Questions related to Infection
A patient with desminopathy (mutation Thr341Pro DES in a heterozygous state) with the progression of the disease has a decrease in taste and smell, immunosuppression, and an increase in IgA in the blood.
Oddly enough, but all this is characteristic of infections, including viral ones. For example, it is known that if the hepatitis C virus is not treated, then death will occur in 20 years.
In the identified case of late onset desminopathy, muscle weakness manifests itself at the age of 30, and death occurs 20 years after the onset of the disease.
Could the desmin mutation in myofibrillar myopathy be caused by an infection?
Perhaps the infection contributes to the progression of desminopathy?
- There is, no country in the world is facing the challenges of COVID- 19. This Corona virushas already infected more than one million people and killed more than 100,000 peopleworldwide. Trends clearly indicate that more people will be infected and killed in the comingweeks. But the large-scale pandemic crisis caused by COVID- 19 has already had asignificant impact on economic sectors, social behaviour, cultural practices, populationdynamics, politics and governance, and importantly public health. I don't think there is asingle researcher in any discipline who would disagree that this is only the beginning of thecrisis and that the impacts of the pandemic will not last for the next couple of decades andwill not change the world order in economic, social, political, cultural and demographicterms.As part of our research on population dynamics and climate change, we have studied theimpacts of different extreme weather events such as floods, cyclones, drought on fertilitydynamics, particularly fertility preference, desired number of children, age at first marriageand gender preference in different areas of Bangladesh affected by different extreme events.Our studies revealed various implications for people affected by different events. Theseinclude high fertility, low contraceptive use and relatively low age at marriage, highpreference for sons and high perceived risk of child death in flood-prone areas. However, thiswas a mix for other areas prone to extreme weather events.In research, we see COVID- 19 as one of the important factors contributing to populationdynamics, and the impacts of infection and death from the virus will influence all areas ofpeople's lives in the future. It can reshape the population and age structure in all countries,which may differ from country to country depending on the impact and severity of the virus.This could influence people's fertility decisions in terms of the experiences (number ofdeaths, age and sex of the dead, perception of the risk of death of young children and youngpeople, infected and stories of death in social networks) they face during the pandemicsituation. Thus, our interest is to explain how the impact of COVID- 19 contributes tofertility dynamics, in particular fertility preference, age at marriage, gender preference,and desired number of children.For COVID- 19, people of different age groups are infected and a portion of each age groupdies. Although people in older age groups die at a much higher rate than other groups, this isnot true for all the countries that now have the highest number of deaths. These days, we canalso see that children aged 0 to 9 have died. Young people between the ages of 20 and 30 and30 to 40 are also infected and dying from the virus. It has also been shown that the proportion of deaths among men is much higher than among women. These changes may influence thedynamics of fertility in the years to come for people who are experienced with the death ofyoung people and young children, especially men. Individuals' or couples' experienceswith death and their perceptions of the risk of their children or young people dyingbecause of the pandemic may help rethink their fertility decisions and influence toincrease fertility preferences, particularly for male children.There are state regulations for as many countries as possible where people have to maintain asocial distance, which means that people will stay at home, and not go to public places andmeet other groups of people. They can go out when they have a valid reason and it is anemergency. Otherwise, there are sanctions in all countries suffering from COVID- 19. In thiscase, people have to stay home and spend time with their families. So couples live togetherand they are much more likely to get closer. They may not have contraception availablebecause of the emergency situation, especially in rural areas because of the lack oftransportation and the lock-in situation. Staying at home day after day can encouragecouples to get closer together as one of the recreational options. There, this leads toincrease conception and high births in the years to come after the control of the virusinfection.There may be another problem with COVID- 19 whereby families who have experiencedinfection with the virus and have lost one or more family members may face socialstigmatization. Families may be labelled and other families or members outside their familymay avoid the families and be less interested in connecting with the families. People ofmarriageable age in affected families may find it difficult to get proposals from families whohave not been infected or who have had stories of death. This may delay their marriage andwomen may lose time from their childbearing age. As a result, it may even delay marriage foryoung people, especially young girls, and young girls may face a delay in their age atmarriage and childbearing. Young girls or boys of marriageable age from uninfected familiesmay receive much more attention and be very demanding in the marriage process comparedto families with infection and death. In this case, people from low-income families whohave suffered economic loss due to COVID- 19 without having been directly infected orhaving infected and experienced the death of a family member may decide to arrange amarriage for their young girls even if they are not 18 years old.
