我国医疗保障制度改革中医院配套改革措施探讨

论述了医疗保障制度改革给医院带来的机遇与挑战,认为医院应采取调整结构,转换运行机制;完善补偿机制;加大宏观调控力度,制订和实施区域卫生规划等配套措施,来适应医疗保障制度的改革。     

Baclofen: reduction of presynaptic calcium influx in the cat spinal cord in vivo

 In the ventral horn of the lumbar spinal cord of cats anaesthetised with pentobarbitone sodium, microelectrophoretically administered (–)-baclofen, but not (+)-baclofen, reversibly reduced the duration of the orthodromic action potential of muscle group Ia afferent terminations, but not those of muscle group I afferent myelinated fibres. The presumably submicromolar concentrations are already known to reversibly reduce excitatory transmitter release from muscle group Ia afferent terminations. Action potential durations were estimated from threshold recovery curves after an orthodromic impulse using an extracellular microstimulation technique. Both of these presynaptic effects of (–)-baclofen were blocked by baclofen antagonists, and neither appeared to be reduced by the potassium channel blocking agents tetraethylammonium and 4-aminopyridine. Tetraethylammonium and 4-aminopyridine also did not significantly modify the reduction by (–)-baclofen of monosynaptic field potentials in the lumbar cord of rats anaesthetised with pentobarbitone sodium. In the cat the maximum reduction by (–)-baclofen of termination action potentials was considerably less than that produced by cadmium ions, which, unlike (–)-baclofen, also reduced the action potential duration of group I myelinated fibres. These findings are consistent with a reduction by (–)-baclofen of the influx of calcium through voltage-activated channels in the membrane of group Ia terminations, a proposal which also accounts for the reduction by (–)-baclofen of the release of GABA at axo-axonic depolarizing synapses on these terminations. The results are discussed in relation to the mode of action of (–)-baclofen and the different sensitivities of transmitter release at various central synapses. Received: 30 May 1996 / Accepted: 11 September 1996     

Meta-analysis of gross insertions causing human genetic disease: novel mutational mechanisms and the role of replication slippage

Although gross insertions (>20 bp) comprise <1% of disease-causing mutations, they nevertheless represent an important category of pathological lesion. In an attempt to study these insertions in a systematic way, 158 gross insertions ranging in size between 21 bp and approximately 10 kb were identified using the Human Gene Mutation Database (www.hgmd.org). A careful meta-analytical study revealed extensive diversity in terms of the nature of the inserted DNA sequence and has provided new insights into the underlying mutational mechanisms. Some 70% of gross insertions were found to represent sequence duplications of different types (tandem, partial tandem, or complex). Although most of the tandem duplications were explicable by simple replication slippage, the three complex duplications appear to result from multiple slippage events. Some 11% of gross insertions were attributable to nonpolyglutamine repeat expansions (including octapeptide repeat expansions in the prion protein gene [PRNP] and polyalanine tract expansions) and evidence is presented to support the contention that these mutations are also caused by replication slippage rather than by unequal crossing over. Some 17% of gross insertions, all >or=276 bp in length, were found to be due to LINE-1 (L1) retrotransposition involving different types of element (L1 trans-driven Alu, L1 direct, and L1 trans-driven SVA). A second example of pathological mitochondrial-nuclear sequence transfer was identified in the USH1C gene but appears to arise via a novel mechanism, trans-replication slippage. Finally, evidence for another novel mechanism of human genetic disease, involving the possible capture of DNA oligonucleotides, is presented in the context of a 26-bp insertion into the ERCC6 gene.     

S-99和S-100止血作用研究

PT、APTT、TT、血小板粘附率和血栓形成试验表明S-99可溶性止血纺织材料和S·100吸收性止血綾的止血效果无显著差异。但是S-99和S-100止血纺织材料的止血机理不尽相同,S-100止血绫主要是通过溶解后的负电性液相激活内源性止血系统;而S-99止血纺织材料主要是通过溶胀胶粒粘附血小板,进而激活血小板。     

迷走神经刺激对家兔高血钾时心室肌单相动作电位及心室肌细胞跨膜电位的影响

本文观察了电刺激迷走神经对家兔商血钾时心室肌单相动作电位(MAP)及单个心室肌细胞跨膜电位(TMP)的影响。结果表明,迷走神经刺激可以改善高血钾引起的心室内传导阻滞,使单相动作电位振幅(MAPA)、单相动作电位0相最大上升速率(MVmax)增加,单相动作电位时程(MAPD)延长,亦使单个心室肌细胞静息电位(RP)、动作电位振幅(APA)和0相最大上升速率(Vmax)增加,动作电位时程(APD)延长。另外,两种记录方法在同一部位的MAPD与APD完全一致。     

