population has been assessed. In this regard, it is noteworthy that a frequently tested population like the one of the players potentially has a number of undetected infections close to zero. This is completely different in the general population where some studies point to numbers of undetected infections in the range of 75-90% with higher values in the young age groups where asymptomatic Covid-19 courses are more frequent. Due to the very short methods description it is not clear which calculations have been carried out for this study. Therefore, we have uncertainties about the numerators of both incidence calculations which makes results hard to interpret.
When we assume (in favour of the authors´ numbers) that the number of undetected infections has been taken into account appropriately by referring to an „infection fatality rate“ from a small area in Germany (a highly questionable method from our perspective) the message would be that hygiene protocols in Germany and England work well. However, studies based on procedures like the ones in this text appear methodologically unsound and should not be published – not even on pre-print servers. Even on such pre-print platforms more thorough descriptions as well as careful interpretations (including the limitations of one´s work) are needed because otherwise misinterpretations may enter the public domain.
Tim Meyer (Conflict of Interest: Chair of the German Task Force "Sports Medicine/Special Match Operations" which has been developing the hygiene protocol for the German football leagues; chair of the medical committees of the DFB and UEFA); Barbara Gärtner (Conflict of Interest: Member of the German Task Force "Sports Medicine/Special Match Operations" which has been developing the hygiene protocol for the German football leagues
On 2021-01-26 14:17:45, user Rune wrote:
How is sensitivity and specificity of 69.7% and 99.5% for RAT calculated?<br /> 87.0% of PCR sensitivity of 90%-95% equals 78%-83%.<br /> 98.6% of PCR specificity of >99% equals >98%.<br /> PCR values according to SST "Information om PCR test for COVID-19 til almen praksis".
On 2022-10-26 10:01:47, user Christian Jauernik wrote:
This study seems to now have been published in the Danish Medical Journal
On 2021-01-27 15:44:21, user Steve Goodacre wrote:
Now published in PLOS ONE<br /> https://journals.plos.org/p...
On 2021-01-30 20:34:38, user kdrl nakle wrote:
Using unreliable data with elementary stats. Looks like a student paper..
On 2021-01-30 23:05:47, user disqus_uZtSLivn1O wrote:
CFR increases when the rate of unscreened infected individuals increases (you mention this yourself). The proportion of positive tests increased sharply in December; an indicator of a higher incidence of unreported cases. This is not an interesting finding in my opinion.
On 2021-02-07 11:26:26, user Luzia wrote:
Such precious excellent news! I am delighted that scientists are researching the benefits of natural remedies like propolis. This helps us to take more responsibility for our own health. Lets be grateful to the bees that they collect and process this natural substance and do all we can to protect them.
On 2021-02-15 13:07:34, user Guido wrote:
State, local governments & complicit media simply ignore this, as unions help shut down rank and file "health & Safety Committee" walkout/sickout strikes. Our Creative Class is speciously distracted by blatantly staged shock & awe by an autocratic duopoly as the most vulnerable are intentionally exposed to the mutated strains, before vaccination is properly evaluated.
On 2021-02-20 09:50:26, user Darren Brown; HIV Physiotherap wrote:
Thank you for this comprehensive study. In your methods you reference inclusion of 2 functioning/disability measurement tools; (a) World Health Organization Disability Assessment Schedule (WHODAS) 2.0; (b) Washington Group (WG) on Disability Statistics. Which WHODAS and WG questionnaires did you use as there are different versions? You have not reported any results from these measures of functioning/disability. Are you able to provide these results either in the main article or supplemental material, as they are very important data.
On 2021-10-10 04:45:03, user kdrl nakle wrote:
10+% of unvaccinated got COVID. Excellent argument for mandatory vaccination of HCW.
On 2021-03-04 05:40:34, user J Sato wrote:
I read this preprint paper and would like to ask if the authors can share the data of BCG vaccinated individuals and unvaccinated individuals.
I understand that this research divides the individual into BCG primed and control primed.<br /> I guess there are BCG vaccinated and unvaccinated individuals among both BCG primed and control primed groups.<br /> I would like to divide the individual into four groups; BCG primed & BCG vaccinated, BCG primed & BCG unvaccinated, control primed & BCG vaccinated, control primed & BCG unvaccinated.<br /> Can you share the data of those?
Kind regards,<br /> Jun Sato
On 2021-03-05 15:18:59, user Suzanne Barnes wrote:
Any opinion on whether protection would be provided from breast milk if offered to an older sibling of 5 years old?
On 2020-11-03 11:20:46, user Thomas de Broucker wrote:
one of my concerns is the validity of so little differences (although significant) of the SD values throughout the results knowing that the minimal pathological value admitted by neuropsychologists is -1,65 of the normal population tests results
On 2020-11-08 21:44:53, user Redouane Qesmi wrote:
This preprint is now published in Chaos, Solitons & Fractals doi: 10.1016/j.chaos.2020.110231 with a new title which is "Impact assessment of containment measure against COVID-19 spread in Morocco".
On 2020-11-11 00:15:13, user kdrl nakle wrote:
This is not to be trusted, we have no idea how the patients were selected (if at all) for SORT <9 and >9 and there is no control group for either. For all we know the results could easily be because of the course of the disease than about remdesivir.
On 2020-11-11 00:17:25, user kdrl nakle wrote:
This paper has no science in it, there is no data in it, mostly typical educational stuff.
On 2020-11-18 16:11:06, user D Greenwood wrote:
Impressive work. But could the finding anti-S and NAbs declines faster in males than in females simply be regression to the mean? The conclusions sound like males end up with lower anti-S and NAbs than females, but the results you present do not show this - they show M3-6 results much the same for males and females. Maybe if you showed the full trajectory over all visits, and analysed these using multilevel models, this would give some support to your claim. As a second point, please update the manuscript to give all estimates and confidence intervals, regardless of statistical significance, e.g. table 2. This way policy makers can combine your results with those of others and you make a greater contribution to science.
On 2020-11-18 18:56:00, user Vincent wrote:
For the sake of science and public trust, it would be highly relevant that the authors of this study would do any of the following: 1) Withdraw their paper and address the comments below (that is the point of posting manuscripts to pre-print servers, allowing peer-review), 2) submit the manuscript to a peer-reviewed journal or 3) transparently state that their findings are erroneous due to errors in the analyses.
These actions would be important especially in the light new evidence (https://www.acpjournals.org... "https://www.acpjournals.org/doi/10.7326/M20-6817)") that, in line with previously conducted RCTs on other respiratory pathogens, shows that surgical facemasks are not effective (with 5% significance level) in preventing transmission to its wearer.
It simply cannot be acceptable that a study like the one by Ollila et al is published without peer-review, receives a lot of media attention, undermines the credibility of other researchers and then when confronted with criticism, no responses are given.
