However, most of the observational studies do not support a significant association between higher nutritional
vitamin D store and increased risk of Cell Cycle inhibitor stone formation. Short-term nutritional vitamin D repletion in stone formers with vitamin D deficiency also does not appear to increase urinary calcium excretion.SummaryThe effect of nutritional vitamin D use in stone formers is still not clear. As vitamin D deficiency is highly prevalent among stone formers, future prospective studies are needed to establish the biological effect, as well as the safety and efficacy of nutritional vitamin D therapy in this unique patient population.”
“The mechanism of increased MTb disease susceptibility in HIV+ persons remains poorly understood. Apoptosis of macrophages in response to MTb represents a critical host defense response, and decreased apoptosis may represent a mechanism of increased susceptibility to MTb in HIV. In the current study,
MTb-mediated apoptosis of human AM was reduced in HIV+ subjects compared with healthy subjects in a TNF-alpha-dependent manner. IL-10 levels in BALF from HIV+ persons were significantly elevated compared with HIV-persons, and exogenous IL-10 reduced MTb-mediated apoptosis in healthy AM, suggesting that IL-10 could mediate decreased apoptosis observed in HIV. Further study showed that IL-10 reduced TNF release in response to MTb in AM through a reduction in TNF mRNA levels, and exogenous TNF could partially reverse
Pevonedistat concentration IL-10-associated effects on AM apoptosis. IL-10 did not influence p-IRAK, I kappa B degradation, or NF-kappa B p65 nuclear translocation in response to MTb, but IL-10 did increase levels of AM BCL-3, an inhibitor of NF-kappa B nuclear activity. BCL-3 knockdown in human macrophages increased MTb-mediated TNF release. Importantly, BCL-3 levels in AM from HIV+ subjects were higher compared with healthy GSK1210151A cell line subjects. Taken together, these data suggest that elevated lung levels of IL-10 may impair MTb-mediated AM apoptosis in HIV through a BCL-3-dependent mechanism. BCL-3 may represent a potential therapeutic target to treat or prevent MTb disease in HIV+ persons. J. Leukoc. Biol. 86: 53-60; 2009.”
“The microbes residing in and on the human body influence human physiology in many ways, particularly through their impact on the metabolism of xenobiotic compounds, including therapeutic drugs, antibiotics, and diet-derived bioactive compounds. Despite the importance of these interactions and the many possibilities for intervention, microbial xenobiotic metabolism remains a largely underexplored component of pharmacology. Here, we discuss the emerging evidence for both direct and indirect effects of the human gut microbiota on xenobiotic metabolism, and the initial links that have been made between specific compounds, diverse members of this complex community, and the microbial genes responsible.