Science topic

Infection - Science topic

Invasion of the host organism by microorganisms that can cause pathological conditions or diseases.
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Hi,
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?
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My problem was solved by switching to another HEK cell line
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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?
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A patient with desminopathy survived Covid-19 six months ago without pneumonia, but with a temporary loss of smell and taste. After Covid-19, we note an accelerated progression of desminopathy, penetration accelerates, new muscles are quickly involved in the pathological process, muscle mass decreases, and heart function worsens. Perhaps the infection or its consequences are somehow connected with the mechanism of progression of desminopathy?
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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.
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I agree with Silke Zimmermann that it is looking more like a crystal below your cells. I would even assume that you can wipe it of and will not see it again. That the cells are blured in the picture, is also a sign, that it it is below and not inside your culture.
kind regards
Soenke
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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?
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5-8 ug/ml is a good condition.
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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!
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Emily Smith Most of microorganisms contaminating lab cultures came from human skin or from soil. Sequence 16S/18S rRNA gene to find the species.
In my experience from commercial diagnostic lab - it is important to fight with contamination every day.
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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?
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In a study, A, B, and Rh+ were found to be more susceptible to COVID-19 infection, whereas blood groups O, AB, and Rh− are at a lower risk of COVID-19 infection. No association was found between blood groups and susceptibility to severity of disease and mortality. https://www.frontiersin.org/articles/10.3389/fcimb.2021.767771/full
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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?
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The following study suggest that cats can also transmit SARS-CoV-2 to humans.
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Hi all,
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
Julien
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The cascade leading to the transcriptional factor activation is short, in the case of the canonical ones (NFkB, IMD). The accumulation of the transcripts is another subject matter. The structure of the promoters of AMPs suggest non immune related transcription factors are likely to bind and interfere with the specific transcription. HIF binding site, for instance, is frequently found nearby these genes, suggesting a potential hindrance upon redox stress.
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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.
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Generally in mild symptomatic infection Paracetamol 650 with Vitamin C , Zinc tablet fir three days ,Prednisolone . For severe acute respiratory syndrome ( SARS-COV-2 ) the patient should be shifted to Hospitals ( ICU management ).
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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?
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Hi, in our practise we routinely do Urine CS one week before PCNl if positive start antibiotics. If urgent need of surgery and patient is asymptomatic TLC is normal, even with urine CS positive we do PCNL with atheist few dose of preoperative antibiotics.
During surgery we do give antibiotics at the time of induction of surgery.
And at the time of stone breaking we guve one dose of amikacin along with lasix.
Post operative we do give antibiotics as required till discharge.
Of Pus during initial puncture we keep PC N for drainage and do surgery later
Thanx
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During covid-19 infection antibodies are developed against virus. Is these antibodies are life long for that strain competing against infections.
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The following study demonstrate that people who recovered from even mild cases of COVID-19 produced antibodies for at least 5 to 7 months.
The full-text of the above article is available online
Thanks!
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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?
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Very interesting to add exposed / qurentined part of SIR -
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There are indications that mouthwashes could reduce the risk of coronavirus transmission. Do you have any solid information about this?
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Patients with better oral hygiene combat Covid-19 symptoms, milder symptoms and less inflammation in their bodies, and recover faster.
📷
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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?
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Yes certainly !!!, it is possible even in vaccinated people, as well as facing to the new varients
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It has been seen that many deaths of older people happened due to coronavirus, younger was found infected and then recovered yet no any case or less cases or children affected by coronavirus was reported. Anyone have any information or suggestions???
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A uncommon but devastating multisystem inflammatory disease affecting children and adolescents has been reported, probably linked to COVID-19.
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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.
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In addition to the Angiotensin receptor, others receptors can be related with COVID-19. Can you provide me some examples?
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Agree with Dr. Sadanand Pandey
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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.
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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?
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You can acquire SSI within 3 months of surgery.
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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
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Immunity level
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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.
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Yes, people develop immunity to the Covid-19 disease after recovery.
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What is the difference between infection of a fracture fixation device and a joint prosthesis? and do they have anything in common? Thank you!
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This mode of questioning allowed me to glean experts’ perspectives from a number of different angles.
Thank you for your invitation and it is a great pleasure to participate in your project.
