On 2021-12-06 16:24:28, user Hank Black wrote:
What cycle levels were used in the PCR tests that were used to determine infections? If those levels we’re above 24, then this paper is irrelevant. If the authors can identify people who had symptomatic Covid disease, and compare that number to current persons symptomatic with Covid disease from the new variant, then this paper might have merit.
On 2022-06-18 09:09:00, user David Escors wrote:
The preprint is still a work in progress before submitting it for publication. It has an error in the definition of the cohort and in Table 1. The correct statement defining the cohort previous to the correction of the manuscript would be :"The majority of patients were smokers, 75% male and the mutational status of the tumors was not evaluated in 96.4% of the patients".
On 2020-04-06 11:27:18, user Eleanor Johns wrote:
"Conclusion: The SARS-CoV-2 prevention needs to focus on the screening of asymptomatic patients in the community with a history of contact with the imported population, especially for children and the elderly population." 28% of infected COVID19 individuals are asymptomatic, as PCR and Antibody testing covered a wide population in a Chinese province. We must test EVERYONE.
On 2020-05-17 16:22:51, user Sinai Immunol Review Project wrote:
Main findings<br /> The impact of SARS-CoV-2 infection and subsequent COVID-19 disease in pregnant women at different trimesters is not well described. The precise influence of a potentially dysregulated antiviral response to this pathogen during pregnancy is unclear, so a better understanding would guide management for pregnant women, who may be more susceptible to infection. Here, Hosier et al. profile a case of a woman with COVID-19 in the second trimester of pregnancy with severe hypertension, elevated liver enzymes, and coagulopathy. These symptoms led to a diagnosis of severe preeclampsia.
The patient initially presented with a high fever, non-productive cough, nausea, diarrhea, diffuse myalgias, anorexia, and malaise. A RT-PCR test for SARS-CoV-2 RNA in a nasopharyngeal swab of the patient was positive. Upon admission, the patient was treated for hypertension, disseminated intravascular coagulopathy, and she eventually elected to terminate via dilation and evacuation. During surgical management and recovery, the patient developed lymphopenia, though she was able to be extubated and weaned to room air on post-operative day 1. The patient was given hydroxychloroquine. Two days later, her coagulation markers improved, and she was discharged.
RT-PCR and sequencing and phylogenetic analyses showed that the placenta and umbilical cord were positive for SARS-CoV-2 RNA, but no other major fetal tissues tested positive. Saliva and urine, collected from the patient, also tested positive, although the oral and nasal swabs did not. Whole genome sequencing of the viral genome isolated from the placenta was phylogenetically similar to those isolated from local cases of SARS-CoV-2 infection and those identified in Europe and Australia.
Serologic testing for patients' antibodies revealed high titers of anti-SARS-CoV-2 IgG and IgM antibodies. These levels were reportedly the highest of the 56 COVID-19 patients admitted to the Yale New Haven Hospital, suggesting that the patient was not unsuccessful in eliciting a humoral response.
Gross pathological examination revealed a marginally adherent blood clot, presenting as a focal placental infarct, while histological analyses using CD3 and CD68 as markers revealed an infiltration of T cells and macrophages, which suggests that fibrin-dense intervillositis may have contributed to the coagulopathy observed in the patient. No necrotic tissue was seen. Immunohistochemistry staining for the SARS-CoV-2 spike protein and in situ hybridization for the SARS-CoV-2 RNA revealed that the infection of fetal tissue was localized preferentially to the syncytiotrophoblasts of the placenta.
Electron microscopy confirmed the presence of viral particles (75-100 nm in diameter) in the cytosol of placental cells.
Limitations<br /> Technical<br /> This report profiles a single patient to describe the impact of COVID-19 in pregnant women. Without a larger sample size, it is difficult to assess, however, how infection or peak disease at a given trimester differentially influence prognosis and clinical outcome. It is also important to note that this patient was diagnosed with an underlying autoimmune disease, psoriasis. It will also be important for future studies to consider the stage of pregnancy and whether COVID infection leads to other pregnancy-related disorders, such as recurring miscarriage, fetal growth restriction and possibly even increase in size of fetus creating challenges for delivery.
Biological<br /> Finally, it is unclear whether these placental cells express the ACE2 receptor. Though electron microscopy, among other methods, identified viral particles in placental cells and indicated SARS-CoV-2 infection of the placenta, the authors did not demonstrate that the syncytiotrophoblasts expressed the ACE2 receptor, which has been shown to be the target of SARS-CoV-2 viral entry into host cells.
Additional considerations<br /> The immunology of pregnancy is not static - the myeloid and T cell repertoire of the placental micro-environment is dynamic throughout the different trimesters. For instance, during the first trimester, trophoblastic cells secrete cytokines and chemokines that promote the recruitment and infiltration of circulating monocytes, neutrophils, NK cells, and T cells (1,2). This trafficking is essential, and disruption of any elements of this signaling axis results in poor pregnancy outcomes (1). Notably, NK cells and monocyte-derived macrophages are responsible for decidual vascular and tissue remodeling (1,2).
The second trimester, however, is described as an anti-inflammatory stage, characterized by the induction of regulatory T cells by decidual CD56brightCD16- NK cells and monocyte-derived macrophages. Interestingly, a population of TH17 cells are also present and expand during the second trimester (1). The third trimester is then marked by a return to an inflammatory phenotype (1). It is unclear how these differential states are influenced by an antiviral response to SARS-CoV-2 infection. The authors reported the presence of macrophages and T cells, but a lack of more specific stains and analyses make it difficult to precisely characterize the immunological anomalies of the placental micro-environment in pregnant women with COVID-19. The role of decidual NK cells is likely to be especially important, given their role in trophoblast-mediated immune modulation during the different trimesters of pregnancy and their role in the antiviral response to viral infections.
Significance<br /> Hypertensive disorders, like preeclampsia, in pregnant women increase the likelihood for complicated pregnancies, and recent studies of the field suggest that dysregulated immune activity may partially be responsible for these outcomes. The trimesters of pregnancy exhibit different immune landscapes, so the presence of certain microbes, including viral pathogens, is likely to perturb homeostatic immune processes that are required for a normal pregnancy. The impact of SARS-CoV-2 infection, therefore, warrants its own investigation, as the health outcomes of COVID-19 are especially poor. The authors report direct infection of the syncytiotrophoblast by SARS-CoV-2. These cells are derived from trophoblasts, which play an important immuno-modulatory role in all three trimesters of pregnancy. So, collectively, given the role of the ACE2 receptor as the target of SARS-CoV-2 viral entry and the involvement of ACE2 in the physiology of preeclampsia, the two pathologies likely share altered immune states and a dysfunctional renin-angiotensin-aldosterone system (RAAS) as etiologies.
This review was undertaken by Matthew D. Park as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn school of medicine, Mount Sinai.
References<br /> 1 Mor, G., Aldo, P., & Alvero, A.B. The unique immunological and microbial aspects of <br /> pregnancy. Nat. Rev. Immunol. 17, 469-482 (2020).<br /> 2 Yockey, L.J., Lucas, C., & Iwasaki, A. Contributions of maternal and fetal antiviral <br /> immunity in congenital disease. Science. 368, 608-612 (2020).
On 2020-06-05 22:06:31, user K Jane wrote:
I think everyone should replace the word antigen with .... Protein or pathogen.?
On 2021-01-29 22:05:04, user José Raymond Herrera wrote:
It's about the predictable anti-inflammatory effect of Colchicine. I don't know if it's better than Dexamethasone already proved useful in those cases. In any event, we're talking about cheap drugs not promoted by big pharma...
On 2021-09-12 01:11:27, user Tracy Beth Høeg, MD, PhD wrote:
If the entries stated they were currently COVID+ they were excluded.
On 2021-09-10 19:50:39, user Roger Seheult wrote:
Were you able to exclude the subjects from VAERS based on SARS-CoV-2 positivity? Was it even known if they had tested positive for SARS-CoV-2?
On 2022-01-14 15:44:35, user Jordan Taylor wrote:
There are at least three major issues in this paper.
The first is a technical issue and probably the most obviously fatal flaw. It was first pointed out (that I could see) by Shih-Hao Yeh, and I think deserves re-emphasising. The authors have badly miscalculated the COVID19 hospitalisation risks for children conditional on comorbid status. They cite a 120 day hospitalisation rate (during moderate viral prevalence) of 255/million children. They note that the hospitalisation risk is 4.7-fold higher for children with comorbidities than for those without. How do we calculate the risk for each subgroup then? In this case, we are told 70% of those hospitalised have commorbidities and 30% do not, so for each 255 hospitalised, 0.3*255 = 76.5 will be healthy and 178.5 will have commorbidities. We can't stop there though as we need to adjust for the size of the background healthy and comorbid populations, which the authors tell us is 67% and 33% respectively. To get rates per million we have 76.5/0.67 = 114.2 among the healthy and 178.5/0.33 = 540.9 among those with comorbidities. They seem to have come up with the 44.4/million and 210.5/million figures based on the assumption that the two have to sum to 255/million, which is just not how it works at all. A basic sanity check should have been "should the risk in the high risk group really be lower than the overall risk?" If the rate of gun deaths is 100/million in the military and 1/million in civilians, you don't just add them together to get an average population gun death rate of 101/million!
The second is more conceptual. The comparison is between a risk from vaccination conditional on vaccination with a risk from infection which is not conditional on infection. In other words, the paper does not answer the question: what is the myocarditis risk of a vaccinated child versus the hospitalisation risk of an infected child? Instead it rather tries to answer the question: what is myocarditis risk of a vaccinated child versus the COVID hospitalisation risk for an average child over a 4 month period at X prevalence rate. Given that the pandemic has already been going on for 2 years now and shows no signs that it will simply disappear, this strikes me as an inappropriate choice.
Another issue is how the claims in the conclusions compare to the data. The authors state that for "boys 12-17 without medical comorbidities, the likelihood of post vaccination dose two CAE is 162.2 and 94.0/million respectively..." (emphasis added) and that this "exceeds their expected 120-day COVID-19 hospitalization rate at both moderate (August 21, 2021 rates) and high COVID-19 hospitalization incidence." However, at no point in the text, data, methods, or the Study Profile supplement (S2) of the paper is a stratification of CAE rates by comorbid status provided. In fact, although they did not provide any code, I was broadly able to reproduce their VAERS myocarditis counts in 12-17 year olds from 01/01/2021-06/18/2021 using the criteria they provide*, and that was without adjusting for comorbidities. So it seems likely to me that they have not separately analyzed "healthy" and comorbid patients and thus have no basis for making claims about effects of vaccination on "boys without medical comorbidities".
If as seems likely they have compared CAE rates among both healthy and unhealthy children with COVID19 hospitalisation rates among only healthy children, this is a big problem. The authors should be challenged to stratify their analysis equally for both COVID19 hospitalisation and vaccination before this paper is actually published.
*I found 277 cases matched the original criteria, however, this was with a number of likely duplications and possibly other data entry erros; as mentioned, the authors' methods were pretty inadequate so we have no way to see whether or how they have cleaned the data.
On 2021-04-12 05:38:07, user ICUC wrote:
What were the results of these breakthrough infections? Were the symptoms severe? Did anyone need hospitalizations? Was there any death?
On 2021-12-21 21:03:38, user Mike B wrote:
Fantastic early news on boosting to increase circulating antibodies to provide Omicron protection. I hope we see a matching case study to correlate clinical data. Although the author declared the limitations regarding waning, it is critical to determine the waning pattern of boosted response.<br /> Taking "likely to be similar" as a starting point, the data appears to show significant loss of circulating antibodies 6 months post vaccination. This a critcal clinical issue in the USA because the high number of elderly/institutional vaxxed early in 2021 and subsequently boosted in Aug/Sept timeframe to enhance protection against Delta. For this highly risk population, boosted protection may already have significantly waned leaving less than expected protection just as Omicron begins to dominate. Without data on waning attached, the study may set false expectations of protection and open questions on continued booster use. <br /> One way to ameliorate the issue is to extend the study, collect samples pre and post a 4th dose at 50 and 100 micrograms. Thus will settle discussion and improve application towards clinical use.
On 2020-10-23 06:01:42, user Martijn Hoogeveen wrote:
Pre-proof is nu online https://authors.elsevier.co...
On 2021-12-06 14:07:04, user Steven Sampson wrote:
Why hasn't this been peer reviewed?
On 2021-09-21 09:06:34, user Muhammad Yousuf wrote:
Notwithstanding the comments this preprint is generating, it would also be interesting to compare three groups in this study with another group who were COVID-19-naive but received 3 doses of Pfizer's vaccine including a booster dose. If the immunity and protection against SARS-CoV-2 is still higher in infected plus vaccinated compared with those having three doses of COVID-19 vaccine, this will indicate that there is immune memory (1) through bone marrow plasma cells at play.
On 2021-09-04 19:09:42, user Ben Veal wrote:
As a qualified statistician who's been doing this stuff for over 20 years, and has worked on several medical studies I think I ought to add my voice to the crowd.<br /> There may be a few things that aren't fully accounted for such as the false positive rate for PCR tests, or unbalanced populations due to deaths of highly vulnerable members of the pre-infected group, but they should not alter the conclusions much. As mentioned by others the false positive rate for PCR tests would have the effect of biasing the risk ratio downwards, not upwards, so we should expect the effect to be even stronger than reported.
As for the potential drop-out issue due to deaths of highly vulnerable people among the pre-infected group; this would only be a problem if there are some unaccounted for cofactors causing that high vulnerability. If this is the case then we can approximately correct for the imbalance by estimating the number of deaths in the pre-infected group based on the known infected mortality rate. <br /> I have done that calculation (see link below), and get a lower bound estimate for the 95% confidence interval of [4.3,11.23] which is still significant.<br /> However, it could make a big difference to the risk of hospitalization (again assuming there are some important cofactors unaccounted for).<br /> https://www.facebook.com/ec...
Another criticism I have read in these comments is that they should have used a conditional model (https://en.wikipedia.org/wi... "https://en.wikipedia.org/wiki/Conditional_logistic_regression)") to account for the matching. Actually a conditional model is used when there is unequal distribution of the treatment groups (pre-infected & vaccinated) within each strata (age, gender, socio-economic status & geographic region), and you are unable to use covariates to control for this. But the matching that they did ensures that this isn't the case. Furthermore they control for all but one of the strata (geographic region) with covariates.
So, overall I trust the overall conclusion; natural immunity from pre-infection is better than vaccination, but not as good as natural immunity + vaccination.