On 2021-08-11 05:37:53, user Rob wrote:
“In May, independent hesitancy risk factors included…having a PhD or <=high school education…”
Definitely the most fascinating aspect of these results. More research needs to be done to try to unpack the dynamics at play here.
On 2021-08-12 12:20:10, user Drewster R wrote:
I would much rather know what their PhD was in as opposed to that they were a PhD. I've met many a Phd without the good sense to change a light bulb.
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.
On 2021-08-20 00:25:35, user troRx wrote:
So where are the "eMethods" they refer to? If this was driven entirely through Facebook, I would have some validity issues with applying it to the general population.
On 2021-08-22 13:09:40, user Dan Elton wrote:
A major reason for hesitancy, which is sadly not mentioned in this paper, is the lack of FDA full approval. Once again the FDA is exhibiting a lot of dysfunction and showing they can't do cost benefit analysis at all. We've had what is effectively the largest Phase IV trial in history yet the FDA won't approve it. The risks are tiny - like a few in a million - like the risk of driving for a few months.
A lot of people are holding out for the full approval. See survey results i tweeted here: https://twitter.com/moreisd...
It's easy to demonstrate that holding up the approval is leading to hundreds of thousands of unnecessary cases and a lot of unnecessary suffering and death.
also see <br /> https://www.slowboring.com/...
On 2021-08-11 20:29:39, user S.O.S_1.20.17 wrote:
Me and my husband are both over age 60, (61 and 62) we both had the Moderna shots and we had a very strong response to the second shot, husband had a 102 degree fever, I had a 101 degree fever or possibly a little higher (my digital thermometer wasn't working right, it was flashing). Anyway we had a strong response. My son who is in his 20's also had the Moderna vaccine and works in a busy supermarket. He was exposed to 3 coworkers who had Covid (they were unvaxxed). My son wore an N95 mask to work. He was tested for Covid on July 21st. The tests, PCR and Rapid both came back negative. My husband travels to NYC on public transit wearing an N95 mask. He has not gotten Covid. Vaccines seem to be working well. We are still avoiding restaurants, my son did go out to restaurants a few times with his friends who are now vaccinated.
On 2021-08-12 12:32:47, user Christopher M. Brown wrote:
This is an interesting study, but one glaring confounder which the authors do not seem to have addressed is age. Older patients, who are much more susceptible to infection and hospitalization, also tend to be the most vaccinated cohort. Additionally, older patients are more likely to be vaccinated with BioNTech than Moderna, given the earlier introduction of that product. Patient age and time since vaccination may also account for a large part of the gap seen between the two vaccines in recent estimated efficacy. An attempt should be made to stratify/analyze these data using age.
On 2021-08-12 13:20:30, user Nicolas Gambardella wrote:
Something seems wrong with the tables 3, 4, 5, reporting efficacy. In most cases (Pfizer OR Moderna) is much lower than (Pfizer PLUS Moderna), as if the cases had received both vaccines. In some cases (Pfizer OR Moderna) is higher than (Pfizer PLUS Moderna). Where are the missing cases coming from? And in some cases it is much lower, like Pfizer=5, Moderna=5, Pfizer OR Moderna=1. <br /> Now, this could be the result of the case matching algorithm?
On 2021-08-13 00:46:51, user Bung Prachya wrote:
The problem lies in the design. With case-control study, you should get only Odd ratio, not %effectiveness.
They said 80% of their population was vaccinated (the numbers seem wrong). If you found that among 1700+ covid patients, only 10 were vaccinated guys, you should think about effectiveness of 95%something.
On 2021-08-13 02:51:57, user Zachary Hadden wrote:
This makes a lot of sense as my post covid experience since last December, recovery has been slow. I coded in ICU, brought back and recovered in 14 days where they started me at 70 liters of Oxygen for 4 days and had a gradual reduction down to 1 liter when I was discharged. No cardiac issues after stress test and echocardiogram. Pulmonary breathing performance tests show I have the lungs of someone that’s been smoking all my life. I’ve never smoked. CT scan shows the lower right lobe is collapsed, but I’ve been told this should not cause my shortness of breath issues. I feel like I have a more constricted airway than pre-covid. My pulmonologist is a joke. I’ve only had one video conference call with him and have had to get these tests scheduled on my own…. even the pulmonary test. I’ve still not had a follow up call since April. There aren’t any more pulmonologist available in my area. I guess if there is any consolation with this study, patients are improving.
On 2021-08-14 21:10:03, user Daniele Sardinha wrote:
10.4236/wjv.2021.113004 <br /> Sardinha, D. , Lobato, D. , Ferreira, A. , Lima, K. , de Paula Souza e Guimarães, R. and Gondim Costa Lima, L. (2021) Analysis of 472,688 Severe Cases of COVID-19 in Brazil Showed Lower Mortality in Those Vaccinated against Influenza. World Journal of Vaccines, 11, 28-32. doi: 10.4236/wjv.2021.113004.<br /> published
On 2021-08-15 12:58:51, user Stephen B. Strum wrote:
I re-read this article in a recent "quest" to understand why we do not have surrogate virus neutralization tests (sVNTs) that are available through national labs such as LabCorp and Quest. An important publication by Goodhue Meyer led me back to the Joyner et al. paper. Here's my overall take on the Joyner paper and the issues at-large.
There appears to be a very excellent correlation between either natural COVID-19 infection or vaccination with the development of virus-neutralizing antibodies (NAbs).
The occurrence of high-titer NAbs correlates well with protection from new infection from COVID-19 and also reduces morbidity when variants of concern (VOC) cause infection in vaccinated individuals. Yet mass testing of the population has not been done because these surrogate tests are not agreed upon as to which one(s) has the greatest sensitivity & specificity for NAbs as determined in plaque reduction neutralization tests (PRNT) assays or wild-type COVID-19 assays, both of which are tedious, expensive, require BSL3 (biosafety level 3) labs and not suitable for high throughput testing.
Yet, as of today, 8/15/21, there exist publications showing good correlation between specific sVNT and plaque reduction neutralization tests (PRNT). In reading over 150 articles on this topic, I have not found any articles so far that have studied the Ab (antibody) test used in the Joyner study (VITROS Anti-SARS-CoV-2 IgG qualitative assay by Ortho. Please help out and identify if such articles have been published (I am still searching).
The FDA authorized an EUA for Ortho's VITROS test above while other assays that published their results were not used to select COVID-19 convalescent plasma (CCP) for treatment purposes.
? So how do we really know what the nAb levels were in the CCP given to patients in the study? The VITROS Ab test used is a qualitative test. At the time of publication I am fairly certain that there were no correlative studies to show that this test was accurately depicting the nAb levels using so-called gold standards.
? How, as Hllda Bastian pointed out do we accept the article at face value without a placebo control? There is a need to go over the structure of this study to ascertain if the differences in survival later reported in 2021 by Joyner et al. are sufficient to look further into CCP and if so, then what is the best way to screen for donors?
