普鲁卡因对缺血性视网膜脉络膜cAMP变化的实验研究

目的 :观察普鲁卡因对缺血性视网膜脉络膜 c AMP变化的研究。方法 :新西兰白兔 10只 2 0只眼 ,孟加拉玫红耳静脉注射后 ,立即用间接检眼镜为光源 ,先后照射双眼鼻侧视网膜脉络膜血管 ,持续 6分钟 ,制成光化学反应的光栓视网膜脉络膜血管阻塞缺血模型。随机分正常组、生理盐水组 ( normal saline,NS)、普鲁卡因组 ( procaine,PR)、樟柳碱组 ( anisodine,AS)和复方樟柳碱组 ( com-pound anisodine,CA) ,各组均治疗 2周 ,每组 4只眼测定 c AMP含量。结果 :缺血后各组 c AMP含量均比正常组降低 ,其中 CA组降低最显 ,次为 PR与 AS组 ,三组与 NS组比均降低显著 P<0 .0 1,PR与 AS组比无显著差异。结论 :由于 CA降低 c AMP比 AS显著P<0 .0 5 ,从而减少肾上脉素合成 ,减轻血管痉挛 ,故 CA的优越性与 PR也降低 c AMP密切相关。     

The enigma of arsenic carcinogenesis: role of metabolism

Inorganic arsenic is considered a high-priority hazard, particularly because of its potential to be a human carcinogen. In exposed human populations, arsenic is associated with tumors of the lung, skin, bladder, and liver. While it is known to be a human carcinogen, carcinogenesis in laboratory animals by this metalloid has never been convincingly demonstrated. Therefore, no animal models exist for studying molecular mechanisms of arsenic carcinogenesis. The apparent human sensitivity, combined with our incomplete understanding about mechanisms of carcinogenic action, create important public health concerns and challenges in risk assessment, which could be met by understanding the role of metabolism in arsenic toxicity and carcinogenesis. This symposium summary covers three critical major areas involving arsenic metabolism: its biodiversity, the role of arsenic metabolism in molecular mechanisms of carcinogenesis, and the impact of arsenic metabolism on human risk assessment. In mammals, arsenic is metabolized to mono- and dimethylated species by methyltransferase enzymes in reactions that require S-adenosyl- methionine (SAM) as the methyl donating cofactor. A remarkable species diversity in arsenic methyltransferase activity may account for the wide variability in sensitivity of humans and animals to arsenic toxicity. Arsenic interferes with DNA methyltransferases, resulting in inactivation of tumor suppressor genes through DNA hypermethylation. Other studies suggest that arsenic-induced malignant transformation is linked to DNA hypomethylation subsequent to depletion of SAM, which results in aberrant gene activation, including oncogenes. Urinary profiles of arsenic metabolites may be a valuable tool for assessing human susceptibility to arsenic carcinogenesis. While controversial, the idea that unique arsenic metabolic properties may explain the apparent non-linear threshold response for arsenic carcinogenesis in humans. In order to address these outstanding issues, further efforts are required to identify an appropriate animal model to elucidate carcinogenic mechanisms of action, and to define dose-response relationships.      

Clinical profile of special children at asha centre

Background: The care of special children suffering from cerebral palsy, deaf mutism, mental retardation (MR) and post encephalitic sequelae etc. is done in the armed forces at “ASHA” centre supported by Army Wives Welfare Association (AWWA).     

Does in situ replacement of a staphylococcal infected vascular graft with a rifampicin impregnated gelatin sealed Dacron graft reduce the incidence of subsequent infection?

BACKGROUND: The aim of this study was to treat methicillin-resistant Staphylococcus aureus (MRSA) or S. epidermidis prosthetic vascular graft infections by in situ replacement with a rifampicin bonded Gelsoft graft. METHODS: Interposition grafts were placed in the internal carotid artery of 56 merino sheep and the graft surface directly inoculated with 10(8) colony forming units (CFU) of MRSA (29) or S. epidermidis (27). At three weeks, grafts were harvested and sheep allocated to three groups. In the MRSA infected group, sheep received grafts soaked in 1.2 mg/ml (12), 10 mg/ml (10) and no (7) rifampicin. For S. epidermidis, sheep received grafts soaked in 1.2 mg/ml (10), 10 mg/ml (9) and no (8) rifampicin. There were two deaths, in the MRSA study group, one each from the rifampicin treated groups. The remaining sheep were euthanased and grafts harvested three weeks following regrafting. Grafts at harvests were assessed for perigraft abscess formation, anastomotic disruption and graft thrombosis. Swabs were taken to assess bacterial growth in the perigraft tissues, and external and internal graft surfaces. A 3-5 mm segment of graft was incubated in a broth medium. For S. epidermidis the remainder of the graft was ground and then incubated in a broth medium. RESULTS: For MRSA, no statistical difference between the groups was reached for any of the measured parameters. For S. epidermidis, a significant reduction was reached for total infected specimens in the 10 mg/ml group compared to both control (p<0.001) and 1.2 mg/ml (p<0.005) groups. Graft reinfection was also less likely to occur with S. epidermidis than MRSA. CONCLUSIONS: In conclusion, replacement of S. epidermidis infected vascular grafts with 10 mg/ml rifampicin soaked Gelsoft graft is effective in reducing subsequent S. epidermidis infection. This conclusion cannot be extended to MRSA infected vascular grafts.