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Infectious Disease Epidemiology - Science topic

Infectious Disease Epidemiology is the study of the patterns, causes, and effects of health and infectious disease conditions in defined populations.
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Is there any evidence to think that is a confined disease?
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The leprosy is highly concentrated around south east asian and briazilan countries. But here and there there are lots of case report from the developed countries too.
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Hanta Virus
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what is period of infectivity of NIPAH virus encephalitis and is there any specisic treatment?
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Dear Dr.Sandip Das,
Nipah virus disease is an emerging zoonosis of public health concern. The infection was was time recorded in pig workers in Malaysia.The incubation period is variable (4 to 18 days). The disease is also reported from India.I have described this viral diease in my book entitled " Zoonoses" published in 2007.
We have published one paper on Nipah virus.
Pal, M. and Abdo, J.2012. Nipah virus disease: A newly emerging viral zoonosis. International Journal of Livestock Research 2: 65-68.
You can easily download from Research Gate or Academia.
With kind regards,
Prof.Dr.Mahendra Pal
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If the leishmaniasis parasite (visceral leishmaniasis) existence is not that much clear in the blood. how the transmission between humans occurs. I mean from where the sand fly can take the amastigotes if it is not available in the blood? For example in Syria it is proved that the the visceral leishmaniasis type is only L.infantum. But we are facing big problems because in spite of spraying the epidemic areas we have 2-3 new cases weekly that means that we have another forms like donovani or tropica that causes VL and the reservoir is human. The other question, Should we treat asymptomatic VL or not.
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Treatment of asymptomatic cases is not recommended for many reasons: drug is toxic, asymptomatic can remain without development of any clinical manifestations for the rest of their live so they dont have the disease and they should not be treated.
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Does anyone has experience in publication with this journal?
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It is not in my field of research, but I checked the Excel file regarding InCites Journal Citation Reports (by Clarivate Analytics) for 2018 year, and was not able to find that Journals in that file. Also I am not able to find it here in ResearchGate... But I found two articles here with full text, published in that journal...
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Especially in a country like India. Tests which are available are time consuming leading to delay in TB/HIV infected patients?
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Thanks for all the tips! This was extremely helpful
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What are the possible negative effects of the low-dosage drug on the people who drink the water? Have there any been studies that look at its effectiveness?
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Thanks for all the tips! This was extremely helpful
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I am working on a research to determine the endemicity classes of different regions in a country which means that each region has to have one endemicity class. I am looking for ways of using different classes for each region to come up with my results
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Thanks for all the tips! This was extremely helpful
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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?
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Thanks for all the tips! This was extremely helpful
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During off the season/winter season, what should be our best strategies for dengue vector control to prevent from next epidemic season? I think Integrated vector management (IVM) strategies should be used round the year. We should continuously use ovitraps to check for seasonal trends, increase or decrease in vector population so that timely use of conventional control methods could be applied. Ovicides like bleach and some botanical extracts might be beneficial. But kindly share your ideas and experiences?
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following
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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? 
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For trends analysis purpose, it is recommended to use the age-standardize YLL rate instead of YLL rate. This is important because the age structure of the population changes over time, so it requires to adjust for age as a confounder factor.
I hope this helps.
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Since the climate is changing, there will be also a change in the adaptive characteristics of bacteria. This question is related to our research topic, "The relationship of the zoonotic diseases in stray dogs and the climate of the Philippines." 
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We do know that Zika virus is causing a pandemic problem that causes microcephaly on newborns. Now upon looking at several websites regarding zika virus, there are certain ways to stop the spread but also dangerous like using Ribavirin which inhibits the synthesis of viral RNA but small dosage can cause birth defects as well as to cause . Will there be a way to find out what other receptors or is there any other receptors it carry other than the E glycoprotein which also carries the function of cell to cell communication on this enveloped virus?
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Research project on possible vector-borne diseases spread by capybaras
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HI See this link 
https://www.ncbi.nlm.nih.gov › NCBI › Literature 
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What are the companies or government bodies in India who can provide international standards for Hepatitis B, C, and HIV which can be used for quantitiative measurement using Real -Time PCR .
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Dear Sir,
You can buy at ABBOTT, ROCHE or BIOMATRICA.
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(1) what is meant by unexpected here .how to detemine the level shifted from endemic to epidemic.
(2) what is the period of surveillance needed to say that this is an outbreak ??
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Additionally a ln epidemic can occur when a disease emerged in a place it never was. Eg the re-emergence of a single case of small pox could be described as an epidemic
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The pathohystological diagnosis is too simple.
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Hodgkin disease is a type of cancer, better saying neoplasm. As for most of neoplasms, the cause - again, better saying the trigger - is not known. Even speaking about viral associated cancers (such as HPV/cervical cancer; HHV-8/Kaposi sarcoma; HTLV-I/ATL, HBV/HCC, etc.), the viral etiology is "nearly" a 100% finding. Of note, not in all cases or always these viruses lead to malignancy in any individual, in other words, a (chronic) infection is necessary but not sufficient.
The presence of a virus or other intra-cellular microorganism can be a trigger of HLs, because in Hodgkin's disease there is classically a "defect" in cell-mediated immunity which is primarily activated by intra-cellular infectious agents. 
For example, it's known that in order to survive in a host organism, T. gondii can induce apoptosis of immune cells (monocytes), initiated from surface receptors and from within the cell. T. gondii suppresses Bak and Bax, and prevents activation of Bax through BimS mechanism, thus regulating the apoptotic processes which may be the first step in the detrimental processes resulting in cell proliferation in HLs. However, I see T. gondii as a risk factor rather than an etiological agent.
Never heard about HL triggered by Koch bacillus, but it's true that there are reported cases of concomitant HL and TB, simultaneous occurrence of both, TB hiding non-HL or mimicking HL. 
Very well said, as chemotherapy doesn't cure viral, bacterial or protozoan infections, microbiological investigations of lymphnodes should be considered in the overall approach of some lymphoma types. Overcoming the old fashion in everything is a difficult job for many, isn't it. 
