The progress in industrialization has blessed mankind with a technologically superior lifestyle but poor management of industrial waste has in turn poisoned nature. One such chemical is carbon tetra chloride (CCl4), which is a potent environmental toxin emitted from chemical industries and its presence in the atmosphere is increasing at an alarming rate. Presence of CCl4 in human body is reported to cause liver damage through free radical mediated inflammatory processes. Kupffer cells present in the liver are potentially more sensitive to oxidative stress than hepatocytes. Kuffer cells produced tumor necrosis factor-α (TNF-α) in response to reactive oxygen species (ROS), that might further cause inflammation or apoptosis. In this study hepatoprotective capacity of antioxidant rich extract of Croton bonplandianus Baill. (CBL) was evaluated on CCl4 induced acute hepatotoxicity in murine model. Hydro-methanolic extract of C. bonplandianus leaf was used for evaluation of free radical scavenging activity. Liver cells of experimental mice were damaged using CCl4 and subsequently hepatoprotective potential of the plant extract was evaluated using series of in-vivo and in-vitro studies. In the hepatoprotective study, silymarin was used as a positive control. Antioxidant enzymes, pro-inflammatory markers, liver enzymatic and biochemical parameters were studied to evaluate hepatoprotective activity of Croton bonplandianus leaf extract. Free radical scavenging activity of CBL extract was also observed in WRL-68 cell line. The phytochemicals identified by GCMS analysis were scrutinized using in-silico molecular docking procedure. The results showed that CBL extract have potent free radical scavenging capacity. The biochemical parameters were over expressed due to CCl4 administration, which were significantly normalized by CBL extract treatment. This finding was also supported by histopathological evidences showing less hepatocellularnecrosis, inflammation and fibrosis in CBL and silymarin treated group, compared to CCl4 group. ROS generated due to H2O2 in WRL-68 cell line were normalize in the highest group (200 μg/ml) when compared with control and negative control (CCl4) group. After molecular docking analysis, it was observed that the compound α-amyrin present in the leaf extract of C. bonplandianus has better potentiality to protect hepatocellular damages than the standard drug Silymarin. The present study provided supportive evidence that CBL extract possesses potent hepatoprotective capacity by ameliorating haloalkane induced liver injury in the murine model. The antioxidant and anti-inflammatory activities also affirm the same. The synergistic effects of the phytochemicals present in CBL are to be credited for all the hepatoprotective activity claimed above.

Background Different methods available for extraction of human genomic DNA suffer from one or more drawbacks including low yield, compromised quality, cost, time consumption, use of toxic organic solvents, and many more. Herein, we aimed to develop a method to extract DNA from 500 μL of fresh or frozen human blood. Methods Five hundred microliters of fresh and frozen human blood samples were used for standardization of the extraction procedure. Absorbance at 260 and 280 nm, respectively, (A260/A280) were estimated to check the quality and quantity of the extracted DNA sample. Qualitative assessment of the extracted DNA was checked by Polymerase Chain reaction and double digestion of the DNA sample. Results Our protocol resulted in average yield of 22±2.97 μg and 20.5±3.97 μg from 500 μL of fresh and frozen blood, respectively, which were comparable to many reference protocols and kits. Conclusion Besides yielding bulk amount of DNA, our protocol is rapid, economical, and avoids toxic organic solvents such as Phenol. Due to unaffected quality, the DNA is suitable for downstream applications. The protocol may also be useful for pursuing basic molecular researches in laboratories having limited funds.

SYNOPSIS A survey is in progress of patients attending the Charing Cross Hospital Migraine Clinic in London. Information collected is stored for retrieval and analysis by computer. This paper reports some initial findings from patients seen during the first 212 years since the clinic opened. Patients registering with such a specialized clinic are not representative of the migraine population at large. Migraine sufferers present to the clinic at all ages from 6 to 70, but in three peaks, at 21–30, 41–45 and 51–55 years. Although onset of migraine tends to be earlier in males than in females, the latter are more likely to present during the first of these peaks. Migraine in younger clinic patients is predominantly classical in type. This predominance declines with increasing age at onset and may reverse when onset is delayed beyond 40. An inverse correlation exists in both sexes between age at onset of classical or common migraine and strength of family history. Females have a strong family history more commonly than males, except in those with onset in childhood. The mother is the more frequently affected parent, but involvement of the father may be associated more closely with early onset. Therefore, although migraine appears predominantly to be a disease of females with a female parental history, in clinic patients with early onset there is a relative preponderance of males and of male parental history.

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Mycobacterium tuberculosis exerts its pathogenic effects mainly via its cell wall glycolipid called Mannosylated Lipoarabinomannan (Man‐LAM), which subverts the cellular inflammatory responses by the suppression of superoxide anion generation in earlier hours, and nitric oxide (NO) generation at later hours of pathogenic invasion. In this paper, we have shown the prophylactic effect of C‐C chemokines, both in vitro and in vivo. Exogenous administration of C‐C chemokines, particularly monocyte chemoattractant protein (MCP)‐1, led to the induction of superoxide anion generation via the restoration of impaired protein kinase C (PKC) signalling in Man‐LAM‐treated macrophages. Monocyte chemoattractant protein‐1 could also potently induce NO generation by upregulation of the proinflammatory cytokines tumour necrosis factor‐α and interleukin‐12 from Man‐LAM‐treated macrophages accompanied by inhibition of anti‐inflammatory responses. Our in vivo observations clearly exhibited effective restoration of impaired PKC signalling as well as proinflammatory cytokine expression by MCP‐1 in Man‐LAM treated as well as M. tuberculosis H37Rv‐infected C57BL/6 mice. We also observed, as direct evidence, that MCP‐1 induced a significant reduction of the number of viable tubercle bacilli in the lungs and spleen of infected mice. Collectively, our findings strongly suggest the effectiveness of MCP‐1 as a potent immunoprophylactic tool for controlling the mycobacterial establishment within the host.