尼古丁依赖的功能影像学研究进展

在过去10年中,随着功能脑影像学技术在物质滥用领域的发展,越来越多的研究者运用这些技术以探讨尼古丁成瘾的神经生物学机制。本文主要总结了尼古丁急、慢性暴露下对脑功能影响的神经脑影像学研究进展,证实了尼古丁依赖与中脑边缘犒赏系统、调节注意、记忆、运动以及联想相关脑环路之间的相关性。这些研究发现将为揭示尼古丁依赖的神经生物学机制提供更多的证据支持,进一步促进今后戒烟治疗的发展。     

物质成瘾Stroop效应研究进展

物质成瘾Stroop任务是考察物质成瘾者对成瘾相关刺激产生注意偏向的一种研究范式。研究者们采用多种实验任务和研究方法,对物质成瘾Stroop干扰产生的心理机制进行了考察,并提出了几种理论解释,但目前这些理论解释之间还存在一定的分歧。最后,本文提出了未来研究的一些建议。     

A low-voltage activated,transient calcium current is responsible for the time-dependent depolarizing inward rectification of rat neocortical neurons in vitro

Intracellular recordings were obtained from rat neocortical neurons in vitro. The current-voltage-relationship of the neuronal membrane was investigated using current- and single-electrode-voltage-clamp techniques. Within the potential range up to 25 mV positive to the resting membrane potential (RMP: –75 to –80 mV) the steady state slope resistance increased with depolarization (i.e. steady state inward rectification in depolarizing direction). Replacement of extracellular NaCl with an equimolar amount of choline chloride resulted in the conversion of the steady state inward rectification to an outward rectification, suggesting the presence of a voltage-dependent, persistent sodium current which generated the steady state inward rectification of these neurons. Intracellularly injected outward current pulses with just subthreshold intensities elicited a transient depolarizing potential which invariably triggered the first action potential upon an increase in current strength. Single-electrode-voltage-clamp measurements reveled that this depolarizing potential was produced by a transient calcium current activated at membrane potentials 15–20 mV positive to the RMP and that this current was responsible for the time-dependent increase in the magnitude of the inward rectification in depolarizing direction in rat neocortical neurons. It may be that, together with the persistent sodium current, this calcium current regulates the excitability of these neurons via the adjustment of the action potential threshold.     

原发性肝癌患者抑郁症状与不成熟防御机制的关系

目的：了解原发性肝癌（PLC）患者的抑郁症状和不成熟防御机制（IDM）的水平，探讨PLC患者的抑郁症状与IDM的关系。方法：采用流调用抑郁自评量表（CES－D）和防御式方式问卷（DSQ）对PLC患者和健康组各100例进行调查。结果：1）PLC患者中49％可能或肯定有抑郁症状，其中23％肯定有抑郁症状，其发生率高于健康组；2）PLC组的CES－D总分高于健康组；3）PLC组比健康组采用较多分裂和潜意显现机制，采用较少抱怨机制；4）肯定有抑郁症状者比无抑郁症状者采用较多IDM；5）两组CES－D总分与IDM均分呈显著正相关，Pearson r为0.473-0.776，其中PLC组为0．473。结论：抑郁症状是PLC患者常见的负性情绪，医护人员应引起重视，并指导患者采用成熟的防御机制代替不成熟防御机制，预防并减轻患者的抑郁症状，以提高患者的生活质量。     

电磁脉冲辐射对猕猴凝血机制影响研究

目的:探讨电磁脉冲对猕猴凝血机制影响。方法:经高场强电磁脉冲源以6×104V/m全身辐照5只猕猴,于照前及照后1、3、7、14、28及90d下肢前静脉采血,采用AYW-8001型血凝仪检测电磁脉冲对动物血浆中TT、PT、APTT及FIB的影响。结果:动物血浆中TT于伤后1d及14～28d延长,APTT于伤后1d延长,FIB含量于伤后14d减少,PT在照射前后无明显变化。结论:电磁脉冲照射可对实验猕猴凝血机制产生影响,可通过TT、APTT延长和FIB含量减少而使机体凝血机制发生障碍。