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According to the WHO case definition, a case of cholera should be suspected when: – in an area where there is a cholera epidemic, a patient aged 2 years or more develops acute watery diarrhea, with or without vomiting. Do you think we should exclude children under the age of 2 years during an outbreak? Do you know any studies/research papers that provide solid evidence to exclude children under 2 years old from the case definition?
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Thank you Prosper for the paper. It is exactly what I was looking for. Basically, in a limited-resource settings where lab tests are not always possible, discounting children under 2 years old from the linelist (surveillance), during an epidemic, underestimates the burden of this disease and would also flaw the surveillance indicators (AR, WIR, CFR...).WHO used to exclude children under 5 years before updating the case definition. I am also searching for studies/articles that provide scientific evidence for this change.
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For mapping study of diphtheria epidemic at nome 1924-1925, I am looking for the pdf of:
THE DIPHTHERIA EPIDEMIC AT NOME
Curtis Welch, M.D.
JAMA. 1925;84(17):1290-1291. doi:10.1001/jama.1925.02660430048031
Somebody with this paper willing to share?
Thanks
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Is it that you are looking for the paper? I hope I find the true one. =)
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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.
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How well could Malaria be controlled in a low socio - economic population? an at risk population, relatively low in all socio - economic index. Can someone provide any relevant studies?
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To avoid repetition, all comments made by colleagues are right. However, malaria control depends mostly on Government policies. We know the ways the disease and vector can be controlled. If the Government will respond to malaria the way they responded to Ebola,  I believe malaria will be eradicated in one year at most.
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I'm looking for a very small electric desktop lab freezer, less than 1 cubic feet in capacity (about the size of a toaster), rated for -20C to temporarily store a few dried blood spot samples prior to shipping. If so, can you please provide the manufacturer and model or perhaps a website link. The only ones I've seen this size are battery only. Thank you. --Jim
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Hi James, How will the blood spots be used?  Here is a great publication that provides some temperature guidance for different biofluids, tissues, etc. to help you determine if you need to keep them cold. 
BIOPRESERVATION AND BIOBANKING
Volume 12, Number 3, 2014
ª Mary Ann Liebert, Inc.
DOI: 10.1089/bio.2013.0084
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I would like to better understand how each of the vaccines we currently recommend work. So essentially my question is about your favorite source for vaccinology, but I am interested in details that are not so readily available in sources like the CDC website. What type of immunity is necessary for protection for each infectious disease we have a vaccine against? Why do we need multiple doses and boosters for certain vaccines? How did we arrive at the conclusion that we need this many dose administrations and boosters (seminal studies)?
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Cosmina, another excellent source of answers to your questions are the World Health Organization's Position Papers on each vaccine. They provide background epidemiology, describe natural immunity and correlates of the protective immune response where they are understood and evidence from efficacy trials that decisions on vaccine introductions and scheduling are based. 
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I am trying to analysis MIRU-VNTR using Genemapper 4.1. I got .fsa file from 3130 genetic analyser and created analysis method. GS 1200 Liz size standard was selected in genemapper. But I have problem with inserting expected sizes and repeats of each loci. Please any one can tell me how to create panel file and bin for MIRU-VNTR in genemapper and can I have step of analysis.
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Dear Sonia 
Thank you so much
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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.
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 Classically, the diagnosis
of syphilis is based on a combination of clinical history,
symptom presentation (if any), and serologic test results,
including non-treponemal and treponemal tests. Nontreponemal
tests (e.g., RPR, VDRL) are typically used
for screening, and measure a non-specific antibody to
treponemal infection. A reactive test can indicate recent
infection, but could be caused by other conditions unrelated
to syphilis. Treponemal tests (e.g., TPPA, TPHA, FTA-ABS,
EIA) detect antibody to syphilis and thus can confirm
exposure to treponemal disease. However, these tests cannot
distinguish venereal infection (syphilis) from non-venereal
treponemal diseases (e.g., yaws, pinta, bejel). Furthermore,
treponemal antibody persists for life, and thus treponemal
tests cannot distinguish between recent, active infection and
previously treated or old, non-contagious infection.
I agree with Dr. Ricardo
2015-cha-guidance-syphilis-testing-lac.pdf
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I am having trouble in understanding the aim of HAART treatment in HIV patients.
Some papers mention that the viral load should be <50 copies/ml while others state that is should be <50 copies/mm^3.
How is this possible, since the units of measure are not the same.
I would appreciate any help.
Examples of references are:
1) Introducing HIV/AIDS Education Into the Electrical Engineering Curriculum at the University of Pretoria. (and all the references therein)
2)The Struggle for Access to Treatment for HIV/AIDS in India
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In simple explanation, HIV RNA copies is a measure of the virus itself, while CD4 count targets the T lymphocytes population.A reduction in HIV RNA copies population is an indication of suppression of viral replication while an increase in CD4 count population is an indication of improvement of immune system.CD4 count is for T lymphocyte while HIV RNA copies is for the virus itself.
Hope this also helps you.Best regards.
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I have noticed that dengue incidence in Barbados have significantly dropped following the first ever chikungunya epidemic in the country.
Barbados is one of the English speaking Caribbean country. It is an island state with a population of around 275000. It is known to be endemic for dengue.
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hi sergei,
yes i do have data? what kind of data would you need, i will be happy to share with you our 8 years data on the epidemiology of dengue in Barbados.
let me know if you would be interested?
alok
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any recent study or clinical trial on the respective manner 
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Dont know about updates but it works good
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Dennis Shanks and Nick White recently reviewed historical data on the interaction of febrile diseases of known etiology and vivax malaria in the lancet. (http://www.sciencedirect.com/science/article/pii/S1473309913700951#). They conclude that among others S. Typhi and P. falciparum may act as stimuli to reactivate hypnozoites. I was wondering how one would most efficiently design a study to address this?