Best wishes,
Cheng
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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
4. Culture
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Vietnam is one of the country where people follows the rules on its own. While healthcare systems of developed countries were collapsing, Vietnam managed to control it by quick strategic testing for all inbound travelers ( testing, isolate, quarantine weeks before other countries started it), aggressive contact tracing, effective public awareness campaign and develop its own testing kits.
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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?
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But it doesn't contain data about all pathogenic bacteria. As I'm searching toxins of Gardrenella vaginalis and couldn't get that.
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#corona in children #coronavaccine
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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.
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Use of a regimen containing hydroxychloroquine or chloroquine (with or without a macrolide) is associated with no evidence of benefit, but instead was associated with an increase in the risk of ventricular arrhythmias and a greater hazard for in-hospital death with COVID-19.
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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!)
Help?
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Aptar Pharma have developed a novel device to substitute Penn Century. The performance achieved is better. You can contact us for information and to purchase one. adam.fischer@aptar.com
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Is this an infection? If so, which one?
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Dear Kibet,
It is not possible to say anything with this picture. We need some basic informations about history of your fish. For example, did you examine any clinical sign of infection? Did you see any abnormality in fish? Was the fish dead before taking photo or you sacrificed fish? If you suspect any parasite, first you must collect the unknown parasite and examine under the light or dissection microscope. Morphological identification and molecular identification should be use for determination of parasite species. You must also get aware of identification features of their life stages and eggs to differentiate them from other parasites. Just morphological identification is not enough. You have to prove that through molecular identification as well as using the specific primers.
Best wishes
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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: ventegodt@livskvalitet.org
Introduction
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.
Conclusions
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.
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Dear Dr. Ventegodt,
Your very interesting question that deserves wider attention got shared in the project:
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Is corona virus capable of infection in the air?
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Please also go through the following attached document.
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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.
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Also, have a look at this useful link.
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We are currently trying to make a list of all antibiotics for Infections.
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The differences between gentamicin and gentamycin is the source that taken for drug formation , gentamicin is synthetic type while gentamycin is natural source.
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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.
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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.
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The link from which Sadanand Pandey has copied/pasted his answer has already been shared by me in this thread before his reply.
Thanks!
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What will be the consequence of the coronavirus vaccine on a patient’s health?
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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.
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I am not sure what you mean by water. Do you mean the composition on the cytosol? (Around 7).
About the virus, the virus seeks the molecular recognition to take place. However, thismight be the mechanism sensed by the innate inmune response, or why the eyes and brain are "difficult" almost hermetic to open (like a lock). The inmune system recognises the proper molecules otherwise we have autoinmune diseases. Allergies are mistakes, but the minor allergies can be corrected with the help of a doctor.
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BMJ now mentions that "Long Covid" symptoms occur:
-Covid foot
-rashes
-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"
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£18.5 million to tackle ‘Long-COVID’ in the community. Imperial College & 2 other study centres.
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Hi all
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.
Also
How please explain what is the normal procedure for FMD diagnosis.
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please, anyone has idea about the optimal parameter for cultivation of BHK cells in Bioreactor ( Agitation, DO, CO2 and PH).
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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?
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Such an indicator could be burdened with a high level of error of correlation between the issue of the scale of development of the SARS-CoV-2 (Covid-19) coronavirus pandemic and the level of international tourist traffic, cross-border business trips and others. The inaccuracy of this type of indicator results from the fact that, apart from the issue of international tourism, there are many other factors determining the scale and pace of the development of successive waves of the SARS-CoV-2 (Covid-19) coronavirus pandemic in individual countries. For example, the level of general public awareness of the principles of compliance with anti-pandemic safety instruments (e.g. wearing protective masks, maintaining social distancing in public places and frequent washing and / or disinfecting hands with disinfectant fluids) and the sense of social solidarity between generations varies from country to country. In addition, there are also significant differences between countries with regard to the commencing or ongoing vaccination programs of citizens against the coronavirus SARS-CoV-2 (Covid-19). There are also significant differences between countries in terms of the imposed anti-pandemic security restrictions, lockdowns imposed on specific industries and sectors, and improvement of crisis management systems and pandemic risk management. Therefore, there are many additional determinants shaping the different level and scale of the development of the SARS-CoV-2 (Covid-19) coronavirus pandemic in individual countries.
