The CLDN5 locus may be involved in the vulnerability to schizophrenia.

The present study was designed to detect three single nucleotide polymorphisms (SNPs) located on 22q11 that was thought as being of particularly importance for genetic research into schizophrenia. We recruited a total of 176 Chinese family trios of Han descent, consisting of mothers, fathers and affected offspring with schizophrenia for the genetic analysis. The transmission disequilibrium test (TDT) showed that of three SNPs, rs10314 in the 3'-untranslated region of the CLDN5 locus was associated with schizophrenia (chi(2) = 4.75, P = 0.029). The other two SNPs, rs1548359 present in the CDC45L locus centromeric of rs10314 and rs739371 in the 5'-flanking region of the CLDN5 locus, did not show such an association. The global chi-square (chi(2)) test showed that the 3-SNP haplotype system was not associated with schizophrenia although the 1-df test for individual haplotypes showed that the rs1548359(C)-rs10314(G)-rs739371(C) haplotype was excessively non-transmitted (chi(2) = 5.32, P = 0.02). Because the claudin proteins are a major component for barrier-forming tight junctions that could play a crucial role in response to changing natural, physiological and pathological conditions, the CLDN5 association with schizophrenia may be an important clue leading to look into a meeting point of genetic and environmental factors.     

通心络胶囊对冠心病治疗效果的临床对照观察

目的观察通心络胶囊对冠心病（CHD）常见临床症状的改善效果。方法对照组维持原有药物治疗不变,治疗组在此基础上加服通心络胶囊4粒/次,3次/日,疗程4周。病人接受观察前进行常规化验检查,检测心率、血压、心功能等指标。疗程结束时对上述指标再进行检查,并观察病人的临床症状改善情况。结果两组病人的胸痛、胸闷、气憋、心悸、乏力等常见临床症状均有改善,且治疗组明显优于对照组（P〈0.05）;治疗组每搏量和心排血量的较对照组提高较为明显（P〈0.01）。结论加服通心络胶囊治疗CHD能增强西药的治疗效果,进一步改善CHD病人的常见临床症状。     

血清低密度脂蛋白胆固醇直接测定与Friedewald公式计算结果比较

采用聚乙烯硫酸（ＰＶＳ）沉淀法测定血清低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）值，同时应用Ｆｒｉｅｄｅｗａｌｄ公式计算ＬＤＬ－Ｃ含量，并对两法结果进行比较分析，提出当甘油三脂（ＴＧ）＜４．５２ｍｍｏｌ／Ｌ时，Ｆ公式计算法可代替ＰＶＳ法，当ＴＧ＞４．５２ｍｍｏｌ／Ｌ时，不宜用Ｆ公式计算ＬＤＬ－Ｃ的值。     

Kinetics and enzyme involvement in the metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in microsomes of rat lung and nasal mucosa.

The rat lung and nasal cavity are two target organs for carcinogenesis by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). In order to characterize further the enzymes involved in the bioactivation of NNK, detailed kinetic and inhibitory studies were conducted with rat lung and nasal mucosa microsomes, and the results were compared with previous studies. The enzymes in rat lung microsomes catalyzed the alpha-hydroxylation, pyridine N-oxidation and carbonyl reduction of NNK. The apparent Km for the formation of the NNK-derived keto aldehyde, NNK-N-oxide, the NNK-derived keto alcohol and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol were 28.8, 10.4, 7.0 and 178.1 microM respectively. In rat nasal microsomes, alpha-hydroxylation was the predominant pathway and the rate was approximately 200 times higher than that in lung microsomes. The apparent Kms for keto aldehyde and keto alcohol formation in rat nasal microsomes were 9.6 and 10.1 microM respectively. The cytochrome P450 inhibitors metyrapone and carbon monoxide markedly inhibited the metabolism of NNK in both rat lung and nasal microsomes. In rat lung microsomes, alpha-naphthoflavone and monospecific antibodies against P450s 1A2, 2A1 and 2B1 inhibited the formation of keto aldehyde by 39, 46, 64 and 23% respectively. In rat nasal microsomes, alpha-naphthoflavone and antibodies against P450s 1A2, 2A1 and 3A inhibited the metabolism of NNK by 80, 35, 20 and 14% respectively. The results indicate that cytochromes P450 play a major role in the metabolic activation of NNK in rat lung and nasal microsomes, and that there are tissue-related differences in NNK metabolism.     