This does not mean governments should put a halt to their vaccination programs since that's obviously going to result in more deaths among the vulnerable, but perhaps it might be wise to reduce the vaccination rate among the less vulnerable people (i.e. young healthy people) so that they can build up natural immunity and be better prepared to fend off new variants from spreading through the population. In fact it ought to now be possible to estimate the optimal proportions of vaccinated & unvaccinated that would result in the lowest risk of contagion spread, given that we can expect to see this virus reappearing every year.
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 2021-09-08 09:07:35, user Kenneth Coville wrote:
As mentioned below the study has many flaws that impact its use for public policy. But that aside even if you accept the study findings the findings were that recovered individuals who forego vaccination are twice as likely to be re diagnosed with Covid as those recovered individuals who obtain vaccination.
Your final para demonstrates one of the biggest problems of the study that the authors can not control that is, the misinterpretation of the results to support a predetermined position.
I support your right to choose on vaccination and at the same time fully oppose the attempts to use studies such as this to justify that choice. The study in fact demonstrates the importance of vaccination to prevent disease, death and economic consequences.
On 2021-08-27 06:06:45, user joseph harrison wrote:
I wonder how this study accounts for people who died from infection from covid, considering that people who die from covid may have some defect in immune response, which has been documented in serveral studies. These immunocompromised people are effectively removed from the infected pool but are still present in the vaccinated pool, where they may not have as strong of an immune response to the vaccine. Furthermore, we are talking about a relatively small increase in breakthrough infection rate 13%, or the difference between a 30% or a ~35% chance. While the study seems well done and interesting to evaluate, I am dissappointed to see it linked on drudge with a headline natural immunity is better than the vaccine, when there are many other ways to potentially explain the small increase in protection from breakthrough infections.
On 2021-10-16 15:36:50, user Alex wrote:
Clearly there are some very logical arguments here and whilst I think it’s absolutely logical that having had COVID is the best defence against COVID and as the virus is in the environment so we are likely to encounter it again can someone tell me why vaccines are effectively being forced on people and recommended for children even though a large number have had the virus and to date is very low risk?
On 2021-09-16 15:11:24, user USA Bottom Line wrote:
Nice analysis. Thanks for presenting it here. Three things to add:<br /> 1. Survivorship bias would exclude people who've died from any cause, the virus, the vaccine, or a third unrelated cause. It would also exclude people who've moved out of the country and possibly those who've become incapacitated. Survivorship bias is not relevant to the results of the study though. It's only relevant to the risk of either getting Covid-19 or getting vaccinated. Once someone has been infected or vaccinated (the vast majority of the Israeli population), it's no longer an issue.<br /> 2. False positives on the initial test for previous infection would bias the results in favor of vaccination. There was no symptomatic requirement on the initial test.<br /> 3. As others have pointed out, it's an open question whether previously infected or vaccinated people would be more likely to seek out future tests. Both groups had reason to believe they were immune, so would have been less likely to get tested for any minor symptoms. The fact that hospitalizations all swing in the same direction and magnitude as the rest of the outcomes is strong supporting evidence for the rest of the outcomes.
On 2021-08-28 22:44:31, user Business wrote:
Have you considered comparing Covid-19 naïve vaccinated vs unvaccinated and Covid-19 previously infected vs Covid-19 naïves?
Also, is the data available for further analysis?
On 2021-09-17 08:01:48, user 4qmmt wrote:
Good points and well said. I am not sure about your statement " it is likely that asymptomatic or lightly symptomatic natural infections that have symptoms more mild than the typical 1 day dose 2 side effects of myalgia, fatigue, chills/fever, etc., will result in lower protection than the vaccine. "
An alternative to your hypothesis is that those with mild symptoms are already well-immunized. An alternative to asymptomatic is of course, mistakenly interpreting a positive PCR as an active infection.
On 2021-09-06 10:07:40, user Erwin Stark wrote:
As the group of previously infected only consists of survivers, there may be a selection bias excluding those having weak immunity
On 2021-12-17 02:13:00, user Stoichastic wrote:
It's a great question, and is known as OAS - original antigenic sin.
The hypothesis is your first (original) exposure to a pathogen and subsequent immune response (antigenic) will be used in perpetuity for that pathogen and related, slightly mutated variants (sin).
The amazing thing about the immune system is it's not only antibodies. It starts with the innate immune system, and there are so many additional components to the adaptive immune system where antibodies kick in, that vaccine influence - and this is only my opinion now - won't really matter in the grand scheme of things.
Trust your immune system. If you're fit and healthy you are probably going to be 100% fine.
Just don't expect the vaccine to prevent infection or transmission - things they were never designed to do. As indicated by Pfizer's own end points noted in their trial documents.
On 2022-12-15 21:37:06, user Yiwen Zhu wrote:
This paper has now been published in Neuroscience & Biobehavioral Reviews Volume 143, December 2022, 104954 (doi: 10.1016/j.neubiorev.2022.104954). Please update the link if possible, thank you! <br /> - Yiwen Zhu
On 2020-04-13 11:38:17, user Sanjiv Vij wrote:
Thank you. My concern is that 205 patients is too small a number and 7 days is too early to be reliable. Will it be possible to get more data from the registry, and, have data that spans admission to death or discharge for as many patients as possible? With regards to how many were on ACE / ARB / Immuno-modulating drugs / Neither[none]. That will help in risk stratification in a more reliable way. Regards Sanjiv
On 2020-09-07 18:33:30, user Sunil Bhopal wrote:
I have read the methods section several times and can't find any description of the tool or administration method for asking about these symptoms. Was this retrospectively done? At what time point? What was the recall period? Who asked the questions? Were they free-answers or multiple choice and so on. My apologies if this is already written up but I can't see it. Best wishes, Sunil Bhopal
On 2020-02-10 08:17:02, user zjuliu wrote:
Firstly I think this should be a milestone for 2019 NCov research because of the work from Academician Zhong and his colleagues. But one thing I need to point out: this paper included patients from Wuhan, Hubei (except Wuhan) and other cities except Hubei, but as we know, it is very different on epidemiological trend, mortality etc when compared with these cohorts. Therefore, I think it is worthy to share this trend on public database so that the scholars can better use these data for further study.
On 2022-12-04 06:38:01, user Jianyu Lai wrote:
This manuscript is now published in Microbiology Spectrum. DOI: https://doi.org/10.1128/spe...
On 2022-01-09 16:15:33, user Greg wrote:
Here is my big bone with the study. The OR given for Omicron susceptibility is 1.04 for the unvaxxed, suggesting that the double-vaxxed were pretty much equally susceptible. Reading the Method, however, it stated that they counted the vaxxed with one dose as unvaxxed. What?! Would that not mean the true unvaxxed were less susceptible to Omicron? Likely!
Also, with vaccine protection waning rapidly, and even for the boosted, it would've been nice to know how vaccination timing was affecting susceptibility. This study did not consider that. Interestingly, the other prior Danish study suggested that after a few months of being double-vaxxed, there was a net negative protection against Omicron.
On 2020-03-21 16:42:23, user Nick wrote:
I attempted to reproduce Tables 2 and 3 (R code included at the end of the post), and obtained these results:<br /> `Table 2, Day 3: reported p=0.005, calculated p=0.0136<br /> Table 2, Day 4: reported p=0.04, calculated p=0.0780<br /> Table 2, Day 5: reported p=0.006, calculated p=0.0148<br /> Table 2, Day 6: reported p=0.001, calculated p=0.0019
Table 3, Day 3: reported p=0.002, calculated p=0.0019<br /> Table 3, Day 4: reported p=0.05, calculated p=0.0429<br /> Table 3, Day 5: reported p=0.002, calculated p=0.0025<br /> Table 3, Day 6: reported p<0.001, calculated p=0.0005`
That is, Table 3 was more or less reproduced, but Table 2 wasn't; most of my p values are around twice the ones in the preprint.
Of the 8 tests, 5 produced warnings because chisq.test() doesn't like cell values of 0 or 1. Using fisher.test() from the "stats" package got rid of the warnings and caused some of the Table 2 p values to move towards the ones in the preprint, but only one (Day 6) got close. It isn't clear to me why one would use Fisher's Exact Test here --- my understanding is that it is not sufficient to invoke per-cell numbers of less than 6, as many authors seem to do, but I don't have a reference to hand for that.
Code:<br /> `t2.d3 <- chisq.test(matrix(c(10, 10, 1, 15), ncol=2))<br /> cat("Table 2, Day 3: reported p=0.005, calculated p=", sprintf("%.4f", t2.d3$p.value), "\n", sep="")
t2.d4 <- chisq.test(matrix(c(12, 8, 4, 12), ncol=2))<br /> cat("Table 2, Day 4: reported p=0.04, calculated p=", sprintf("%.4f", t2.d4$p.value), "\n", sep="")
t2.d5 <- chisq.test(matrix(c(13, 7, 3, 13), ncol=2))<br /> cat("Table 2, Day 5: reported p=0.006, calculated p=", sprintf("%.4f", t2.d5$p.value), "\n", sep="")
t2.d6 <- chisq.test(matrix(c(14, 6, 2, 14), ncol=2))<br /> cat("Table 2, Day 6: reported p=0.001, calculated p=", sprintf("%.4f", t2.d6$p.value), "\n", sep="")
t3.d3 <- chisq.test(matrix(c(1, 15, 5, 9, 5, 1), ncol=3))<br /> cat("Table 3, Day 3: reported p=0.002, calculated p=", sprintf("%.4f", t3.d3$p.value), "\n", sep="")
t3.d4 <- chisq.test(matrix(c(4, 12, 7, 7, 5, 1), ncol=3))<br /> cat("Table 3, Day 4: reported p=0.05, calculated p=", sprintf("%.4f", t3.d4$p.value), "\n", sep="")
t3.d5 <- chisq.test(matrix(c(3, 13, 7, 7, 6, 0), ncol=3))<br /> cat("Table 3, Day 5: reported p=0.002, calculated p=", sprintf("%.4f", t3.d5$p.value), "\n", sep="")
t3.d6 <- chisq.test(matrix(c(2, 14, 8, 6, 6, 0), ncol=3))<br /> cat("Table 3, Day 6: reported p<0.001, calculated p=", sprintf("%.4f", t3.d6$p.value), "\n", sep="")`
On 2020-09-07 16:03:04, user Joe B wrote:
We don't know how long ago the vitamin D levels were obtained in these patients. This is especially true in the COVID patients, because we have no idea if they truly were "deficient" at the time of their infection. Additionally, you never tell us in the methods that you were going to examine supplementation, and how you were going to do that (and assure adherence). Can vitamin supplements not be purchased over the counter in the countries involved in this study? Finally, I assume you categorized people by "sex" and not "gender" as sex if the term used for male/female DNA based differences.
On 2021-08-03 14:16:09, user Dimich wrote:
Since the conclusion about the infections is based on PCR testing, it is pointless. PCR tests do not check if the person is infected or not, but confirm presence of SARS-CoV-2 genetic material in the sample, which may not be associated with the infection, but can be a randomly inhaled viruses or leftover of previous asymptomatic infection.<br /> Two references on PCR testing subject:<br /> https://www.nejm.org/doi/fu...<br /> https://www.journalofinfect...
On 2021-08-12 16:15:34, user pedro paulo castro wrote:
I would say DEATH is a crucial component of the relative risk of intervention, and therefore instances of death should be more appropriately parsed, don't you think?
On 2021-08-11 18:43:00, user questionable02848 wrote:
I am interested in seeing a similar study done on Recovered versus Vaccinated cases over some years. It is **theoretically** possible that Recovery (despite original virus death rate) confers greater defense than Vaccinated (despite lower original virus death rate) because Recovery forms a superior, longer-lasting, or greater-breadth immune response. This is important to consider for coronavirus specifically due to its tendency to mutate. The studies I have seen indicate that the Recovered do have a greater immunity than the Vaccinated, as studied here: https://www.biorxiv.org/con...
And so, if Recovered do in fact fare better when exposed to mutations, we really want to know this before we vaccinate the young, who do not face a statistically significant threat from coronavirus but have many years ahead of them facing its mutations.
On 2021-08-01 20:08:35, user Billium wrote:
After six months monitoring >45,000 patients, there were 14 deaths in the placebo group and 15 deaths in the vaccine group. This not only demonstrates lack of efficacy in the most important endpoint, but highlights the extremely low fatality rate of Covid-19 in most people.
On 2020-10-27 03:23:50, user Anonymous wrote:
Great analysis and synthesis of ideas pertaining to EV isolation. The utilization of EV-like liposomes are certainly supportive of the argument for NBI methods and back-up the validity of that isolation method. The only source of confusion I encountered were the error bars in the figures being quite variable in relation to the claimed increased or decreased biomarkers without much note of their presence. In a clinical setting, can one truly indicate a difference between ALS and SBMA, for example, if data pertaining to EVs/biomarkers tend to fall within those error bars? What is the implication here for misdiagnosis?
On 2020-04-22 12:29:26, user rupesh chaturvedi wrote:
Well immunity is outcome of humoral immune response. In these model authors assume that all the subjects infected with virus would generate a sustainable and durable IgG response. Where is data? Do we have data to show after infection how much immunity is generated? <br /> Please see a recent study from China. If 30% do not have antibody response then the at best case we will reach below 70%. I do not not if that will be really a Herd Immunity.<br /> Biological phenomena based models need to adjust the dynamics for the variables of biological process. A linear models should not be used to make policy decision unless backed up by understanding of biological events.<br /> Rupesh
On 2020-08-21 13:38:24, user Susan Levenstein wrote:
If I understand the paper correctly, its most striking result is the isolation of Patient 1's virus from the VIVAS air sampler located 4.8 m away. But according to the Figure, Patient 1 had to walk right past that air sampler, closer than 1 m, every time he went to the bathroom. Couldn't that be a simpler explanation for how it picked up his virus?
On 2020-07-12 18:19:53, user Doug Vaughan wrote:
Very interesting study. PAI-1 provides a site of convergence for risk (age, obesity, diabetes) and mechanisms driving thrombosis (inflammation, activated renin-angiotensin system, endothelial dysfunction) in patients with COVID-19. Failure of the endogenous clot-dissolving system is most likely a key contributor to morbidity and mortality as demonstrated here. Just last week, we secured an IND from the FDA to begin testing of a novel orally-active inhibitor of PAI-1 (TM5614) in high-risk patients with COVID-19. This Phase 2 study will enable the first use of this drug in USA.
On 2021-09-20 08:53:46, user NMN wrote:
"Where is the proof the delta variant was isolated?"<br /> They never claimed that they isolated the delta variant, so this question seems a bit silly.<br /> They sequenced the virus in the initial sample, and found that they could "culture a virus" from the sample (that is, there was a progressive cytopathic effect).<br /> Are you really asking where is the proof that they were culturing virus from the samples?
On 2021-08-24 05:00:47, user Crawdaunt wrote:
The nice figure looks nice. But uploading the raw data used to generate it would be great.