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Consider a hypothetical experiment: You would want a susceptible population (i.e. one with hypnozoites present), then randomly expose half of them to some agent that may lead to reactivation, after which we observe the difference in reactivation over time between two the groups.
In the absence of RCTs, I would look for population where the exposure to the factors on interest is as close to random as possible. This is what is so elegant about the paper by Shanks and White's use of military populations: The exposure to various potential exposures is not a consequences of endogenous characteristics of the individual soldier, but is determined by where the soldier is stationed.
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The FDA and our federal health authority among many others have recently asked for a four weeks deferral period for blood donors coming back from regions infested by the vector and the virus.
However, since infections may be asymptomatic in blood donors, how is it guaranteed that infected donors do not harbour the virus in third spaces and in danger of a long lasting viraemia?
Do you have any specific thoughts regarding this topic?
Thank you very much in advance! 
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My dear friends. I think that high commited blood transfusion specialists like ourselves are actually paying attention very carefully and closely about the insurgence of this quite unknown virus. There is no doubt that it is very important, particularly for pregnant women, and for them, all attention must be driven from authorities in order to avoid new cases. But most importantly, if we do not fight the real culprit, the mosquito, we will certainly lose not only this battle, but the whole war. Unfortunately, this I haven´t seen not only in my country, but in several places.  This is a great forum for discussion. Regards
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Zika virus is considered to be more or less restricted to tropical countries. However, transmission might be possible when a competent vector (Aedes species) is present. But, the presence of a vector is not sufficient. Warm summer periods might bring favourable conditions for transmission via ektothermal insects also outside of the tropics. With climate warming, these regions are likely to increase in extent. As far as I know, there is no knowledge on the EIP (extrinsic incubation period), which would be needed to assess whether  regions and periods with the risk for transmission will evolve. Are there any hard facts, data, exeriments that can be used or applied to this virus.
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There is  limited knowledge on the EIP (extrinsic incubation period) in the field, which would be needed to assess whether  regions and periods with the risk for transmission will evolve. Are there any hard facts, data, experiments that can be used or applied to this virus. The two papers that might gives a first answer under fixed lab conditions are  (see graphics)
Li MI, Wong PS, Ng LC, Tan CH. Oral susceptibility of Singapore Aedes (Stegomyia) aegypti (Linnaeus) to Zika virus. PLoS Negl Trop Dis. 2012;6(8):e1792.
Wong PS, Li MZ, Chong CS, Ng LC, Tan CH. Aedes (Stegomyia) albopictus (Skuse): a potential vector of Zika virus in Singapore. PLoS Negl Trop Dis. 2013 Aug;7(8):e2348.
Friendly greetings from Stockholm. B.
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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.
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We may not be able to determine the geographic origin of the whole "species" Seratia marcesens but if there are specifc pathogenic variants of the species which have recently begun causing a disease in humans or plants, it could very well be possible to trace where the most recent source of this spread was.  This may cost many millions of dollars or much less, depending on many aspects of the "outbreak" and the natural range of the organism.   Some recent examples of this type of tracing are found by studying for example how the source of the enteropahtogenic E. coli (STEC serotype 0104H4-2011) which killed people in Europe in May-June 2011, was traced. 
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Prevalence cross sectional study?
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Hello Juan,
since both HIV and HCV are chronic illnesses and do not resolve, prevalence from different points in time would be an acceptable measure of the disease burden. However,  that being said, at the country level, the design and number of samples tested will have a very strong effect on the prevalence-especially since the transmission of these diseases is not homogeneous. Furthermore, because they are chronic the age of the individuals sampled is also important since as they age, people have a higher chance of being exposed over time. This is very important when trying to compare different countries to each other. This an age adjusted prevalence of HIV and HCV could be useful to assess the disease burden. 
Thus is a great research topic, since both have common exposure pathways!
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  • please all key actors
  • their potential contributions to risks of eating food infected with Campylobacter
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Food Standards Agency very important, for example see this survey from earlier in 2015 about chickens in supermarkets 
Obviously the farming industry, and food retail industry too. 
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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?
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Dear Eric
There is an interesting paper you may be want to read:
Am J Pathol. 1988 Apr; 131(1): 48–52.
PMCID: PMC1880566
Immunoelectron microscopy of Schüffner's dots in Plasmodium vivax-infected human erythrocytes.
P. V. Udagama, C. T. Atkinson, J. S. Peiris, P. H. David, K. N. Mendis, and M. Aikawa
I attache the PDF.
Finally, please if you consider this answer appropriate, please upvote it using the green up arrow click. Thanks.
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I have a series of increases in death arising from a suspected series of outbreaks of an unknown agent.
The suspicion is that the agent is relatively difficult to transmit and relies heavily on chance to initiate a mass effect.
How do I test the hypothesis that a high increase in deaths is typically followed by a low increase in deaths in the following outbreak and vice versa?
See attached chart.
See also http://www.hcaf.biz/emergencyadmissions.html  for further detail of these infectious-like events
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Dear Thomas, Many thanks for the reply. Probably a little more complex as there seem to be interactions with influenza, however, seemingly a new type of outbreak. See attached. Cheers Rod
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 Krentz HB, MacDonald J, Gill MJ.  High mortality among human immunodeficiency virus (HIV)-infected individuals before accessing or linking to HIV care: a missing outcome in the cascade of care?  Open Forum Infectious Diseases.  2014 1 (1)
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Not sure if we can do this in England - will ask valerie Delpech at PHE. Excellent paper John!
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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
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I think that this link may be useful for you.
Pathogenesis of human cytomegalovirus infection and ...
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de G Gerna - ‎2004 - ‎Cité 93 fois - ‎Autres articles
In acquired immunodeficiency syndrome patients with human cytomegalovirus (HCMV), disseminated infection, and end-organ disease, autopsy findings show ...