预移植在胚胎移植中的意义

目的 :评价预移植在胚胎移植中的作用。　方法 :在超声波引导下胚胎移植 114个周期 ,其中 10 1个周期进行预移植。比较预移植与未预移植周期临床妊娠率和胚胎种植率 ;按预移植与实际胚胎放置深度差值分组 ,并比较两组妊娠率和胚胎种植率。　结果 :预移植周期与未预移植周期临床妊娠率和种植率统计学差异无显著性(5 9.4 1%和 6 1.5 4 % ,35 .81%和 31.4 3% ,P均 >0 .0 5 ) ;按预移植与实际胚胎放置深度差值分组后 ,两组妊娠率和种植率统计学差异也无显著性 (6 1.5 4 %和 5 8.6 7% ,4 0 .79%和 34.0 9% ,P均 >0 .0 5 )。　结论 :在胚胎移植技术中 ,预移植不能准确指引胚胎移植深度     

脾脏肿块的超声诊断

目的 :探讨脾脏肿块的超声表现及鉴别要点。材料和方法 :回顾性分析 76例脾脏肿块患者的超声检查资料 ,分析脾脏肿块的大小、数目、边界、内部回声等多种超声表现。结果 :76例脾脏肿块中有 3例错构瘤 ,10例血管瘤 ,16例淋巴瘤 ,2例淋巴管瘤 ,4例血管肉瘤 ,11例脾转移瘤 ,16例脾囊肿 ,4例脾梗死 ,3例脾血肿 ,5例脾脓肿 ,2例付脾 ,其超声表现各具特征。结论 :超声检查可早期发现并区别脾脏肿块的囊、实性 ,借助彩色血流显像可进一步鉴别良、恶性病灶。     

股骨头缺血坏死的低场MRI评价

目的: 分析股骨头缺血坏死(ANFH)低场MRI征象,评价ANFH的MRI分期及其关节积液的分级.材料和方法:在分析50例正常髋MRI基础上回顾性对照分析51例(90个股骨头)ANFH的低场MRI和X线平片资料.结果:90个ANFH中,20个(22 %) X线平片为阴性;64个(71%)MRI示"脂肪强度征"即坏死区内或近侧可见类似皮下脂肪样信号.按照 Hungerford分期:0期9个,Ⅰ期13个,Ⅱ期31个,Ⅲ期26个,Ⅳ期11个.ANFH引起的关节积液多为2～3级(60个髋,占67%);Ⅲ、Ⅳ期ANFH合并关节积液量比0～Ⅱ期明显多(P＜0.005).结论:低场MRI能够准确显示ANFH的范围、程度、信号特征及其关节积液的情况,并能够对早期ANFH作出可靠诊断;"脂肪强度征"为低场MRI的特征性表现,对诊断ANFH有非常重要的价值.     

Inhibitory effect of glycyrrhiza uralensis fish and chelidonium majus L on gastrocarcinogenesis induced by N-methyl-N′-nitron-N-nitrosoguanidine

In order to investigate the antagonistic effect of Glycyrrhiza Uralensis Fish (GUF) and Chelidonium maJus L (CML) on gastrccarcinogenesis induced by MNNG in Wastar rats, we treated the rats with MNNG alone (group 1) and with MNNG plus GUF and CML (group 2 and 3) respectively. The incidence of infiltrating adenocarcinoma of the glandular stomach and duodenum in group 2 was significantly lower than that in group 1 (26.7% vs. 67.8%). The differentiation and aggressivenees of carcinomas occured in group 2 were much better and mild than those in group 1. Present study also demonstrated that the inhibitory effect of CML on proliferation of human stomach carcinoma cell line MGC-803 was very remarkable; in addition, GUF and CML were able to antagonise the mutagenic activation of MNNG. These results suggest that GUF and CML may be empoyed in prevention of gastric carcinoma.     

Effects of thiamine deficiency on hepatic cytochromes P450 and drug-metabolizing enzyme activities

To elucidate the mechanisms by which thiamine deficiency affects hepatic microsomal monooxygenase activities, the effect of thiamine deficiency on two constitutive cytochrome P450 isozymes, P450IIE1 and P450IIC11, was investigated, using weanling male Sprague-Dawley rats. The clinical signs of thiamine deficiency were apparent after feeding a thiamine-deficient diet for 3 weeks. Thiamine deficiency caused an increase in P450IIE1, which was determined by N-nitrosodimethylamine demethylase assay and immunoquantitation of P450IIE1. This increase in the P450IIE1 level was mainly attributed to thiamine deficiency per se but not to dietary restriction. Ketone bodies were not elevated in thiamine-deficient rats, whereas ketone bodies were elevated and may have served as inducing factors in calorically restricted pair-fed animals. Injections of pyruvate or pyrithiamine in addition to thiamine deficiency did not potentiate the induction effect. On the other hand, thiamine deficiency did not affect the level of P450IIC11 during the 3 weeks of feeding the thiamine-deficient diet. In addition, thiamine deficiency increased cytosolic glutathione S-transferase activity but not steroid isomerase activity. The present study demonstrates the specificity of thiamine deficiency per se in the induction of P450IIE1 which does not involve an increase in the ketone body level.