On 2021-07-26 03:48:27, user George Orwell wrote:
Carvallo study showed that PPE alone was ineffective at preventing PCR positive cases among HCW. 58% of HCW tested weekly over 2 months tested positive.
On 2021-09-17 16:27:49, user Daniel Keyes wrote:
I commented previously that the apparently long delay in peer review is understandable, and typical for many journals. However, given the extremely high profile of this article, it should have been considered for expedited review. Now even "regular" review seems to be taking rather long. This could be due to reviewer delay, reviewers or editors requiring a large number of changes, or it may even reflect a general reluctance to publish an article with this conclusion.
On 2021-09-01 12:20:26, user Jack Roberts wrote:
There is NO peer reviewed study on benefits of getting a vaccine when previously infected. ONLY PEER REVIEWED studies that show people who have had the virus have long lasting immunity.. Some say lifetime.
On 2021-12-31 14:09:18, user Allan Randrup Thomsen wrote:
Any publish evidence that ADE augments infection? To my knowlegde, it only affects pathology/severity cf. Dengue. ADE primarily incereases infection of Fc receptor bearing cells, are sufficient numbers of these cells found in the upper respiratory tract to substantially participate in augmenting the infection? I doubt it considering the availability of ACE2 receptors on epithelial cells in this region.
On 2022-01-04 01:55:09, user HenkPoley wrote:
The people who go to test, are people who have symptoms, or had contact with infected people. So their positivity percentage is much higher than the general population.
If all of Ireland had symptoms or were in contact with an infected person. Then your false "100% of the population is infected within a week" statement would be true.
In reality not all the Irish are currently sick. And most of those who are not sick do not get a test.
On 2020-02-13 05:13:34, user Ogi Dido wrote:
Singapore has special case of transmission. There are meeting of one company that some one as carrier spreading the virus to other meeting member. That's why Singapore evident is higher than the model prediction. meanwhile for Thailand the evidence below the model. It seem the model must be corrected again, excluded Singapore or give a note. Also for Japan recent days there are outbreak in two cruising ship,
On 2020-11-14 04:23:20, user Rich Kibbee wrote:
Error, this pdf lists a Centricon 70 Plus 100 kDa filter ...the first version lists it at 10 kDa.
On 2021-11-04 07:51:30, user kdrl nakle wrote:
Pretty much a nail in the coffin for international use of Sinovac vaccine unless it is for free.
On 2020-04-08 23:11:42, user stephen zhang wrote:
Now published in Psychiatry Research. Check it out:
On 2021-04-28 10:31:51, user Steve Winter wrote:
In terms of Altmetric attention score, this potentially includes both positive and negative comments on social media. Did you account for this in your analysis? This is an important limitation when it comes to interpretation of Altmetric scores, and could be discussed in your manuscript.
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 2020-06-28 14:17:39, user Munir Hazbun wrote:
Congratulations with your results . We have published in Critical Care Exploration very encouraging results with a higher dose of MP. We learned early that at high dose MP work very well for rescue we have not have any prone position need and outcome are about 10% mortality in about 60 patients so far. Certainly optimal nursing and respiratory strategies are necessary for example we are not using propofol and use recruitment lung strategies
On 2020-06-29 05:59:53, user Andrew Craigie wrote:
Many of the confounders listed are known or suspected to be associated with low vitamin D, including ethnicity, obesity, diabetes, old age and deprivation. Adjusting for these will therefore incorrectly mask out the relationship between Covid-19 severity and low vitamin D. It's a bit like concluding that high sugar intake is not associated with early death after adjusting for confounding factors like obesity, diabetes, heart disease & tooth decay.
Using 10 year old vitamin D level data also renders the data meaningless. More relevant is what each patient's vitamin D level was at the point of diagnosis, and this is the data we should urgently be gathering to evaluate the relationship.
On 2020-05-26 07:22:53, user Yashawant Gothankar wrote:
The important thing to consider here is the author of the paper does NOT say that Ivermectin should be ruled out.
Positive outcome of this research would have been identifying what concentration/dose can work to counter covid19 infection in humans.
Ivermectin is one of the most promising candidate currently under investigation world over.More data is expected from human trials being conducted.
Some of the most interesting results and progress is coming form human trials conducted in Bangladesh using combination of Ivermectin and Doxycycline . It looks like BD doctors have figured out the Ivermectin doses need to be administered for human trials.
Refer following links:
https://www.ibtimes.sg/mira...
On 2021-06-07 12:30:38, user UNG wrote:
Covishield vaccine is essentially spike protein, while Covaxin was whole virus. I don't understand why the antibody titre was measured against only spike protein? also one should used multiple brand kit (at least two) to get the fair idea of the antibody titre.
On 2020-08-24 17:31:53, user Mercer Creed wrote:
Where is the information regarding controls?
On 2020-04-17 18:38:09, user Marm Kilpatrick wrote:
Can you please provide a more detailed breakdown of the ages of those sampled and the general pop? Grouping 19-64 year-olds obscures a potentially enormous amount of variation. It's also not clear why you didn't adjust estimates for age. The justification appears to be that your sample sizes were too small. Without adjustments for age it's not clear how one can make an accurate estimate of fatality ratios given the substantial age effects for COVID-19.<br /> Can you also present the results by age group (with finer age groupings - e.g. decades or 5yr incements)?<br /> Could you also present results based on prior symptoms? It seems quite likely that individuals w/ COVID-19 symptoms would be more likely to be recruited into study.<br /> Could you report the sensitivity results for your known samples at Stanford by IgG and IgM like you present the manufacturer data? This would help the reader understand the discrepancies.
Finally, it seems likely that socio-economic status of Facebook users and non-facebook users likely differs. It doesn't appear that you collected this data and yet it seems like it could significantly influence the results. Can you discuss this issue in Discussion?
Thanks!<br /> marm
On 2020-04-17 22:20:15, user Teddy Weverka wrote:
To take this test, people had to violate the ORDER OF THE HEALTH OFFICER OF THE COUNTY OF SANTA CLARA DIRECTING ALL INDIVIDUALS LIVING IN THE COUNTY TO CONTINUE SHELTERING AT THEIR PLACE OF RESIDENCE EXCEPT FOR ESSENTIAL NEEDS. What do you bet that people willing to violate that order have a higher prevalence of covid-19 antibodies? The paper ought to mention this source of bias.
On 2020-04-23 21:22:01, user erkin wrote:
I have listened to Ioannidis interview (April the 3rd one) and he even challenges the existing death numbers as inflated due to the psychological environment, he says like every death followed by a respiratory complaint is counted as covid without testing etc.
On 2020-04-25 01:20:57, user Brent Tharp wrote:
The CDC info shows that solely from confirmed cases, nearly 20% of those that have been tested are positive. That does not include asymptomatic people, who would rarely seek testing, nor would they be allowed to have a test given limited resources, nor does it include those who would have tested positive because the virus is no longer in their system (i.e., they would only test positive for antibodies). The real infection level is well over 20% now, just proving that the distancing measures have had virtually no impact on contagion, and further that this "killer" is pretty weak.
On 2021-02-01 01:14:00, user gogettem wrote:
Sam Moore is quoted in Telegraph as trying to justify extending lockdown post vaccination saying “The vaccines are not going be 100 per cent effective at stopping serious disease. So if you manage to get, say, 85 per cent of people to take it and it turns out to be 90 per cent effective, that's still 25 per cent of people who could die from it, which is a lot of people," But if the Case Fatality Rate for Covid is 1% overall and the most vulnerable will be vaccinated first, then the CFR for the 25% will be much less - let’s be pessimistic and say 0.1%. So only 0.025% could die from it. A lower rate than annual flu. Even at 1% the impact will only be 0.25%, still tiny. No way this can justify the carnage lockdown is inflicting on jobs, lives, people’s futures in the devastated private sector. How can we have any confidence in the response to Covid when we hear this kind of exaggerated fearmongering from those driving it?
On 2020-04-15 14:38:14, user Lawrence Mayer wrote:
I am very suspicious of articles that are data driven but do not allow us to see the data. Why aren't papers like this being submitted to peer-reviewed journals? They are guaranteeing two week turn around from submission to posted on line.
I suggest people interested in learning about what has been reviewed by at least one expert join our discussion group on clinical epidemiology and science. We are over 2000 clinicians and epidemiologists discussing the latest empirical results on Covid19
Lawrence S. Mayer, MD, MS, PhD<br /> Faculty Associate<br /> Harvard University<br /> Professor Emeritus of Public Health, Medicine and Biostatistics
On 2020-04-28 14:00:55, user Sinai Immunol Review Project wrote:
Main Findings<br /> This preprint sought to compare the daily deaths in countries using CQ/HCQ as a treatment from the beginning of the COVID-19 pandemic to those that did not. From a list of 60 countries in descending order by number of confirmed cases, 16 countries were selected for inclusion into either the high CQ/HCQ production or use group, versus not. Countries were included if they met the criteria for having data from the day of the 3rd death in the entire country and the daily deaths for the 10 days immediately following, until both groups were populated with a list of 16 (Figure 1: Table with the CQ/HCQ group list; Figure 2: Table with the “control” group list). For each group of countries, the average daily deaths were determined, and the curves projected to illustrate trajectories. In Figure 3, the author suggests that the deaths in the countries belonging to the control group follow an exponential curve, while the progression of average daily deaths in the countries with greater use of CQ/HCQ follow a polynomial curve.
The author then applies Auto Regressive Integrated Moving Average (ARIMA), a modeling tool used for time-series forecasting (i.e., predicting the future trajectory of data over time using the data from previous time points as predictors in a linear regression). The Auto Regressive component refers to each difference between two previous time points that make the model “stationary” (current – previous); the Moving Average is the number of forecast errors from calculating these differences that should go in the model. The author uses ARIMA to predict the next 10 days of mean deaths for the CQ/HCQ list (Figure 6) and the control countries (Figure 8). In figures 9 and 10, autocorrelations of residuals are performed to determine internal validity of the model, here defined as no significant autocorrelations.<br /> In conjunction, the author argues that these findings support major differences in death rates between countries that use/mass produce CQ/HCQ versus those that do not.
Limitations<br /> The title of this study refers to itself as an ecological study, an observational study in which the data are defined at the population level, rather than individual. Although this study design allows for rapid hypothesis testing in large datasets, a robust ecological study should account for as many known risk-modifying factors or confounders as possible. Subsequently, any results should be reviewed under strict criteria for causality, since there is high probability of the outcomes falling under the definition of ecological fallacy, which occurs when inferences about individuals are determined from inferences about a group to which they belong.
This study conflated the use and mass production of CQ/HCQ at the start of the COVID-19 pandemic in each respective country, with that country’s direct pandemic response. It is never explained whether use or production is the key output for any given country, which are vastly different metrics. The author fails to consider other reasons for having existing infrastructure for the mass production of drugs like hydroxychloroquine, whether the country was a global supplier of the medication (India), or is a region where malaria is endemic (India, Pakistan, Indonesia, Malaysia, South Korea), which may correlate to both chloroquine production and use. Notably, the countries from which studies of HCQ in the treatment of COVID-19 have been predominantly performed (China, France, USA), are all in the control list of countries. Additionally, the data for cases and deaths were collected from reports accessed from https://www.worldometers.in... data were not selected from the top countries using a methodological approach, but rather skipping certain countries to use only the most complete death data for the timeframe of interest, allowing for bias introduced by the reporting of each individual country.
With regards to the statistical methods applied, namely ARIMA, they are non-standard practices for interpreting the results of an ecological study. The first problem with this, in my opinion, is that the message will be difficult to interpret and criticize for many scientists, as ARIMA will be unfamiliar to most in the biological sciences. Further, the models applied (Table 4) do not take into account any confounders, which is a requirement for robust analysis of an ecological study. There are only 3 variables in this type of model: p, the autoregressive coefficient, q, the moving average coefficient, and d, the difference between points in the time-series. Any flaws or bias inherent to the input data are then upheld and propagated by the model, which does not allow for any other variable that would contribute to the risk of death.
Significance<br /> The faults of the stratification of countries into the groups proposed in this study, together with the unorthodox application of ARIMA modeling, make it challenging to accept the conclusion that the author draws in this study. The apparent decrease in death rate in countries with a high production/use/either/or of CQ/HCQ could be due to any number of other factors for which this study did not account. The top 5 countries in both confirmed cases and reported deaths are all in the control list, which has no relationship to the amount of CQ/HCQ production within those countries yet skews the data to make the dynamics of death rate appear more dramatic.
Reviewed by Rachel Levantovsky as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn School of Medicine at Mount Sinai.
On 2020-04-25 14:05:52, user Rosemary TATE wrote:
Hi, I dont see the STROBE guidelines checklist uploaded, although you ticked yes to this<br /> "I have followed all appropriate research reporting guidelines and uploaded the relevant EQUATOR Network research reporting checklist(s) and other pertinent material as supplementary files, if applicable. "<br /> A lot of people seem to ignore these but they are important and any good journal will require them.<br /> Can you please upload? Many thanks.
On 2025-03-06 13:21:04, user Matteo Pozzi wrote:
Here is the accepted version of the manuscript: https://www.nature.com/articles/s41598-024-79602-w
On 2021-09-10 15:53:12, user Israel Kochin M.D. wrote:
Page 20 of the PDF- "a AU/mL values for anti-spike IgG and anti-RBD IgG can be converted to the WHO international standard (NIBSC code 20/136) using the following<br /> conversion factors: Spike: BAU/mL = AU/mL x 0.00645 RBD: BAU/mL = AU/mL x 0.00798. BAU/ml: Binding antibody units per millilitre." https://www.medrxiv.org/con...
On 2023-04-02 19:09:38, user GL wrote:
This systematic Review is lacking of protocol in PROSPERO. It says that follow PRISMA guidelines but it does not.
Therefore the findings are biased.
I would recommend the authors to follow more rigorously the PRISMA 2020 Guidelines or in case delete the term "systematic".
On 2021-06-24 09:15:57, user KKRay wrote:
Why no data from April?
On 2021-06-13 20:13:06, user Christopher Knittel wrote:
I would like to receive the underlying data and code for this paper. The paper states a CSV is available, but there are no contact details for the authors listed. Please let me know an email address that I can use to get access to the data. Thank you.
On 2021-06-14 19:06:53, user justtravis wrote:
Duly noted. Please apply each of your above criticisms to blanket administration of vaccines...?
