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The present study shows that TNF-alpha-induced activation of the NF kappaB pathway plays a critical role in cardiomyocyte apoptosis. IL-10 prevents TNF-alpha-induced NF kappaB activation and pro-apoptotic changes in cardiomyocytes by inhibiting IKK phosphorylation through the activation of ERK 1/2 MAPK.

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It is known that TNF-alpha increases the production of ROS and decreases antioxidant enzymes, resulting in an increase in oxidative stress. IL-10 appears to modulate these effects. The present study investigated the role of p38 and ERK1/2 MAPKs in mediating the interplay of TNF-alpha and IL-10 in regulating oxidative stress and cardiac myocyte apoptosis in Sprague-Dawley male rats. Isolated adult cardiac myocytes were exposed to TNF-alpha (10 ng/ml), IL-10 (10 ng/ml), and IL-10 + TNF-alpha (ratio 1) for 4 h. H(2)O(2) (100 microM) as a positive control and the antioxidant Trolox (20 micromol/l) were used to confirm the involvement of oxidative stress. H(2)O(2) treatment increased oxidative stress and apoptosis; TNF-alpha mimicked these effects. Exposure to TNF-alpha significantly increased ROS production, caused cell injury, and increased the number of apoptotic cells and Bax-to-Bcl-xl ratio. This change was associated with an increase in the phospho-p38 MAPK-to-total p38 MAPK ratio and a decrease in the phospho-ERK1/2-to-total ERK1/2 ratio. IL-10 treatment by itself had no effect on these parameters, but it prevented the above-listed changes caused by TNF-alpha. The antioxidant Trolox modulated TNF-alpha-induced changes in Bax/Bcl-xl, cell injury, and MAPKs. Preexposure of cells to the p38 MAPK inhibitor SB-203580 prevented TNF-alpha-induced changes. Inhibition of the ERK pathway with PD-98059 attenuated the protective role of IL-10 against TNF-alpha-induced apoptosis. This study provides evidence in support of the essential role of p38 and ERK1/2 MAPKs in the interactive role of TNF-alpha and IL-10 in cardiac myocyte apoptosis.

Empirical antimicrobial therapy Targeted antimicrobial therapy usage, underlining the need for antibiotic stewardship to promote evidence-based practice.

Ubiquitous presence of cypermethrin as a contaminant in surface stream and soil necessitates to develop potential bioremediation methods to degrade and eliminate this pollutant from the environment. A cypermethrin utilizing bacterial strain (MIC, 450  ppm) was isolated from the soil of pesticide contaminated agriculture field and characterized by using polyphasic approach. On molecular basis bacterial isolate showed 98% homology with Bacillus subtilis strain 1D. Under optimized growth conditions, bacteria showed 95% degradation of cypermethrin after 15 days and the end products of cypermethrin biodegradation under aerobic conditions were cyclododecylamine, phenol, 3-(2,2-dichloroethenyl 2,2-dimethyl cyclopropane carboxylate,1-decanol,chloroacetic acid, acetic acid, cyclopentan palmitoleic acid, and decanoic acid. Amplification of esterase (700 bp) and laccase (1200 bp) genes was confirmed by PCR which showed a possible role of these enzymes in biodegradation of cypermethrin. In the presence of cypermethrin Km value(s) of both the enzymes was low than the control. A nobel cypermethrin degradation pathway followed by B. subtilis was proposed on the basis of characterization of biodegraded products of cypermethrin using GC-MS. Cypermethrin biodegradation ability of Bacillus subtilis strain 1D without producing any toxic end product reveals the potential of this organism in cleaning of pesticide contaminated soil and water.