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81.

Background

Fulminant hepatic failure (FHF) is clinical syndrome with very poor prognosis and high mortality there is urgent need for the development of safe and non-toxic hepatoprotective agents for the adequate management of hepatitis. Hepatoprotective effect of the Lepidium sativum ethanolic extract (LSEE) was assessed by D-galactosamine-induced/lipopolysaccharide (400 mg/kg and 30 μg/kg) liver damage model in rats.

Methods

Hepatoprotective activity of LSEE (150 and 300 mg/kg) and silymarin on D-GalN/LPS induced FHF in rat was assessed using several liver function enzyme parameters. Antioxidant properties as antioxidant stress enzymes were assessed in hepatic Liver as well as mRNA expression of cytokines genes such as TNF-α, IL-6, and IL-10 and stress related genes iNOS and HO-1 were determined by RT-PCR. Protein expression of apoptotic genes were evaluated through western blot. MPO and NF-κB DNA-binding activity was analyzed by ELISA. The magnitude of hepatic impairment was investigated through histopathological evaluation.

Results

Marked amelioration of hepatic injuries by attenuation of serum and lipid peroxidation has been observed as comparable with silymarin (25 mg/kg p.o). D-GalN/LPS induced significant decrease in oxidative stress markers protein level, and albumin. LSEE significantly down-regulated the D-GalN/LPS induced pro-inflammatory cytokines TNFα and IL-6 mRNA expression in dose dependent fashion about 0.47 and 0.26 fold and up-regulates the IL-10 by 1.9 and 2.8 fold, respectively. While encourages hepatoprotective activity by down-regulating mRNA expression of iNOS and HO-1. MPO activity and NF-κB DNA-binding effect significantly increased and was mitigated by LSEE in a dose-dependent style as paralleled with silymarin.

Conclusion

Our data suggests that pretreatment of LSEE down regulates the caspase 3 and up-regulates the BCl2 protein expression. The above findings revealed that Lepidium sativum has significant hepatoprotective activity.
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Social Psychiatry and Psychiatric Epidemiology - Refugees may be at risk of experiencing a complicated form of bereavement. As yet, however, the nosological status of this putative category across...  相似文献   
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Stem cells mediate tissue repair throughout the lifespan of an organism. However, the ability of stem cells to mitigate catastrophic damage, such as that sustained after major myocardial infarction is inadequate to rebuild the heart and restore functional capacity. However, capitalizing on the ability of these cells to attenuate damage in the myocardium, various maneuvers that enhance repair mechanisms to improve cardiac structure and function after injury are being investigated. These studies have led to discovery of various factors that mediate cardioprotection and enhance endogenous repair by 1) salvaging surviving myocardium, 2) promoting homing of stem cells and 3) increasing survival and proliferation of stem cell populations at the site of injury. Herein we report upon a downstream target of Akt kinase, named Pim-1, which promotes cardioprotective signaling and enhances cardiac structure and function after pathological injury. The compilation of studies presented here supports use of Pim-1 to enhance long-term myocardial repair after pathological damage. This article is part of a special issue entitled “Key Signaling Molecules in Hypertrophy and Heart Failure.”  相似文献   
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Background  

Recently there is a growing concern about stress during undergraduate medical training. However, studies about the same are lacking from Pakistani medical schools. The objectives of our study were to assess perceived stress, sources of stress and their severity and to assess the determinants of stressed cases.  相似文献   
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Bone is an anisotropic structure which can be compared to a composite material. Discontinuities within its microstructure may provide stress concentration sites for crack initiation, but act as a barrier to its propagation. This study looks specifically at the relationship between crack length and propagation in compact bone. Beam-shaped bone samples from sheep radii were prepared and stained with fluorochrome dyes and tested in cyclic fatigue under four-point bending in an INSTRON 1341 servo-hydraulic fatigue-testing machine. Samples were tested at a frequency of 30 Hz and stress range of 100 MPa under load control. Specimens were sectioned transversely using a diamond saw, slides prepared and examined using epifluorescence microscopy. Cracks in transverse sections were classified in terms of their location relative to cement lines surrounding secondary osteons. Mean crack length, crack numerical density and crack surface density were examined. Short microcracks (100 microm or less) were stopped at the cement lines surrounding osteons, microcracks of intermediate length (100-300 microm) were deflected as they hit the cement line, and microcracks that were able to penetrate through cement lines were longer (> 400 microm). These data show that bone microstructure allows the initiation of microcracks but acts as a barrier to crack propagation.  相似文献   
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Objective: Focussing on maternal/newborn health and vascular diseases, to review NSW Health's reporting, by Aboriginal status, against national performance indicators relevant to preventable chronic diseases. Methods: We reviewed seven indicator documents and the Australian Institute of Health and Welfare Chronic Disease Indicator Database to identify national indicators. Indicators from six NSW Health reports were then compared with these national indicators to assess reporting by Aboriginal status and region. Results: NSW Health routinely reports against six maternal/newborn indicators and fourteen vascular national indicators. Five of the former report performance by both Aboriginal status and region. Eight of the latter report by Aboriginal status, one of which (diabetes hospitalisations) also reports by region. Indicator quality and breadth was substantially limited by under‐enumeration of Aboriginal status, small or potentially unrepresentative samples, inadequate longitudinal or regional data and few primary health care indicators. Notwithstanding these limitations, we found wide and persistent disparities in outcomes for Aboriginal people for all indicators in all regions. Conclusions: NSW Health reports adequately, by Aboriginal status, for maternal/newborn health monitoring (albeit constrained by under‐enumeration), but provides limited information about vascular health. A minimum, national chronic disease indicator dataset against which all jurisdictions would report performance by Aboriginal status and region is needed. Improved monitoring requires sustained efforts to address under‐enumeration, better survey sampling, and population representative data from the primary care system.  相似文献   
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