On 2021-07-13 19:11:26, user StephenWV wrote:
Stephen Smith suggested this study could be used by other studies for evaluation. How does it mesh with this study of Hydroxychloroquine alone and hydroxychloroquine with azithromycin when receiving hydroxychloroquine within the first 24 hours of admission.<br /> Treatment with hydroxychloroquine, azithromycin, and combination in patients hospitalized with COVID-19 - International Journal of Infectious Diseases (ijidonline.com) https://www.ijidonline.com/... <br /> This shows a reduction in morbidity of 290%
On 2020-03-04 19:29:21, user David Do wrote:
Somebody researched on this yet ? Somebody should confirm this.
On 2021-10-18 00:30:55, user Prescott Comptr wrote:
hasn't there been enough time for a peer review?
On 2021-08-30 23:32:13, user Patrick Auta wrote:
Thank you
On 2019-07-23 17:47:15, user GuyguyKabundi Tshima wrote:
EVOLUTION OF THE EBOLA EPIDEMIC IN THE PROVINCES OF NORTH KIVU AND ITURI
Monday, July 22, 2019
The epidemiological situation of the Ebola Virus Disease dated 21 July 2019:
Since the beginning of the epidemic, the cumulative number of cases is 2,592, of which 2,498 are confirmed and 94 are probable. In total, there were 1,743 deaths (1,649 confirmed and 94 probable) and 729 people healed.<br /> 272 suspected cases under investigation;<br /> 14 new confirmed cases, including 10 in Beni, 2 in Mandima, 1 in Oicha and 1 in Mutwanga;<br /> 6 new confirmed case deaths:<br /> 3 community deaths including 1 in Beni, 1 in Mandima and 1 in Mutwanga;<br /> 3 deaths at the Ebola Treatment Center of Beni.
Change in coordination of the response to Ebola Virus Disease<br /> A new arrangement of the Presidency of the Republic announced this Saturday, July 20, 2019, the establishment of a technical secretary under the direct supervision of the Head of State to coordinate the response against the Ebola Virus Dpsease in North Kivu and Ituri. This technical secretary is headed by Professor Jean-Jacques Muyembe, who was also chairman of the laboratory committee in coordinating the current response since August 2018.<br /> As a result, all communications related to the response will now be managed directly by the Presidency.
Source: The press team of the Ministry of Health.
On 2019-11-16 01:59:42, user Guyguy wrote:
EVOLUTION OF THE EPIDEMIC IN THE PROVINCES OF NORTH KIVU AND ITURI AS AT 14 NOVEMBER 2019
Friday, November 15, 2019
• Since the beginning of the epidemic, the cumulative number of cases is 3,292, of which 3,174 are confirmed and 118 are probable. In total, there were 2,195 deaths (2077 confirmed and 118 probable) and 1070 people healed.<br /> • 508 suspected cases under investigation;<br /> • No new confirmed cases;<br /> • 2 new deaths of confirmed cases in North Kivu, including 1 in Beni and 1 in Mabalako;<br /> • 3 healed people released from CTE in North Kivu in Mabalako;<br /> • No health worker is among the new confirmed cases. The cumulative number of confirmed / probable cases among health workers is 163 (5% of all confirmed / probable cases), including 41 deaths;
NEWS
Continuation of vaccination with the 2nd Ebola vaccine in two health zones of Karisimbi in Goma
• Vaccination continues in the health zones of Majengo and Kahembe in Karisimbi (Goma);<br /> • A total of 40 people were vaccinated, including 34 adults and 6 children under 18;<br /> • This vaccination began on Thursday, November 14, 2019 with the Ad26.ZEBOV / MVA-BN-Filo vaccine, produced by Janssen Pharmaceuticals for Johnson & Johnson. This second vaccine was approved on 22 October 2019 by the Ethics Committee of the School of Public Health of the University of Kinshasa and 23 October 2019 by the National Ethics Committee.
VACCINATION
• 40 people were vaccinated with the 2nd Ad26.ZEBOV / MVA-BN-Filo vaccine (Johnson & Johnson) in the two Health Zones of Karisimbi in Goma;<br /> • Since the start of vaccination on August 8, 2018 with the rVSV-ZEBOV vaccine, 252,249 people have been vaccinated;<br /> • Approved October 22, 2019 by the Ethics Committee of the School of Public Health of the University of Kinshasa and October 23, 2019 by the National Ethics Committee, the second vaccine, called Ad26.ZEBOV / MVA-BN -Filo, is produced by Janssen Pharmaceuticals for Johnson & Johnson.<br /> • This new vaccine comes in addition to the first, the rVSV-ZEBOV, the vaccine used until then (since August 08, 2018) in this epidemic. Manufactured by the pharmaceutical group Merck, after approval of the Ethics Committee on May 20, 2018, it has recently been approved.
MONITORING AT ENTRY POINTS
• A 38-year-old woman from Beni for Nzanga in Mutwanga, North Kivu, high-risk contact was intercepted at PK5 checkpoint (PoC) in Beni. She is in contact with a source case notified to Beni on 03 November 2019;<br /> • Since the beginning of the epidemic, the total number of checked travelers (temperature increase) at the sanitary control points up to 13 November is 116,622,388 ;<br /> • To date, a total of 112 entry points (PoE) and sanitary control points (PoCs) have been set up in the provinces of North Kivu and Ituri to protect the country's major cities and prevent the spread of the epidemic in neighboring countries.
As a reminder, the recommendations of the MULTISECTORAL COMMITTEE OF THE RESPONSE TO EBOLA VIRUS DISEASE are as follows:
On 2019-10-16 12:34:53, user GuyguyKabundi Tshima wrote:
EVOLUTION OF THE EPIDEMIC IN THE PROVINCES OF NORTH KIVU AND ITURI AS OF OCTOBER 10, 2019<br /> Friday, October 11, 2019<br /> Since the beginning of the epidemic, the cumulative number of cases is 3,210, of which 3,096 confirmed and 114 probable. In total, there were 2,146 deaths (2032 confirmed and 114 probable) and 1028 people healed.<br /> 422 suspected cases under investigation;<br /> 2 new case confirmed at CTE in Ituri in Mandima;<br /> 2 new confirmed deaths, including 1 in North Kivu in Mabalako and 1 in Ituri in Mandima;<br /> 1 person healed out of CTE in Ituri in Mambasa;<br /> No health workers are among the newly confirmed cases. The cumulative number of confirmed / probable cases among health workers is 161 (5% of all confirmed / probable cases), including 41 deaths.
NEWS
President Félix-Antoine Tshisekedi Tshilombo submits to sanitary control for the prevention of #Ebola Virus Disease at Beni Airport<br /> - The Head of State, Coordinator of the Multisectoral Committee for the Ebola Virus Epidemic Response (CMRE), President Félix-Antoine Tshisekedi Tshilombo and his delegation were welcomed on Thursday, October 10, 2019 by the monitoring team at the entry points / sanitary control at Mavivi Airport in Beni, North Kivu Province. President Tshisekedi and his team have gone through all stages of health control at this point of entry to prevent Ebola Virus Disease;<br /> - The Ebola Virus Epidemic Response Coordination Team and a few members of the CMRE Technical Secretariat have been staying in Mambasa, Ituri province since Wednesday. It is in this part of the Democratic Republic of Congo that the last confirmed cases of #Ebola Virus Disease are concentrated;<br /> - This team, made up of the different experts in Ebola Virus Disease, has moved closer to Mambasa to coordinate closely the activities of the response;<br /> - Since they have been there, several activities have taken place, among which the release of 5 cured people from the ETC and a big meeting with all the partners of the response present in this sub-coordination. This meeting stems from the orientations to end the epidemic in this part of the DRC.
VACCINATION
MONITORING AT ENTRY POINTS
As a reminder, the recommendations of the MULTISECTORAL COMMITTEE OF THE RESPONSE TO EBOLA VIRUS DISEASE are as follows:
On 2020-06-05 20:58:26, user eduardo wrote:
Comment from author: new version (uploaded 04 June 2020) updated parameters based on new data; the main difference with the first version is that the "CID" critical delay is now shorter, but nothing changed qualitatively.
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 2021-12-15 18:08:42, user Gaute wrote:
Does the unvaccinated include people that are to fragile to receive the vaccine ???
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 2021-07-04 15:46:32, user AF wrote:
The authors fail to describe the online questionnaire - did it restrict the set of symptoms that were able to be reported? Did it allow entry of non-predefined symptoms? Did it include a severity scale for each reported symptom? The precise questioning schema might have a very significant effect on the results which seem obviously in contradiction to e.g. UK ONS data.
On 2021-07-13 23:50:52, user Pedro Viana wrote:
Now published on Epilepsia: https://doi.org/10.1111/epi...
On 2021-10-11 05:16:51, user Jonathan Sobel wrote:
Dear Dr Buekers,<br /> Thanks a lot for your interest in our work and your supportive comment. Your work is indeed inspiring and we will cite it in a revised version of our manuscript.<br /> Best Regards,
On 2021-03-24 15:21:57, user evacguy wrote:
I am pleased to annouce that this paper was accepted by the Journal of Travel Medicine following peer review on 11/02/21. It is noted that none of the findings, results or conclusions from the first draft have changed. The authors thank the reviewers for their insightful comments and suggested changes which improved our paper. The peer reviewed paper can be freely downloaded using the following link: https://doi.org/10.1093/jtm...
On 2021-09-29 01:16:54, user Alberto wrote:
So on 2 September the total severe cases was 629 (hospitals and ICUs at the verge of collapse), and the estimation if 0% of the population had been vaccinated is that there would have been 5182 severe cases in the country. And this during the summer. I don't have the figure at hand of how many severe cases were on 2 September 2020, when 0% of the population was vaccinated, but it may have been around 250-300? It's hard to know what exact effect mass vaccination is having that leads to these kind of absurd results, but it would be worth looking at it in detail.
On 2025-08-21 08:10:06, user Taukim Xu wrote:
Comments from the authors-01:
Since the preprint was made available, we have been honored to receive numerous publication invitations from various journals. We would like to express our sincere gratitude for your interest and recognition of our work.<br /> However, we feel it is important to clarify that this manuscript is currently under consideration at another journal. Therefore, we are unable to submit it to your publication at this time.
Dr. Taukim Xu
On 2024-05-08 14:58:49, user mira wrote:
Thank you for carrying out this research. This preprint needs to be published so people and the medical world can finally stop gaslighting us and telling us it's "just eczema". I have been suffering for years with TSA and after quitting steroids my life has been terribly changed because of TSW. We are so overlooked, desperate for knowledge and solutions, we are a suffering community.
On 2024-05-10 04:50:19, user Kaitlin Lee wrote:
Thank you for this long overdue research. It gives me hope that in the near future TSW will be universally diagnosable, treatable, and most importantly, prevented. I have had eczema for ten years, just a few patches here and there, which never interfered with my livelihood. Now 5 months into TSW, so many things have been put on hold for me. People suffering from TSW need treatment and support and medical professionals need to start acknowledging this condition.
On 2024-04-27 20:26:14, user Sarah Simpson wrote:
Thank you for this important study. I have been suffering with topical steroid withdrawal for over 20 months after 35+ years of use for my atopic dermatitis which only got worse. My skin is now finally healing after the cessation of all medication. We need more research and for doctors to know more about this iatrogenic condition
On 2024-04-28 10:09:53, user Menucha Bernstein wrote:
As someone going through TSW this is of unimaginable importance. My gp has never heard of tsw before and so leaves me without any validity of what I'm going through and leaves me without possible remedies. This research would help have an impact by spreading more awareness for doctors and give patients that official diagnosis which is so important.
On 2020-08-03 20:14:42, user Sluggo67 wrote:
I may be missing it, but I didn't see any updated summary results on the GitHub repo. I only see the two sets of 95% CI's as reported in Abstract version 1 (5% to 25%) and version 2 (2% to 15%). I'm intrigued by the statement that 'results are consistent across time periods' even though the CI's exhibited sizable changes between the two posted versions from April. Are the authors able to post results (at least CI) from the daily updates?
On 2021-06-25 10:42:32, user helene banoun wrote:
Congratulations for your work!
It would be interesting to study also the mutations related to the immune system not located on the spike like those on orf3 and orf8
https://www.karger.com/Arti... <br /> Evolution of SARS-CoV-2: review of mutations, role of the host immune system ?<br /> Banoun H, Nephron (2021 Apr 28:1-12)
On 2021-08-20 15:55:33, user Dime wrote:
(1) Yes, and those who were vaxed following infection carry a higher viral load upon re-infection than the previously infected unvaxed. In fact, the viral load of the infected/vaxed group upon re-infection is closer to the unvaxed/first-time infection than to the unvaxed/re-infection group.
(2) Yes, many, and they are showing efficacy wanes over time, especially to the variants.
On 2025-09-02 10:12:20, user Audouze wrote:
Now published in Toxicology ( https://doi.org/10.1016/j.tox.2025.154225) "https://doi.org/10.1016/j.tox.2025.154225)")
On 2021-09-14 09:00:20, user Alberto wrote:
"Incidence rates were estimated in the 28 days post first-dose vaccine, 90 days post-COVID-19". I think that this study will be much more informative once you can gather the data to estimate incidence rates between the first dose and 90 days post-second dose of the vaccines.
On 2023-07-21 14:12:39, user Gaël Nicolas wrote:
I think that this variant is definitely a strong contributor to AD. However, the pedigrees also show that the patients with DNA available and carrying the variant, also carry one APOE4 allele. Actually, APOE4 segregates as good as SORL1 in these pedigrees! All affected individuals with DNA available are SORL1+/APOE4+. One unaffected individual is SORL1+/APOE4- (family 1) and one unaffected individual is SORL1-/APOE4+ (family 2). To be clear, I have absolutely no doubt of a major role of the SORL1 variant here, but I feel that this is very much consistent with a more complex inheritance and not purely autosomal dominant, as shown in our penetrance paper (Schramm et al., Genome Medicine 2022, PMID 35761418)
Interestingly, we have the same variant in three independant families from France (one of them is mentioned in this preprint). Although there is an obvious aggregation of AD cases in the families, there is a huge diversity of ages of onset and younger cases have a positive family history in both branches, suggesting the contribution of additional factors. Some of them are APOE4+ but not the 2 youngest probands. This may suggest the contribution of undetected contributing variants along with SORL1.
Overall, our penetrance paper (Schramm et al., 2022) and many pedigrees suggest a contribution of additional factors with SORL1 variants and that SORL1 alone may not be sufficient / fully penetrant. We have clear evidence for APOE4, as this is a common allele, but we know that there are many other other AD-associated variants, especially rare variants, among known variants (as families with SORL1+ABCA7 as we previously reported in Campion et al., Acta Neuropath 2019, PMID 30911827) and in other papers and, obviously, not yet known variants.
I thus recommend to use such results with great caution for genetic counseling, as we still don't exactly know how variants in other genes may drastically change an age of onset from 50 to 75-80 for example, or to absence of AD (as also shown for some truncating variants, as in Campion et al., 2019 where a mother transmitted a truncating a truncating variant and was unaffected with AD at age 95 years).
