High HIV prevalence and risk behaviors in men who have sex with men in Chennai, India

OBJECTIVE: To estimate HIV and sexually transmitted disease (STD) prevalence and behavioral risk characteristics of men who have sex with men (MSM) in Chennai, India. METHODS: A cross-sectional population-based random sample survey was conducted in 2001. Randomly selected residents of 30 slums in Chennai were interviewed for behavioral risk factors through face-to-face interviews. Sera and urine were examined for syphilis, HIV-1, gonorrhea, and chlamydia. Logistic regression analyses were used to assess associations between MSM status and HIV infection and to identify risk characteristics of MSM. RESULTS: Of 774 men, 46 reported (5.9%) sex with other men. MSM were more likely to be seropositive for HIV (odds ratio [OR] = 8.57; 95% confidence interval [CI]: 1.83, 40.23) and were more likely to have a history of STD (OR = 2.66; 95% CI: 1.18, 6.02) than non-MSM. Men who used illicit drugs in past 3 months (adjusted odds ratio [AOR] = 4.01; 95% CI: 1.92, 8.41), ever exchanged money for sex (AOR = 3.93; 95% CI: 1.97, 7.84), or were ever tested for HIV (AOR = 3.72; 95% CI: 1.34, 10.34) were significantly more likely to report sex with men. CONCLUSIONS: MSM in Chennai slums are at high risk for HIV. HIV prevention strategies aimed at changing unsafe drug and sexual practices should target the general population of men, with specific attention to areas with high rates of MSM.     

Immune reconstitution inflammatory syndrome in association with HIV/AIDS and tuberculosis: Views over hidden possibilities

Background  

CD4+ T lymphocyte (CD4) cell count testing is the standard method for determining eligibility for antiretroviral therapy (ART), but is not widely available in sub-Saharan Africa. Total lymphocyte counts (TLCs) have not proven sufficiently accurate in identifying subjects with low CD4 counts. We developed clinical algorithms using TLCs, hemoglobin (Hb), and body mass index (BMI) to identify patients who require ART.     

Attenuation of Aluminum Chloride-Induced Neuroinflammation and Caspase Activation Through the AKT/GSK-3β Pathway by Hesperidin in Wistar Rats

Hesperidin, a flavanoglycone abundantly present in citrus fruits, is reported to have antioxidant, anti-inflammatory, and neuroprotective properties. Previous reports from our laboratory indicated the neuroprotective effect of hesperidin against aluminum chloride (AlCl₃)-induced memory loss, acetylcholine esterase hyperactivity, oxidative stress, and enhanced expression of amyloid β protein biosynthesis-related markers. However, their role on AlCl₃-induced inflammation, caspase activation, Tau pathology, altered Akt/GSK 3β signaling pathway, and Aβ clearance marker has not yet been fully elucidated. Intraperitonial injection of AlCl₃ (100 mg/kg body weight) for 60 days significantly elevated the expressions of insulin-degrading enzyme (IDE), cyclin-dependent kinase 5 (CDK 5), and phosphoTau (pTau); inflammatory markers such as glial fibrillary acidic protein (GFAP), ionized calcium-binding adapter molecule 1 (Iba-1), NF-kB, cyclooxygenase-2 (COX-2), interleukin (IL)-1β, IL-4, IL-6, tumor necrosis factor-alpha (TNF-α), inducible nitric oxide synthase (iNOS); and apoptotic markers including cytosolic cytochrome c (cyto c), caspase-3, caspase-8, and caspase-9, and lowered expressions of mitochondrial cyto c, phospho-Akt (pAkt) and phospho-glycogen synthase kinase-3β (pGSK-3β) in the hippocampus and cortex. Co-administration of hesperidin to AlCl₃ rats for 60 days significantly ameliorated the aluminum-induced pathological changes. The behavioral studies also supported the above findings. Our results imply that treatment with hesperidin might be a potent option for treating the symptoms of cognitive impairment in Alzheimer’s disease by targeting its most prominent hallmarks.     

Transmission of "a" determinant variants of hepatitis B virus in immunized babies born to HBsAg carrier mothers

Hepatitis B virus (HBV) surface antigen mutations may lead to immune escape and eventually cause failure of immunization. In this report, we identified immune escape variants in immunized babies born to hepatitis B surface antigen (HBsAg) carrier mothers. A total of 68 babies were followed up for 2 years after the full course of vaccination; 2.9% (2/68) of babies were found to be infected with the variant HBV in spite of preexisting antibody to surface antigen (anti-HBs) at 24 months post immunization. Both infants were positive for HBV-DNA; sequencing results of the "a" determinant region of the surface gene revealed that both babies had point mutations at a different nucleotide position resulting in various amino acid substitutions. In addition, an intriguing variant having an addition-deletion mutation was observed in one of the babies. This is the first report to show the addition-deletion variant of HBV in India. However, the immunological significance of the above HBV variants needs to be further elucidated.     