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Drug resistant enteric fever is a harsh reality; with resistance to fluoroquinolones, cotrimoxazole, ampicillin, amoxycillin on the rise. So what is the place of aminoglycosides in the treatment of enteric fever? Could you please cite recent research done in this area? Thanks in advance !
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Aminoglycosides are ineffective for intracellular organisms (as Salmonella often is) and therefore as pointed out by Easow, do not lead to a clinical cure. Quinolone resistance is over 50% in the Indian sub-continent so Ceftriaxone is the current drug of choice. 
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Is it possible to make an estimation of Hepatitis B Virus prevalence in a society depending on the data collected during blood donation and sample examination ??
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Thanks Ernest, but can we extrapolate the results somehow?? 
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Hi everyone
Can I ask whether MALDI can detect organism straight from the positive bottle without first growing the colony/colonies?
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Barnini, S., Ghelardi, E., Brucculeri, V., Morici, P., and Lupetti, A. (2015). Rapid and reliable identification of Gram-negative bacteria and Gram-positive cocci by deposition of bacteria harvested from blood cultures onto the MALDI-TOF plate. BMC microbiology 15, 124.
Carbonnelle, E., Mesquita, C., Bille, E., Day, N., Dauphin, B., Beretti, J.-L., Ferroni, A., Gutmann, L., and Nassif, X. (2011). MALDI-TOF mass spectrometry tools for bacterial identification in clinical microbiology laboratory. Clin Biochem 44, 104-109.
Deak, E., Charlton, C.L., Bobenchik, A.M., Miller, S.A., Pollett, S., McHardy, I.H., Wu, M.T., and Garner, O.B. (2015). Comparison of the Vitek MS and Bruker Microflex LT MALDI-TOF MS platforms for routine identification of commonly isolated bacteria and yeast in the clinical microbiology laboratory. Diagn Microbiol Infect Dis 81, 27-33.
Kohlmann, R., Hoffmann, A., Geis, G., and Gatermann, S. (2015). MALDI-TOF mass spectrometry following short incubation on a solid medium is a valuable tool for rapid pathogen identification from positive blood cultures. Int J Med Microbiol 305, 469-479.
Schneiderhan, W., Grundt, A., Wörner, S., Findeisen, P., and Neumaier, M. (2013). Work flow analysis of around-the-clock processing of blood culture samples and integrated MALDI-TOF mass spectrometry analysis for the diagnosis of bloodstream infections. Clin Chem 59, 1649-1656.
Singhal, N., Kumar, M., Kanaujia, P.K., and Virdi, J.S. (2015). MALDI-TOF mass spectrometry: an emerging technology for microbial identification and diagnosis. Front Microbiol 6, 791.
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Dear researchers,
I come across some papers in Epidemiology field where they use geometric mean concentration for antibody titer. I wonder why do we want to use geometric mean concentration, what is the advantage(s) and disadvantage(s) of using this calculation for antibody titer.
Also if any one can suggest a good reference to read about it, I would really appreciate.
Thank you.
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Antibody effects are often tested by observing reactions at concentrations which are multiples of each other  eg 2x, 4x,8x, 16x  or 10x, 100x,1000x. This imples the logarithms of the concentrations increase arithmetically.In a series of observations the logarithms give a more symmetical distribution for whicn an arithmetic mean is appropriate. The arithmetic mean of the logs is the log geometric mean(GM)
log GM = 1/n { logx1 + logx2 + logx3.....logx}
            = log[{x1x2x3   xn} 1/n.]
so GM ={x1 x2 x3 ....xn} 1/n
The technique can be used for other observations following a log normal type of distribution, eg occupational and environmental dust  exposures
See eg Armitage and Berry Statistical Methods in Medical Research 2nd ed 1987 p 31-33.
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for example polio and RCH has been given enough emphasis for social mobilization and development communication. Tropical diseases and especially leprosy have rarely been addressed with such vitality. can mass level mobilization and awareness creation about the disease be helpful in eradicating?
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Apart from awareness creation about basic symptoms of disease, a lot needs to be done in the area of stigmatization. Infected persons especially females may be reluctant to seek medical help because of stigmatization, and this will hinder control efforts. So emphasis of the social mobilization should rest more on sustained, simple and repetitive information to discourage discrimination against infected and affected persons. This is very vital. Advocacy visits to political leaders and government should engender the desired shift in priority from curative to preventive programs such as community mobilization for adequate participation. In other words, advocacy can lead to political will and commitment by Government in favour of leprosy control and eradication.
also be carried
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I am planning a bibliometrics analysis of the scientific output of influenza to know the trend this topic, over Web of Science database.
Thank you
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In my research group, we are discussing about what is a scenario in the preparedness logic of government in order to prevent pandemics. 
Specifically, we want to know: 
  • How is defined scenarios by bio-experts?
  • What are the root of this concept in biosecurity and biosurveillance projects?
  • How does it works? 
  • It is true that scenarios are based in imagination?
I have written about it in my blog: http://bit.ly/1CvUeeL
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Beware early warning systems that are based on wrong information!   H5N1 was first identified in 1997 in Hong Kong, but was stamped it out successfully. When it appeared again in SW Asia mainland in 2003, the CDC embarked on pandemic plan that could be downloaded by any country, state, or municipality.  The package was called "FluAid", and allowed predictions of cases, hospitalizations, and deaths.  The problem was that as of 2003-2005 the only hard evidence of "recent" case fatality rates were to be found from the 1957 and 1968 pandemics of "HK flu" and "Asian flu", where the CFR was approx. 0.1%-0.2% (1-2 per thousand).  BUT from 2003 onwards, the human cases of H5N1 infection had shown a global CFR of between 50-60%!   The vast discrepancy in lethality is astonishing. As the human cases steadily increased between 2003 to 2009, the global CFR did not drop below 50% and still remains at that level to this day.  The most lethal pandemic to date in human history was the 1918 A/H1N1 which harvested at least 40-50 million in those countries that were keeping records, and this was at a CFR of 2.5%. Almost a hundred years later, when respiratory virus can  travel at the speed of a modern jet, H5N1 appears with a CFR  20 times greater that 1918, and we chose to use a CFR that is 20 times LESS than 1918,  Fortunately, the pandemic that did appear next (2009/H1H1) was generally another very mild entity, but one shudders to think how unprepared we would have been (and still are) should H5N1 or H7N9 mutate enough to wreak havoc.  Curiously, the CDC realized the error around 2006, when they announced an adjustment in FluAid calculations to reflect a "mortality rate" (not CFR)of 1%.  Most people missed the subtle switch: a MR of 1% with a Attack rate of 30% gives you a CFR of 3.3%, certainly an improvement on the previous CFR estimate of 0.1%, and closer to the 1918 CFR of 2.5%, but still a long way from reality and 50%.