? Why are not donors selected using a sVNT that has been shown to have high correlative value vs. PRNT such as cPASS by GenScript?
? Why are not donors selected by cPASS results from those vaccinated with Pfizer or Moderna where the cPASS results can be shown to be protective against VoC such as Delta Variant (B.1.617.2)?
? Note that I am not a virologist, but a hematologist/oncologist that also happens to be immunocompromised. I assessed my nAb status with an sVNT that has been commercially available across the USA: LabCorp test code 164090: SARS-CoV-2 Semi-Quantitative Total Antibody, Spike using Roche Elecsys on a cobas 601 analyzer. With testing at one month post-Pfizer #2, my total levels were > 250 U/ml, but at 4 months later they had decreased to 59 U/ml. If these Ab levels continue to fall I will be one of the functionally un-vaccinated or under-vaccinated. This is a large group of patients in the world and a potential breeding ground for more vicious VoC. <br /> Stephen B. Strum, MD, FACP <br /> sbstrum@gmail.com
On 2021-08-16 04:13:39, user liutasx wrote:
RNA isn't infectious virus, so if it's 43 time more RNA, how much is more infectious virus in that sample?<br /> How was standardize upper epithelium cells count in measurements? During different phase of infection different amount of virus is produced, how accounted for this variable?
On 2021-08-20 12:28:35, user Marco wrote:
This article is now published on Scientific Reports: https://www.nature.com/arti...
On 2021-08-21 06:47:01, user Heba A. A. Ibrahim wrote:
The dataset link is broken https://github.com/datadist... , can you provide another link for it ?
On 2021-08-23 08:47:36, user Medhat Khattar wrote:
How is it correct to have used only saline as placebo injection, when the composition of the vaccine includes a range of compounds, most notably lipids?
On 2021-08-25 17:36:55, user Bill wrote:
Well, that is it then. If you have had COVID, you do not need to get the vaccine. Only 10% of those that had it would have difficulty fighting it after 9 months! More studies say similar -- real science right here folks.<br /> https://www.nih.gov/news-ev...<br /> https://www.nature.com/arti...
On 2021-08-26 11:46:43, user Mike Kruskamp wrote:
NIH/CDC/IDSA recommend to treat patients with OS of 6 at baseline due to that being the group with statistical benefit at day 28. Will you please evaluate that same population at day 60? The current analysis at day 60 is in the entire study population which is not consistent with the 28 day analysis or guideline recommendations.
On 2021-08-27 01:55:40, user Private for now wrote:
Great work. We need more of this and updates vs variants for infection and serious disease efficacy correlates. Not sure how many people would want a personalized booster schedule created, but this type of data is foundational.
On 2021-08-27 23:57:15, user Chris Woolley wrote:
Is your sample biased? A snowball sample has reported that the nurses have worked more hours than normal. Isn’t it human nature to over-exaggerate hours worked. Would it have been better to just get the factual data from the hospitals if possible?
Just looking at the nurses that worked 31-40 hours. 1/3 worked more than contracted and 15% of these claimed to have high stress. Does this not mean that only 5% of full time workers have had extra stress during COVID? Shouldn’t that be the headline?
On 2021-08-31 05:02:22, user kdrl nakle wrote:
Since contact tracing depends heavily on the level of community transmissions there is no way it can be used successfully in the situation where that level is high. The most effective measure in that situation is vaccination regardless of mathematical models.
On 2021-08-09 21:08:09, user Richter David Oliver wrote:
One major flaw of this and the "Dresden"-study is the "self-reported" questionaire. Introspection is not a scientific measurement. Particularly extremely common symptoms like "tiredness" or "headache" are not suitable to diagnose any particular condition and are basically treated as reliable long-covid markers in the study. Also age -groups around 6, most likely did not fill out the questionaire themselves. A study like this would greatly benefit from data like respirometry or any quantifiable physiological or biochemical parameter that can be objectively measured. This would also allow a single/double blinded design.
On 2022-11-04 00:15:41, user Brian Mowrey wrote:
Study design inadvertently results in the 3rd-dosed experiencing their "primary Omicron" infections mere weeks after injection. Bias for lower viral loads, antibody masking, and higher false positivity rates (because lower overall infection rates), which the 1-to-1 matching cannot fix. Adjusting for the 90-day delay between positive test and "follow up" start:
"Median duration between the third dose and [primary Omicron test] was [34] days (IQR, [13-53] days), and between the second dose and [primary Omicron test] was [244] days (IQR, [196-281] days)"
Oops.
On 2022-11-07 07:35:58, user Renier Mendoza wrote:
Now published in AIMS Mathematics:
On 2022-11-08 00:00:25, user japhetk wrote:
This preprint makes the wrong comparison.<br /> It is possible for there to be more than one cause of death in the Ministry of Health, Labour and Welfare's report of suspected post-vaccination deaths. Myocarditis and myocardial infarction can be the cause of death even if myocarditis is listed.<br /> Demographic causes of death, on the other hand, list only one underlying cause of death: there can only be one cause of death per death. Therefore, it is not possible to compare the frequency of occurrence of the two.<br /> Also in terms of demographics, in 2021 there are 155 deaths from acute myocarditis I40; in 2020 there are 168; in 2019, 162; in 2018, 177; and in 2017, 167. Why are there the fewest deaths from acute myocarditis I40 in 2021 in the last five years if deaths from myocarditis caused by vaccines are identical to deaths from demographic I40 as the underlying cause?<br /> So from this you can see that the authors have clearly made the wrong comparisons and drawn the wrong conclusions.
Translated with www.DeepL.com/Translator (free version)
On 2022-12-09 22:42:39, user Josipa Domjanovic wrote:
This is an interesting and well-written randomized controlled trial that examined the effect of intradialytic exercise on the survival of patients undergoing treatment with intermittent hemodialysis. The main findings suggest that intradialytic exercise improves survival in this population. The methodology of this study is robust and the results are well-presented, but there are several important constraints that should be acknowledged.
Major remarks:
Minor remarks:<br /> - The authors are encouraged to correct the typos and improve the textual flow throughout the manuscript. Paragraphs should be justified.
Nevertheless, this well-organized study warrants publication so it could act as an incentive to start similar ones on a larger sample and with a longer follow-up, which could lead to change in the treatment practice of these patients.
On 2022-12-22 13:04:03, user Howard Waitzkin wrote:
Here is another peer-reviewed article from the same project. Constructive comments welcome. Thanks.
Howard Waitzkin
Fassler E, Larkin A, Rajasekharan Nayar K, Waitzkin H. Using absolute risk reduction to guide the equitable distribution of COVID-19 vaccines. BMJ Evid Based Med 2022. doi:10.1136/bmjebm-2021-111789. [Epub ahead of print: 07 Mar 2022
On 2022-12-27 18:27:33, user Bahrad Sokhansanj wrote:
A peer-reviewed version of this manuscript has now been published: Sokhansanj BA, Zhao Z, Rosen GL. Interpretable and Predictive Deep Neural Network Modeling of the SARS-CoV-2 Spike Protein Sequence to Predict COVID-19 Disease Severity. Biology (Basel). 2022 Dec 8;11(12):1786. PMID: 36552295; PMCID: PMC9774807. https://doi.org/10.3390/bio....
