周亚滨教授运用六经辨证治疗心病证治经验

周亚滨教授从“伤寒最多心病”立意,通过总结《伤寒论》一书对于心病的脉证及遣方用药,指出六经辨证体系对于心病证治具有指导意义。六经辨证是涵盖了八纲以及脏腑经络辨证的学说,能够指导着脏腑经络生理、病理变化的辨证论治。文章整理周亚滨教授在基于六经病证分论的基础上,临证上运用六经辨证思维论治心病的辨证经验,用药上可概括以和、温、补、清、下法为多。     

杜元灏教授针刺治疗失眠经验

失眠是由各种原因导致的入睡困难和(或)睡眠维持困难的睡眠障碍,主要特征是睡眠感不满意,属于中医学"不得眠""不寐"范畴。传统多从心、肝、胆、脾、胃、肾论治该病,杜元灏教授认为脏腑机能失调,气血不和,阳不能入阴,阴不能涵阳,神不守舍而致失眠。重视"脑为元神之腑"的理论,且因督脉入络脑,夹脊穴为五脏六腑之气转输、流注之处,杜教授多强调从脑、督脉以及夹脊穴论治失眠,为针刺治疗失眠提供新思路。     

李松林副主任医师治疗肾小球肾炎的经验

李松林副主任医师将肾小球肾炎的病机概括为湿、热、毒、瘀、虚等方面，在中医辨证的基础上，结合现代医学对其病因和发病机理的认识及中草药药理作用，针对不同的病理机制和临床表现，提出清热解毒法，活血化瘀法，调补脾肾法，扶正固本法，并视症有机结合，恰当治疗，疗效显著。     

血清补体系统在流行性出血热患者中的变化及其意义

应用单向免疫扩散法测定了流行性出血热(EHF)患者的7种补体成份和血浆素原(Pg).结果表明,CT脂酶抑制剂在少尿期、多尿期和恢复期均高于正常(P<0.01);补体C_1q在多尿期高于正常(P<0.01);补体C_4在发热期和少尿期低于正常(P<0.01),以后逐渐恢复正常;补体C_3,C_5和C_9的变化与C_4相似;B因子在少尿期低于正常(P<0.01),在多尿期高于正常(P<0.05);Pg始终高于正常水平但在少尿期有回降.说明EHF患者不仅有补体经典途径的识别阶段、活化阶段和膜攻击阶段的变化,而且亦有旁路激活,其活化程度与病情有关.     

Linear relationship between the maintenance of hippocampal long-term potentiation and retention of an associative memory.

The hypothesis that the maintenance or decay of an associative memory trace after an extended retention interval is a function of the residual strength of the synapses originally strengthened during learning was examined in a classical conditioning paradigm in which high-frequency stimulation of a hippocampal input--the medial perforant path--served as a conditioned stimulus. Rats received perforant path stimulus-foot shock pairings while engaged in a previously acquired food-motivated lever-pressing task. Conditioned suppression of lever pressing was the behavioral measure of learning and retention of the association. Stimulus trains to the perforant path at an intensity above the threshold for eliciting a population spike induced long-term potentiation of synaptic transmission in the dentate gyrus. Synaptic potentials recorded extracellularly in the dentate gyrus were subsequently monitored for 31 days to examine quantitatively the decay of synaptic potentiation, a period after which retention of the learned association was assessed. All rats learned the association to a similar extent and displayed equivalent amounts of long-term potentiation by the end of conditioning. A slowly decaying function of synaptic potentiation was observed in remembering rats, i.e., rats with high retention performance after the 31-day learning-to-retention interval, while forgetting was associated with a rapid decay of long-term potentiation. Behavioral performance at the long-term memory test was linearly correlated with the amplitude of long-term potentiation maintained just prior to the retention test. The results favor the hypothesis that long-term associative memory depends, at least in part, on the maintenance of elevated synaptic strengths in the pathway activated during learning and suggest a role for the lasting component of long-term potentiation in the maintenance of memory.     