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Since the MERS Coronavirus infection is endemic on the Arabic peninsula and now transfered by single patient to South Korea: Do you defer travelers coming back from these regions for a specific period (e.g. 4 weeks after return) from donating blood in your country? 
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In response to colleagues’ inquiries about any relevance to blood donors of recent MERS-CoV spread to the Korean peninsula, the following reflects what recently came from colleagues in the US and Europe. So far, there has been no evidence of parenteral transmission published. No specific intervention related to blood donors has been recommended, and there are no new recommendations related to ongoing transmission in the Middle East or the outbreak in South Korea at this time. Donors must be well on the day of donation, and in the unlikely event that a history of MERS-CoV infection is provided by a donor, they should be fully recovered before being accepted for phlebotomy.
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Given the relatively rapid progression in areas of Brazil (8 states until yesterday) in approximately one month, how faster or when would be expect to have cases of Zika in other countries of the region? Would be similar to chikungunya?, when ending 2013 cases were reported in some Caribbean islands and some months later we received in other countries in the region. I felt we, as region, were not prepared for CHIK. Not even yet, physicians and research groups are doing properly in the most efficient way, even those working in dengue, and now we will face Zika.
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You might already have cases of Zika and not know it.  The huge difference between Zika and chikungunya is the percentage of people who get sick.  Actually Zika seems like dengue in that both viruses are unlikely to cause someone to be so sick as to present at a clinic.  If you look at the statistics from some longer studies it seems like with Zika maybe less than 20% of people present.  This and the fact that it seems similar to chikungunya and dengue there was a great probability that Zika was being missed over the last year or so.
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Please include experiences on how to obtain ethical approval and informed consent for research among sexual minorities (LGBTI) in a country where the practices are illegal. Thank you
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The key is to outreach the population. In Guatemala, we're building an experience to increase coverage in MSM. Is important to mention that in Guatemala isn't an unfreandly legal system for LGBTI, however stigma is a major concern in our context.
The close work with a community based organization, and promotion through social network as Facebook, Twitter; and "gay apps" such as Grindr and Manhunt; are an important strategy to contact MSM. 
Also, Mpowerment model 
Here are some publications that may help you:
Goldenberg T, McDougal JS, Sullivan SP, Stekler DJ, Stephenson R. Preferences for a Mobile HIV Prevention App for Men Who Have Sex With Men. JMIR mHealth uHealth [Internet].
Young SD, Szekeres G, Coates T. The Relationship between Online Social Networking and Sexual Risk Behaviors among Men Who Have Sex with Men (MSM). PLoS One. 2013;8(5):15–8.
Usher D, Frye V, Shinnick J, Greene E, Baez E, Benitez J, et al. Recruitment by a Geospatial Networking Application for Research and Practice: The New York City Experience. JAIDS J Acquir Immune Defic Syndr [Internet]. 2014;67(5).
Suthar AB, Ford N, Bachanas PJ, Wong VJ, Rajan JS, Saltzman AK, et al. Towards Universal Voluntary HIV Testing and Counselling: A Systematic Review and Meta-Analysis of Community-Based Approaches. PLoS Med. 2013;10(8).
Kegeles SM, Hays RB, Coates TJ. The Mpowerment project: A community-level HIV prevention intervention for young gay men. Am J Public Health. 1996;86(8 I):1129–36.
Kahn JG, Kegeles SM, Hays R, Beltzer N. Cost-Effectiveness of the Mpowerment Project, a Community-Level Intervention for Young Gay Men. JAIDS J Acquir Immune Defic Syndr [Internet]. 2001;27(5)
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If the methodology of the study is sound, can you just conclude by saying that being diabetic does not confer an extra risk of being predisposed to latent TB infection (in contrast to having tuberculosis)? Or does this mean that the levels of latent TB in the community is overwhelmingly large that it is almost similar to levels in diabetics?
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LTBI reflects exposure to tuberculosis disease. It would be surprising if diabetics had a higher or lower exposure to tuberculosis disease. From the available research, one would expect diabetics to have a higher chance to develop active disease.
The interesting question is: Will those diabetics exposed to TB have a higher chance of developing active disease than non-diabetics? I think you have the potential for a fascinating longitudinal study!
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I am intended to pursue my Ph.D dissertation on dengue epidemic, please suggest some suitable measures in public health domain.  
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do u want to study epidemic or epidemiology?
As if it is epidemic first do secondary data analysis of earlier epidemic in relation to various determinants   to prepare preparedness methodology for predicting epidemic   
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I have a disease data set along with environmental data of five years of different cities in Pakistan. I want to develop a disease prediction model and visualize it using the maps of those cities that where which environmental variables are explaining the maximum variability in disease development?
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As said before, you need to use Goegraphical Information Software (GIS)
QGIS is good and free but you need to read the documentation to make good use of it. As a start and if you only need simple data visualization (say, cases on a map, perhaps in different categories), I recommend using the website called http://www.spatialepidemiology.net/
It is free and very simple to use
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There is significant amount of hospital based research with loads of biomedical research institutes. I am curious to know if there is evidence showing the benefits of hospital based research to the health of populations, training of health workers and clinical care (the easy bit).