On 2023-01-06 03:26:21, user Danuta Skowronski wrote:
The peer-reviewed publication of this paper with the Canadian Medical Association Journal (CMAJ) is freely available as of December 5, 2022, at the following link : https://www.cmaj.ca/content...
On 2023-01-06 18:49:46, user Ahmet Tas wrote:
Important Notice<br /> In this preliminary version, signal analysis is suboptimal due to inadequately designed filter for raw signal smoothing. Moving average method with inappropriately wide window length has caused blunted waveform peaks. For the actual study, authors have re-analyzed the PPG signals with an accordingly designed Savitzky - Golay filter.
Importantly, comparisons between subgroups remained the same since all data had undergone the same processing (filtering).
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
On 2023-02-07 08:39:11, user Frauke Mattner wrote:
Hi, congratulation to your very informative preprint. I am just looking for a figure comparing vaccinated with non-vaccinated persons. Could you still add it? You defined vaccination as at least one shot obtained. Could you also provide data for thoses being at least two-fold or triple-fold vaccinated ?
On 2023-03-06 09:52:44, user baba aurhum wrote:
Now published in Communications Medicine: https://www.nature.com/arti...
On 2023-03-08 22:43:36, user Daniel Davis wrote:
This paper has been published in the journal Delirium: doi:10.56392/001c.36822
On 2023-03-09 12:14:10, user Guido van Wingen wrote:
Great study showing that high quality multimodal MRI data does not improve classification performance beyond multicenter resting-state fMRI as reported for two other large cohorts (REST-meta-MDD with N=2338 and PsyMRI with N=1039): https://www.nature.com/arti...
On 2023-03-21 09:47:06, user Aamir Fahira wrote:
Hello Cato Romero<br /> How you computed MAF for summary statistics using UK BioBank, can you please share reference method or your code
On 2023-04-11 00:51:25, user Xianyong Yin wrote:
We did a similar analysis between vitamin D and psoriasis. We achieved similar results at https://pubmed.ncbi.nlm.nih...
On 2023-04-20 05:53:06, user José F. Català-Senent wrote:
Hello everyone,
I am glad to inform you that the preprint has been published in the journal Neurobiology of Disease: https://doi.org/10.1016/j.n....
On 2023-05-11 08:01:12, user Siri Fløgstad Svensson wrote:
This paper has now been publised in Neuro-Oncology Advances:<br /> https://academic.oup.com/no...
On 2023-07-06 06:27:06, user Dimitrios Karagiannakis wrote:
I declare that our article entitled "Prevalence of cirrhotic cardiomyopathy according to different diagnostic criteria. Alterations in ultrasonographic parameters of both left and right ventricles before and after stress" has been published in Annals of Gastroenterology <br /> Dimitrios S Karagiannakis <br /> Corresponding author<br /> Email: dkarag@med.uoa.gr
On 2023-07-21 21:15:45, user zmil wrote:
Worth noting that the deletion reported in this pre-print appears likely to be the pre-integration site of a transposable element insertion. That is, the minor allele is not a true deletion, but rather the major allele is an *insertion,* specifically of an Alu element. See twitter thread here: https://twitter.com/genomer...
On 2023-08-14 20:23:31, user Peter Lange wrote:
This paper reports the prevalence of common symptoms in the population after covid-19. There is no control group. The paper is therefore of no utility and no conclusions can be drawn. The authors should make some effort to derive useful comparisons before attempting to publish.
On 2023-08-21 16:51:06, user Maria Vanderléia Araujo Maximi wrote:
This review resulted from the graduate-level course "How to Read and Evaluate Scientific Papers and Preprints" from the University of São Paulo, which aimed to provide students with the opportunity to review scientific articles, develop critical and constructive discussions on the endless frontiers of knowledge, and understand the peer review process.<br /> The preprint titled “Differential modulation of attentional ERPs in smoked and insufflated cocaine-dependent associated with neuropsychological performance” associated the cocaine consumption with reduced attentional event-related potentials (ERPs, namely P3a and P3b, indicating bottom-up and top-down deficits respectively. In this study was evaluated these ERPs considering the route of cocaine administration. <br /> This study had the hypothesis that smoked cocaine dependent (SCD) would exhibit reduced modulation of the P3a, while both SCD and insufflated cocaine dependent (ICD) would show reduced modulation of the P3b.<br /> The authors examined the differences in the P3a and P3b potential between SCD and ICD, and their relationship with neuropsychological performance.<br /> Below are some suggestions for revisions pertaining to the various sections of the manuscript.<br /> Abstract: The abstract provides a nice summary of the study.<br /> Introduction: The introduction section would be strengthened by further discussion, such as including a description of differences between schooling and SCD and/or ICD use, and their relationship with neuropsychological performance.<br /> Methods: If possible, it would be important to have information about how long the participant has been a cocaine user.<br /> Results: Descriptive statistics are good, including mean age, biological sex and education for the study group and comparison group. Additionally, if available, the authors are encouraged to include participants’ handedness. Missing data, if any, should be indicated in this results section. <br /> The preprint could be improved by expanding the comparisons and analyzes obtained from data on schooling and use of SCD or ICD. It could also be improved by emphasizing the need for these findings to be known and shared with the scientific community. This way, the authors would be able to analyze schooling and use of SCD and/or ICD, granting a deeper assessment of this information.<br /> Discussion: Limitations of the study have been pertinently included in the discussion section.<br /> The content of this research is very interesting, innovative and may have implications for the relationship between differential modulation of attentional ERPs in smoked and insufflated cocaine-dependent and neuropsychological performance.
On 2023-09-04 21:32:53, user Joilson Xavier wrote:
This study is now published in Nature Communications doi:10.1038/s41467-023-40099-y
On 2023-09-11 12:43:46, user youni wrote:
Can chronotype be discerned from activity tracking data or self-report?
Might chronotype account for a portion of variance in the association with mortality?
Would interpretation vary if the sleep-wake schedule (reported as circadian rhythmicity) were dictated by 'lifestyle" choices versus genetic chronotype?
On 2023-09-21 10:06:53, user Glenn Tisman, M.D. wrote:
Beautiful work. Great team cooperation. Possibly gives credence to some of those swearing that high-dose B12 helps their symptoms of various neurologic disorders in spite of normal serum B12 levels. I wonder if our paper "https://www.academia.edu/68..." in 1993 revealing that XRT and or chemotherapy drugs (e.g. Hydrea) cause a decrease in HOLOTCII may add to the discussion. Neuropathy in patients on various chemo and XRT (e.g. Hydrea) and non chemotherapy drugs (statins said to induce subtle EMG signs of peripheral neuropathy in 40% of patients) may add to the discussion. Glenn Tisman, M.D.