On 2020-03-31 16:51:49, user Parmjeet Randhawa wrote:
I think the subject of this<br /> manuscript deserves further discussion as it has obvious implications for organ<br /> transplant. I would like to make the following points: <br /> Overall, the evidence<br /> presented certainly raises concern about the ability of COVID-19 to infect the kidney.<br /> However, the implications of this finding are such that more rigorous immunohistochemistry<br /> controls are very desirable. Normal kidney and renal sections form unrelated<br /> autopsies showed no antibody staining, but it would be important to rule out non-specific<br /> staining in damaged tissue. I have personally seen such non-specific staining<br /> with C5b-9 antibodies. Therefore, negative controls should include tissues with<br /> acute tubular necrosis and interstitial nephritis not related to COVID-19
Electron microscopy can<br /> certainly be done on paraffin embedded tissue, since viruses survive formalin fixation<br /> quite well. That would make the case watertight and provide really convincing<br /> evidence that COVID-19 can infect tubular epithelium.<br /> To further define the<br /> spectrum of renal injury in COVID-19 infection, the cases with proteuria reported<br /> in this draft manuscript should undergo systematic urine sediment examination<br /> with special reference to presence of inflammatory debris, casts, viral cytopathic<br /> effect and ultrastructural evidence of viral particles.<br /> Even if renal infection is further<br /> confirmed, one should keep in mind that the kidney pathology presented may only<br /> occur in a minority of patients with very severe infection. Renal dysfunction<br /> in the setting of viral pneumonia can be due to pre-renal factors, medications,<br /> cardiac-renal syndrome, and other comorbidities. The risk of transmission of COVID-19<br /> from an unrecognized infected donor to a recipient may be much lower via kidney<br /> compared to lung transplantation.<br /> Further research is needed to quantify that risk in numeric terms and come up<br /> with more precise risk estimates of COVID-19 transmission via organ transplantation.<br /> Parmjeet Randhawa,<br /> Professor of Pathology,<br /> Division of Transplantation Pathology, <br /> University of Pittsburgh and The Thomas E Starzl<br /> Transplantation Institute, <br /> Pittsburgh, PA, USA
On 2020-12-11 18:07:58, user Thierry Grenet wrote:
Another discussion of the trajectories is given here : https://bmcmedresmethodol.b....
On 2021-01-27 15:14:20, user Florence Paré wrote:
How do you account for the possibility of COVID infections disproportionately occurring later in the period under study (due to rapidly rising numbers of infections), whereas influenza and respiratory tract infections may tend to slightly go down over the period due to distancing measures? This seems to risk introducing a confounding variable - mental health deterioration due to social distancing and pandemic-related anxiety. Did you or do you intend to make adjustments to the control cohorts to match the distribution of events over the period under study?
On 2020-05-17 22:42:10, user Arvind Gulati wrote:
It's NIH study of 2000 patients not adding zinc, it's a shame.
On 2021-11-16 17:30:31, user Marcelo Sauaf wrote:
Authors using ONLY the term "faster" about the viral cleareance while this "faster" meant mere 2 DAYS less than unvaccinated evidentiate their POLITICAL bias on the subject. Why don't they QUANTIFY in the conclusion the "faster" was mere 2 days less than unvaxxed - AND that the contagious phase (PCR ct = 25) is tipically up to 9 days ??
On 2020-09-14 19:25:30, user Vincent Fleury wrote:
Can you provide the distribution by age of the deaths, I can't find it in the paper. What I read is that there are 8 times more people in the stratum age>65yo, while the mortality is only 3 to 4 times higher. If mortality occurs only in the >65yo, then this work shows 1-that HCQ is not given to elderlies and 2-potentially that HCQ is actually harmful.
On 2022-02-08 07:46:02, user kdrl nakle wrote:
Absolutely catastrophic. Too sad. All those nurses were likely infecting other patients and their own family members.
On 2022-01-13 07:22:11, user Tomer Yona wrote:
What measurement tools did you use to assess depression, anxiety and OCD disorders?
On 2025-07-15 16:59:57, user zlmark wrote:
The preprint relies on survey data that shows clear evidence of sampling protocol violations, including improper household selection, failure to screen for residency, and geographic deviations confirmed by GPS data.
In several cases, inconsistencies appear to have been retroactively edited to align with protocol.
Data from two teams—Gaza9 and Gaza3—raise particular concern, with demographic anomalies and mortality figures that suggest possible manipulation or fabrication.
These issues compromise the representativeness of the sample and call into question the reliability of the resulting estimates.
A full analysis of these issues is available here: <br /> https://markzlochin.substack.com/p/design-vs-execution-in-gaza-mortality
On 2020-11-20 02:26:46, user Prasad Kasibhatla wrote:
Interesting.. scaling reported median risk (2e-6) for individual touches by average touches per day (336), gives a transmission risk by fomites of 10-12% over a 6 month period (roughly length of pandemic ). Seems high .. so my scaling must not be appropriate. Any thoughts?
On 2021-08-24 05:03:58, user rusbowden wrote:
Hi Tim --All we can do is get the information out there. I have a very good friend who is 82 and very active, always has been. He wears a mask, will double mask, has been vaccinated, and also has some trouble breathing. We need to protect him, not by taking his liberty away -- not that we could -- but by insisting on getting the information out. But, he takes all precautions. There's nothing about him that makes him anything but smarter than you or me for being 82, a well to do, retired business man, who still dabbles in his craft. His wife has a serious respiratory ailment, and the unmasked and unvaccinated people have driven her into being a shut in. She is a shut in because of insistent stupidity and uncaring media messages and the effects it has on couch potatoes. There is no other reason than viral covidiocy for this along with using ad hominem attacks to replace real research findings. Here's the kicker. They have a son who comes by often, who buys into the paranoia of a government conspiracy narrative, the helplessness of wearing what is told to him by smirking talking heads to be ineffective masks and now vaccines, not to mention the fear of vaccinating when government and big pharma are out to get everyone and so would never care to test properly, so he's told. He's a grandfather himself, who is putting the entire beautiful big family at risk because of these false narratives. They try to talk sense into him, but the anti-mask and anti-vax conversation that is supported by what he believes to be news shows on TV, has him like cement, mixed up and set. In the mean time, their innocent victims are dying by the millions across the globe -- and we're up to a million excess deaths in the USA now, because of Covid. It's the false narratives that are killing us.
On 2021-08-03 01:50:28, user Lance56 wrote:
You premise is wrong out of the gate. Covid-19 is airborne, no longer those big droplets described by Fauci...Here is a double blind study from Denmark showing masks wearing both inside and outside does not protect you from getting or spreading covid-19. I can cite many more studies show the uselessness of wearing a face mask to protect against a virus that is smaller then the mask can even filter.
On 2021-06-13 23:02:58, user Deplorable D wrote:
I work in a closed environment that is run 24/7 with approximately 100 people rotating through various shifts. About 25 people per shift and our personnel overlap with each other. Nobody wore masks, and nobody social distanced. We work 12-hour shifts and sit about 3 feet apart in one large room. There are no offices, nor are there cubicles. There are no windows, so the idea of fresh air and breezes is nullified. We also take our meals at our workstations, so there is no one going outside the facility during their shift either. A total of 5 people were declared COVID positive in the past 18 months, and we were tested regularly. Aside: most of the workers fall into a co-morbidity factor: obese, diabetic, alcoholic, etc.
If SARS-CoV-2 was as infectious as we are told, and masks are the way to protect each other, then why were there so few cases? My workplace is literally a petri dish of the worst possible scenario for the spread of COVID.
On 2021-07-23 04:36:35, user robert brown wrote:
Masks work. This is a statement of fact. I can make this statement because viruses must follow physical laws. So until you or anyone else can provide a body of evidence showing that viruses are not bound by physical laws you have no argument. We do however need to deal with that body of evidence how is it some studies reach a conclusion that’s opposed to reality? By having a fatal flaw. This study has it. The goal is to determine if masks are effective. So why are they studying if people are actually wearing them? Assuming that a mandate means higher mask usage is a bad assumption. Assuming no mandate lowers usage is another bad assumption. Assuming that areas with and without mandates are closed systems is a really bad assumption. Yet for this study and indeed the body of evidence you claim supports the masks don’t work conclusion to work as intended and be capable of answering the question all these things would need to be true. And as someone who has traveled through areas with and without mandates I can say none of those appear to be true. So how do masks work? This is important to understand many people assume that the goal is filtration but it’s not. Sure a cloth or paper mask can filter a lot of droplets and the particles with them but that’s not the primary mechanism here. How does a sail catch the wind? The air is perfectly capable of passing right through a cloth sail so how does that work? Air is a fluid which for our purposes means it takes the path of least resistance. If you take the carrier of a virus no mask and just normal breathing droplets containing viral particles will quickly spread out into the surrounding area where they will be inhaled by others thus infecting them as well. However if you have some sort of barrier in place like say a mask the air will quickly loose energy the droplets as well and they will fall quickly and for the most part harmlessly to the ground. Why mandates and not just choice? Well if you could not guess by the description the mechanic at play isn’t filtration. Yes a cloth or paper mask can capture some droplets but respiration has a vacuum element and if someone infected without a mask is spewing particles people around them are still going to suck those in. So the function of a mask isn’t to protect yourself it’s to protect other people. That wraps up this mini lecture any questions?
On 2020-04-02 16:55:14, user VWFeature wrote:
What happens if instead of "assuming full social distancing through May 2020" we see what's actually happening? (Deaths go way up.)<br /> What's the assumption of death rates when hospitals and ICUs exceed capacity?
When no beds are available, a reasonable assumption would be that 80% of people needing hospital, and 100% of those needing ICU would die.
This study keeps getting cited as "best possible outcome." It's intellectually dishonest to present a "best possible" without a "most likely" and "worst case" projection.
This study is already inducing a false sense of security. This is the BEST POSSIBLE outcome. The most likely is far worse.
On 2021-12-14 21:01:11, user jayne doh wrote:
has this paper been submitted to a peer reviewed journal?
On 2022-03-01 05:15:31, user Nun Daled Yud wrote:
clearly serial daily or twice daily testing is needed for patients who would benefit from the early antiviral treatments particularly aged care facilities .
On 2025-05-28 23:11:26, user Evolutionary Health Group wrote:
We at the Evolutionary Health Group ( http://evoheal.github.io/) "http://evoheal.github.io/)") really enjoyed this paper. Here are our highlights.
Investment in ensemble forecasts resulted in better calibration and less variable predictions
Work bridged the gap between theory and policy; builds infrastructure for future data integration
Climate zone analysis balanced the desire for model generalizability, the need for sufficient historical data to characterize each zone, and the risks of unrealistically grouping diverse regions together.
Limitations of individual models including the provision of confidence intervals was honestly presented
On 2020-05-29 01:07:52, user Vincent CaliforniaVinny Lewis wrote:
I appreciate your input Doctor SK Gupta. I'm interested in this topic and your opening statement addressed some of my questions: 1) How much was given? 2) At what interval? 3) What was the age of the patient? 4) Did the patient have any pre-existing conditions or comorbidities? 5) Was the patient mild. moderate, severe or critical? I would think all of these play a significant role in determining the efficacy of a therapy,
In Regards to SARS-CoV2:
1) Is it appropriate to cite a Chloroquine study to determine the efficacy of Hydroxychlorquine as I have beard qualified sources claim they are not the same drug but the latter a derivative of the former?
2) Is it appropriate to cite the efficacy of either Hydroxychloroquine or Chloroquine in the study of SARS-Cov and assume it automatically translates to SARS-CoV2. I read a 2020 study that concluded that 2019-nCoV is 96.3% related by genomic sequence to the BatCoV RaTG13 [a separate genetic lineage to the Coronavirus family] and that “Full-genome sequence analysis of 2019-nCoV revealed that it belongs to betacoronavirus, but it is divergent from SARS-CoV and MERS-CoV that caused epidemics in the past. The 2019-nCoV together with the Bat_SARS-like coronavirus forms a distinct lineage within the subgenus of the sarbecovirus.”
Thansk for your time.
https://www.sciencedirect.c... <br /> Volume 79, April 2020, 104212
On 2020-03-27 15:14:04, user Kevin Hall wrote:
Why does this model calculate deaths as being proportional to the time-delayed fraction of the population not susceptible to infection z rather than the time delayed fraction of the infected population y? See equation 3.
On 2023-03-06 09:52:44, user baba aurhum wrote:
Now published in Communications Medicine: https://www.nature.com/arti...
On 2025-09-19 04:08:22, user Jane Dunlap wrote:
Indigenous tribes in the US? How do they compare?
On 2021-08-03 02:27:45, user Kathy Cardy Thompson wrote:
My daughter has a genetic disorder SLC30A9, she is Australian, and comes from 2 parents not related. Has had this fault for years now. There are also kids in England and to date approx 14 kids in total world wide. If you search you will see they are of mixed cultures, so not predominantly African American. My daughter has dealt with issues from SLC30A9 gene now and it’s destroying her life, America also were contacted and knew about my daughter before this report was published.
On 2021-06-10 14:31:53, user Jeff Krantz wrote:
I would really like to know the lab you went to. Quest Diagnostics doesn't have a quantitative test for C19. Thank you
On 2021-12-09 11:47:30, user King Lam Hui wrote:
Is this under review or something?
On 2022-05-23 16:01:08, user John Dough wrote:
Very nice work. I have a suggestion that is a relatively easy fix. I suggest you change from gender to sex. Gender is a social construct while sex is biological and my understanding is you studied sex here.
On 2021-02-23 20:17:28, user AJ wrote:
Regarding public health measures selecting for mutations-<br /> the effect is nil; those mutations must exist in order to perpetuate, and if a mutation confers a transmissibility advantage it will outcompete according to this relativity regardless of the mitigations in place. This is a virus transmitted through lungs and by air- we are not going to start growing gills and swimming and neither will it. It is bound by the laws of physics.
The daily survivorship/ incubation period is also long. In order for a mutation to reduce transmissibility by affecting/incapacitating the host the effect would need to be massive.
The S strain, the relatively slow one that was not as virulent is gone. It had a lower R and was not as virulent. The tendency of these mutations is clear, and is shown by the Weizmann institute.
On 2021-03-27 10:07:56, user Terrapon wrote:
This article has been accepted for publication in Neurosurgery published by Oxford University Press.
On 2021-02-10 20:18:58, user Isaac See wrote:
The article has been accepted by Clinical Infectious Diseases and can be found (ahead of publication in print) at https://academic.oup.com/ci...