1) Is the pediatric age group (<18) more or less susceptible to acquiring CoV-2 infection than other age groups?
2) Why does CoV-2 infection in the pediatric age group (<18) present as asymptomatic in nearly all cases?
3) Do asymptomatic children (<18 yrs) who are positive for CoV-2 by URT RNA test transmit the infection, and if so, is the route of transmission a respiratory route, or an oral route, or both?
4) Do asymptomatic children (<18 yrs) who are positive for CoV-2 by URT RNA test transmit the infection if their status is IgM+ IgG-, IgM+ IgG+, or both?
5) Is infection with CoV-2 acquired from a pediatric (<18) source always, rarely, or sometimes associated with COVID in adults?
When staining with hematoxylin and eosin of a muscle biopsy from a patient with T341P desminopathy, we observe accumulations of inclusions similar to nuclei (arrows in figures 1 and 2, x280). And outside of these accumulations - adipose tissue, which used to be muscle tissue. There are no such massive accumulations of inclusions in adjacent muscle fibers. We assume that clusters of inclusions are not nuclei? Figure 2 is the inverted figure 1.
I need to know the best absorbance value that correlates the growth of Agrobacterium that can be used to infect plant callus. I have tried with 1.0 at 600 nm infection which helped me to transform the callus successfully but Agrobacterium overgrows seems to be resistant even to cefotaxime (even at the highest concentration)
For a long time people drank or ate medicinal herbs from nature or the forest to maintain the health of their bodies.
I'm transducing Ly1 and L363 cell lines using our standard protocol for retroviral transduction. The cells are successfully transduced as evidenced by GFP expression. However, after 4-5 days they start dying off and look really stressed. I'm suspecting polybrene since we've got a new batch. The cells look really weird, irregular and start forming clumps which they don't normally do in standard cell culture. I've tried using the same polybrene concentration (8ug/ml) in standard culture medium without the virus to check toxicity and it appears that it is decreased. Which concentrations do you normally use? Should I make a polybrene concentration curve to find the minimal nontoxic condition?
Can anyone recognize what kind of infection do we have here in the picture? In the picture, the focus is in a different Z axis than the cells, the cells are blured in the picture.
Media has been changed 3 ago and it is not dryed (if there is a doubt regarding it). Cells itself grow normaly, meaning cells still adherent.
I have tried different concentrations of polybrene during experiment but as AML cells are difficult to transfect so could not determine which is the best concentration? To what extent it causes the cell toxicity to death?
Hi everyone! We have a bit of a problem in our lab where every now and again we get a very strange contamination in TC (please see attached photos/ videos). Our work is completely pen/strep free with no added antibiotics, but this contamination looks like no bacteria I have seen before. The movement is also very strange and sometimes they can be seen almost cartwheeling/ doing 360 degree spins in the flask. I would just love to know if anyone has experienced this before and what I can do to make sure it doesn't happen again. Thanks so much in advance!
My question revolves around the degree of infection (onset), appearance of symptoms, the extent of illness and the possible outcome among COVID-19 patients. Do their respective blood groups as well as the specific rhesus factor make any considerable differences?
Which Animal species can transmit the Coronavirus (COVID-19) to humans?
What are the animals incriminated to transmit COVID-19 to humans and how we deal with them to avoid infection?