On 2023-11-03 11:35:08, user Alex wrote:
Some elements seem to be misquoted or false in the introduction, and collected pubmed data only in french language does not actually reflect published data with selected keywords, discussion in this thread :
On 2023-11-15 15:22:22, user Ryon wrote:
The analysis evaluating off-label use of hormonal therapy in OC is fascinating. The methods of adjustment for known, quantifiable variables via IPTW is valid. However, this work could be improved by a discussion of unknown confounders that might have affected the observed associations. For instance, in breast cancer and prostate cancer, the decision to give hormonal therapy or chemotherapy is very influenced by patient frailty, for which ECOG scores are a crude measure. Things like total disease burden, sites of metastases, etc, which are difficult to quantify and sometimes not included in the FH database would be things that should be absolutely considered. More granular commentary of what variables are balanced / imbalanced, and variables that could affect treatment assignment other than the ones quantified, and likely direction of residual bias, are needed for more thorough evaluation of whether the reported analysis supports the hypothesis of off-label effectiveness of these drugs.
On 2023-11-20 10:05:27, user Koen Wortelboer wrote:
This preprint was published in September 2023 in Nature Communications and can be found via this DOI: https://doi.org/10.1038/s41...
Citation:<br /> Wortelboer, K., de Jonge, P.A., Scheithauer, T.P.M. et al. Phage-microbe dynamics after sterile faecal filtrate transplantation in individuals with metabolic syndrome: a double-blind, randomised, placebo-controlled clinical trial assessing efficacy and safety. Nat Commun 14, 5600 (2023).
On 2023-12-10 17:31:49, user Scott Lear wrote:
I have several serious concerns with the study and manuscript:
This is an observational study and despite what is written in the manuscript, an observational study cannot lead to the clear conclusions the authors suggest the results indicate. The authors should temper their interpretation of the results and take into account the below.
The authors do not address their findings in the context of the 1000s of other observational studies indicating activity (and at high levels) has consistently been associated with reduce risk for premature mortality.
The authors state previous studies have not robustly adjusted for other lifestyle measures. This is untrue. Many of the existing observational studies have robustly adjusted for the measures the authors of this study say weren't done (and have done so for decades). Here are a few:
https://pubmed.ncbi.nlm.nih...<br /> https://pubmed.ncbi.nlm.nih...<br /> https://pubmed.ncbi.nlm.nih...
All of these studies (there are many more) had more robust adjustment than the present one and found that high levels of activity either provided further risk reduction or a plateau but no reduced risk reduction. The last study had 30 years of follow-up and 15 points of LTPA assessment- a point that the authors of the current study infer that their study is the only study to have a long follow-up.
Self-reported questionnaires to assess LTPA are not as accurate as the authors indicate. While questionnaires are used in many studies, they tend to overestimate activity levels compared to objective measures such as accelerometers (plenty of studies to support this). They also are not accurate in distinguishing different levels of intensity of activity which is also pertinent to consider. Lastly, the study only assessed leisure time activity ignoring occupational, household and transport activities. Given the surveys were done in 1975, 1981 and 1990, this is likely to be a substantial amount of activity missed (as all jobs were more active back then, than now). There is no indication in the Methods how the participants were put into the four activity groups (sedentary to highly active).
The biological ageing was based only on a sub-sample of 5% of the study population. There is no description in the methods how this sub-sample<br /> was selected. Was it random, and thus possibly representative of the larger cohort, or was a convenience or selective sample that could introduce bias?
BMI was self-reported, and again, there is ample literature to indicate self-reported BMI underestimates true BMI and this is greatest in those with higher BMI. In addition, if one is looking to assess the true affect of LTPA, BMI should not be adjusted for as it is in the causal path between LTPA and mortality.
We have good quality randomized trials from the 1980s in cardiac rehab that indicate the benefit of structured exercise on <br /> reducing early death (and leading to greater lifespan) in people with heart disease. While the authors quote a single study (#5) stating RCTs <br /> have not shown activity to result in longer life, the study quoted is not a real study but rather a commentary. The advantage of the RCTs from the 1980s is the lack of pharmacological management of participants in usual care because statins and anti-hypertensives where either not around or readily prescribed at the time. More recent RCTs have control groups that are optimally medically managed.
On 2023-12-26 14:48:44, user Donald R. Forsdyke wrote:
LATE ONSET POST-VACCINATION MYOCARDITIS
The acceleration of SARS-CoV-2 vaccine research post-2020 was so rapid that preprint postings became the norm for many of us working in the field. This preprint of Watson et al. (1) describing 3 case histories is in line with previous preprints describing single case histories (2, 3). It now appears that late-onset post-vaccination myocarditis in elderly subjects can be either overt (symptomatic; 1, 2) or cryptic (not symptomatic; 3).
The cases described here (1) developed symptoms of myocarditis several weeks after vaccination and a few weeks after initiating anti-PD-1 treatment (Immune checkpoint blockade; ICB). The latter would have decreased constraints on autoimmune phenomena. The reported period following vaccination prior to symptom onset, coincides with that reported early in the pandemic by Guatam et al. (2) for a subject with a previous cardiac condition (prior morbidity). It also concides with the post-vaccination periods that preceded protracted, yet asymptomatic, transient dips in blood pressure (BP) in a normal subject, which has been attributed to myocarditis (3).
In the latter case, an episode of cardiac fibrillation during a run, prompted a retrospective analysis of blood pressure (BP) readings for the period when five sequential anti-SARS-CoV-3 vaccinations has been given (3). This resulted in the unexpected discovery of the extreme BP dips that progressively increased in extent with successive vaccinations. A cause-and-effect relationship was evident. The myocarditis was cryptic and was deemed likely to remain so, unless the subject had made excessive demands on cardiac function (e.g., vigorous exercise). Alternatively, the delicate balance between normal immunity and autoimmunity might have been shifted as in (1), or a comorbidity might have emerged as in (2).
The present preprint begins by stating that association between vaccination and myocarditis is rare and affects younger subjects (1). The other preprints suggest the existence of a vulnerable population-subset that may include many elderly subjects and may be less rare than is generally understood. A “crowd sourcing” follow up has been suggested (3,4).
1.Watson RA, Ye W, Taylor CA, Jungkurth E, Cooper R, Tong O, et al. Severe acute myositis and myocarditis upon initiation of six-weekly Pembrolizumab post-COVID-19 mRNA vaccination. medRxiv 2023; doi.org/10.1101/2023.11.24....<br /> 2.Gautam N, Saluja P, Fudim M, Jambhekar K, Pandey T, Al'Aref S. A late presentation of COVID-19 vaccine-induced myocarditis. Cureus 2021; 13: e17890.<br /> 3.Forsdyke DR. Cryptic evidence on underreporting of mRNA vaccine-induced cardiomyositis in the elderly: a need to modify antihypertensive therapy. Qeios Here<br /> 4.Forsdyke DR. Physician-scientist-patients who barketh not. The quantified self movement and crowd-sourcing research. J Eval Clin Pract 2015; 21: 1024–1027.