Best regards, Have a nice day, Stay healthy!
Dariusz Prokopowicz
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Iodin as a liquid form proved it is effectiveness against SARS COV2 infection, so how can the dentist use it in clinical manner with minimal side effects?
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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?
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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
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The second COVID-19 infection is more severe than the first one.
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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?
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Most symptoms of covid are related to immune dysregulation. reason for this is incomplete clearance of virus and it's the virus debries which acts as target for immune system stimulation. Luckily children tend to clear virus faster and as there's not much debries left after a week, mmune stimulation does not happen hence mild symptoms. Children do suffer from multi systemic inflammatory syndrome (MISC)
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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.
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I following the best answer.
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What are the side effects of COVID-19 Infection during Pregnancy?
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That is depends on mTOR pathway
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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?
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There is no vaccine for severe acute respiratory syndrome coronavirus (SARS-CoV or SARS-CoV-1).
Thanks!
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There is some drugs, which helps for coronavirus infection - for example chloroquine, tocilizumab, remdesivir, teicoplanin etc. Do you know any other drugs for coronavirus?
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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?
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In the earliest stages of infection, before the host has mounted an effective immune response, anti-SARS-CoV-2 antibody-based therapies may have their greatest likelihood of having an effect. In this regard, although there are insufficient data from clinical trials to recommend either for or against the use of any specific therapy in this setting, preliminary data suggests that outpatients may benefit from receiving anti-SARS-CoV-2 monoclonal antibodies early in the course of infection. The anti-SARS-CoV-2 monoclonal antibodies bamlanivimab and casirivimab plus imdevimab are available through Emergency Use Authorizations for outpatients who are at high risk for disease progression.
Remdesivir, an antiviral agent, is currently the only drug that is approved by the Food and Drug Administration for the treatment of COVID-19. It is recommended for use in hospitalized patients who require supplemental oxygen. However, it is not routinely recommended for patients who require mechanical ventilation due to the lack of data showing benefit at this advanced stage of the disease.
Dexamethasone, a corticosteroid, has been found to improve survival in hospitalized patients who require supplemental oxygen, with the greatest effect observed in patients who require mechanical ventilation. Therefore, the use of dexamethasone is strongly recommended in this setting.
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I am planning to start with infection of my target cells with and I was wondering what would be the easiest method to quantify the virus titer so I could conclude about the optimal MOI? Any kind of protocol would be very much appreciated!
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Hi Kristina,
It is not the easiest, but I would recommend the TCID50 method, whereby a series of dilutions (I like to use 10 4-fold dilutions in quadruplicate) of your stock can be used to infect your target cells in a 96-well plate. Ideally, you would use the same target cells in your other assays to determine if a well has been infected. If this is not possible, the appropriate reporter cell line will have to be determined.
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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.
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Use carbon with the solution of your inoculum and scratch the leaves with the help of a cotton cloth.
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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
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You may be right. If you consider that healing is permanent and thus obviates the risk of subsequent infection, then his one month healing rate pertains. However, healing is not binary, because most wounds heal with a scar that is inferior in quality to native tissue. As a result, many wounds recur after appearing to be healed due to recurrent trauma or illness. Consider the fact that venous stasis ulcers of the ankle have a high relapse rate while an injury to the scalp heals rapidly after injury with minimal incidence of infection or recurrence. The main differentiating factor is the quality of blood flow and delivery of oxygen. Hypoxia is characteristic of the ankle due to its dependent position when we stand or sit.
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Hi everyone !
Norway population is 5,432,580 I am confused how to implement the assumption "20% of people infectious with SARS-CoV-2 do not have symptoms".
What is the formula used to get the number of masks needed to wear to prevent 1 infection?
Thank you for your time
Frederik
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Nice intesresting formula
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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.
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You can differentiate SARS-CoV-2 infection from other diseases through nasopharyngeal swab with research of viral RNA
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Infections and colonization or contamination criteria?
If you know a paper to review, I was wonder if you can introduce me.