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The advantage of hospital-based research is that the technical manpower & laboratory facilities are available to diagnose Illness and do research at hospitals . Regarding Infectious diseases , symptomatic ( mild & severe ) patients can be evaluated & treated in hospitals only . The Incidence data of any Infectious disease can be easily obtained from hospitals . The prevalence data can be designed for community , by utilizing the hospital data . Most of research publications on severe Infectious data come from hospitals only .
  My personal experience on human leptospirosis in India is based on hospital data only . The primary reason being availability of clinical material & laboratory facilities to diagnose the disease in hospital . This is relevant for developing countries , where there is shortage of skilled manpower & finance to do community based research . It was possible for me to design guidelines for diagnosis & management of leptospirosis , based on my hospital experience for community practice also.
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The target audience is virally unsuppressed HIV-positive gay-identified men in the U.S. who have had condomless anal sex with HIV-negative or unknown status male partners.
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We can create one by using PPT or keynote. 
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I am interesting in finding prevalence/incidence rates of specific opportunistic infections of young age groups (not adult) from before and after the start of the AIDS epidemic (~1980). 
In particular I am looking for trends in: Tuberculosis, Cryptosporidium, and Non-Typhi Salmonella. 
Does anyone know if such data exists and where I can find it? I would want to look in an area where HIV/AIDS is widespread, so somewhere in Sub-Saharan Africa would be ideal (or the whole region). 
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Hi Oliver,
the time individual computers started being used in a whitespread fashion (and, thus: 'easy data collecting' emerged) stretches from the beginning 90'ies in the industrialized world and a bit later in African countries. Hence, before that decade, there was virtually nothing  in this respect, at least not in a representative fashion and/or the amount you are intending to obtain here. Sorry to say, the only slim chance would be to contact the respective officers at WHO.
good luck for your endeavour!
Sibylle
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Bovine brucellosis is endemic in Africa but very scarce information on predominant biotype in specific regions
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Brucella abortus biovar 1 has been isolated by some members of Brucellosis Research Department, Animal Health Research Institute, Egypt from milk, supramammary and retropharyngeal lymph nodes and identified by convenient bacteriology, MLVA  and MALDI-TOF mass spectrometry (MS). We used to have Brucella abortus biovar 3, but it has been a while since we last isolated it 
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I would like to know what is the best approach between prevented number of cases for every 1000 vaccinated individuals and the decreasing lethality of cholera in the vaccinated region when it comes to assess the Oral Cholera Vaccine Efficacy during a mass vaccination campaign in Sub Saharan Africa.
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It might be a ''before-after" study. Incidence rate of cholera using person-time determined before (risk in exposed) and after (risk in unexposed) vaccination campaign can be compared. The number of preventable cases is calculated as follows : number of person-time in exposed group * risk difference.  The etiologic fraction in exposed to assess the vaccine efficacy is : (RR-1)/RR = (number of preventable cases)/(number of cases in exposed group = (risk difference)/(risk in exposed).
NB : RR = risk ratio.
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Are there any online tools or free programs? Please suggest the name of program or website thank you so much.
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If you present a sample image, it can give a better idea as a lot of tools may be used and more people can give ideas, if you give the image that you want to create.
But I am giving a few sites that may be useful.
Also see ChemBio if it may be useful. Appears they give one year free license for research purposes.
Regards,
Dr. Akilesh. R
India
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To all interested parties,
My name is Nelson Karp, MD and I am an HIV/Aids researcher who works on the development of drugs and vaccines for patients.
I have numerous published patents:http://www.endhivtoday.org/united-states.html
We are at a point in our research that funding is required for the USPTO applications and to further both the research and the submission of the patents to potential drug manufacturers.
This is an area in which I have no expertise and am hoping to find some information and/or someone who has experience in this field.
Thank you.
Feel free to contact me anytime 
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Nelson - a somewhat broad question -  but one that can be answered 'in parts' - so you may get quite a few responses in this thread. I would 'start' by suggesting that, despite your lack of experience in grant writing, you are best to consider the nature and scope of your team initially. It may well not be a good idea to put yourself forward as Chief Investigator (CI) or Principle Investigator (PI). Grant proposal reviewers need to assess the ability of the investigators in the research team to undertake the research. Therefore, proposals require some information about the research team (e.g. name, qualifications, employment position) as a minimum. In some instances (e.g. NHMRC grants), a short biography (research track record) and publications list are necessary for each investigator. All authors on the research team should provide intellectual capital to the research project in a 'ranked order'; that is, they must actively participate in the project and contribute to the generation of knowledge. Following some unfortunate episodes of ‘honorary authorship’ to persons in authority who provided no academic input to the research and related publications, there are now guidelines on authorship, sponsorship and accountability, issued by, among others, the International Committee of Medical Journal Editors (ICMJE) (Halperin et al. 2005), and Universities Australia http://www.universitiesaustralia.edu.au/. These types of resources may well assist in working through the grant process
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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?
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Dear Dr. Hegazy,
The 2009 WHO guidelines entitled "WHO policy on Tuberculosis infection control in health-care facilities, congregate settings and households"  described all the different components on this topic  (http://www.who.int/tb/publications/2009/infection_control/en/). In addition, you can find specific recommendations related to building design in the following document: "TBCTA. IMPLEMENTING the WHO Policy on TB Infection Control in Health-Care Facilities, Congregate Settings and Households. A framework to plan, implement and scale-up TB infection control activities at country, facility and community level. November 2010. (http://www.tbcta.org)."
All the best,
Dr. Daniel Chemtob (Former WHO Medical Officer in charge at the Geneva WHO/HQ  of TB infection control worlwide)
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In the 1940s and 1950s there have been cases of malaria in the south of the Atlantic Forest biome, however, never read anything about the Pampa biome.
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Malaria is going to be consider "erradicated" in Argentina soon.
Endemic areas were no the NORTH WEST, near bolivia, not near the pampas. 
