Questions related to Immunology of Infectious Diseases
we had a case of right parotid swelling, misdiagnosed as malignancy.Excision of lymph node revealed the diagnosis of Kimura's.
Hi guys. Im growing MCF7 cells treated with 1ng/ml TGFb for two weeks. But once after cell passaging, their phenotype changed to a flat, round and large shape which is different from their normal cell shape (See the attahced file). Im wondering what conditions might cause the consequence? Thanks for your help!
The laboratory blood picture in typhoid fever is generally characterized by leucopenia with neutropenia, and relative lymphocytosis. However, one study found true lymphopenia in typhoid fever following lab investigations. What could be the reason behind lymphopenia found in this study? Does true lymphopenia occur in typhoid fever?Why?
Could this lymphopenia occur due to haemophagocytosis (not HLP) or hemophagocytic histiocytosis?
Detection of new infections from relapses in vivax malaria elimination programme is a big challenge, as a routine diagnostic method that can distinguish these cases from there. Please help us out if you have experience in this field.
Aphthous Ulcer is common during stressful condition. As reactivation of HSV is always associated with decreased immunity due to any cause. Decreased immunity is most common during prolong stress and so we can imply aphthous ulcer to reactivation of HSV. Recurrence of stress is common and so recurrence of aphthous ulcer also common. This recurrence can be prevented by levamisole for many years.
Does average years of life loss (AYLL) can be used to monitor the progress of a particular disease over time? If so, does it require to be age-adjusted? What does an increasing AYLL over time suggest?
For my experiment we infect B6 mice with Plasmodium berghei parasites (IP injection) and after 6 days we measure the percentage of infection = the amount of red blood cells that are infected with our parasites. Last time we did this by making a Giemsa stain of a blood smear from the infected mice. Because this is so much work we were looking for a faster method to determine parasitemia. This week I tried labeling with sybr green. So I took a drop of blood from the mice, added sybr green and CD45 (to stain lymphocytes) and then measured the sample by flow cytometry. The first experiment was fine, I got about the same percentages of infection on the FACS as by counting on the microscope. However, today the results were really bad and I don't now the reason. Does any one already has done this? Or does anyone knows another method to stain DNA of parasites to determine the percentage of infection by flow cytometry? Hoescht is unusable because we don't have an UV laser.
I hope someone can help ;-)
How do you coat an antibody on a nitrocellulose membrane in order to develop immunology parasite antigens diagnostic strips?
We have one HIV positive patient who got failed on first line ART regimen with TDF/ TFC/ EFV, then we need to switch to AZT,3TC,lop/rit (in line with WHO HIV guideline). The patient is also having HBV co-infection, hence we want to keep TDF in that regimen such as TDF,3TC,AZT,lop/rit.
But in our country stock, we do not have a separate tablet of AZT nor TDF . Then the patient will need to take( TDF+3TC) + ( AZT+3TC) + lop/rit. We are concerned about high dose ( 600mg) of 3TC. Are there any study related with 3TC high dose toxicity? Please advice. Thanks
I was recently working on the inflammatory factor expression variances between WT and knockout mice by inducing LPS. But I didn't get a convincible result by detecting several IFs. I was wondering if anyone knows the accurate relationship between the inflammatory response and the dose of LPS as well as the injection time. I will deeply appreciate your reply.
As you know, there are many contributing factors in developing Hepatocellular cancer in hepatitis C patients which some of them are immune mediated factors. TLR4 is one of the immune mediated factors. I'm studying about its role in developing HCC IN HCV patients. I need your experience in this regard or your point of view.
Infectivity relates to how a pathogen is able to establish infection in a healthy but susceptible host and it positively correlates with virulence. Methods to measure infectivity if specific and sensitive will aid prion research.
Hello! I ligated a DNA in E. coli DH5 alpha, but I got low absorbance of bacteria, it was 0.066 at A500 nm. How will this affect the outcome of the agar culture?
Sorry for my english, i'm native spanish. Thanks.
as you know there are some biomarkers which are introduced for different aspects in Glioblastoma (GBM). As I studied, each one has some deficiencies in diagnosis, prognosis or other aspects of the disease. Do you have any new data in this regard?
We've seen an up regulation of CD27 on both CD4+ T cell and CD8+ T cell subsets in multiple tissues in the body. However, in reading I'm getting a mixed bag of what this could mean for the cells. How does CD27 expression relate to memory phenotype and antigen recall?