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Contamination: contamination is the presence of non-proliferating organisms on the surface of a wound
Colonization: presence of multiplying micro-organisms on the surface of a wound, but with no immune response from the host
Infection: presence of multiplying organisms with associated immune response and clinical signs of inflammation
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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?
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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)?
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That's a very relevant question, madam. I really think that the complications due to covid 19 are partly dependent on the genetics of the host. This obviously explains that infected people don't suffer the infection in the same way, hence the interest of integrating human genetics into our thinking to better understand and predict the complications of this disease.
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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).
Please advise.
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Rather than just "association", look at "interaction".
CHAID (chi-square-automatic-interaction-detection) also known as "decision trees", similar to CART (classification and regression trees) analysis is a method that I would recommend.
If you set infection (or not) as the dichotomous dependent target variable being predicted by the multivariate independent predictors (Age, Gender, any other attributes, etc.) CHAID modeling will produce a "c-statistic" , similar to BLR (binary logistic regression) that can be used to calculate and plot the area under the receiver operating characteristic (AUROC) curve, same as BLR, as a way to evaluate how good the model is (at the admitted risk of over fitting).
But when exploring data for significant content, you want a method that will rapidly identify and suggest the best candidates for inclusion in the well defined final trimmed model that consists only of independently predictive variables.
With the CHAID method, the model alpha threshold can be preemptively set at any level. Setting alpha at greater than 0.05 as the threshold for hierarchical branching results in more branches, lower than 0.05 results in fewer branches. The higher up the branch occurs in the resulting tree cascade, the more powerful the factor is. Similar to Odds Ratio (OR) in BLR, the higher the OR, the more variation that the IV factor is explaining in the DV, and the more important the variable is. The BLR method is also recommended if your sample size is large enough to support the assumptions of the BLR model. CHAID (like all the chi-square tests) will work with smaller data sets (30 - 40 observations) whereas BLR usually will not.
Scale or ordinals (Age days, weeks, months, years; weight, height, etc. ; non-linear weighted scales: none 0, low 1, medium 3, high 9) also work in CHAID "as is". Findings can always be reproduced at each tree "branch" by using either the "Likelihood Ratio" or "Pearson" chi-square method, and of course, Fisher Exact.
CHAID is way underutilized (my opinion). The "branching" in the tree shows the hierarchical interactions that are embedded in the data, at the given level of statistical significance (alpha) that has been specified for the model.
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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).
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I suggest to read:
Environmental Infection Control in Intensive Care Units at Gaza Governorates
  • January 2014
  • 📷Khalid Khadoura
  • 📷Samir A. Afifi
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There are some news about repeated infection of COVID 19. RT-PCR test result becomes positive for the second time after recovering from the disease. There may be a chance that the presence of RNA fragments of disintegrated/non viable virus that is detected by RT-PCR test which leads to the misconception of repeated infection. Immune system needs time to clear off the viral load and its associated contents from the body. The time required varies depending on several factors viz. individual immunity, genetic factor. It can only be confirmed by assaying the replication ability or infectivity of the virus isolated from those patients.
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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?
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It is possible to use fuzzy logic algorithms to predict COVID-19 but you need an appropriate dataset and need to consult with a physician.
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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.
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Thank you so much dear, Tathagata Dey for this useful and valuable explanation.
I should read the attached articles carefully.
Thanks again Sir and hopping you have a healthy life.
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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?
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I agree with the excellent and comprehensive answers from Mary CR Wilson.
Just to add recurrent UTI's occurring in the context of an incomplete course of antibiotics, and /or resistance to the prescribed antibiotic, anatomical bladder abnormalities (diverticulae, calculus), functional -vesico-urethral reflux, renal calyx- pyelonephrosis, calculi, underlying co-morbidities (diabetes) and perimenopausal changes in estrogen levels.
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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?
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Nucleic acid from SARS-CoV 2 can be amplified from samples collected in water waste. It's been used as a marker for community spread of COVID-19 by some researchers. So yes, there is SARS-CoV 2 in the environment. But to your point, whether the viruses recovered from those samples are live replication competent viruses is still not clear to me. It is possible that what's amplified during the RT-PCR is just RNA from dead viruses. Answering this question will require to isolate from the waste produced and grow SARS-CoV 2 in the proper cell culture systems.