On 2024-01-08 18:05:42, user jhick059 wrote:
This article was published in the peer-reviewed journal Cureus Journal of Medical Science on Dec. 14, 2023: https://doi.org/10.7759/cur...
On 2024-01-16 13:30:11, user Jan Egger wrote:
The paper has been published in CMPB from Elsevier:<br /> https://www.sciencedirect.c...
On 2024-02-26 15:44:36, user Anthony Dallosso wrote:
Hi - supp figure S3 is mentioned in the text but I can't see it in the Supplementary info link. Is this available somewhere please?
On 2024-02-26 17:17:40, user Ciarán McInerney wrote:
Please, explain the<br /> situation that warranted the Bonferroni correction, and explain precisely how<br /> you came to the threshold of 0.01. The Bonferroni correction scales the level<br /> of significance by the number of comparisons being made. With 19,314 candidate<br /> features, this would make for a staggeringly small Bonferroni correction of<br /> 0.00005.
On 2024-04-27 23:54:27, user Dee McDonald wrote:
Currently suffering from TSW for 17 months and agree this study is extremely valuable insight into the condition. It is difficult to communicate how life changing this condition is to experience, and any progress we can make in recognizing it, can be an aid in preventing its occurrence for others in the future. It is hideous to experience! Furthermore, TSW communities find dermatologists denying the condition exists, make it additionally challenging. So few resources are available to help patients (or victims of practitioners over prescribing) one must be self educated and advocate for their case continually to get any medical assistance. <br /> I am fascinated by the science of these skin abnormalities, and how I can potentially induce more affective healing. It is studies like this that will make a huge impact in treatment of the TSW condition.
On 2024-05-03 17:29:02, user Jackie Kilpatrick wrote:
I have been through this hellish condition, experiencing all of the classic symptoms which differentiate it from eczema, including inability to control body temperature, bone deep incessant itch ( I slept in boxing gloves, ffs!), hair loss, insomnia, full red sleeve, oozing and flaking. I was told by doctors that the condition doesn’t exist. My consultant dermatologist said “if you don’t want my drugs, why are you here?” and when I said that I was hoping we could discuss other ways to maintain skin health like PH or microbiome issues she said scathingly that I and ‘my internet’ would know far more about that than she. <br /> For too long there has been a total disconnect between patients suffering a condition which not even medieval torture professionals could have dreamt up and a medical profession refusing to see the growing mountain of irrefutable even while anecdotal evidence emerging globally from social media. With the new video technology now available to all the number of brave selfless souls documenting in almost scientific detail what they are going through means that this, maybe one of the biggest medical scandals of all time, will soon be properly exposed for all to see. Proper research will support what all of us sufferers already know, the medical community will be forced to become as informed as their patients… imagine! … and maybe these horrendous drugs will be used as an absolute desperate measure of last resort rather than being doled out like sweeties for the most minor of complaints. More research and quickly please. Be the people who break this story properly and stand up for all the benighted souls burning in agony in their own skin.
On 2024-05-10 18:06:25, user Adam Jones wrote:
Now published in Computers in Biology and Medicine doi: 10.1016/j.compbiomed.2024.108545
On 2024-07-01 17:32:52, user Cristian Riccio wrote:
Hello, there is a typo in the title. "half-a-million" -> "half a million"
On 2024-07-26 14:15:20, user Gauthier wrote:
This preprint has now been published in the Journal of Dentistry: https://doi.org/10.1016/j.jdent.2024.105130
On 2024-09-13 06:49:57, user Shicheng Guo wrote:
Really impressive work! Congratulations!! I am wondering will the pLoF based burden test result will be included in this study?
On 2024-10-04 15:29:55, user Santiago Vasco wrote:
This preprint has been published as a peer-reviewed article in Revista de Gestão Social e Ambiental. The link to the published article is: https://doi.org/10.24857/rgsa.v18n10-074
On 2024-10-07 13:30:05, user Dimy Fluyau wrote:
Preprint is published.<br /> Fluyau, D.; Kailasam, V.K.; Revadigar, N. Rapid and Prolonged Antidepressant and Antianxiety Effects of Psychedelics and 3,4-Methylenedioxy-methamphetamine—A Systematic Review and Meta-Analysis. Psychoactives 2024, 3, 476-490. https://doi.org/10.3390/psychoactives3040029
On 2024-10-09 14:55:31, user Emma Chambers wrote:
This is now published in the peer-review journal npj Vaccines and the link to the paper can be found here https://www.nature.com/articles/s41541-024-00878-0
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.
On 2024-12-03 15:27:15, user Guerard Byrne wrote:
The authors use Goat IgG to block Fc-receptors prior to the flow cross match. If goat IgG contains Gal antigen (likely) then this effectively adds Gal antigen to the GTKO cell surface. Staining the cells after FC-blocking with anti-Gal antibody, or GSIB-4 lectin could determine if this is a problem.
On 2024-12-05 16:47:19, user Anna Carolina Viduani wrote:
This is an excellent and highly relevant paper for Brazilian researchers and practitioners—congratulations on such an impactful contribution!
I have just one very minor observation: while there is indeed a Dourados in Minas Gerais (MG), I believe the city referenced on page 10, particularly in relation to the suicide rate in Indigenous communities, is actually Dourados in Mato Grosso do Sul (MS).
On 2024-12-11 21:15:30, user Basheer Abdullah Marzoog wrote:
the paper is published https://www.mdpi.com/2227-9059/12/12/2814
On 2024-12-13 13:28:40, user Mahalul Azam wrote:
This article now published at http://dx.doi.org/10.2174/0118749445361291241129094132
On 2024-12-14 16:10:34, user Yann Kull wrote:
First of all, thank you to the researchers for advancing biomedical research on Long COVID.
Here are some notes I had:
individuals meeting long COVID criteria were defined as those who (1) reported presence of COVID-19 symptoms that could not be explained by alternative diagnoses; (2) reported ongoing significant impact on day-to-day activities; or (3) had any diagnosis codes of long COVID in their electronic health records. Primary analyses used population controls (i.e., all non-cases)
What irks me about this selection is it is completely unclear what happens to people that develop post COVID cases of ME/CFS, POTS, or other common labels often included in long COVID subtypes.
Does that count as an “alternative diagnosis” which means they aren’t in the study cohort. If so it might end up being a weird exclusion of more severe ME and POTS cases resulting from COVID because they are more likely to be separately diagnosed, while including mild ones under the long COVID label? This makes the data quite messy, and it worries me the long COVID label is doing more harm than good at this point. Studying a heterogeneous set of conditions resulting from a viral infection, perhaps through different mechanisms, as a single entity, will likely dilute useful subtype level findings.