I am currently studying on the affinity of artificial antibacterial peptides to plasmid DNA of Pseudomonas aeruginosa. Is it possible to use SYTOX Green stain as part of the gel retardation assay (gel electrophoresis; possibly to replace ethidium bromide in the loading buffer)? Thank you for pondering or answering my question.
I already know the work of Miller and co-authors (2001, 2007) about the lived experiences of pwMS taking interferons and glatiramer acetat.
Do you know of any other studies?
Hi. I am planning to test about macropinocytosis ability of RAW264.7 cells
But, I didn't know Which bacteria of shigella and samonella would be more invaded to RAW 264.7 cells.
If you would do this experiment, Which bacteria would you use for this test?
Please let me know your brilliant thinking.
Please, someone using the inverse algorithm with rapid tests for serological diagnosis of syphilis could clarify me why it is considered positive (and require treatment) a case that is positive by a rapid treponemal test, non-reactive by VDRL or RPR, and positive by TPPA or TPHA; if it is marker of previous syphilis treated? Only in the case of a patient with late manifestations of syphilis could be interpreted these results as a positive case, but not in an asymptomatic patient.
I used limiting dilution assay for the quantification of parasite burden in the spleen of vaccinated mice post challenged with Leishmania parasite. I need some useful information to use the ELIDA software for data analysis because this has been widely used for analysis in several studies.
Serratia marcescens is a broad host-range pathogen and is capable of opportunistic infections of humans. As a member of the Enterobacteriaceae, it is related to Escherichia and Shigella, Salmonella and Yersinia. It is implicated in a wide range of serious infections including pneumonia, lower respiratory tract infection, urinary tract infection, bloodstream infection, wound infection and meningitis. The organism has also been described as an important cause of ocular infection with high incidence in contact lens-related keratitis.
Hello! Has anyone experience in storing field collected insects (mosquitoes in tropical climates) for insect and included parasites RNA/DNA extraction (using TRIzol/TRIreagent method) and qPCR analysis? No cold chain involved and as cheap as possible. Reviewing the literature I thought about comparing the effect of RNAlater, RNAfix (homemade RNAlater), methylated ethanol or FTA cards. I was wondering whether there are other methods that more cost-effective as possible? Many thanks!
Dear colleagues, could anyone provide information regarding risks of malaria during 1-month field trip in Northern Laos at June - July? We plan to stay at the campground in forested river valleys.
Many peoples in our district East Godavari and in Agency area having no awareness on Aids and HIV. So that we are planning to aware the children and people from their School level. Itself so we are selecting some Z.P School and A.P.S.W. R Schools and we go for awareness programs and camps to educate the children. And we are also planning to make an HIV Anti- group. We select some children and conduct some competitions, seminars and workshops and aware them against HIV and Aids.
We are requesting you for the fund needed for our plan and requesting for the addresses of any other organizations who are supporting us.
I inoculum 5X10^3 pfu H1N1 influenza virus to mice through intranasal injection, but the result shows that no matter after 48 hrs, 72 hrs or 96 hrs, the virus titer of mice lung tissue still remains in 5x10^3 pfu or even less(From plaques assay results). Are there any possible reasons that cause this problem?
Direct virus titer test through MDCK cells did not show this problem, only in mice lung tissue. Thanks.
Endotoxin can possibly be neutralized in vivo by diverse substances. The endotoxin- neutalizing substance complex must be removed from the body before it could cause CD14-TLR4-mediated activation of leukocytes and release of inflammatory cytokines leading to ill-effects of endotoxemia. A single mechanism or it will depend on the type of the complex formed?
I receive conflicting information whether Field stain can show Schuffner dots in malaria parasites.
Information online on this are limited.
What is your knowledge on this?
I am currently looking for research on any clinical study of the direct correlation between oil extraction and specific diseases in Africa, such as cancer, asthma or other respiratory illnesses in Africa.
Have been documenting an international series of infectious-like events in which deaths and medical admissions simultaneously rise in what can be best described as a rectangular wave effect. Have written a review attempting to link CMV to these suspected outbreaks. Any thoughts or suggestions would be welcome along with potential research which could be relevant. Many thanks for your valuable time. Kind Regards Rod
P.S. even if CMV is not the direct agent I would be highly surprised if it were not taking opportunistic advantage as it does in HIV/AIDS
I have isolated human neutrophils (from blood) in the inactivated condition for parasite infection study. I need to fix the cells for staining protocol. I have used 1% and 4% paraformaldehyde. I am getting more ghost cells during staining protocol. What should I use for fixing cells? Also I need it to grow on coverslip. What is the method used for adhering neutrophils on glass coverslip?