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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
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Hi Christian there are quite a few virulence factors and
Stefan Zimmermann
covered most of them. There are also cell adhesion factors important in colonization such as CadF which binds to fibronectin triggering a signalling process that eventually leads to cell internalisation.
An often forgotten virulence factor are genes/proteins involved in bile resistance and stress conditions. Campylobacter is a fragile organism but is also very capable of surviving bile salts and heavy metals found in the GIT due to the multidrug efflux pump (cme) it harbors. It can also survive various stresses encountered along the food chain such as oxidative stress (katA, AhpC) and heat shock (dnaJ).
To be honest, there are quite a few virulence factors involved in Campylobacter pathogenicity and a lot more than has been covered here. The good news is that there are a ton of reviews that have covered this area so you won't have any issue finding more on this topic. In the meantime I recommend this excellent review:
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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?
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Agro. tumefaciens is used for getting transgenic shoots.
Agro. Rhizogenes strains are used to get those "crazy" roots, growing by themselves with no hormones added.
Either way: if you use one of the Agros you always have to go thru cleaning the shoots or roots thru antibiotics.
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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?
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Hi Hadi
Looking at your question, I only think of Virus-Like-Particles (VLPs) which are non-infectious. Look at this article which might be of your interest
Best,
Kiran
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If an immunodeficient/immunocompromised patient gets infection with the SARS-CoV2 virus, what could be the usual outcome?
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My question is related to bacteria associated with skin and soft tissue infection
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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.
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the A bacterial suspension of Escherichia coli is made according to the 0.5 McFarland turbidity standard and an even lawn of bacteria was made on the Mueller Hinton agar petri plate (90mm). The screening for ESBL Escherichia coli is performed using ceftazidime (30 μg) disk and ceftazidime resistant strains are considered as screen positives. DDST is performed by using disks containing amoxicillin/ clavulanate on Mueller-Hinton agar plate at a 20 mm distance from the indicator drugs; ceftazidime (30 μg) and cefotaxime (30 μg). ESBL production is seen by the clavulanate mediated enhancement of the activity of the indicator drug as a keyhole effect.11
11. Clinical and Laboratory Standards Institute (CLSI) Performance standards for antimicrobial susceptibility tests . 20th ed. approved standard, CLSI document M100-S20. vol. 30. Wayne, PA: CLSI; 2010.
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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
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commonest is sore throat and headache. While the other reported ENT manifestations include pharyngeal erythema , nasal congestion , runny nose or rhinorrhea , upper respiratory tract infection (URTI), and tonsil enlargement.
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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?
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I agree with Dr.Anoop Mohanty that Vibrio choleare, the causative agent of cholera, was probably the first waterborne bacterium.John Snow is credited who first investigated the outbreak of cholera in London during 1854. Since than the disease is reported from many countries of the world including India.
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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?
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How trauma and fear of infection can affect brain functions and structures?
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The neurotransmitters maybe negatively affected.
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Hi,
I want to transduce UC-MSCs with lentivirus luciferase (79692-G (G418), which is 5x10^6 TU/ml) and I want to test different multiplicity of infection (MOI) and different amount of time for transduction and I'm wondering if someone has experience doing this? Would MOI of 2 be too little? What about 100? Is that too much, and the cells would get high chance to die? Also what about doing 4h of transduction? is this too little? Thanks for any advice!
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I've realized David Schad has given you key suggestions. I've been doing something similar in the past few weeks, and the nature protocol paper below has been my guideline. Take a look at it, and it may guide you step by step!
All the best!
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Hey :)
I'm growing MV4-11 and THP1 suspension cells with Pen-strep.
I have been having troubles for the last month growing my cells, which I attributed to an infection in my medium. The media changed color to pink and was turbulent (Fig1)
After changing everything and cleaning the incubator I thawed new cells and began again. Now after I infected my cells with a concentrated lentivirus the cells again appeared very stressed and I think that I saw, using a light microscope, moving white elongated things in between my cells . Using a different microscope I took Fig2. Does anyone know what is the thing infecting my cells? is it even an infection? what should I do about it?
any help would be much appreciated!
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Giving again antibiotics or antimycotics to the contaminated culture doesn't help at all. You need to take again new cells and use new medium containing the antibiotics and antimycotic mix.