I want to know the kinetics of a transcriptomic response to infection. I am interested in the earliest time points, how minutes does it take a cell to activate a gene upon infection?
Thank you for your insights
If possible, active participation for the purpose of collecting the types of drugs used, as well as medicinal plants, each according to their country, mentioning the country, and thank you for your kind cooperation.
UTI and maybe sepsis are occasionally encountered after URS and PCNL. From your daily practice What are the possible strategies to prevent infection after RIRS or PCNL?
During covid-19 infection antibodies are developed against virus. Is these antibodies are life long for that strain competing against infections.
In epidemiology modelling, in order to calibrate such a model, we require discrete observations of the population compartments functions. If we neglect the underreporting and other issues (such as vital dynamics etc.), observing the most compartments sizes is relatively easy. The infected (I) population is the integrated newly infections per day, reduced by the integrated removed. It is the case with the removed (R) compartment, which is constituted by the integrated newly recovered and deceased per day. In the classical SIR model, again rejecting the possibility of reinfection, the susceptible (S) class is calculated as the whole population, reduced by the infected and removed. Statistics is also collected for other compartments as quarantined (Q), hospitalized (H) and so on.
But how to measure the exposed (E) population share? Is there any (real world) statistics, or how to calculate it from the existing data?
What is the possible diagnosis and management for the following case?
Healthy male 43 years old, infected with corona virus ... had 4 days of fever (38-39.5) with fatigue and sore throat for 1 day (with no other symptoms) managed by antipyretics only
D-dimer on 7th day 3600 (normal less than 500), WBC and lymphocyte count normal. CRP 130mg/dl (normal less than 10)
Oxygen saturation between 92-95 (by pulse oximeter)
Chest X-ray normal (CT scan was not done)
Started then rivaroxaban 10mg once daily ....
2 days after start rivaroxaban (9 days from the infection) d-dimer reduced to 2000 ... CRP 90
4 days from rivaroxaban (11 days from infection) O2 saturation by pulse oximeter was between 84-90 (with no dyspnea and fever and no fatigue (very well activity)) ...
on fifth day from starting rivaroxaban (13 day from infection) d - dimer 2100 (increased from the 2nd day) and CRP reduced to 14 (normal less than 10) Oxygen saturation 92-95%
What is the reason behind that? is it pulmonary embolism? or is it acceptable?
Is there any need to start therapeutic anticoagulant dose? or there is a need to Oxygen therapy or anti viral therapy?
Hello to all
About 3 months ago, I asked this question, but I didn't get a comprehensive answer.
Can a person who has had Coronavirus disease (COVID-19) get infected again?
These days I was reading a lot of articles about coronavirus and hypertension.
Is known that S protein of coronavirus use ACE2 as receptor to entry in the cell, a protein related to renin-angiotensin system. On the other hand, there are anti-hypertensive drugs that increase the expression of ACE2 (vasodilator function). Could they be facilitating th cell infection? Other explanation could be that the virus is blocking this protein, so increasing the blood pressure and afecting the sick.
Drugs that increase ACE2 levels could facilitate infection (although this is not totally clear, Li et al, J. Virol, 2004), but once infected, they would prevent sever lung infection, since the infection lowers ACE2 levels (Inai et al, Nature 2005, Exp. Physiol. 2008). Would not be better give another antihypertensive drug during the epidemic? (beta-blockers, calcium antagonists, diuretics, ...) Perhaps prevent the masive infection, and once one hypertensive is infected would be better give those that increase ACE2 levels, so preventing the onset of severe lung disease.
I would like to reunite those interested in estimating using different approach the true underlying number of SARS-CoV-2 infected individuals. This is important since this number give us an idea about those undetected individuals spreading the infection and causing deaths amongst the elderly and individuals with preexisting health conditions.
What is the most common type of surgical site infection?
How do surgical site infections occur?
Can you get an infection 2 months after surgery?
What kind of infection can you get after surgery?
How common are surgical site infections?
What are the signs of sepsis after surgery?