The START (“Strategic Timing of AntiRetroviral Treatment”) study was a randomized, controlled clinical trial designed to more clearly define the optimal time for HIV- infected individuals to begin antiretroviral therapy. The study was stopped early (May 2015) and showed that starting antiretroviral therapy early prevents a combination of outcomes that includes AIDS events (such as AIDS-related cancer) and serious non-AIDS events (major cardiovascular, renal and liver disease, non-AIDS cancer, and death not attributable to AIDS).
In India, currently we start ART at a CD4 count <350 and even here grapple with a significant percentage of treatment failures due to poor adherence. If every HIV individual were to be started on ART right at diagnosis or quite early in disease, besides economic difficulty, would we not have a large percentage of drug failures (and resistance) in a few years. Would an upward revision of initiating ART at CD4 of 500 or even greater be a good choice, considering drug resistance and poor adherence issues, despite scientific evidence of early therapy being beneficial in RCT.
malaria researchers and parasitologists : How can sex hormones influence the outcome of cerebral malaria pathology in humans and mice?
malaria researchers, microbiologists and neuroscientists, how can I detect blood brain barrier breakdown during cerebral malaria in mice other than Evan's blue injection technique?
When the animal is challenged intranasaly or intratracheally will there be any clinical signs in animal? I challenged calves intranasally with 5ml of inoculum containing 109 cfu/ml but observed no clinical signs. Also no clinical signs were produced when the calves were challenged intratracheally with 109 cfu. So in such case will there be any immune response?
I have difficulty to transduce unstimulated T cells using VSVG-lentiviral vector. A lot of papers mention that measles virus glycoprotein pseudotyped lentiviral vector is a good option. However, I cannot find any commercial kit. Any suggestions? Many thanks.
We are looking at LPS levels in serum in certain infections and as controls we use serum from healthy individuals. All healthy individuals were fasting for 12 hours and blood was separated in class II safety cabinets with sterile tips. However, the highest LPS levels were detected in healthy individuals and in most the levels were >1000ng/ml which is more than the upper detection limit of the ELISA.
Why do we get such high levels in healthy individuals?
I have a question
how many ug of protein from inactivated influenza virus simply to immunize (1 swine) help me please, I don’t know what to do I look everywhere and I do not find the information
With my protocol for purification virus I have only 70ug/ml (total protein SIV), IM NOT SURE if 70ug/ml is sufficient to immune 1 swine with 3 booster
I'm working with Salmonella enterice serovar Typhimurium and when I orally infect mice, I observe 10% of mice having strong dizziness. This bacteria is known to infect systemic tissues such as mesenteric lymph nodes, peyer's patches, spleen and liver but what about the dizziness phenotype? Is Salmonella able to infect the internal ear? Or is there any other explanation for this?
Many thanks in advance for your help!
Dear friends, Suppose if I am interested in finding relationships among symptoms of meningitis across certain test characteristics, can I put test characteristics (CSF test) in levels. For instance, CSF cell count as level 1, level 2 level 3 and etc. or CSFtotal protein levels as level 1, level 2, level 3 and etc.
Thanks in advance....
In several clinical settings such as pancreatitis and trauma, a secondary infection can be frequent and often causes death. I wonder if the body in a hyperactivated status would amplify the detrimental effect of bacterial infection. Is there any literatures on this aspect?
I would like to immunize different groups of OT-1 mice with SIINFEKL and some variants we have made to determine if there is a difference in T-cell response. The OT-1 model is attractive because all the CD8 T-cells are specific. They are great in vitro tools or for adoptive transfer, but can you directly immunize an OT-1 mouse? The alternative is to use B6 mice, but we have a lot of OT-1 on hand and I'd get a lot more cells from them.
is there any research or evidence that advocate locating highly infectious wards in hospital design...is there any scientific evidence about the preferred location regarding the floors (upper vs lower floors).. i found one research that recommends locating infectious patients in the uppermost floors for the prevention of airborne infection transmission... is there any other researches?
I wold like to test some newly synthesized compounds as aminopeptidase M1 (PfAM1) inhibitors and antimalarial agent. Can any one evaluate our compounds in scientific collaboration or tell me where can I run the biological evaluation?
