14 research outputs found
Immune reconstitution inflammatory syndrome in association with HIV/AIDS and tuberculosis: Views over hidden possibilities-0
<p><b>Copyright information:</b></p><p>Taken from "Immune reconstitution inflammatory syndrome in association with HIV/AIDS and tuberculosis: Views over hidden possibilities"</p><p>http://www.aidsrestherapy.com/content/4/1/29</p><p>AIDS Research and Therapy 2007;4():29-29.</p><p>Published online 30 Nov 2007</p><p>PMCID:PMC2216023.</p><p></p>ion. Initiation of HAART in the subject leads to abrupt restoration of CD4+ T-cells and almost any pathogen-specific immune response. IRIS developers have a high burden of LPS and proinflammatory cytokines produced against LPS could result in an exaggerated, nonspecific attack on latent mycobacterial antigens that are presented in the local lymph nodes leading to localized inflammation. We also hypothesize that subjects that do not develop IRIS could have developed either tolerance (anergy) to persistent LPS and tubercle antigens or could have normal FOXP3+ gene (not shown) and that those with defective FOXP3+ gene or enormous plasma LPS could be vulnerable to IRIS (as demonstrated by researchers that defective FOXP3+ gene is associated with increased risk for inflammatory conditions). (Bold lines indicate the availability of clinical/experimental evidence and dashed lines indicate the possible mechanism)
HIV testing and counseling services in 2001 among low volume (<10 HIV tests per month) and high volume laboratories (>10 HIV tests per month) (N = 1031).
<p>HIV testing and counseling services in 2001 among low volume (<10 HIV tests per month) and high volume laboratories (>10 HIV tests per month) (N = 1031).</p
Changing patterns in HIV testing, counseling, and clinical services from 2001 to 2006 (N = 90).
<p>Changing patterns in HIV testing, counseling, and clinical services from 2001 to 2006 (N = 90).</p
Estimates of the force of infection (λ, summed across all serotypes) and R<sub>0</sub> obtained from catalytic models fit to dengue age-specific seroprevalence data.
<p>*We fit models with increasing number of parameters. Thus, while model A assumes that the force of infection has been constant historically, models B and C allow for periods with different transmission intensity.</p><p><sup>†</sup> p-value of a likelihood ratio test comparing model B vs. model A.</p><p><sup>γ</sup>p-value of a likelihood ratio test comparing model C vs. model B.</p><p>Estimates of the force of infection (λ, summed across all serotypes) and R<sub>0</sub> obtained from catalytic models fit to dengue age-specific seroprevalence data.</p
Results of multiple logistic regression of the association between seropositivity to Chikungunya/Dengue/Both with household and individual factors.
<p>*Income categories are described in <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0003906#pntd.0003906.t002" target="_blank">table 2</a></p><p>Results of the best fitting model (based on AIC) for each outcome are shown. All models included a random effect for location.</p
Population attributable fractions of severe liver stiffness/cirrhosis among total population and persons with chronic HCV infection.
<p>Population attributable fractions of severe liver stiffness/cirrhosis among total population and persons with chronic HCV infection.</p
Characteristics of participants.
<p>* Self reported</p><p>Characteristics of participants.</p
Distribution of liver stiffness by HIV and HCV status.
<p>Distribution of liver stiffness by HIV and HCV status.</p
Map of Chennai showing population density estimates and the 50 locations sampled in the study.
<p>Map of Chennai showing population density estimates and the 50 locations sampled in the study.</p
Selected characteristics of participating households (n = 438).
<p>*Includes data from two additional households that answered questionnaire but did not provide blood samples</p><p><sup>†</sup>Participants were allowed to list up to 2 sources</p><p>Selected characteristics of participating households (n = 438).</p