There is currently no evidence that people who have recovered from COVID-19 and have antibodies are protected from a second infection. The development of immunity to a pathogen through natural infection is a multi-step process.
What is the difference between infection of a fracture fixation device and a joint prosthesis? and do they have anything in common? Thank you!
As we know the immune system in both children and adult is impaired. The question is that why the covid-virus infection is very rare in children compare to young and adult people
Vietnam has no more new confirmed cases over the past three weeks. A total of 16 cases were treated.
Number of factors should be considered
1. Government's Actions
2. Systems and Individual levels
3. Evidence-based approaches
How to determine which bacterial virulence factor (bacterial toxins or cell wall components) in relevance to human sepsis or bacterial infection will interact or regulate my target protein of interest. I have examined with LPS treatment in a dose and time dependent fashion. However, I did not notice any difference in expression. Are there any panel of bacterial virulence factors commercially available or bioinformatically possible?
Recently, a study published in France showed that combination of Hydroxychloroquine with Azithromycin could help to treat patients with COVID-19. As we know that Azithromycin is an antibiotic belonging to Macrolid family that is usually used to treat Bacterial infection. Hence, I am wondering how Azithromycin could help in treating Viral infection. My thought is it is more related to Pharmacokinetic/Pharmacodynamic in which Azithromycin might helps to increase the absorption and boost the effect of Hydroxychloroquine by making it more effective and prone to attach COVID-19 virus. I would like to hear your opinions and thoughts regarding this matter.
I'm currently working on a lung infection model for a project, and have tried EVERY method we can find for consistent intratracheal administration of our infection (biolite, small tubing down the trachea, catheters, feeding needles, you name it we've researched it.) It seems like the Penn Century microspray device is the top of the line in a well distributed and consistent infection and/or treatment, and we really want to use one.
Unfortunately we cant find one, anywhere. They went out of business in 2015. If your lab has one you rarely use, we'd love to buy it. We'd prefer not to purchase the $2000 one from Bio-Equip in China, they aren't licensed by penn century and we don't know what quality we would get (if you've ordered this other version, please tell me about it!)
Dear colleques, I would like your feedback on this:
COVID-19 test: The antibody-based test does not work when the innate immune system fights the infection
Søren Ventegodt, MD, MMedSci, EU-MSc-CAM
Quality-of-Life Research Center, Copenhagen and Research Clinic for Holistic Medicine, Psychology, and Sexology, Copenhagen, Denmark
Correspondence: Søren Ventegodt, MD, MMedSci, EU-MSc-CAM, Quality-of-Life Research Center, Schlegels Allé 4, 5tv, 1807 Frb C, Copenhagen, Denmark. Email: email@example.com
There are two lines of immunological defense in the vertebrate immune system: The innate and adaptive immune system. These two are related, the innate being the evolutionary oldest, and the functional basis of the adaptive immune system. The innate immune system is able to handle small and local infections. A small bolus of Corona COVID-19 virus, say about 20 viral units, in small, airborne drops from the breath of a healthy infected person, is normally handled without any symptoms. Still this gives immunological learning and immunity. If the innate immune system is handling the small boluses of virus, there is no antibodies to detect. This means that only the people who have a weak innate immune system will have a symptomatic infection which calls for the second line of the immune defense, the adaptive immune system response with antibodies. It is therefore very likely that every single person living in a city is being infected with COVID-19. Therefore, the number of infected people are likely to be 100 times larger than estimated from random population tests testing for Corona (inclusive COVID-19) using antibody tests. Therefore, all the numbers of infection fatality rates (IFR) we are collecting these days from all countries must be set 100 times lover than estimated by World Health Organization and other authorities using the present Corona test to estimate the mortality of COVID-19. Furthermore, if we include the resent findings from large autopsy studies of people who died with COVID-19 showing that there are no people dying from COVID-19, we are forced to set IFR=0.