On 2025-03-25 15:51:39, user Kristjan Norland wrote:
This manuscript has now been published in JACC: https://www.jacc.org/doi/10.1016/j.jacc.2024.06.052
On 2021-01-29 18:20:06, user Neal wrote:
I think it's worth looking at institutional conflict-the possibility that the institution that they work for has received major donations from interests that have some potential financial gain possible from negative results for Ivermectin. That would explain the strange results and methodologies of this study, such as 1. Including large studies as having "no data" 2. Selective negative individual outcomes from trials which did have positive results 3. Meta-analysis showing the exact opposite conclusion.
In an age when medical science may be highly corrupted by financial inducements, this needs to be scrutinized carefully. There are all too many "studies" or "Meta-analyses" that seem to have strange data, especially when an inexpensive treatment or prophylaxis threatens an expensive one.
On 2020-04-06 12:54:12, user xdoomx wrote:
Here in South Africa we probably have the highest possible rate of infection in the world due to the high density most of our low income population live in. However, we currently have only 11 deaths out of 1685 cases. We also have an EXTREMELY low testing rate, so bear that in mind. There could be thousands of people infected we don't know about.<br /> The BCG vaccination has been rigorously in place for all newborns since 1973. It is estimated that at least 70% of the population have had it, at most 90%.
On 2019-07-21 03:12:01, user Guyguy wrote:
EVOLUTION OF THE EBOLA EPIDEMIC IN THE PROVINCES OF NORTH KIVU AND ITURI
Saturday, July 20th, 2019
The epidemiological situation of the Ebola Virus Disease dated 19 July 2019:<br /> Since the beginning of the epidemic, the cumulative number of cases is 2,564, 2,470 confirmed and 94 probable. In total, there were 1,728 deaths (1,634 confirmed and 94 probable) and 726 people healed.<br /> 392 suspected cases under investigation;<br /> 18 new confirmed cases, including 7 in Beni, 3 in Mandima, 3 in Mabalako, 1 in Vuhovi, 1 in Butembo, 1 in Mambasa, 1 in Lubero and 1 in Masereka;<br /> 13 new confirmed cases deaths:<br /> 8 community deaths, including 4 in Beni, 2 in Mandima, 1 in Mabalako and 1 in Masereka;<br /> 5 Ebola Treatment Center (ETC) deaths, 2 in Mabalako, 2 in Beni and 1 in Katwa;<br /> 5 people recovered from ETCs, including 3 in Beni and 2 in Katwa.
NEWS
Minister of Health visits Beni<br /> The Minister of Health, Dr. Oly Ilunga Kalenga spent the day of Friday, July 19, 2019 in Beni where he visited the various field teams and the transit center whose capacity will be increased in the coming days.<br /> Following the resurgence of patients in Beni, Dr. Oly Ilunga said that one of the key lessons learned in this tenth epidemic is to rely on the health system. "If we really want to solve this epidemic and have a lasting impact, we need to strengthen the health system by working with the actors in this system and with the community," he said adding that this is how we can quickly stop this new outbreak in the city of Beni.<br /> He recalled that the declaration of this epidemic as an international public health emergency requires other countries to strengthen border surveillance, while for the response, the declaration recognizes the work that is being done and the performance of the response. managed to contain the epidemic in an extremely complex context.<br /> This statement also stresses the need for a response with greater coordination and consultation. Another point that Minister Oly Ilunga always insists on is the accountability of all actors on the ground, the sharing of information, the measurement of performance, and the use of data to guide and improve actions on ground.
168,746 Vaccinated persons.
76,632,731 Controlled people.
138 Contaminated health workers<br /> The cumulative number of confirmed / probable cases among health workers is 138 (5% of all confirmed / probable cases) including 41 deaths.
Source: Ministry of Health press team on the state of the response to the Ebola epidemic in the Democratic Republic of the Congo
On 2021-08-21 17:14:03, user Alan wrote:
How will increased vaccination make a difference if the efficacy is as is being reported less than 50%? Once one is infected it does not appear to reduce one's odds of being hospitalized. So if the efficacy approaches zero, there would be zero benefit to being vaccinated, with the currently available vaccines.
On 2020-10-16 12:17:32, user Criticical Opinion wrote:
Unfortunately it is not clear if there was a difference between a diagnosis of OSA vs treatment for OSA, severity or degree of OSA, or type of treatment for OSA. Without this information, the utility of these findings is questionable at best.
On 2020-08-27 13:14:41, user Fernanda Di Genio wrote:
This preprint brings the same results of the preprint of Watanabe previously published more than one month ago:<br /> https://arxiv.org/abs/2007....
On 2021-11-29 13:08:12, user TheBigWakaWaka wrote:
There's something that needs explanation.
In table S2, the raw <br /> ratios of unvaccinated cases over unvaccinated person-time (45% vs 55%, <br /> single dose vaccinated cases over single dose person-time (24% vs 19%), <br /> and double dose vaccinated cases over double dose person-time (30% vs <br /> 26%) are pretty close.
Nevertheless, the Cox coefficients indicate<br /> a strong difference. This means that very strong confounding effects <br /> are at play here: this would need commenting. Usually such a strong <br /> difference between "corrected" effects and raw effects indicates a <br /> weakness in the study, that should at least be commented.Based <br /> upon the raw ratios one would think there's no effect of extra <br /> vaccination ; based upon the Cox coefficients, there's a very strong <br /> effect.
On 2020-08-10 11:48:29, user memini wrote:
The assumption of constant case ascertainment (Line 474) in these countries from March through June is a critical one. It is probably most accurate in Portugal where health systems were least overwhelmed and which has the most testing per covid-19 death. Portugal's dashboard reports <100 tests processed per day to >10,000 tests per day over this period, so it is unlikely that the assumption of constant case ascertainment is sound in Portugal or in the other three countries.
The authors could show whether similar parameters fit a more realistic time series of infections (estimated from deaths). Alternatively, simulated infection trajectories could be filtered by a reasonable estimate of how case ascertainment varied over time before estimating parameters.
Also, Fig S1 shows gamma distributions with CV=0.5, 1, 2; but best fits give CV = 2, 3 or 4 for these countries (Table S1). The relative susceptibility of the median person for those distributions is 0.17, .01, and 0.0001. Given the narrow confidence intervals in Table S1, authors could hypothesize how susceptibility in Portugal could be so much more variable than England, for instance.
On 2020-12-14 08:49:55, user Patrick Schmidt wrote:
Interesting connection between network models and standard inference on contact tracing data.
I have a paper showing that the tendency of superspreading can be estimated without contact tracing data from aggregated surveillance data alone. In line with the results here, I estimate a dispersion of 0.61 (95%-CI: [0.49, 0.77]) for Germany in spring 2020.
On 2024-02-05 00:31:50, user disqus_qMy1DU5jUb wrote:
The preprint challenges the validity of two modelling papers by comparing COVID-19 mortality data across Japanese prefectures, assuming these differences reflect the impact of varying vaccination coverages. This comparison is flawed due to unaccounted variables like population density, demographics, urbanization, and epidemic stages. Moreover, it overlooks the interconnectivity between prefectures in virus spread. The critique simplistically equates, for example, Tokyo and Saitama as identical except for their vaccination rates, which is highly questionable.
On 2020-10-27 12:08:10, user BigRed wrote:
The study rests on its the definition of "cost" and the definition use in the paper is extremely questionable. The authors equate the economic costs with the estimated decline in GDP. The GDP has a handful of now widely discussed methodological weaknesses -- such as that polluting production is as much a part of the GDP as the elimination of that pollution, or that the production of advertising has a positive impact on the GDP -- that stem from the fact that everything that is sold and bought is valued (with the well-known side effects that socially useful services such as housework and volunteerism are not included).<br /> But this cost accounting then becomes blurred because the authors look at the "costs" of hospital care without making a clear distinction between the two. If the latter costs are expenditures of private persons, they could have a negative effect on their financial situation, which can be reduced or even completely neutralized by the state with support payments. If the authors refer to costs for drugs, equipment and personnel that are paid directly by the state, there are no negative financial effects for private individuals at all (at least as long as the state does not pay for these expenses in foreign currency).<br /> In both cases, however, hospital costs are NOT costs in the sense of GDP reductions - on the contrary, any payment for a drug, a ventilator, or a nurse's salary is positively reflected in GDP. (that the chronically ill are good for GDP is another absurdity of GDP calculation)
The fact that the total "costs" are so ambiguously defined also means that the per capita costs as a figure are rather worthless and not suitable as a basis for debate.
A much more interesting approach would be "quality of life" considerations, which the authors very briefly touch on: a complete lockdown without unconditional salary compensation for part-time unemployed people has serious consequences for their quality of life; the same applies to small (micro) enterprises, especially those that depend on daily customer traffic. These companies need non-repayable support to ensure their continued existence and minimize the financial damage to their owners. Psychologically, lockdown experiences in various countries have shown that depression increased, as did anxiety, the perception of being lonely and resulting drug abuse of all kinds, especially among people who were already socially isolated before.
In other words, there are many important aspects to the question of "national lockdown vs. test-trace-isolate" and especially the question of how isolation and prevention of certain economic activities should be designed, but a headline-grabbing 45M US$ per life saved is not one of them.
On 2020-03-26 02:27:01, user Cristian Orrego wrote:
Its a small sample, right, but it doesnt seem to unvalidate the study. The only thing that i think in this case (if i read it right) that could be wrongly interpreted would be the conclusion. Because the sample of the sick people was obtained in the hospitals, so maybe the O type doesnt have less chance to get the virus, but insted it has less probabilities of develop synthoms that get people into the hospitals. So maybe the virus attack them (O type) with less severity. New studies should get infected people from random tested people among the general population to confirm if the O type gets lower rates of infection or the O type gets lower rates of worsening sympthoms once infected.
On 2020-02-29 22:14:11, user Meat house man wrote:
Thank you for this in this dynamic situation..let me know which journal it gets published in.<br /> I agree with your conclusion re R0..
On 2020-05-22 16:36:33, user ryccoh wrote:
You could have high regional variability. Percentage of smokers, air pollution, different strain, age demographics, diet, exercise habits, even ethnicity could play a factor we just don't know a lot yet.
On 2020-05-22 00:41:34, user Spaceman3 wrote:
Something critical that hasn't been asked to my knowledge is what percentage of counted Covid-19 deaths could be attributed to flu or other illnesses? Why is no one asking this question? It's as if the very sketchy data on fatalities is taken as gospel and there are no error bars.
On 2020-05-25 21:46:44, user ben marafino wrote:
Interesting finding. However, the study, as designed currently, does not exclude the possibility that the drop in mortality rate in April was principally driven by increased testing picking up more out-of-hospital, and thus less severe, cases. What proportion of the sample was hospitalized in April versus March?
On 2020-07-09 09:39:14, user ABCD2020 wrote:
Can Dexamethasone be used alongwith Remdesivir?
On 2023-08-22 14:47:23, user SRamin wrote:
I wonder if there is something different about individuals who get the bivalent vaccine versus individuals who do not that may explain the outcome observed in this study. <br /> 1) For example, perhaps individuals who received the bivalent vaccine work in a "higher risk" environment (ex. Doctors and nurses with direct patient contact) and those who did not get the bivalent vaccine worked in a "lower risk environment" (housekeeping/sanitation/cafeteria workers/laundry services). Perceived occupational risk would self-select for the exposure of interest and if perceived occupation risk matches actual risk then we would expect that bivalent vaccinated individuals would experience higher incident covid-19 rates because of higher risk of exposure. I see that one of the covariates of interest was "job location" which I presume refers to the physical location of employment in Ohio, but I think it is important to collect data on employee job type (direct patient contact vs indirect patient contact) and adjust for this in the multivariate models. <br /> 2) Another potential explanation for these results could be that individuals who received the bivalent vaccine versus those who did not had perceived an added protection and were more willing to place themselves in "riskier situations" for contracting COVID (perhaps bivalent vaccine recipients are more likely to eat out at restaurants or shop in public because of perceived added protection) or they may have felt less inclined to follow other COVID-19 infection prevention methods (less likely to wear masks or wash hands because of perceived protective benefit from the vaccine).
On 2020-03-25 00:18:42, user Sinai Immunol Review Project wrote:
Summary of Findings: <br /> - Retrospective study of 59 patients assayed key function indicators of the kidney–including urine protein, blood urea nitrogen (BUN), plasma creatinine (Cre), and renal CT scan data. <br /> - Found that 34% of patients developed massive albuminuria on the first day of admission, and 63% developed proteinuria during their stay in hospital; and 19% of patients had high plasma creatinine, especially the terminal cases. <br /> -CT analyses of 27 patients showed all patients to have abnormal kidney damage; indicate that inflammation and edema of the renal parenchyma very common.
Limitations: <br /> -No analysis of immunity-dependent damage and cytokines in blood/plasma/urine. Will be worth correlating disease progression with cytokine production, immune activity and kidney function. <br /> -Extrapolating to earlier SARS-CoV studies provides the only rationale for viral-damage in kidney and resultant pathologic immune response (understandable for this clinical study).
Importance/Relevance: <br /> -Multiple lines of evidence along this study’s finding point to the idea that renal impairment/injury is a key risk factor in 2019-nCoV patients similar to what has been reported for SARS-CoV [1]; this may be one of the major causes of virally-induced damage and contribute to multi-organ failure. <br /> -ACE2 expression in kidney proximal tubule epithelia and bladder epithelia (https://doi.org/10.1101/2020.02.08.939892) support these clinical findings. <br /> -Study argues for closely monitoring kidney function, and applying potential interventions including continuous renal replacement therapies (CRRT) for protecting kidney functions as early as possible, particularly for those with rising plasma creatinine.
References:
Review by Samarth Hegde as part of a project by students, postdocs and faculty at the <br /> Immunology Institute of the Icahn school of medicine, Mount Sinai.
On 2020-05-05 21:07:04, user Bozo wrote:
Please review this preprint...figure 2 in the appendix says it all.
On 2021-03-28 05:46:23, user Kareem Choucair wrote:
This article really shows what it is like to be a medical student and the crucial role that partaking in research has in their training. I greatly believe that the implementation of an evidence-based approach in exploring this topic has been used excellently and it has really compounded how research participation is one of the most crucial parts of generating an outstanding physician. Hopefully compulsory research modules become more prevalent as a result within medical schools globally. Well done altogether.
On 2022-07-28 13:28:19, user ??????? ?????? wrote:
This preprint has been published in the Journal of Medical Virology here: https://onlinelibrary.wiley...<br /> The title was slightly changed which I guess is why it was not picked up automatically.
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 2021-05-21 20:59:55, user Harold Thimbleby wrote:
From harold@thimbleby.net
I mailed the author for correspondence constructively two weeks ago but I have had no reply.