不同婴儿食品铝含量的测定

本文应用原子吸收光谱法测定母乳、牛奶、奶粉及不同喂养方式婴儿血清中锌、铜、铁及铝含量。母乳中锌、铜、铁含量均较牛奶丰富，铝含量低于牛奶；奶粉中锌、铜、铁含量高于牛奶，与母乳无显著差异，铝含量高于牛奶。母乳、牛奶及奶粉喂养的贫血患儿血清铝含量无显著差异，均明显低于铝中毒的血清铝水平。     

运用中国古典音乐应对胃癌病人的术前焦虑

[目的 ]探讨中国古典音乐治疗胃癌病人术前焦虑的作用。 [方法 ]随机将 60例早期胃癌病人分成实验组和对照组。两组均给予解释、指导、鼓励、安慰等支持性治疗 ,实验组再给予音乐治疗。应用Zung氏焦虑自评量表 (SAS)对两组病人进行评估。 [结果 ]两组病人在支持性治疗前焦虑评分比较无统计学意义 ,而实验组病人在给予音乐治疗后焦虑分值比对照组有统计学意义(P <0 .0 5 )。 [结论 ]中国古典音乐影响人的情绪行为 ,从而引起愉快、舒适的情绪 ,有改善和调整人的大脑皮层的功能     

方剑乔教授针药结合治疗类风湿性关节炎的临床思辨特色与治疗经验

[目的] 介绍方剑乔教授针药结合治疗类风湿性关节炎的临床思辨特色及其临证经验。[方法] 通过整理、回顾、分析方教授治疗类风湿性关节炎的相关文献及医案,从中医病因病机和治则治法等方面,总结归纳方教授治疗类风湿性关节炎的学术经验,并列举医案一则予以佐证。[结果] 临床思辨上,方教授认为“痰、瘀、虚交错”为该病的基本病机,治疗宜针药结合,主要起到同效相须、异效互补和反效制约的作用。临证治疗上,方教授强调,针刺宜整体治疗与局部穴位兼顾,须重视经络辨证。合理应用电针,疼痛急性发作期电针频率多选择“先高后低”,先100 Hz/10～15 min,后2 Hz/30 min;慢性疼痛期电针治疗多选择疏密波(2/100 Hz)。用药强调精准辨证,在该病四种基本证型的基础上提出了阴虚湿热兼证的概念,确立了滋阴清热、通络止痛的治疗大法。倡导适时采用经皮穴位电刺激治疗,其操作简单,携带方便,在镇痛方面具有明显的优势。所举病案采用西药甲氨蝶呤片抑制免疫,稳定病情;中药以祛风除湿为主,佐以藤类药通络行窜、祛风止痛;电针治疗选择频率为2/100 Hz的疏密波调和气血、通络止痛。经治疗后,患者症状缓解,相关指标趋于正常。[结论] 方剑乔教授根据本病的病因病机及临床特点进行辨证论治,针药并重,中西医取长补短,临床特色鲜明,治疗效果显著,值得临床借鉴和推广。     

Identification of 16 novel mutations in the argininosuccinate synthetase gene and genotype-phenotype correlation in 38 classical citrullinemia patients

Classical citrullinemia (CTLN1), a rare autosomal recessive disorder, is caused by mutations of the argininosuccinate synthetase (ASS) gene, localized on chromosome 9q34.1. ASS functions as a rate-limiting enzyme in the urea cycle. Previously, we identified 32 mutations in the ASS gene of CTLN1 patients mainly in Japan and the United States, and to date 34 different mutations have been described in 50 families worldwide. In the present study, we report ASS mutations detected in 35 additional CTLN1 families from 11 countries. By analyzing the entire coding sequence and the intron-exon boundaries of the ASS gene using RT-PCR and/or genomic DNA-PCR, we have identified 16 novel mutations (two different 1-bp deletions, a 67-bp insertion, and 13 missense) and have detected 12 known mutations. Altogether, 50 different mutations (seven deletion, three splice site, one duplication, two nonsense, and 37 missense) in 85 CTLN1 families were identified. On the basis of primary sequence comparisons with the crystal structure of E. coli ASS protein, it may be concluded that any of the 37 missense mutations found at 30 different positions led to structural and functional impairments of the human ASS protein. It has been found that three mutations are particularly frequent: IVS6-2A>G in 23 families (Japan: 20 and Korea: three), G390R in 18 families (Turkey: six, U.S.: five, Spain: three, Israel: one, Austria: one, Canada: one, and Bolivia: one), and R304W in 10 families (Japan: nine and Turkey: one). Most mutations of the ASS gene are "private" and are distributed throughout the gene, except for exons 5 and 12-14. It seems that the clinical course of the patients with truncated mutations or the G390R mutation is early-onset/severe. The phenotype of the patients with certain missense mutations (G362V or W179R) is more late-onset/mild. Eight patients with R86H, A118T, R265H, or K310R mutations were adult/late-onset and four of them showed severe symptoms during pregnancy or postpartum. However, it is still difficult to prove the genotype-phenotype correlation, because many patients were compound heterozygotes (with two different mutations), lived in different environments at the time of diagnosis, and/or had several treatment regimes or various knowledge of the disease.