The data seems to be coming from the 2023 long COVID GWAS using the COVID Host biobank. Who’s major finding was an association with FOXP4 Locus
FOXP4 has been previously associated with COVID-19 severity6, lung function8, and cancers9, suggesting a broader role for lung function in the pathophysiology of Long COVID.
This suggests the signals they are picking up are likely related to susceptibility to lung damage from COVID, Post-ICU syndrome and the such. In this context, this study’s association with clotting genes makes more sense, and perhaps points to the fact even if there is a buildup of evidence behind the microclot data, it likely isn’t going to be relevant for post-COVID ME/CFS.
On 2025-01-20 17:02:49, user Lucy Mackrell wrote:
An updated version of this article has been published in BMJ Open: https://bmjopen.bmj.com/content/14/12/e089021
On 2025-02-17 11:02:33, user Sebastian Röner wrote:
The paper has been published by GigaScience in December 2024.<br /> DOI: https://doi.org/10.1093/gigascience/giae102 <br /> PMCID: https://pmc.ncbi.nlm.nih.gov/articles/PMC11659977/
On 2025-03-15 20:32:14, user Hani Molaie wrote:
The failure to critically address alternative factors such as economic sanctions and healthcare capacity further weakens the argument, as these variables likely play a significant role in shaping public health outcomes in addition to political populism.
On 2025-04-05 17:39:07, user Ellie Murray wrote:
My 2023 public peer-review comments of this article can be found at: https://epiellie.substack.com/p/from-the-archive-shingles-vaccine
The tl;dr: although I would love this hypothesis to be true, there are a number of methodological concerns I have with this analysis which leave me unconvinced.
On 2025-04-16 08:57:01, user Idan Menashe wrote:
This manuscript has now been published here: DOI: 10.1186/s11689-024-09573-6
On 2025-04-17 08:53:34, user Nitzan Paldi wrote:
For this research project to be considered valid, a few items are missing and should be provided by the authors. The most pertinent outstanding issues are:<br /> 1) The analysis of wMel was done in the months July-October, but the 2023 and 2024 summer wMel prevalence data is missing. This is important because almost all previous studies, including those done in Niteroi, have shown a very large dip in Wolbachia detection in the summer. <br /> 2) The analysis done to demonstrate the impact on dengue compares an arbitrary 10 year-period and takes into account the extremely high 2013 outbreak in Niteroi to demonstrate how Niteroi moved from one of the highest dengue cities in the state of Rio to the lower part of the spectrum. However, the period from 2013 onwards marks a massive reduction of dengue regardless of intervention or non-intervention status, and is identical in almost all >100k population cities in a 100 km radius around Niteroi. Moreover, the adjacent city of San Goncalo, that had half the level of dengue in the 2024 outbreak, had an almost identical reduction since the 2013 epidemic and all of this without any connection to Wolbachia releases. <br /> 3) The authors compare the dengue cases of Niteroi in 2024 with other cities in the state, but do not make a comparison with the city of Rio, across the bay, where another massive Wolbachia project had no impact on the prevalence of dengue in 2024, and resulted in a massive dengue epidemic of 1300 cases per 100k population. Omitting, or more likely “conveniently forgetting” this project underscores the unacceptable “cherry picking” of this manuscript. <br /> When these comparisons with the adjacent cities of San Goncalo (no Wolbachia – low dengue, half from Niteroi in 2024), and Rio de Janeiro (massive Wolbachia project- identical high epidemic dengue to non-intervention areas) are both taken into consideration, the conclusion is that the Wolbachia project had no demonstrable impact on dengue prevalence.
On 2025-05-09 19:16:34, user Tom Hähnel wrote:
Accepted publication: 10.1002/mdc3.70094
On 2025-06-13 08:49:30, user TU wrote:
From an author of Ref.60: Thank you for your citation of our work on DOCK8 (Life Sci Alliance, 2021). The structure reported is DOCK8 DHR-1 domain, which binds PI(4,5)P2. I believe that the relevant structure in your context is rather DOCK8-DHR2/Cdc42 reported in another work: DOI: 10.1182/blood-2012-01-407098. Please check it.
On 2025-07-30 10:53:20, user Esther van Kleef wrote:
This preprint has been accepted for publication in Eurosurveillance and is awaiting final editing.
On 2022-06-07 20:44:20, user Iver Juster wrote:
Suggestion: Table 4 shows state of subjective recovery at various time points according to various forms of treatment. Suggest making it clear that the top 3 rows together sum up the 23 subjects, and the 4th row (IVIG) is a subset of the 23, who had not recovered by months 5-9, and were given IVIG. PS: Really good to see post-vaccination sequelae investigated; much to learn about how immune responses go awry here.
On 2022-06-11 16:21:38, user Miles Markus wrote:
RHETORICAL QUESTION: Is there a possibility that drug-treatment-based estimates of "relapse" percentages (such as are given in the article) might not be entirely accurate? Just asking. SEE: Markus MB. 2022. Theoretical origin of genetically homologous Plasmodium vivax malarial recurrences. Southern African Journal of Infectious Diseases 37 (1): a369. https://doi.org/10.4102/saj....
On 2022-07-25 08:51:05, user Abdullah A. Al-Shammari wrote:
This study has been published. The published version of this manuscript can be found here
On 2022-07-26 03:01:00, user Phil Pellett wrote:
This is an interesting and potentially important paper. It is worth noting that Yang et al. published a possibly related article in Journal of Infectious Diseases in 2019, “Evaluating for Human Herpesvirus 6 in the Liver Explants of Children With Liver Failure of Unknown Etiology” (PMID 30418598). I wrote an accompanying commentary (PMID 30496434). Searching Pubmed with "liver failure, hhv-6" turns up several other papers that connect to the subject. It seems prudent to expand the background of the paper to include mention of this literature.<br /> Best wishes,<br /> Phil
On 2022-07-26 17:55:22, user Matthew Whitaker wrote:
This paper has now been published in Nature Communications: https://www.nature.com/arti...
On 2022-08-01 17:42:19, user Nils Yang wrote:
Published at Lancet Child & Adolescent Health https://doi.org/10.1016/S23...
On 2022-08-03 13:35:17, user V Morris wrote:
Abstract needs editing for clarity, i.e., this "In all, 243 subjects were infected with COVID-19, of whom 97 had been wearing masks and 146 had not. " where no data on total number of people in studies is provided so it could be interpreted as masks not being very effective in preventing infection.
On 2022-08-13 14:11:20, user Vijay Iyer PhD wrote:
Thank you to all the authors for this contribution towards understanding Long Covid.
