Experimental and Modeling Investigation of the Effectof H2S Addition to Methane on the Ignition and Oxidation at High Pressures

The autoignition and oxidation behavior of CH₄/H₂S mixtures has been studied experimentally in a rapid compression machine (RCM) and a high-pressure flow reactor. The RCM measurements show that the addition of 1% H₂S to methane reduces the autoignition delay time by a factor of 2 at pressures ranging from 30 to 80 bar and temperatures from 930 to 1050 K. The flow reactor experiments performed at 50 bar show that, for stoichiometric conditions, a large fraction of H₂S is already consumed at 600 K, while temperatures above 750 K are needed to oxidize 10% methane. A detailed chemical kinetic model has been established, describing the oxidation of CH₄ and H₂S as well as the formation and consumption of organosulfuric species. Computations with the model show good agreement with the ignition measurements, provided that reactions of H₂S and SH with peroxides (HO₂ and CH₃OO) are constrained. A comparison of the flow reactor data to modeling predictions shows satisfactory agreement under stoichiometric conditions, while at very reducing conditions, the model underestimates the consumption of both H₂S and CH₄. Similar to the RCM experiments, the presence of H₂S is predicted to promote oxidation of methane. Analysis of the calculations indicates a significant interaction between the oxidation chemistry of H₂S and CH₄, but this chemistry is not well understood at present. More work is desirable on the reactions of H₂S and SH with peroxides (HO₂ and CH₃OO) and the formation and consumption of organosulfuric compounds

Vitamin D in autoimmunity: Molecular mechanisms and therapeutic potential

Over the last three decades, it has become clear that the role of vitamin D goes beyond the regulation of calcium homeostasis and bone health. An important extraskeletal effect of vitamin D is the modulation of the immune system. In the context of autoimmune diseases, this is illustrated by correlations of vitamin D status and genetic polymorphisms in the vitamin D receptor with the incidence and severity of the disease. These correlations warrant investigation into the potential use of vitamin D in the treatment of patients with autoimmune diseases. In recent years, several clinical trials have been performed to investigate the therapeutic value of vitamin D in multiple sclerosis, rheumatoid arthritis, Crohn's disease, type I diabetes, and systemic lupus erythematosus. Additionally, a second angle of investigation has focused on unraveling the molecular pathways used by vitamin D in order to find new potential therapeutic targets. This review will not only provide an overview of the clinical trials that have been performed but also discuss the current knowledge about the molecular mechanisms underlying the immunomodulatory effects of vitamin D and how these advances can be used in the treatment of autoimmune diseases

Irreversible renal damage after transient renin-angiotensin system stimulation:involvement of an AT1-receptor mediated immune response

Transient activation of the renin-angiotensin system (RAS) induces irreversible renal damage causing sustained elevation in blood pressure (BP) in Cyp1a1-Ren2 transgenic rats. In our current study we hypothesized that activation of the AT1-receptor (AT1R) leads to a T-cell response causing irreversible impairment of renal function and hypertension. Cyp1a1-Ren2 rats harbor a construct for activation of the RAS by indole-3-carbinol (I3C). Rats were fed a I3C diet between 4-8 weeks of age to induce hypertension. Next, I3C was withdrawn and rats were followed-up for another 12 weeks. Additional groups received losartan (20 mg/kg/day) or hydralazine (100 mg/kg/day) treatment between 4-8 weeks. Rats were placed for 24h in metabolic cages before determining BP at week 8, 12 and 20. At these ages, subsets of animals were sacrificed and the presence of kidney T-cell subpopulations was investigated by immunohistochemistry and molecular marker analysis. The development of sustained hypertension was completely prevented by losartan, whereas hydralazine only caused a partial decrease in BP. Markers of renal damage: KIM-1 and osteopontin were highly expressed in urine and kidney samples of I3C-treated rats, even until 20 weeks of age. Additionally, renal expression of regulatory-T cells (Tregs) was highly increased in I3C-treated rats, whereas the expression of T-helper 1 (Th1) cells demonstrated a strong decrease. Losartan prevented these effects completely, whereas hydralazine was unable to affect these changes. In young Cyp1a1-Ren2 rats AT1R activation leads to induction of an immune response, causing a shift from Th1-cells to Tregs, contributing to the development of irreversible renal damage and hypertension