I assume you can read spanish, so check this: 
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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
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You can, may be draw examples from the Indian model, although not completely integrated in its true sense currently. The National AIDS Control program nevertheless has worked progressively towards integration and now envisages to integrate the AIDS program completely in to the national health mission. Integration as I understand occurs at various levels and for various program components of the AIDS program. If your question is about the prevention and treatment component of HIV/AIDS then the answer would be yes it can be integrated one hundred percent. For example, testing for HIV can occur at any general laboratory, in most cases it would not require specialised training or equipment that is not manageable by a certified general laboratory technician. Now the larger problem I assume could be when we talk of the treatment component. If PLHIV have access to ARV medications provided by the government then it could be challenging, in terms of the capacities of the medical officers to provide standardized care based on the guidelines and also the laboratory support for periodic CD4 testing. Our experience in India is that integration is a slow drawn process especially for a concentrated epidemic such as ours. And, most off it depends on the existing public health infrastructure.
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Snounou. G and any person with info. Thanks
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this should be plenty of DNA to give a a band even with the outer PCR. lets see the results of the nested PCR.
good luck
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Besides the type of epidemic how do we determine the overall severity (i.e mild moderate severe)?
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You can also use a software called "Spectrum" from UNAIDS. When you enter certain parameters, it can produce some prediction about HIV magnitudes.
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I am conducting a qualitative study on HIV/AIDS medication adherence and compliance and seek contributions on how to gather relevant information.
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From your question, you indicate that adherence to HIV and AIDS medicines in Nigeria is high and there are some factors that have been shown to contribute to that, i believe you want to establish which factors may be adapted into strategies for sustained high adherence.
Since you want to conduct a qualitative research, interview with the patients, health care providers, managers, caregivers and community organization representatives (such as support groups and home based care groups)  may be the way to go. You could use semi-structured questionnaires and focused group discussions and your questions should include some of the factors identified to result in high adherence and seek from the participants what they should be done. In your interviews you should have representation in terms of gender, age and if possible, duration on therapy. 
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Dear all,
kindly give your valuable suggestion as i am going to design patient Education Material with Holistic Approach. for HIV-AIDS Patients.
Thanks in Advance
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Our experiences shows that more inter active is more effective .Side effects of ART and how to cope with it is very important for patients' adherence, other important based on our study is family stigma that should be targeted by IEC approaches.
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I am developing an ELISA for Porcine Epidemic Diarrhea Virus (PEDV). I have in-house PEDV controls that agree on both ELISA and IFA. However, when testing cross-reactivity, Porcine Respiratory Coronavirus (PRCV) is cross reactive on my ELISA to PEDV antigen. Yet, in an IFA for PEDV, PRCV serum does not cross-react. In addition, NVSL (commercial resource) positive control for PEDV comes up negative on my ELISA but positive on my IFA. Why might this be when I am using the same serum samples and the same PEDV antigen for both tests? 
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Dear Chelsey,
I just realized your request and the answers above are really facing major aspects correctly. I would just  like to emphazise another aspect of your ELISA. For every immunoassay the intended use is important. This aspect is highly relevant in terms of the second aspect mentioned by Hans Lutz. If you like to recognize in a serological format those sera, which have high affinity antibodies against the virus antigen (So the "patients" had a "clear and targeted" immune response.), your assay should perform different compared to the situation where you want to see weak infection status with only low affinity antibodies. (But some of those "individuals" don't have or had a relevant infection and don't need any treatment of whatsoever. Most of them had only contact with a cross-reacting antigen and not with the virus, you like to investigate.). If you are interested in a serological assay, which clearly and without any doubt detects only sera after infection and after a real response from the immune system, you should develop your assay in a way that low to medium affinity binding does not occur at all. This makes a serological assay highly reliable, but on the other hand not sensitive during the first few days of infection.
Low to medium affinity binding is the major cause for cross-reactivities. And so if you optimize your assay to show only high affinity binding effects and not low to medium affinity binding - which is done by choosing the assay diluent - you will most probably get rid of any cross-reactivities.
But if you like to have an assay, which also gives a signal from the weakest immune response, that would mean, that your assay will have to show also low affinity binding effects. In that case you will not get rid of cross-reactivities and other potential interference effects, but you will have positive results even in earlier stages and with weaker immune responses (maybe false-positives due to cross-reactitivies of unknown molecular reasons). In other words: a serological assay either gives nearly no false-positives and is very reliable to detect a strong infection reaction, but you maybe loose the first days of infection as false-negatives. Or your assay will detect all potential infections, but will show many false-positives due to cross-reactivities and interference. Both assay types are good and well-done, but it is important to differentiate and to understand which assay gives the one or the other kind or answer. For many diseases and situations the weak immune response is not relevant. Unfortunately most kit manufacturers and also scientist do not realize and mention this difference in the intended use and the answer of an assay.
Again: It is a question of your research task, whether you should avoid potential interference due to cross-reactivity and similar effects or not. You can avoid it by using interference-reducing assay diluents or antibody diluents. But this is not always good to do so.
Furthermore I would like to add a comment to the point 1 of Hans Lutz, which is in general correct, but it maybe doesn't fix the complexity of coating to ELISA plates. If you coat molecules on an ELISA plate you will normally not get a monolayer of molecules, which are "directed" like polar or non-polar. In fact you normally get a completely uncontrollable and complex layer of molecules, which are in part monolayer in part double- or multilayered and which are oriented in any thinkable and non-thinkable direction. As a result only very few of the coated molecules (regardless whether you coat proteins or peptides or antibodies in other kinds of ELISA) will be presented in a way that binding to other molecules like antibodies will be possible. For example in an extremely good optimized sandwich ELISA only 4-8 % of all coated capture antibodies can bind to the target molecule. All the other coating antibodies are either denatured or misoriented or both. So it is not the case that your capture molecules on an ELISA plate will be completely oriented according to the polarity of plate and molecule. You will also see all other orientations and in most cases even multilayer and complexes of molecules. There are only few options to change this situation, which is difficult to control. One option is choosing different pH values during the coating process. You will get very good results in many cases with a Coating Buffer at pH 9.6, but sometimes pH 7.2 (or maybe others) will give you different results in your ELISA. Normally you can't predict the outcome. Just test different pH-values during coating and you will sometimes get different results in your assay.