A first-pass set of comments on the manuscript:<br /> * Fig 3 has 10 subpanels (A-J) but the caption references 11 subpanels (A-K)<br /> * Acronym CVC in Fig 4 does not appear to be defined <br /> * The phrase "double positive CD4+ and CD8+" T-cells may cause confusion in the field. Manuscript appears to be referencing their IL-4/IL-6 positivity. Some ME/CFS researchers (Selin & Gil) have meanwhile found hybrid CD4+CD8+ T-cells, which they also refer to as "double positive".<br /> * No commentary is given wrt why Galectin is chosen for the suggested "minimal set" of biomarkers over the various CCL & LCN markers with higher spearman rho wrt LCPS<br /> * Some commentary may be warranted of any lower significance distinction between the HC & CC cohorts with your models. There appears to be weak separability based on cortisol in Fig 6F. This may be a small hint towards the possibility of subclinical LC.
On 2022-09-14 16:39:34, user Dr. Amy wrote:
In press https://pubmed.ncbi.nlm.nih...
On 2022-09-22 05:17:40, user Mehrdad Pedram wrote:
A peer-reviewed version of the above article has been E-published online ahead of print by the Journal of Autism and Developmental Disorders back on February 27, 2022:
https://link.springer.com/a...
Panahi Y, Salasar Moghaddam F, Babaei K, Eftekhar M, Shervin Badv R, Eskandari MR, Vafaee-Shahi M, Pezeshk H, Pedram M. Sexual Dimorphism in Telomere Length in Childhood Autism. J Autism Dev Disord. 2022 Feb 27. doi: 10.1007/s10803-022-05486-2. Epub ahead of print. PMID: 35220523.
On 2022-09-29 15:48:37, user Gabriel Costa wrote:
Update: The work can now me cited in BMJ EBM. https://ebm.bmj.com/content...
The abstract is published but not the full paper, we're still working on ramifications of the main analysis.
On 2022-10-10 15:27:53, user Brian Mowrey wrote:
"We do not interpret the associations between vaccination and long COVID here as causal, as we fail to fully account for two important conditions: unconfoundedness and latent variables."
Too bad this is not what will be reported.
This is a nicely-designed paper, but even with the adjustment it seems hazardous to compare a Delta-infection-heavy unvaccinated cohort with an Omicron-infection-heavy vaccinated cohort. It would be nice to see unadjusted, but time-segregated results here.
And while the adjustment *may* reduce the risk that this skew is reflected in the results, it diminishes the relevance for the vaccinated. Most so-called breakthrough infections are Omicron infections. So the specific Long Covid Efficacy for Omicron should be shown.
Likewise for age group - is the protective association consistent for young and old, or is only the latter powering it? Again, it would be nice to just see the unadjusted, age-segregated results. But there's no apparent raw data to allow the reader to parse this (eTable 7 doesn't distinguish "With Long Covid" by vax status.
On 2020-07-15 17:27:42, user Nicholas DeVito wrote:
The authors identify this trial as NCT04438629.
This registry entry is available here: https://clinicaltrials.gov/...
This entry does not mention treatment with Baricitinib at all. Can the authors please update their clinical trial registry entry to accurately reflect the treatments under consideration in this study?
On 2020-07-17 00:16:55, user NickSJ wrote:
So as I understand it, these were all already hospitalized patients, and there is no mention of using zinc in conjunction. In the NYU study, hospitalized patients who used a combination of HCQ and zinc were 44% less likely to die, but on HCQ alone, there was no significant difference in mortality.
On 2020-07-17 15:30:31, user Kamran Kadkhoda wrote:
Great study! This has implications for vaccines; we already know people lose Abs in early convalescence... see : Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections...in Nature Med.
On 2020-07-18 10:11:08, user Richard Harrison wrote:
Much to discuss in this paper, including whether the hypothesis of a uniform prevalence across the country is consistent with more plentiful new confirmed cases data at LTLA level (showing significant variations in rates even in May), confidence limits on estimated R, possible self selection bias (related to low response rate), apparent differential response rates, and implications of high false negative swab rates for Test, Trace and Isolate strategy. Useful confirmation of a number of things, including high pre-/asymptomatic %, significant % of children infected and high infection rate of care home workers, with important recommendation for continuance of 'social distancing' measures.
On 2020-07-18 11:46:21, user Benjamin Kirkup wrote:
Could you address the observations [ie. https://www.medrxiv.org/con...] of viral loads up to 10^11 viruses per ml saliva?
On 2020-07-18 12:58:04, user Anand Srinivasan wrote:
I understand that the risk calculations are done with the assumption of 1E8 RNA copies per mL of viral load in the saliva. I would like to know whether the risk estimates are directly proportional to the viral load (whether linear or non-linear dependency). Also, if the viral concentration in the saliva is lower by two orders of magnitude (1E6 RNA copies per mL), then what will be risk for the same conditions described in this pre-print? <br /> Thanks and Regards.
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?
On 2020-07-21 02:10:17, user Paul Gordon wrote:
Hi, thanks for posting this. I see that this is in press at JCM, congratulations. Might it be worth noting that the described mutation occurs not just in the 8 described genomes in the manuscript, but also these 7 in GISAID?
Belgium/rega-0423297/2020 <br /> Belgium/rega-0423298/2020<br /> Belgium/rega-0423299/2020<br /> Belgium/rega-0423300/2020<br /> Belgium/rega-0423301/2020<br /> Belgium/rega-0423302/2020<br /> Belgium/rega-0423303/2020
Or is this a resampling of some of those same genomes? Thanks for any clarification you can provide.
On 2020-07-21 11:21:52, user Hagai Perets wrote:
This study: https://arxiv.org/abs/2007.... might explain these results. If a preceding strain provided immunity and began elsewhere in China, one would expect a correletion with two positions - one direct (Wuhan) and one inverse with the origin of the preceding strain.
On 2020-07-21 16:01:20, user OxImmuno Literature Initiative wrote:
On 2020-07-21 21:34:31, user Deborah Verran wrote:
Interesting development. Although a systematic review on this topic may be of interest the constraints posed by resorting to summarising the already published literature may limit it's utility in practice. Other groups of professionals are now undertaking the process of developing and posting guidelines in order to assist clinicians who are being faced with making decisions on such patients during the pandemic https://journals.lww.com/jb...
On 2020-07-22 09:51:25, user Peiying Hong wrote:
what was the spiked SARS-CoV-2 in the recovery test? Is it the gene product or actual SARS-CoV-2? Given that the wastewater may contain SARS-CoV-2, how can recovery efficiency be determined without accounting for those SARS-CoV-2 that are already present in the sample?
On 2020-06-23 08:22:43, user Julii Brainard wrote:
108-102 = 6. 6/108 rounds to 6%, so OR 0.94 is correct as change in risk from no exposure to exposure (exposure = wearing masks). We checked all the raw case/sample numbers using ITT and the numbers are correct so the OR & 95%CI are correctly calculated for primary prevention RCTs. -Dr. Julii Brainard, UEA