A number of definitions are found in publications ranging from 6 days to 14 days. Most frequent definitions mention 7 and 14 days. Some use onset of symptoms as staring point. Others use first detection of virus material as starting point. The end of shedding is usually defined by the last detection of viral material followed by negative sampling results. Usual duration of shedding (about 6 days) should probably be considered when the definition is chosen. Any suggestions?
I've been using the commercial Rotavirus ELISAs to detect murine adapted (EDIM and EC wild-type) strains of Rotavirus A, however their sensitivity for this application is quite low - though obviously they are perfectly fine for detecting human rotavirus A infection as viral shedding is so much greater than mice.
Does anyone know of a good sandwich ELISA antibody pair (viral capture and detection) that I can use to detect the relatively low shedding from adult mice? Ideally the detection antibody would be labelled with biotin or directly with HRP / AP.
Appreciate the help.
due to accelerating roll-out of ARV , HIV/AIDS services are integrated into PHC in order to increase the access of ARV by people living with HIV. however there is ongoing shortage of material and human resource
We are interested in sera samples from literally all soil-transmitted helminths and filarial parasites, with a top priority placed on hookworm infected patients, to use sera in screening in immunoassays for vaccine development. Thank you.
Viruses are using cell machinery for its amplification. After enough number of replication cycle it leaves cell and attack next cell. Is there any chance of changing pH of that infected cell during amplification process? I mean whether pH values of cell is increasing at the time of its genome replication and translation process and pH value decreases when cell is dying because of degrading enzymes.
I am conducting a qualitative study on HIV/AIDS medication adherence and compliance and seek contributions on how to gather relevant information.
I am looking for a researcher working on Babesiosis to collaborate with, in order to detect IgG antibodies on human and bovine serum samples from Colombia. Any suggestion?
We work with murine model to study Plasmodium berghei NK65 infection, wich causes lung damage in C57BL/6 mice, but some times I don't see this fenotipe. I would like to use 4-aminobenzoic acid to improve the parasites growth , but I don't know if its work.
We have used subcutaneous route for MTB infection in mice. We have observed lung bacilli burden at 30 days after infection. I just want to know any supplementary evidence to support my result.
I need to grow influenza viruses from respiratory samples prior to sequencing (due to low viral load), but i don´t know if I can assume for evaluating data the genetic changes that would happen with adapting these viruses to MDCK cells or embrionated eggs.
Should prednisolone be used in the management of immune reconstitution inflammatory syndrome in patients with HIV/AIDS?
in the most viral infection experiment, it is common sense that prior to inoculate virus, cells cultures are washed in order to get rid of serum, in some cases, even after infection, the medium are serum free. as I known, for example, flu A viral infection needs plasminogen and its NA protein cooperate to cleavage flu HA protein or exogenous trypsin to cleavage HA. but why in the many experiments, serum were not added, because calf or human serum contain plasminogen.
Maternal diagnosis of VZV was based on clinical symptoms and signs, positive specific IgM and IgG and positive PCR for VZV on samples from cutaneous lesions.
The newborn, was born at 37+5 weeks and IgG and IgM for VZV were tested two times in different laboratories.
No evidence of immunodeficency in mother and child.
We are trying to optimize dried blood spot specimens to quantitatively measure measles IgG in human samples. At low antibody titers, we are getting a lot of non-specific binding. I believe it is due to residual RBC and hemoglobin in eluates. Does anyone have any ideas on how to get rid of the excess RBC and Hemoglobin in whole blood samples? Does centrifugation help get rid of RBCs? I elute samples in 250ul of elution buffer and cannot dilute the samples any further.
Thanks in advance.
I want to dissociate virus bound to antibody onto the Protein G sepharose high performance columns. Can anyone suggest a simple protocol which will enable me to separate them while keeping them intact? I came across some suggestions, like using KSCN or 0.1-0.4M MgCl2. I don't want to use any kit for the purpose. Any help will be appreciated. Thanks in advance.
I am interested in the dynamics of the cellular immune response during Leishmania infection, particularly with regards to immune cell recruitment to the site of inoculation. What is the earliest time-point at which antigen-specific CD4+ T cells are present at the site of inoculation? Could you recommend any papers which have used flow cytometry or imaging methods to investigate this in mouse models?
I am doing a research study on the impact of parental attitudinal barriers on Infleunza immunization in the pediactric population. Does anyone have or know of a tool I can convert into survey monkey on facebook with consented permission?