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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Dear Colleague,
I hope this message finds you well. Polybrene (hexadimethrine bromide) is commonly used to enhance the efficiency of viral transduction, particularly with retroviruses and lentiviruses, by reducing the charge repulsion between the virus and the cell surface. However, polybrene toxicity can sometimes be an issue, manifesting as reduced cell viability or altered cell behavior. Here are some insights and troubleshooting tips to address polybrene toxicity during viral transduction:
Understanding Polybrene Toxicity
  1. Mechanism of Toxicity:Cell Membrane Interaction: Polybrene interacts with the cell membrane to facilitate viral entry. At higher concentrations, this interaction can disrupt membrane integrity, leading to cell toxicity. Cell Type Sensitivity: Different cell types have varying sensitivities to polybrene. Some cells tolerate higher concentrations, while others are more susceptible to its toxic effects.
Troubleshooting and Mitigating Polybrene Toxicity
  1. Optimizing Polybrene Concentration:Concentration Range: Polybrene is typically used at concentrations ranging from 2 to 10 µg/mL. Start with a lower concentration (e.g., 2 µg/mL) and gradually increase it while monitoring cell viability. Cell Type Specificity: Determine the optimal concentration for your specific cell type. Perform a titration assay to find the highest concentration that enhances transduction efficiency without causing significant toxicity.
  2. Shortening Exposure Time:Reduced Exposure: Limit the exposure time of cells to polybrene. Shorter incubation periods (e.g., 2-4 hours) can reduce toxicity while still enhancing transduction efficiency. Wash Steps: After the desired exposure period, wash the cells thoroughly to remove any residual polybrene, replacing it with fresh culture medium.
  3. Using Alternatives or Supplements:Poloxamer 407 (Pluronic F-68): This non-ionic surfactant can be used as an alternative to polybrene to enhance viral transduction with reduced toxicity. Serum Supplementation: Ensure that your culture medium contains serum (e.g., 10% fetal bovine serum), which can help mitigate the toxic effects of polybrene by providing protective factors.
  4. Monitoring and Validating:Cell Viability Assays: Use viability assays (e.g., MTT, CellTiter-Glo) to quantitatively assess the impact of polybrene on cell health. This helps in optimizing the concentration and exposure time. Transduction Efficiency: Evaluate the efficiency of viral transduction by measuring the expression of the reporter gene or transgene (e.g., GFP, luciferase) to ensure that reduced polybrene toxicity does not compromise transduction efficacy.
Example Protocol for Polybrene Optimization
  1. Cell Seeding: Seed your cells in a 24-well plate at a density that allows them to reach 70-80% confluency the next day.
  2. Polybrene Titration: Prepare a series of polybrene concentrations (e.g., 0, 2, 4, 6, 8, 10 µg/mL) in your viral supernatant or culture medium.
  3. Viral Transduction:Add the viral supernatant containing the different concentrations of polybrene to the cells. Incubate the cells for 2-4 hours at 37°C. After incubation, replace the medium with fresh culture medium without polybrene.
  4. Assessment:Cell Viability: Assess cell viability 24-48 hours post-transduction using a viability assay. Transduction Efficiency: Measure the expression of the transgene 48-72 hours post-transduction to determine the optimal polybrene concentration.
By carefully optimizing the polybrene concentration and exposure time, you can enhance viral transduction efficiency while minimizing toxicity to your cells.
Should you have any further questions or require additional assistance, please feel free to reach out.
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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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Dear Esteemed Colleague,
Greetings. I trust this message finds you deeply engaged in your research and seeking answers to complex questions within the realm of genetics and molecular pathology. Your inquiry regarding the potential role of infection in causing desmin mutations in myofibrillar myopathy is both intriguing and indicative of a keen scientific mind exploring the multifaceted nature of genetic disorders.
To address your question with the precision and clarity it deserves, it is crucial to first understand the nature of myofibrillar myopathies and the role of desmin within this context. Myofibrillar myopathies are a group of neuromuscular disorders characterized by the progressive weakening of muscles and the disintegration of muscle fibers at a cellular level. Desmin, a type of intermediate filament protein, plays a pivotal role in maintaining the structural integrity and function of muscle cells. Mutations in the DES gene, which encodes the desmin protein, are directly linked to certain forms of myofibrillar myopathy.
The genesis of these mutations, particularly those affecting the desmin protein, is primarily genetic, resulting from inherited or de novo mutations in the DES gene. These mutations lead to the production of an abnormal desmin protein, which disrupts the normal architecture of muscle cells, leading to the symptoms associated with myofibrillar myopathy.
Addressing the specific question of whether an infection could cause desmin mutations, it is essential to differentiate between the origins of genetic mutations and factors that may exacerbate the phenotype of a genetic disorder. Genetic mutations, including those affecting the desmin gene, arise from alterations in the DNA sequence. These alterations can be inherited from parents, occur spontaneously during DNA replication, or be induced by certain environmental factors, such as exposure to specific chemicals or radiation. Infections, while capable of causing a wide array of health issues, do not directly induce genetic mutations in the DNA sequence of the genes like DES. However, it is conceivable that certain infections could exacerbate the clinical manifestations of myofibrillar myopathy in individuals already predisposed or carrying a desmin mutation, by stressing the muscular system or triggering inflammatory responses that may further compromise muscle function.