It is well known to all immunologists that there are two lines of immunological defense in the vertebrate immune system: The innate and adaptive immune system (1-4). It is also well known how these two are related, the innate being the evolutionary oldest, and the functional basis of the adaptive immune system.
The innate immune system in COVID-19
The innate immune system is able to handle small and local infections, so if you have a small bolus of virus, say about 20 viral units in small, airborne drops from the breath of a healthy infected person, this is normally handled without any symptoms (1-5). Still it seems to give immunological learning as the about 100 different viruses, that constantly attacks the human airways in new forms because of mutations are easily handled.
In COVID-19 this understanding is essential, as it explains how a population of mammals can become immune to the hundreds of viruses they co-evolve with (5). While this seems to be basic textbook knowledge for immunologists it seems to be unknown to the health authorities that these days want to base the number of infected people on antibody tests. If the innate immune system is handling the small boluses of virus, there is no antibodies to find (1-5). This means that only the people who have a weak innate immune system will have a symptomatic infection which calls for the second line of immune defense, the adaptive immune system response with antibodies (1-5).
It means that what you find with the test for COVID-19 with antibodies is the number of people in the population that either have a weak innate immune system, or who got a massive amount of virus so that the innate immune system could not handle it.
The IFRs are calculated to orders (100 times) to large everywhere because of this error
The consequence of this is that the number of COVID-19 infected is counted 100 times to small and the infection mortality rate (IFR) is calculated 100 times to large.
The IFR is the ratio: people dead by COVID-19/people infected by COVID-19. In estimating this number it is worth remembering that the people who have specialized in autopsies of people dying with COVID-19, like professor Klaus Püschel, have concluded that nobody is actually dying from COVID-19 (6).
Combining the likelihood that every single person living in a city together with other people is getting infected with COVID-19 as healthy infected people are spreading the small drops with small amounts of viruses effectively, and the fact that the experts doing autopsies of the dead people testing positive for COVID-19 are not finding anybody dying from COVID-19, we are forced to set the IMF=0.
Translated to our understanding, COVID-19 is not deadly at all. Nobody dies from an infection with COVID-19, because everybody is already immune, due to countless exposures to Corona virus in the past. Because the infection was symptomless (subclinical) and handled without problems by our innate immune system, we did not notice, and thus we do not realize that we are immune. Thus the fear of COVID-19, and all the measures to prevent the infection, are totally and absolutely without any scientific foundation and justification.
As yet, no one has found the animal that gave people Covid-19. The Center for Disease Control (CDC) points out that at this time, there is no evidence that animals play a significant role in spreading SARS-CoV-2, the virus that causes COVID-19, to people.
SARS-CoV-2 is unprecedented in its combined characteristics: its long period of asymptomatic infection, high transmissibility, significant lethality in high-risk populations, being well-adapted to human cells since its emergence, and having the ability to hijack human innate immunity and bind with high affinity to the human ACE2 receptor.
The reason why we should try hard to figure out the origin of Covid-19 is to inform our efforts to prevent another pandemic like this from happening again. This one was an unfortunate and terrible accident. We should badly want to avoid a second occurrence. We can be blamed for allowing a second one like it if we do not work together soon to find the origin. Right now it appears likely it came directly or indirectly from bats. But specifics would better help us to avoid a second pandemic disaster. Furthermore time is not our friend in finding the origin and sooner is better before information is lost. We need all countries to support a real epidemiological investigation by an unbiased team of scientists given access and authority to take the investigation where ever it leads – possibly to patient zero or to the CoV-2 animal source.
I found a patient who has alopecia areata, it started a month back. He is found to have H.pylori infection. i wonder if there is relation between the two.