So first decide, which kind of question your assay should answer and then optimize your assay to answer exactly this question (avoiding of low to medium affinity binding or not, ...). You should keep in mind that you can get two completely different assays with the same antigens and antibodies, if you change aspects like coating procedure, assay diluent, incubation times.
Best wishes
Tobias
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We have recently isolated HAdV-57. However, we do not know if this virus is isolated from many countries? We do know they have been isolated in Russia and China. 
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I don't know about the HAdv,but now i'm isolating the swine Adv by PK15 (a kind of cell from swine kidney cellline)and now i have got the type 3 and type 4.Acutually the HAdv desease is known to have a strong  influence in people,especially for children,but not in swine, so We hope we can get the the information of the SAdv.
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I can easily find the basic reproduction number of deadly, or serious infectious microbes such as HIV, Ebola, rubella, TB, and MRSA. However, it is more difficult to find it for other microbes. So, is the basic reproduction number of at least one strain of all infectious microorganisms available? if yes, what is the most reliable reference collecting them; if no, what is the criteria upon which we decide we should estimate the basic reproduction number. Also, for known basic reproduction number of different strains of a single species, are they significantly different (for instance, MRSA , VRSA, and other sensitive staph. aureus do they have a different R0). Thank you
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Actually, I need a reliable reference that I can releate to when needed, also if you have any info. About the 
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I've carried out a survival analysis. I have a dataset of live singleton deliveries over a few year period (~203, 000 deliveries, 1, 512 events). I'd like to be able to calculate the C-statistic/C-index for my proc phreg model. I have found various macros online to do this, and have them up and running. However, I am concerned that even though I take care of the clustering of children within mothers (mothers could have more than 1 live singleton birth in this three year period) using the covsandwich (aggregate) option, I'm not sure that the macros calculating C-index take clustering into account. I can see that they calculate the usable pairs, concordant and discordant pairs that go into the C-index calculation, but it's not clear they account for clustering. What would you have to do to account for clustering in the C-index calculations or is it sufficient that I used the predicated survival values from a cluster adjusted proc phreg to then calculate the C-index? I should note that the amount of clustering in my data is probably not significant - there are slightly less than 10% of deliveries are a second or third delivery for the mother.
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Dear  Herzog,
It's a practical method with R
Best regards
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What is the reason for the epidemic of severe Plasmodium vivax malaria in East Africa?
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It might be, but that is very unlikely given that the reduction of P. falciparum is mostly related to the effect of the many interventions implemented in the region that are also efficient against P vivax. Epidemiologically, you will need to increase the population at risk (susceptible subjects ~ Duffy positives) as well as the population of mosquitoes that are efficient P. vivax vectors to close the malaria cycle. Both can be driven by migration, which occurs often and very intensively in some African regions. I do believe that this will offer you a partial answer to your question, although I'm afraid that the reality is far more complex than that. Africa offers a very favorable environment for vivax malaria transmission so once we have more subjects that are protected against it there is no reason to don't expect more P vivax malaria cases.
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Lots has been written about quarantine and closing borders domestically (US) but not much else.
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Hi Brandon,
I think that rather than thinking about "domestic" ethical issues in connection with the Ebola epidemic, we should focus on the epidemic as further evidence of Globalization diminishing the relevance of the nation-state and its imaginary boundaries.  We live in a time of fluid borders and porous nationalities brought on by ease of travel, technological innovations, an aggressive global media and an equally obdurate "global civil society" made up of transnational NGOs.  This denies us the intellectual luxury of viewing global issues such as HIV/AIDS, global warming and, now, Ebola from the narrow lens of a domestic crisis.
Remember how the 2008 "domestic" financial crisis brought on by "domestic" hubris in the U.S.  financial industry ("securitization," toxic loans, etc.) spread like wildfire to the rest of the world?  While I have described the morally challenged financial industry in terms of the weaknesses of domestic regulatory agencies (see "After Shame...." among my RG publications), I definitely do not view the lack of moral fiber in the financial industry as a "domestic ethical issue".  Indeed, it reflects a pandemic of global amorality brought on by the enhanced respectability of "Neoliberalism" as a euphemism for moral decay.
Gwen
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Mers
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MERS CoV is always  transmitted from dromedaries to humans. From protein bio assays it is clear that antiboides to MERS CoV are very common in camels.  But virus is also detected in camels and humans with MERS by competitive assays.  No doubt  humans also link with MERS and camels epidemioloically..
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When we do studies concerning association between infectious disease and climate change, do you think it is better to use onset dates rather than notified dates and why? I might prefer to use onset dates, what do you think?
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You should strive for onset date of infection, if you can obtain it.  But agree with Wittert: use accurate, consistent  information. Ideally you would adjust for lag time if you are not using onset date. How you adjust needs to be thoughtful. 
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To be used at 0, 3 and 6 monthly intervals.
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It depends on the population you are studying (e.g. adults vs adolescents etc). I would suggest checking out the CAPS website (University of California, San Francisco) - they have a lot of survey instruments for HIV researchers, prevention planners etc - as long as you cite CAPS as your source. 
Hope this helps!
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I am in a need of some literature on TUNEL method. Can anybody help me?
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Hi Achini,
Please find the following protocol for tissue staining. I am forwarding you both colorimetric and fluorometric staining protocol.
Best Luck.
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Olivia Horna-Campos' papers show that Peruvians who spend more time on public transport have increased risk of TB infection and disease. Is anyone aware of empirical studies conducted in Sub Saharan Africa exploring the link between use of indoor public space and TB? I can find very few. I am reviewing the literature and need test papers to ensure my search terms are capturing relevant work.
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