In conclusion, while infections can have significant impacts on overall health and may interact in complex ways with genetic disorders, the mutations in the DES gene that cause myofibrillar myopathy are not directly caused by infections. The mutations are genetic in origin, and the relationship between infections and the severity or progression of myofibrillar myopathy would be more accurately viewed through the lens of infection exacerbating pre-existing conditions rather than causing the genetic mutation itself.
I hope this elucidation addresses your inquiry comprehensively. Should you have further questions or require additional clarification, please feel free to reach out.
Warm regards.
This protocol list might provide further insights to address this issue.
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Freshwater shrimps of the genus Neocaridina which are kept in captivity (aquarium) have "dirty" gills (visible through the transparent carapace). The "parasite" was not motile. Mortality was recorded. Is it a parasite, bacterial infection or what is it?
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In the picture you sent, it doesn't look like a parasite of any type of animal. This object is more like dirt or moss attached to the gills. If it is true that the object is moss, then it is still classified as a phytoparasite. You have to confirm the object first before drawing conclusions.
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The patient is being kept alive by 100% O2 input.
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Reviving lungs that have been infected by the swine flu virus, or any influenza virus, largely depends on the severity of the infection and the damage incurred. Influenza A virus H1N1, commonly known as swine flu, can range from a mild to severe respiratory illness, and the body's ability to recover varies significantly among individuals. Here are several key points regarding recovery and treatment:
Mild to Moderate Infections
  • Immune Response: In cases of mild to moderate infection, the body's immune system can often clear the virus effectively on its own. Supportive care and symptomatic treatment may be all that's required.
  • Antiviral Medications: Drugs like oseltamivir (Tamiflu) or zanamivir (Relenza) can be prescribed to reduce the severity and duration of symptoms, especially if taken within the first 48 hours of symptom onset.
Severe Infections and Lung Damage
  • Hospital Care: Severe cases, particularly those involving significant lung damage or complications like pneumonia, may require hospitalization. Treatment can include antiviral therapy, antibiotics (to prevent or treat secondary bacterial infections), oxygen therapy, and sometimes mechanical ventilation support.
  • Recovery and Rehabilitation: Recovery from severe lung infection may involve a prolonged period of rehabilitation. The lungs can heal from the damage over time, but the recovery process can vary widely and may take weeks to months. Some individuals may experience long-term respiratory issues following a severe influenza infection.
Preventive Measures
  • Vaccination: Getting vaccinated against the influenza virus is a key preventive measure that can reduce the risk of severe infection and complications.
  • Hygiene Practices: Regular hand washing, wearing masks during outbreaks, and avoiding close contact with infected individuals can also help prevent the spread of the virus.
Experimental and Supportive Therapies
  • In cases of severe lung damage, experimental therapies such as ECMO (extracorporeal membrane oxygenation) may be used. ECMO is a life-support technique that oxygenates the blood outside the body, allowing the lungs to rest and heal.
  • Research into regenerative medicine and stem cell therapy offers potential future treatments for repairing lung tissue damaged by viral infections, though these are still in the experimental stages.
Conclusion
While the body can often recover from mild to moderate swine flu infections with appropriate care, severe infections requiring hospitalization can result in significant lung damage that necessitates more intensive treatment and a longer recovery period. The extent to which lungs can "revive" or heal depends on the severity of the damage, the overall health of the individual, and the treatments applied. Continuous advances in medical treatments and supportive care improve outcomes for those affected by severe influenza infections.
l Reviewing the protocols listed here may offer further guidance in addressing this issue
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Can anyone share a link to a publication in which this is announced as a novelty? I am curious who first invented this kind of protection against infectious transmissions from patients to drugstore staff. I'm curious how old this idea is.
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  • 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.
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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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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.
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Dear Geir Bjorklund, Duc M. Hoang, John Hildyard, thank you very much for your answers and recommendations!
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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)
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You can see the latest research
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For a long time people drank or ate medicinal herbs from nature or the forest to maintain the health of their bodies.
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I think that sage (المريمية) is very useful to drink every day for the strengthening the immune system.
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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 thousands of ponds (a small body of still water formed naturally or by artificial means.) in Bangladesh. People in rural Bangladesh used to have their bath in those ponds. Is it possible to be infected with COVID-19 during bathing when COVID-19 patients in their asymptomatic state are using the same ponds for a bath (as COVID-19 patients can transmit the disease in the asymptomatic state)?
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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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New Model for the COVID-19 Reported Cases and Deaths of Ghana in Accelerated Spread and Prediction of the Delayed Phase
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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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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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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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Interesting. As a teacher in contact with relatively large numbers of children it is not unusual to contract colds and flus regularly. Children appear to be great carriers of viruses but not as susceptible to them.
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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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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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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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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 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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Is this an infection? If so, which one?
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I would perform DNA barcoding for these vesicles. You may use fish-COI primers, otherwise invertebrate barcodes can be really useful. This can be really fast and accurate..Cheers!
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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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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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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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The search was successful. I recommend looking at the US patent, which proposes to treat eyes for a viral infection
Perhaps a drop of heavy water in the nose is a good prevention of COVID-19 fever. This is a hypothesis, not a recommendation, and needs to be investigated.
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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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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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My question is related to bacteria associated with skin and soft tissue infection
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A simple method that give a suggestive answer is to plate the bacteria onto Mannitol Salt Agar (MSA) and it is selective for the Staph (can grow on salt) and normally inhibits Strep. Also, Staph aureus produces acid from the mannitol and so can be identified as it would be a major cause of these skin infections.
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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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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.