Ethnic variation in certain hematological and biochemical reference intervals in a south Indian healthy adult population

BACKGROUND: We established the biochemical and hematological reference intervals among a south Indian healthy adult population attending an HIV referral centre in Chennai, southern India. METHODS: In a cross sectional study, 213 study subjects (129 male and 84 female) were studied between March and August 2005. All of the parameters were analyzed using standard hematological and biochemical techniques. RESULTS: Certain biochemical (viz. total bilirubin, alanine transaminase, albumin, creatinine, total protein, lipid profile, creatine phosphokinase, uric acid and lactate) and hematological (mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration and lymphocyte levels) parameters presented higher upper limits. In addition, the upper limits of white blood cell count, platelet count, hematocrit, red blood cell count and hemoglobin level were low in comparison to the currently reported ranges. CONCLUSION: Ethnic variation in reference intervals was observed in certain biochemical and hematological analytes in a south Indian adult population.     

Astrocyte-T cell crosstalk regulates region-specific neuroinflammation

During multiple sclerosis (MS), an inflammatory and neurodegenerative disease of the central nervous system (CNS), symptoms, and outcomes are determined by the location of inflammatory lesions. While we and others have shown that T cell cytokines differentially regulate leukocyte entry into perivascular spaces and regional parenchymal localization in murine models of MS, the molecular mechanisms of this latter process are poorly understood. Here, we demonstrate that astrocytes exhibit region-specific responses to T cell cytokines that promote hindbrain versus spinal cord neuroinflammation. Analysis of cytokine receptor expression in human astrocytes showed region-specific responsiveness to Th1 and Th17 inflammatory cytokines. Consistent with this, human and murine astrocytes treated with these cytokines exhibit differential expression of the T cell localizing molecules VCAM-1 and CXCR7 that is both cytokine and CNS region-specific. Using in vivo models of spinal cord versus brain stem trafficking of myelin-specific T cells and astrocyte-specific deletion strategies, we confirmed that Th1 and Th17 cytokines differentially regulate astrocyte expression of VCAM-1 and CXCR7 in these locations. Finally, stereotaxic injection of individual cytokines into the hindbrain or spinal cord revealed region- and cytokine-specific modulation of localizing cue expression by astrocytes. These findings identify a role for inflammatory cytokines in mediating local astrocyte-dependent mechanisms of immune cell trafficking within the CNS during neuroinflammation.     

Monosodium glutamate affects the temporal characteristics of biochemical variables in Wistar rats

Monosodium glutamate (MSG) was administrated chronically for 60 days to Wistar rats and 24 h rhythms of glucose, cholesterol, total protein and alkaline phosphatase were studied. MSG treatment was found to cause acrophase delays in the glucose and alkaline phosphatase rhythms and advances in acrophases of cholesterol and total protein levels. Amplitude and mesor values of these rhythms were found to be altered during MSG treatment. Glutamate levels in the brain were found to be significantly increased, which could alter these biochemical rhythms by modulating the transmission in retinohypothalamic tract and in the hypothalamic nuclei, probably including suprachiasmatic nuclei.     

Melatonin synergizes with low doses of L‐DOPA to improve dendritic spine density in the mouse striatum in experimental Parkinsonism

The dopamine precursor, L‐3,4‐dihydroxyphenylalanine (L‐DOPA), is the preferred drug for Parkinson's disease, but long‐term treatment results in the drug‐induced dyskinesias and other side effects. This study was undertaken to examine whether melatonin could potentiate low dose L‐DOPA effects in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐induced experimental parkinsonism. Mice were treated with the parkinsonian neurotoxin, MPTP, and different doses of melatonin and low doses of L‐DOPA. Behavior, striatal histology, and dopamine metabolism were evaluated on the 7th day. MPTP‐induced striatal dopamine loss was not modified by melatonin administration (10–30 mg/kg; i.p. at 10‐hr intervals, 6 times; or at 2‐hr intervals, by day). However, low doses of L‐DOPA (5 mg/kg, by oral gavage) administered alone or along with melatonin (10 mg/kg, i.p.) twice everyday for 2 days, 10 hr apart, after two doses of MPTP significantly attenuated striatal dopamine loss and provided improvements in both catalepsy and akinesia. Additionally, Golgi‐impregnated striatal sections showed preservation of the medium spiny neurons, which have been damaged in MPTP‐treated mouse. The results demonstrated that melatonin, but not L‐DOPA, restored spine density and spine morphology of medium spiny neurons in the striatum and suggest that melatonin could be an ideal adjuvant to L‐DOPA therapy in Parkinson's disease, and by the use of this neurohormone, it is possible to bring down the therapeutic doses of L‐DOPA.