Information on questions commonly asked
Written by Saif Badran and Suhail A. Doi
The attached file has hyperlinks
Covid-19 is such a threat because it can kill healthy adults in addition to elderly people with existing health problems and because it is transmitted efficiently with an infected person spreading the disease to two or three others (R0 about 2-3). Many people will shed the virus when only mildly ill or even when they are presymptomatic, meaning the asymptomatic phase of the disease. Such cases may be considered to have asymptomatic infection, but they usually, in the majority of cases, end up being presymptomatic on the date of identification/report but do go on to develop disease. The proportion of truly asymptomatic infections is unclear but appears to be relatively rare and does not appear to be a major driver of transmission in the ongoing pandemic for this reason. Most of such patients are identified through contact tracing and will have some clinical progression on follow-up. As an example, in a study of 23 patients who tested positive, 13 had asymptomatic infection of whom 10 patients developed symptoms seven days later. In another study of 24 asymptomatic patients identified through contact tracing, only 7 remained free of clinical abnormalities, were younger (median 14 y) and had clearance of virus within 2 – 15 days. The other 17 developed clinical or imaging evidence of disease.
The most common symptoms that presymptomatic subjects go on to develop are fever (almost everyone), fatigue and dry cough. However, fever might be very low grade <100.4°F/38°C in up to a fifth of (especially younger) patients. Although not highlighted in the initial cohort studies from China, smell and taste abnormalities (eg, anosmia and dysgeusia) have also been reported as common symptoms in patients with COVID-19. Why some infections are truly asymptomatic or very mild is unknown. Age may be a factor and even symptomatic infection in children appears to be mild. In a small study of 10 children in China, symptom onset from exposure was within 2 – 10 days and clinical illness was mild: 8 had fever and the two without fever had a cough. Another report of 36 paediatric patients concurred with mild or moderate type of COVID-19, and there is a danger that the large proportion of very mild cases may lead to difficulty in identifying cases or missed cases.
The milder cases in younger patients is postulated to be tied to the aging lung environment where aged lungs counter the usual immune reaction with some tamping down of inflammation to avoid overreacting to environmental pollutants. Therefore the innate response is delayed in the elderly, ends up playing catch-up and is exuberant leading to severe disease. There are other explanations, but by and large children are able to clear the infection more efficiently and rapidly.
I read a review paper on СOVID. See the file. There is nothing about the
role of water in the process of infection and treatment from СOVID. How does a virus receive information from a cell that it can be attacked? How orders are transmitted in a cell about the beginning and end of complex processes of synthesis of biological molecules. Meanwhile, the role of water as a matrix of these processes is very great. Using the simplest models of the hydrophobic process, we have shown that in the water of the body, which is responsible for the hydrophobic interaction, there should be a large contribution of the water zero point energy (ZPE). A simple ZPE model is a harmonic oscillator whose energy is quantized. ZPE is a quantum phenomenon. The presence of ZPE in the body can be easily checked by the isotope effect. If there is a ZPE contribution in the cell water, then there must be an isotope effect.
To do this, you need to do the following experiment. To a certain concentration, humans and mice tolerate D2O well. It is necessary to select this concentration and compare the infection with COVID without the addition of D2O and with H2O.
I have not found any such research. If someone has such opportunities, I will consult in detail.
BMJ now mentions that "Long Covid" symptoms occur:
-numb hands/feet after sleeping
Covid symptoms are still occurring 6 months after infection in "mild cases that have NOT gone to hospital
PHOSP-Covid at Leicester Uni to study log term effects
see fb "Long Covid Support Group"
How can we differentiate in the laboratory an FMD positive result using ELISA or PCR. FMD antibodies positive samples may be because of vaccination or past infection.
How please explain what is the normal procedure for FMD diagnosis.
Given the current level of infection and spatial distribution, after controlling government responsiveness to control, can the level and rate of infection serve as proxy for countries level of international integration or connectedness?
Corona is spreading so quickly killing hundreds ,
ronaviruses (CoV) are a large family of viruses that cause illness ranging from the common cold to more severe diseases such as Middle East Respiratory Syndrome (MERS-CoV) and Severe Acute Respiratory Syndrome (SARS-CoV). A novel coronavirus (nCoV) is a new strain that has not been previously identified in humans.
