We evaluated the risk of human immunodeficiency virus (HIV) transmission among serodiscordant couples with low adherence to antiretroviral therapy (ART).Data of heterosexual couples/partners in 2010 were extracted from an Internet-based system. Participants were then followed over the course of a year with 6- and 12-month assessments. Prevalence and density of HIV seroconversion were calculated for spouses/partners who did not have a positive HIV test results at baseline. We calculated the transmission odds ratio (OR) value stratified by personal characteristics and behavioral correlates at 6- and 12-month follow-up, as well as seroconversion in spouses/partners over the year.A total of 5544 HIV/AIDS patients and their spouses/partners were recruited in this cohort. Incidence of HIV seroconversion among HIV-negative spouse/partner was 63.7/100 person years (PYs) (430/674.9) at the 6-month follow-up and 33.2/100PYs (567/1707.1PYs) at 12 months. The OR value of transmission from female to male was 2.1 times higher than from male to females at 6 months and 2.3 times higher at 12 months (P < .001). The 55- to 64-year age group was most likely to transmit HIV to their spouses/partners, 2.2 times greater than the participants who were 65 years and older. Married participants were 2.4 times higher at 6 months and 2.5 times higher at 12 months to transmit HIV than divorced/widowed participants. Lastly, transmission among illiterate participants was 6.7 times higher at 6 months and 2.3 times higher at 12 months than those with an educational attainment of community college or above.High HIV seroconversion was observed in this cohort. Spouses/partners who were male had the highest risk of HIV acquisition; those aged 55 to 64 years, having married status, and are HIV-positive with less education were more likely to transmit HIV.

Diabetic neuropathy is a common complication of diabetes. It occurs in approximately 10?20% of patients with diabetes, or roughly 40?50% patients with diabetic neuropathy. However, the pathogenesis of diabetic neuropathic pain is still largely unknown. Several animal models have been used to study the underlying mechanisms for this complication. Some commonly used animal models include streptozotocin-induced rat and mouse models, diet/nutrition-induced models, combination of chemically- and nutrition-induced model, Zucker diabetic fatty rat model, type 1 insulinopenic BB/Wor and type 2 hyperinsulinemic diabetic BBZDR/Wor rat models, and transgenic/knock-out models. Even though the manifestations of diabetic neuropathic pain vary from thermal or chemical hyperalgesia, thermal or chemical hypoalgeia, allodynia, to spontaneous pain, some pathogenesis factors are shared among these symptoms. Increased AR activity, oxidative-nitrosative stress, protein kinase C, PARP and ACE activations, C-peptide deficiency, impaired neurotrophism, and proinflammatory responses have been identified in the development of diabetic neuropathic pain. This review discusses selected animal models for diabetic neuropathic pain, as well as some commonly shared pathways in these models.

Background Tuberculosis (TB) and Acquired Immune Deficiency Syndrome (AIDS) are leading causes of death globally. However, little is known about the long-term mortality risk and the timeline of death in those co-infected with human immunodeficiency virus (HIV) and Mycobacterium tuberculosis (MTB). This study sought to understand the long-term mortality risk, factors, and the timeline of death in those with HIV-Mycobacterium tuberculosis (MTB) coinfection, particularly in those with insufficient TB treatment. Methods TB-cause specific deaths were classified using a modified ‘Coding of Cause of Death in HIV’ protocol. A longitudinal cross-registration-system checking approach was used to confirm HIV/MTB co-infection between two observational cohorts. Mortality from the end of TB treatment (6 months) to post-treatment year (PTY) 5 (60 months) was investigated by different TB treatment outcomes. General linear models were used to estimate the mean mortality at each time-point and change between time-points. Cox’s proportional hazard regressions measured the mortality hazard risk (HR) at each time-point. The Mantel-Haenszel stratification was used to identify mortality risk factors. Mortality density was calculated by person year of follow-up. Results At the end point, mortality among patients with HIV/MTB coinfection was 34.7%. From the end of TB treatment to PTY5, mortality and loss of person years among individuals with TB treatment failure, missing, and adverse events (TBFMA) were significantly higher than those who had TB cure (TBC) and TB complete regimen (TBCR). Compared to individuals with TBC and with TBCR, individuals with TBFMA tended to die earlier and their mortality was significantly higher (HRTBFMA-TBC = 3.0, 95% confidence interval: 2.5–3.6, HRTBFMA-TBCR = 2.9, 95% CI: 2.5–3.4, P < 0.0001). Those who were naïve to antiretroviral therapy, were farmers, had lower CD4 counts (≤200 cells/μL) and were ≥ 50 years of age were at the highest risk of mortality. Mortality risk for participants with TBFMA was significantly higher across all stratifications except those with a CD4 count of ≤200 cells/μL. Conclusions Earlier and long-term mortality among those with HIV/MTB co-infection is a significant problem when TB treatment fails or is inadequate.