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Objective: To investigate the effects of inhalation of hydrogen gas on cognitive impairment induced by transient cerebral ischemia and its potential mechanism. Methods: Two-vessel occlusion rat model was used to produce 10-minute transient global cerebral ischemia. One hundred and twenty male Wistar rats were randomly divided into sham, sham+H2, ischemia, and ischemia+H2 groups (n=30 each group). Inhalation of 2% hydrogen gas was performed immediately at the end of operation and lasted for 3 hours. Cognitive function of rats was evaluated via Morris water maze. Neuronal damage in the CA1 region was quantified according to their morphological changes revealed by hematoxylin-eosin staining. The levels of oxidative stress products malondialdehyde (MDA) and 8-iso-prostaglandin F2alpha, and the activities of anti-oxidative enzymes catalase and superoxide dismutase were measured to investigate the effects of inhalation of hydrogen gas on oxidative stress. Results: Inhalation of hydrogen gas decreased significantly the average latency of the ischemic rats in finding hidden platform and elongated markedly their retention in the target quadrant. The neuronal density 3.3±2.1 cells/mm in CA1 region of the ischemic rats increased to 21.7±2.6 cells/mm after they were treated with hydrogen gas. Moreover, hydrogen gas made higher levels of MDA and 8-iso-PGF2α in the ischemic rats attenuate to 3.2±0.2, 3.5±0.5, 3.4±0.3 and 26.4±2.3, 28.2±2.6, 26.8±2.1 at reperfusion 4, 24, and 72 hours, respectively (P,0.01 versus ischemia group at each indicated time). By contrast, the activities of superoxide dismutase and catalase damaged by ischemia/reperfusion recovered to 129.7±14.8, 100.5±12.2 and 11.4±0.8, 9.6±1.1 at reperfusion 24 and 72 hours, respectively (P<0.01 versus ischemia group at each indicated time). Conclusion: Inhalation of hydrogen gas could attenuate cognitive impairment in the ischemic rats. This protection is associated with decreased neuronal death in CA1 region and inhibition of oxidative stress. [ABSTRACT FROM AUTHOR]

Glioma still remains a major health problem in the world. Celastrol has been proved to be an effective natural proteasome inhibitor and was used for treatment of autoimmune disease, chronic inflammation and neurodegenerative disease. However, its effect on glioma is unclear. In this study, we investigated the therapeutic effects of celastrol on C6 glioma cells. The results demonstrated that celastrol inhibited cell proliferation in a time- and dose-dependent manner, suppressed proteasome chymotrypsin-like activity and induced apoptosis and cell cycle arrest at G2/M phase in C6 cells. Proapoptosis proteins bax and caspase-3 were up-regulated, as well as cell cycle G2/M-related proteins cyclin B1, p21 and p27. Conversely, anti-apoptosis proteins bcl-2 and XIAP and cell cycle regulator cyclin-dependent kinase 2 were down-regulated. Taken together, our data suggest that celastrol can suppress proteasome activity and induce apoptosis and cell cycle arrest in C6 glioma cells, which make it be a potential drug for glioma. [ABSTRACT FROM AUTHOR]

Abstract: Colonic perforation is an extremely rare complication following ventriculoperitoneal (VP) shunting. The common treatment is to remove the perforating catheter and replace it with a new one. Here we report a case of colonic perforation from VP shunting in a 2-year, 8-month-old boy who presented with the distal end of the shunt catheter protruding out of his anus. The distal catheter was removed via the anus and the perforation repaired transanally. The patient's postoperative course was uneventful. This case reminds us that we should not make another rush to perform a new shunt operation unless there are some manifestations of hydrocephalus. Potential mechanisms of migration and its management strategy are discussed. [Copyright &y& Elsevier]

Summary: Gliomas are malignant primary brain tumors with high morbidity. This tumor has a feature of resistance to chemotherapy and radiotherapy and the underlying mechanism is not yet clear. Autophagy is an evolutionarily conserved process of cytoplasm and cellular organelle in lysosome degradation. Under poor conditions, cells use autophagy to recycle cellular components to sustain metabolism and to prevent the accumulation of damaged, toxic proteins and organelles. More and more recent experimental results suggest that autophagy allows tumor cells survive gene therapy, chemotherapy or nutrient deficient environment. Therefore, we propose the hypothesis that autophagy may be one of the factors influencing on malignant glioma’s resistance to therapy. Although there is not yet reaching an agreement about the effects of autophagy on tumor cells survival and death and much more studies are needed to prove the effects of autophagy on malignant gliomas, it gives us a new direction to investigate the mechanism underlying therapy resistance of malignant gliomas. [Copyright &y& Elsevier]

Abstract: We describe a rare scalp malignant peripheral nerve sheath tumor (MPNST) with cranial destruction and intracranial extension in a 52-year-old male with neurofibromatosis type 1 (NF1). The scalp tumor measured 22cm×18cm, with local surface ulceration. Skin examination revealed many café-au-lait spots and small, hard dermal nodules on the trunk. CT scans revealed the scalp tumor to have heterogeneous density with partial destruction of the right parietal cranium; on T1-weighted MRI the scalp tumor displayed heterogeneous hypointensity, whereas on T2-weighted and fluid-attenuated inversion recovery MRI it was hyperintense. The tumor was excised totally and the scalp reconstructed using a skin flap isolated from the lateral aspect of the left thigh. Histological examination confirmed that the tumor was an MPNST. The patient recovered uneventfully and was well at the 6-month follow-up, with no local or other tumor recurrence noted. [ABSTRACT FROM AUTHOR]

Summary: Brain ischemia has been an important risk factor for human being health, there is no effective medicine can be used to protect delayed neuronal injury or death secondary to blood reperfusion following ischemia. Recent discovery shows protein aggregation is an important factor resulting in ischemia-induced neuron death. Therefore, we propose the hypothesis that inhibiting protein aggregation may be an effective way to prevent delayed neuronal death after transient ischemia. At present, in vitro studies show some chemicals such as 4PBA (sodium 4-phenylbutyrate) and trehalose have the features of antagonizing protein aggregation in vitro. Moreover, polyQ-binding peptide (QBP1), geldanamycin, amino acids and amino acid derivatives have been also used in vitro to decrease aggregation and to increase protein stability. Although in vivo and systematical study should be performed to evaluate their effects of anti-protein aggregation, this enlightening us on using them to protect ischemic-induced neuronal death, and find new potential chemicals or methods which could be effective in keeping protein stable and prevent forming aggregates. [Copyright &y& Elsevier]