鞘内注射氨甲喋呤219例总结

鞘内注射氨甲喋呤（MTX）广泛用于白血病患儿的中枢神经系统白血病（CNSL）预防，但同时也可引起少数毒性反应，我科对1974年至1996年间住院的白血病患儿219例进行鞘内注射MTX1096人次所发生的毒性反应做了细致的观察，总结如下：临床资料住院患儿219例，其中男126例，占57．5％，女93例，占42．5％；年龄3个月－14岁；急性淋巴细胞白血病（ALL）111例，占50．7％；急性髓性白血病（AML）99例，占45．2％；淋巴肉瘤白血病9例，占4．1％。全部病例均经临床表现、血象、骨髓象而确诊，CNSL预防均采用单纯药物鞘注MTX每次10－12mg／m…     

新的一年再接再厉

时间荏苒,转眼间2006年已经过去,每当新年来临之际,我们都会想起多年来关心和支持本刊的新老朋友,感谢您多年来对本刊的支持与厚爱!     

输血译苑：红细胞置换和静脉输注Rh免疫球蛋白防止D＋红细胞免疫

输血治疗须避免育龄D-妇女接受D＋红细胞，但在一些偶然情况下，如差错，紧急情况或D-红细胞储存缺乏，D-育龄妇女就可能输入D＋红细胞。是否产生免疫及抗体的水平由患者的免疫状态及输入D＋红细胞的数量决定，数量越多越容易产生免疫。但导致免疫的准确剂量尚不清楚。众所周知，D＋细胞具有免疫原性，如果不采取措施，免疫的风险（输入1单位D＋红细胞达80％）是相当高的，对此目前很少有指导性措施。     

颅内血肿微创清除术后并发上消化道出血的分析与护理

目的探讨高血压脑出血颅内血肿微创清除术后并发上消化道出血的原因,并提出针对性的护理措施。方法对66例高血压脑出血颅内血肿微创清除术后并发上消化道出血的原因进行回顾性分析。结果发现高血压脑出血微创术后并发上消化道出血的诱发因素与高血压脑出血的出血量、出血部位、发病时的意识程度及激素的应用有关。结论积极预防诱发因素,加强临床观察及护理,及早发现上消化道出血,早期采取有效措施,对提高治愈率有着十分重要的作用。     

Perspectives on the Mechanism of Action of Electroconvulsive Therapy: Anticonvulsant, Peptidergic, c-fos Proto-oncogene Effects

Although the mechanism of action of electroconvulsive therapy (ECT) in affective illness has remained elusive, it is hoped that the consideration of mechanisms underlying the anticonvulsant efficacy of ECT will provide new insights into its biochemical and neuroanatomical substrates. In the amygdala-kindling model, electroconvulsive seizures (ECS) inhibit both the development and completed phases of kindled seizure evolution, and therefore, ECS is a more potent anticonvulsant modality than carbamazepine, which inhibits only completed kindled seizures. Carbamazepine is increasingly recognized for its acute and prophylactic efficacy in bipolar affective illness. Thus, comparing and contrasting effects of ECS and carbamazepine may provide insights into overlapping mechanisms of anticonvulsant and psychotropic action. Anticonvulsant effects of ECS have been most closely linked to endogenous opiate substances, perhaps acting on delta-opiate receptors, but a wide variety of other neurotransmitter and peptidergic effects are also potential candidates. Electroconvulsive seizures in mice activate the proto-oncogene c-fos in many discrete areas of brain, including a variety of limbic sites, the ventromedial nucleus of the hypothalamus, and the cerebellum. As such, c-fos induction may provide both an anatomical map of areas potentially activated by ECS and a potential mechanism for initiating a sequence of events that may be important to the mechanism of action of ECT. Although the anticonvulsant effects of ECT may ultimately prove to be separable from those mediating its therapeutic effects in affective illness, seizures and anticonvulsant effects provide easily measurable endpoints for preclinical and clinical studies. Given this clarity of effect, potential anticonvulsant mechanisms can rapidly be identified, enabling direct testing of whether or not these same mechanisms are also critical to the therapeutic effects of ECT in affective illness.