Coronaviruses are zoonotic, meaning they are transmitted between animals and people. Detailed investigations found that SARS-CoV was transmitted from civet cats to humans and MERS-CoV from dromedary camels to humans. Several known coronaviruses are circulating in animals that have not yet infected humans.
Common signs of infection include respiratory symptoms, fever, cough, shortness of breath and breathing difficulties. In more severe cases, infection can cause pneumonia, severe acute respiratory syndrome, kidney failure and even death.
Standard recommendations to prevent infection spread include regular hand washing, covering mouth and nose when coughing and sneezing, thoroughly cooking meat and eggs. Avoid close contact with anyone showing symptoms of respiratory illness such as coughing and sneezing.
So is corona endemic or still to be overcome?
Using available data ,the median time from onset to clinical recovery for mild case approximately 2 weeks and 3 _6 weeks for patients with sever or critical disease. Are patients who recovered from COVID_19 immune from disease or may have viral relapse or re infection?
Clinical, recurrence,relapse,re infection
The affected fish (O. niloticus) are three months old. The infected fish were taken for a public display after which this infection started. Water quality parameter for the tank where the fish were stocked are as follows:
D.O. - 6.3 mg/l at 86% sat
Temperature - 25°C
Ph - 8.25
The infection was observed to start from blinding one eye then spread to the other, then the fish stops feeding and dies. The fish died after two weeks from the time of the first observation of infection.
I've been looking for SARS-COV1 vaccine efficacy and found that there was a lot of work done for developing a vaccine. The question is : since COVID19 shows similarities with the SARS-COV1, has any publication reported a level of immunization against COVID19 in the people who had previous SARS-COV1 infection?
There is some drugs, which helps for coronavirus infection - for example chloroquine, tocilizumab, remdesivir, teicoplanin etc. Do you know any other drugs for coronavirus?
I'm looking for different COVID-19 regimens that are being used for in-hospital patients.
Which are used for critical patients and which are for patients that are more mildly symptomatic?
When was the suggestion of each regimen by authorities?
We are trying to get literature on race determination of ALS of tobacco and we want to have an idea of inoculation methods and optimum conditions for ALS. We have not managed to establish ALS infection on tobacco for more than 5 years now.
I have a Markov model from a colleague for wound healing. 4 stages open infcetd closed and deathd death. The paper used to inform the transition data has monthly healing rate over 6 months and an overall infection rate within those 6 months.
My colleague used the month 1 healing data for the transition probability and calculated a monthly probability for infection. I do not underttand why the firtst months healing data was suitable rather than calculating from using all of the healing data at months 1,2,3,4,5,and 6.
My colleague is no longer here and no-one else can explain. I am concerned our out come is wrong due to wrong data being used. we are using a time horison of 5 and then 10 years.
thanks for any advice
Many people with COVID-19 have mild, flu-like symptoms, which are rather common and need to be distinguished from similar symptoms caused by common cold viruses and from allergic symptoms during springtime. How can we differentiate between covid-19 and common clod viruses.
As far as I understand, without a working version of ACE2, SARS-CoV-2 is essentially locked out of a person's immune system. Are there already some tests available on genetic forms of ACE2 that enable high inborn resistance to SARS-CoV-2 infection (similarly to CCR5-delta 32 and HIV)?
chi-square or Fisher exact test
I have a statistical question about chi-square and/or Fisher exact test.
I have a cohort data studying the cause of infection in BRD with variables such as age, gender, breed etc; where each cattle could have single or co-infection from a total of 11 common bacteria or viruses. Thus, the category may not be fully discrete with a single cattle having positive outcome for more than 1 infection.
I wanted to study the association of each of the 11 infections (yes or no) with age and other above listed factors using a chi-square or fisher exact tests?