I am a professor of computer science. The Excel spreadsheet is, sadly, appalling and needs a lot of professional work to be believable. There is no useful documentation about how it is intended to work. It is obscure and impossible to check. I doubt it is correct, unless evidence can be provided. In short, the results described in this paper cannot be relied on or used for any public health purposes.
Have any of the authors carefully reviewed the spreadsheet? Any independent parties? If so I think the paper should say so.
Best wishes, though, with this important work.
-Harold
On 2021-06-17 16:40:52, user S Venkata Mohan wrote:
This pre-print has been peer-reviewed and published in ‘Environmental Technology & Innovation’, doi.org/10.1016/j.eti.2021.....
On 2020-05-18 09:46:36, user 1ashu1 wrote:
There seems an error in the calculation presented in the abstract, authors should consider to correct this in the revision: "Combining COVID-19 patient data and prior work on Vit D and CRP levels, we show that the risk of severe COVID-19 cases among patients with severe Vit D deficiency is 17.3% while the equivalent figure for patients with normal Vit D levels is 14.6% (a reduction of 15.6%)."
On 2020-06-10 19:55:05, user Sebastian Rosemann wrote:
Dear authors,
this is an interesting overview-study. However, many questions concerning the quality of the data and a systematical question arise.
How do the authors assure that the uniform reporting delay of ~10 days reflects the real pandemic curve by e.g. comparing published reproduction rates against the rates used to estimate the effects of NPIs? How do the authors deal with overestimating certain NPIs when comparing their impact rates to local observations?
For the german numbers we have the following discrepancy:<br /> The estimated reproduction number is based on reported cases using a delay of ~10 days from infection to confirmation. This seems not appropriate as a study from germany and the discussion around it shows.<br /> If simply using the reported cases curve one may get wrong drop rates for NPIs.<br /> This Science-study first used the reported cases:
https://science.sciencemag....
As stated by the authors in a technical note the drop-rates are quite different if one uses the real epi-curve with exact symptom-onset (if available):
https://github.com/Priesema...
Figure 19 shows a model based three-change-point approach and the impact.<br /> Figure 16 shows the same model fitting the curve with reported cases.<br /> Mind the drop rate of the first invention (which was cancellation of gatherings > 1000).
The reproduction numbers in this study lead to a totally different conclusion as changes in R are not correct and gatherings < 1000 as first NPI are not introduced correctly which gives the closing of schools an overestimated impact.
A closer look at the reproduction number of the netherlands reveals the same.<br /> Drops are visible but not in this intensity:<br /> https://www.rivm.nl/documen...
A look around intervention dates in different countries brings up questions concerning the quality of these data. Some of the findings to discuss are the following:
Belgium:<br /> Large gatherings were effectively cancelled since around march 10th and 13th<br /> https://en.wikipedia.org/wi...
Bulgaria:<br /> 10 out of 28 regions closed on march 4th<br /> https://www.bnr.bg/en/post/...<br /> General closage happended on march 13th<br /> https://en.wikipedia.org/wi...
Germany:<br /> Gatherings > 1000 were effectively cancelled since march 9th, one week before closing schools.<br /> https://en.wikipedia.org/wi...<br /> Closing schools was announced on march 13th but startet on march 16th.
Finland:<br /> https://www.reuters.com/art...<br /> Mainly closed since march 18th.
On 2020-03-14 08:04:28, user Stefano Gaburro wrote:
Minimal viral titer for infection: thanks for this great piece of work that allows governmental bodies to give suggestion. One question: the viral titer decreases over time meaning it could be detected but no longer infectious. Have you determined the minimal titer of virus to determine an infection?
On 2025-08-26 18:45:14, user Laura Hemmer wrote:
Thank you to this expert group on undertaking this needed and carefully-executed initiative to help improve diagnostic accuracy of IONM studies! I have a few minor comments as follow below for your consideration.
-In the discussion in the Introduction that lists applicable guidelines, the updated ASNM SSEP position statement published in 2024 could also be a helpful reference here for completeness and particularly for its discussion regarding anesthetic and physiologic factors that can impact SSEPs as well the section on interpretation and outcomes, which has some discussion on the interpretation of reversible evoked potential changes. (J Clin Monit Comput. 2024 Oct;38(5):1003-1042.)
-In the methods section, “STARD dementia” should likely have a reference noted.
-Please pay attention to the tense used for the portion regarding community engagement and feedback (e.g. abstract methods notes Phase 3 will include broader community…” as is starting to occur now, but then the results portion in the abstract somehow notes what was already emphasized by community feedback. Similarly, the Results Overview in the manuscript seems to indicate the results of community engagement and dissemination, even though it appears community engagement is just now occurring.) This may be confusing for readers.
-Phase 3 in the Abstract Methods portion notes that this will include broader community feedback, but in the manuscript, it appears community feedback is actually Part 4 of Phase 2 (“Community Engagement and Consensus Building” and Phase 3 is actually the dissemination of the final checklist. Please clarify.
-In the Results section, part #2, please consider if additional details of your assessment of adherence to the STARD checklist across 12 peer-reviewed publications should be made more fully available, such as adding these 12 references to Supplementary Content.
-Is the Results section, part #4 accurate yet (i.e. already officially endorsed by 3 international societies) or just anticipated still? These societies will need to be stated before publication.
-For anesthesia reporting in IONM studies, consider if more details regarding anesthetic technique could be useful. For example, what if additional anesthetic adjunctive/multimodal agents are also incorporated into the anesthetic regimen beyond just TIVA, inhalational, or mixed? We know from the literature, for example, that ketamine in different doses can impact MEP amplitude differently. Also, inhalational amount (e.g. MAC) should be noted when a “mixed” inhalational and intravenous hypnotic anesthetic regimen in being administered, as further evoked potential signal degradation would generally be expected with higher MAC levels.
-Some of the anesthetic reporting details discussed in the results section are really more physiological details, so should the heading be something like “Anesthesia and Physiologic Reporting in IONM Studies” instead of just “Anesthesia Reporting in IONM studies” perhaps?
-For patient demographics, in addition to the examples given in the document, including height, weight, etc., please consider noting that studies should also include other pertinent medical comorbidities for IONM purposes, such as the presence of diabetes mellitus and associated neuropathy which may make it harder to obtain robust baseline evoked potentials. Table 2 notes “clinical characteristics”, but I wonder if medical comorbidities that would be particularly pertinent to IONM and that may make even obtaining adequate, robust baseline signals difficult should be more clearly stated in the document and/or Table 2? It is helpful that Table 2, in the clinical characteristics of participants section (#20), does state that baseline IONM data should be reported.
-Reversibility of IONM changes is well covered by the authors in its own dedicated section within the Results section of the manuscript. Recommendations by the authors on how to best handle all evoked potential deteriorations is also clearly given in the same area of the results section. This important discussion and recommendation by the group, gets a little diluted and confusing when it is re-addressed shortly afterwards still in the results section under “Alternate evaluation framework in IONM”. Please consider if the repetition here is fully needed, or perhaps this area could refer back to the very well-stated section previous in “Reversibility of IONM changes”? Also the section “Alternate evaluation framework in IONM” might benefit from more clear recommendations from the expert working group.
-Consider if, from the 3rd sentence to the end of the 1st paragraph in the Discussion section, is actually needed. It is pretty redundant from earlier coverage in the document. For conciseness, could move the 2nd paragraph content to just after the 2nd sentence in the 1st paragraph in the Discussion section if desired.
-Anesthesia techniques definition is very basic in Table 1. For readers who do not carefully read the manuscript and refer more to the Tables only, should more detail be given here or at least could note to see the manuscript text content? Similarly, no mention of anesthesia appears in Table 2, which is the actual checklist being presented. Since standardized reporting of anesthesia-related variables is critical for IONM diagnostic accuracy studies, should anesthesia reporting information appear in the Table 2 checklist?
-Should studies be asked to more clearly state how it was determined that adequate baseline evoked potential signals were present (reporting of IONM baseline data is recommended in Table 2 #20, which is good). What about in the case of intracranial surgery and the concern for stimulation occurring below the area where ischemia could occur (potentially leading to false negatives)?
-I do not see the supplementary material currently noted in the document on Medrxiv for review, so I have not reviewed this supplementary content.
-Minor typographical/grammatical errors noted by me have been directly submitted to one of the working group members.
Sincerely,<br /> Laura Hemmer, M.D.
On 2021-06-13 20:25:12, user Gaurav Pandey wrote:
This article has now been published at https://www.nature.com/arti...
On 2020-04-19 09:51:55, user Arne Elofsson wrote:
Just a note (from Arne): It is clear that our predictions for Sweden (done a week ago) were quite wrong (as it earlier models), the exponential increase in deaths in Sweden has not materialized. This will be made clear in a revised version - along with further analysis.
On 2020-08-24 15:23:42, user Ivan Berlin wrote:
Very nice study, maybe the first one that includes a control group.<br /> The authors do not discuss the intriguing discrepancy in the results that is that hospitalization for COVID-19 is less likely among NRT users compared to non-users but mortality is substantially higher. Is it conceivable that NRT users (proxy of smokers) are less likely to be hospitalized than nonsmokers? A selection bias potentially originating from the fact that smokers have more respiratory (and other) symptoms than nonsmokers leading to reduced hospitalization rate of smokers by health care providers. If this is likely, then hospitalization cannot be a proxy of COVID-19 severity.
On 2025-05-13 14:50:33, user Jasmohan Bajaj wrote:
this is now published in Clinical and Translational Gastroenterology https://journals.lww.com/ctg/abstract/9900/a_national_survey_shows_a_dilemma_towards_sbp.397.aspx
On 2025-10-15 20:49:15, user jpirruccello wrote:
This has been published; please see https://pubmed.ncbi.nlm.nih.gov/37019578/
On 2020-07-12 16:00:48, user Marco Confalonieri wrote:
Miriam, thank you for your observation: you're right.<br /> Actually, the reported registration number for ClinicalTrials.gov at page 3 is correct (NCT04323592). Nevertheless, at page 5 of the same manuscript there was a typo (a 9 more). <br /> The link to our study at ClinicalTrials.gov is https://clinicaltrials.gov/...<br /> Kind regards<br /> Marco
On 2020-06-22 19:04:41, user Unknown wrote:
I'm not sure if you were already aware, but John Ioannidis (and others) wrote something similar to what you are describing in the 6-11-20 article at this link:
On 2020-03-13 11:54:03, user Murat Von Marit wrote:
For what temperature is the time you set?<br /> 4C? 20C? 40?<br /> And what about Textile,Fabric,Clothes?
On 2020-06-18 18:59:17, user mike wrote:
I read a earlier MSM version of this report last week. Somehow the firm conclusion was that none of the recorded infections studied were come by by touching " infected " surfaces. I can't, even reading between the lines, find that conclusion in the pdf.
On 2020-04-11 07:57:42, user Jean Perron wrote:
This paper appears to be a hoax. Most evidently, the data on Figure 5 is not at all from Reference 17 and does not correspond to the Covid-19 age association of any country. But the whole premise of the paper is flawed: CFR cannot be compared among countries without modeling test strategies (more tests lowers CFR both mathematically and as a management tool), and modeling the spread of the disease (for many reasons CFR increases as the disease spreads, e.g. people take time to die). Finally, among-country association between vitamin D defiency and CFR does not constitute evidence of causality: a lot of things differ between Germans and Italians. (Last: the paper is very poorly written and full of errors and typos).
On 2020-06-29 19:23:20, user Thomas Ichim wrote:
What do you guys think of using QuadraMune? AT least it is natural
On 2020-05-16 02:45:51, user Sinai Immunol Review Project wrote:
Functional alteration of innate T cells in critically ill Covid-19 patients
Jouan Y et al., medRxic 2020.05.03.20089300; doi: https://doi.org/10.1101/202...
Keywords<br /> • Innate T cells (MAIT, iNT, ?? T cells)
• Critically ill COVID-19 patients
• SARS-CoV-2
Main findings<br /> Innate T cells are a heterogeneous group of immune cells, including mucosal-associated invariant T cells (MAIT), NKT cells (NKT) and ?? T cells, which differ from conventional T cells based on their unique features considered characteristic of both the innate and adaptive immune system. In this preprint, Jouan et al. aimed to address the potential contribution of innate T cells to COVID-19 lung immunopathology. SARS-CoV-2 PCR-positive ICU patients, diagnosed with severe COVID-19 according to clinical symptoms, were enrolled in a prospective study on average within 10 days of disease onset, and were immunologically followed up for two weeks. Of 30 patients, 24 presented with ARDS with the need for invasive mechanical ventilation either at the time of ICU admission (n=20) or later on (n=4); to maintain sufficient systemic oxygenation, one patient further required extracorporeal membrane oxygenation (ECMO), whereas another patient succumbed to disease two days post study inclusion. By the end of the observation period, 15 individuals could be discharged from ICU, while 9/14 ICU patients remained on invasive mechanical ventilation. Similar to several recent reports, the authors observed COVID-19-associated mild to severe lymphopenia, which correlated with disease severity, as well as concomitantly higher neutrophil-to-lymphocyte ratios when compared to age- and sex-matched healthy controls (n=20). Likewise, albeit relatively low overall, plasma levels of the proinflammatory cytokines IL-1?, IL-6, IL-1R? and IFN-?2, a marker of the antiviral type I IFN response, were found to be higher in COVID-19 patients vs. healthy individuals (n=10). Of particular note, these cytokines were further increased in endotracheal aspirate (ETA) supernatants relative to whole blood samples obtained from the same patients (n=20), suggesting locally enhanced airway inflammation at the time of ICU admission. Moreover, analyzing relative frequencies of circulating innate T cells in COVID-19 ICU patients (n=30) vs. age-/sex-matched healthy controls (n=20), the authors report a profound decrease in MAIT (ca. 6-fold; identified by 5-OP-RU loaded MR1 tetramer vs. unloaded control tetramer) as well as in iNKT cells (ca. 7 fold; identified by PBS-57 glycolipid-loaded CD1d tetramer vs. unloaded control tetramer), while ?? T cell frequencies remained largely stable (with the exception of a slight decrease in the V?2 subset as well as a likely increase in the V?3 subset). Interestingly, both MAIT and ?? T cell were detected in early ETA samples of 12/21 ICU patients on invasive mechanical ventilation, whereas iNKT cells were seemingly absent. Of importance, relative MAIT but not ?? T numbers were increased in ETA specimens when compared to whole blood samples obtained from the same donors, suggesting enhanced airway recruitment in contrast to potential extravasation processes as a result of inflammation-induced capillary leakage. Accordingly, the presence of innate T cells was restricted to ETA samples containing high levels of chemo-attractive CXCL10 and CXCL12. Moreover, very basic phenotypic analysis of blood-circulating innate T cells by flow cytometry revealed increased activation based on enhanced expression of CD69 and PD-1 in COVID-19 vs. healthy controls, as well as a potential trend towards exhaustion based on continuous PD-1 expression observed after repeated sampling. Enhanced levels of CD69 and PD-1 were further associated with high levels of plasma Il-18, which has been previously linked to innate T cell activation in viral infections (https://www.jimmunol.org/co... "https://www.jimmunol.org/content/194/8/3890)"). In line with the above observations, innate T cell-expressed activation markers were found to be higher at the presumable site of inflammation as compared to peripheral circulation. Additionally, functional analysis of circulating MAIT, iNKT, and ?? T cell in COVID-19 vs. healthy controls showed substantially reduced IFN? along with slightly increased production of IL-17a following stimulation with PMA/Ionomycin, corroborating a potential tendency of peripheral cellular exhaustion. Conversely, both IFN? and IL-17a were increased in ETA over plasma samples in COVID-19 ICU patients and levels of both cytokines were equally higher in those ETA specimens containing innate T cells suggesting that these cells contribute to local airway proinflammatory cytokine production. Most importantly, while repeated sampling revealed a further decrease of CD69+ activated circulatory MAIT, iNKT, and ?? T in COVID-19 over time, the authors observed that higher frequencies of activated circulatory MAIT and iNKT cells on day 7 correlated moderately with increased PaO2/FiO2 ratios, indicative of preserved lung oxygenation, thus suggesting that activation of innate T cells in early COVID-19 may be used as a predictor of disease severity.
Limitations<br /> Technical/biological<br /> In addition to the relatively small study size, it remains somewhat unclear how many ICU patients were included in some experiments pertaining to ETA sample collection. Furthermore, a more stringent clinical characterization of enrolled patients (in addition to basic information presented in table 1) would add further impact to the observations made here regarding the potential role of innate T cells in critical COVID-19 as well as regarding any further association with ARDS severity, death or clinical course in general. To adequately address some of these questions, larger studies including patients across all clinical stages as well as early-onset and longitudinal sampling will be needed. Similarly, it would be of great interest to further examine kinetics of both potential innate T cell migration to inflamed airways and general function by means of repeated sampling. Additionally, extended flow-cytometric phenotyping of both circulatory and airway innate T cells will be needed to further characterize these populations beyond their basic activation status. In this context, general gating strategies should be included in the supplemental.
General<br /> Throughout the manuscript, some references pertaining to specific figures or their content are incorrect. For example, supplementary figure 1A shows a COVID-19 lung CT scan, but no healthy control scan as suggested by the complementary figure legend. Data on plasma and ETA IL-1R? levels are displayed in figure 1 E & F, not in supplementary figure 1B as stated in the manuscript. Supplementary figure 1B does not exist. Similarly, some of the literature references seem to have been mixed up (cf. reference 16 on the role of MAIT cells in diabetes and obesity vs. on the role of type I IFN responses as cited in manuscript; reference 23 is missing).
Significance<br /> Innate T cells have been previously shown to mediate potent antiviral immune mechanisms in both mouse and human studies (reviewed in https://link.springer.com/c... "https://link.springer.com/content/pdf/10.1007/s11684-017-0606-8.pdf)"). Observations made here generally corroborate limited data reported in two recent preprints (https://www.biorxiv.org/con... https://www.medrxiv.org/con... "https://www.medrxiv.org/content/10.1101/2020.04.05.20046433v1.full.pdf)") on activation status and frequencies of ?? T in COVID-19 patients. Notably, this preprint by Jouan et al. is first to assess basic functional changes of circulatory innate T cells (including MAIT, iNKT and ?? T subsets) as well as frequencies and limited phenotypic analysis of airway innate T cells in critical COVID-19. Further studies including larger cohorts of patients of variable disease are now needed to conclusively determine the role of innate T cells in COVID-19 immunopathology.
This review was undertaken by Verena van der Heide as part of a project by students, postdocs and faculty at the Precision Immunology Institute of the Icahn School of Medicine at Mount Sinai.
On 2021-04-14 16:38:58, user Anke Huels wrote:
This work has been published in The Lancet's EClinical Medicine: https://www.thelancet.com/j... (open access)
On 2021-06-13 01:39:10, user cathyx wrote:
You are using relative risk reduction instead of absolute risk reduction in your calculations. <br /> Therefore, your analysis is flawed.
On 2024-06-16 14:15:45, user Praba wrote:
Dear Authors, this paper is interesting. Congratulations to all authors. Could you please give complete details about the FnCas9 purification (How much vol of culture was used to purify the proteins that was shown in Suppl Fig 9 and what was the yield obtained at the end. These information are not trivial and they are important for the researchers who follow the paper. Hope you will append the details.
On 2021-12-20 09:12:23, user andreiyd wrote:
Soon you will not have uninfected cohort. And even now I don't know how they could actually determine who was infected and who wasn't. At least in my context I barely now anyone who was not infected. And from those who don't have a positive test who knows if they were asymptomatic or were never infected? Nucleocapsid anti bodies wain even faster than anti spike and many didn't even developed such. You can't reliably distinguish between not infected and infected but not tested. Then we will have now this new variant which seems to be a lot milder (so even more undetected/untested infections) and a lot more transmissible which means less and less people in the non infected and non vaccinated cohort. Then you have vaccinations which are continuously increasing which again shrink your cohort.
On 2020-07-13 11:08:47, user Andrew D'Silva wrote:
In any infection IgM responses converting to IgG responses fall over time and rise when there is a secondary antigen exposure. Why do these findings suggest that there is loss of immunity with declining neutralising antibody levels? Surely the questions are: what happens after secondary antigen exposure? Do the neutralising antibody levels rise again? Do they protect from developing the same clinical disease again? Do they affect severity of disease after second exposure?
On 2021-07-01 02:18:40, user akcita wrote:
I was hoping that there would be obvious conflicts of Interest. Alas, it seems the Authors barely reviewed their own study and left it to a technical editor, and the viewing public to fix their bad science...
On 2024-02-09 18:56:46, user Adriano Aguzzi wrote:
It was brought to my attention that this manuscript contains an error. In Figure 2D, the band representing tau immunoreactivity is duplicated between the 2nd and the 10th lane. The raw data of the uncropped blot from which Figure 2D is derived (Supplemental Fig. S1) provides the correct images. The transposition error in Fig. 2D has no impact on the interpretation of the results and will be corrected in a future version of this manuscript. Adriano Aguzzi
On 2021-12-09 21:54:04, user 1969er Kornwestheim wrote:
Any Infos about peer reviewing?
On 2021-10-10 04:51:38, user kdrl nakle wrote:
Your samples are too small for the sweeping conclusion you made about the variant outcome comparison.
On 2022-01-12 15:14:05, user ABR wrote:
This "study", like most other non-peer-reviewed ones being cited by the media, makes no attempt to control for vaccination status. Simply put, if Omicron cases consist of 80% vaccinated and 20% unvaccinated, whereas Delta cases consist of 20% vaccinated and 80% unvaccinated, then you will expect that out of all omicron patients, a smaller percentage is going to get severe disease, simply because more of them have been vaccinated, which we know protects against severe disease. TLDR, there is NO information here, move on.
On 2024-01-17 20:36:43, user Karen Eddleman wrote:
In the acknowledgements section, there is a sentence that appears in both paragraphs: "The All of Us Research Program would not be possible without the partnership of contributions made by its participants."
Also, the correct spelling should be "principal" in this sentence: "See the supplementary information for a roster of past and present All of Us principle investigators."
On 2020-08-12 17:28:58, user Lee Rague wrote:
This study has been recently published as follow:
Labrague, L. J., & de los Santos, J. (2020). COVID-19 anxiety among frontline nurses: predictive role of organisational support, personal resilience and social support. Journal of Nursing Management.
On 2020-04-30 08:59:22, user Skerdi wrote:
It would be great if you could compute the RAASi/nonRAASi difference adjusted for the relevant comorbidities you cite (age, gender, ICU entry on day of admission, serum ferritin, insulin-dependent diabetes mellitus and cardiac arrhythmia history).
This would help give a sense of whether RAASi are likely to work only if taken chronically before encountering Covid-19 (in which case their effect adjusted on clinical baseline would shrink or disappear) or if they could also work when started after disease onset (if adjustment for clinical baseline does not erase their effect).
On 2020-04-27 17:01:13, user Paul Floto wrote:
It should be worthy of research to examine whether copper compounds are as toxic to the virus causing COVID-19 as they are to poliovirus. Since the toxicity level of copper to humans is already well established, if a lower level is effective against viral protease, then drug development could be quite rapid.
A letter that appeared online recently in the New England Journal of Medicine demonstrated that the COVID-19 virus had a shorter life span on a copper surface than on many other materials.
Since copper has an essential role in human health, it might be possible that the growth of the COVID-19 virus is impacted by the copper level in the host organism. Copper levels vary significantly by diet, and are significantly reduced by even small quantities of molybdenum in the diet.
Widely varying rates of infection and death might be explained by variation in typical copper levels in the diet which would influence serum level of copper in blood and tissue. Has any measurement of serum copper level been made in patients with differing response to COVID-19 infection?
On 2023-02-18 07:18:25, user Anikó Lovik wrote:
This preprint has now been published in an extended and revised version in PLOS One: https://doi.org/10.1371/jou...
On 2020-04-17 15:27:19, user Oleg Gasul wrote:
There is big difference. <br /> https://interaktiv.morgenpo...<br /> You can paint map of the DDR in past :-)
On 2021-10-18 09:01:15, user Jan Masleid wrote:
https://www.youtube.com/wat... <br /> Let's Review Novavax Phase III Interim Results (Released on Oct 11th 2021)<br /> Oct 17, 2021<br /> Drbeen Medical Lectures<br /> 420K subscribers<br /> Finally Novavax Phase III Trial Interim Results
On 2021-02-24 01:18:23, user algebra wrote:
Anecdotes of people who had Covid months ago and got the vaccine are alarming. Acquaintances report the side effects of the second shot were worse than the disease itself. Are these people reporting their reactions? No they just tough it out. They were told to expect side effects. How many of them are out there? Does anybody know? <br /> My own physician has been hearing some of these stories and suggests waiting.
On 2020-10-21 19:18:46, user Alan Wilson wrote:
I would recommend the authors to check other recently published ASRM abstracts in the topic:
On 2020-05-31 13:21:46, user Pete Jones wrote:
Nice. Although I don't think the SVOP guys would be happy to not to be mentioned ( https://tvst.arvojournals.o... )
I take your point about calibration being key ("discrete eye movement perimetry is heavily reliant on optimal instrument calibration: if the average calibration error exceeds the ROI radius of each target, it is very well possible to have completely invalid maps."), and funnily enough this was precisely the problem when they tried SVOP at moorfields ( <br /> https://pubmed.ncbi.nlm.nih... ).
It isn't true, however, that calibration need be 'optimal'. And it isn't necessarily the case that one needs to use rigid/binary ROIs (I originally used a probabilistic [Maximum Likelihood] estimator, and still do for the calibration stage. It caused more problems than it solved for the main test stage though, where a simple ROI is often sufficient). But yeah, calibration is certainly a huge and constant challenge.
On 2020-03-05 12:08:26, user Luna Liu wrote:
DOI: 10.1002/path.1560<br /> In this article, they haven't found SARS virus in tesis but in distal convoluted renal tubule.
On 2020-04-10 09:17:04, user Rosemary TATE wrote:
Authors could you please provide me with the CSV data file that I requested in an email to the corresponding author on Monday. Or better still could you please upload it?<br /> Thanks
On 2022-10-25 02:28:09, user Zainab Sikander wrote:
I would like to start with saying thank you for addressing the issues of comorbidity and overlapping symptoms in your research paper. It is a big problem for psychologists and psychiatrists to accurately make a diagnosis. This study makes me believe there is a solution and maybe this can be used in an actual medical setting to diagnose patients accurately. This brings me to my question, which system did you use for defining the symptoms and disease? I know about DSM-5 having criteria for diagnosis and the diagnosis has to be based on the most updated revised version of it, so what was used for this study? The summaries from the brain bank were how old and if they were defined based on a system like the DSM? Also, I would like to see a more depth study on mental illnesses. My initial impression was that those will be discussed in as much depth but they weren't focused on as much. Is there going to be a future research? Will this tool be upgraded and approved to use in behavioral health centers and medical settings?
On 2020-07-16 20:34:30, user David Halvorson wrote:
This paper should not be published in its present form. The following statement is totally without a factual basis; "Thus, it is not clear that the risk of getting infected during a flight is any higher than the risk associated with everyday activities during the pandemic." It is obvious to most of the air traveling population of the world that the risk associated with flying is much greater than the risk associated with everyday activities. The large number of people in close proximity violate two of the few tools available to us according to health professionals. On another note, it is obvious that emptying 1/3 of the seats would reduce the number of passengers and similarly reduce the risk.
On 2020-03-30 18:56:07, user Preci Genome wrote:
https://www.medrxiv.org/con...<br /> Another related papers was also published recently.
On 2021-06-08 06:26:59, user Holger Lundstrom wrote:
Hello Suzy,
The results do not suggest that carrageenan interferes with the PCR assay in this case. The rate of "symptoms with negative PCR" is approximately the same in both groups. If there was interference, this rate would be skewed towards the experimental group.
The difference in those infected vs. those protected, however, seems comparably small. Percent-wise it is a lot, viewed as total numbers it is not convincing.
On 2021-03-17 10:51:20, user D Greenwood wrote:
The trials registry protocol suggests n=507 symptomatic cases would be recruited and followed up, to "characterise prevalence and severity of organ volume change and damage in patients recovering from COVID-19 disease". Yet the preprint appears to focus on n=201 individuals still "symptomatic after recovery" and it is therefore not surprising that nearly 100% of them report symptoms, as this appears to be the eligibility criteria for the paper. Either that, or a substantial deviation from the published protocol. I therefore agree with previous comments on the importance of clarifying the recruitment process and inclusion/exclusion criteria so we know what the denominator is here. There is some benefit in knowing what the % of organ damage is in people with continuing symptoms, but the crucial question that health services and strategic leaders need to know is what this is as a % of all cases, or at least as a % of symptomatic cases. I hope that a revised version of this paper will make that clearer.
On 2022-01-16 13:18:04, user Clint Digger wrote:
And the vaccination rate in Quebec?
On 2021-08-20 12:21:27, user Jodi Schneider wrote:
Additional breakthrough infection data (from states that are collecting more info than the CDC is expecting) could be useful for comparison and contextualization in discussion. https://www.kff.org/policy-...
On 2020-12-27 21:03:59, user CO2lover wrote:
I wonder if those samples are ever tested for influenza?