What is the best way to analyze this? Should I run 11 tests one by one for each infection against one factor each? I will run post hoc tests with two variables if I have more than two variables (such as age).
Hello!, I'm just looking for the most common bacterial infection that causes Ventilator-associated Pneumonia? (also includes the mode of transmission via inhalation route, if possible).
I have no prior experience in the field of medicine, but am curious of the application of fuzzy logic algorithms in medical diagnosis. Would experts in this field believe it is possible to use fuzzy logic to predict a person's infection rate or environment risk based on inputs such as body temp, sanitation, places visited, etc?
Lately, many articles are telling about the spread of infection by mutated D614G strain. We've also performed some bioinformatics studies to find the same results.
We've found that places with higher d614g strain tend to have a higher infection rate and higher fatality ratio. Also, we've shown the gradual increase of d614G in abundance with time.
I wanted to discuss the wet lab verifications of this.
Also, a further question can be raised that is, what is the probability of such mutations in future?
There can be more informative discussions about this from this cell paper:
I believe it will be a good point to know what the scientific community thinks about D614G.
Urinary Tract Infection is more likely to occur in young women especially those who are sexually active or pregnant, which puts them at a higher risk for the infection. It can be a single-episode of Urinary Tract Infection or a recurrent UTI. The incidences of Enterococcus faecalis and Escherichia coli shows to be significantly higher in patients with infection than those who had single-episode urinary tract infection. E. faecalis is known to be the most common and make structural changes. Adherent E. coli is also more likely to have an important role in the etiology of young women who have recurrent UTI. Both of these bacteria are known to cause mild to serious diseases. So the question is, what clinical signs and symptoms will distinguish recurrent UTI from a single-episode UTI?
With increasing number of people infected with Covid-19 globally, and huge increase in mask use, more virus contaminated hospital wastes is being produced and dumped in waste disposal sites. Many countries do not have environmental law regulations for the disposal of such wastes. How will it affect human health and infection, especially in rural areas?
Infection of Campylobacter jejuni is characterized by a self-limiting diarrhea that often begins with abdominal pain which last between 2 to 10 days. I want to know the specific pathogenicity and virulence factors contributing to it
I want to establish hairy roots of my plant for abiotic stress treatment, but I want to do it without involvement of Agrobacterium. In every previously done research works, researchers have used the bacterium A. tumefaciens for infection and generation of roots. is there any other simple method which doesnt involve the bacteria?
I'm currently trying to develop a biosensor to detect covid19 infection. However, I don't want to be exposed to the real virus for a real practical test. Is there any way, to simulate viruses so that a researcher can use these simulators without worrying so much about being infected?
If an immunodeficient/immunocompromised patient gets infection with the SARS-CoV2 virus, what could be the usual outcome?
ESBL stands for extended spectrum beta-lactamase. It's an enzyme found in some strains of bacteria. ESBL-producing bacteria can't be killed by many of the antibiotics that doctors use to treat infections, like penicillins and some cephalosporins. This makes it harder to treat.
many patient come with out nay symptoms or sings for corona infection, they come to clinic with only congestion on pharynges and they clinically diagnosis as corona infection is that right ???? can you explain that i do not think that its right
I have seen that some groups use CSFE to stain some parasite species before infect cells to detect percetage of infected cells. Could I use CSFE to stain Trypanosoma cruzi and measure infection in cells? Someone have experience and advises?
There are a lot of known waterborne bacterias but what is the first waterborne bacteria to be discovered? What is the manifestation of the infection?
I'm investigating scRNA-seq as a way of measuring how different cell types respond to virus infection. To do this the transcriptome would be used to determine 1) cell type and 2) virus infection. Many viruses are notorious for suppressing host transcription, which might interfere with transcriptome analysis. All scRNA-seq data I've found with virus infection is done in cell lines or flow sorted cells (supporting my suspicion). Has anyone done scRNA-seq in virus infected organoids, tissues, mixed cells, etc. or can anyone point me toward useful publications?