听力测试中短文听写的应试技巧

复合式听写比听力选择题更强调语言综合运用能力。全面打好语言基本功是提高听写能力的重要途径。但听写训练具有自身的科学性和技巧性，多练加巧练可以取得事半功倍的成效。     

王焕禄老中医治疗哮喘发作期的用药经验

王焕禄老中医在长期的临床实践中，总结出治疗哮喘病的一些用药体会，兹介绍如下，以飨读者。     

卵巢肿瘤合并副肿瘤性综合征

卵巢肿瘤合并副肿瘤性综合征（ovarian tumor associated with paraneoplastic syndrome）并非罕见,但由于此综合征往往先于肿瘤出现,而因肿瘤病灶小或隐匿不易被发现,常被临床医师所忽略,导致肿瘤未能得到及时诊断和治疗.＂paraneoplastic syndrome＂一词有译为副肿瘤性综合征、副肿瘤综合征、副癌综合征、肿瘤外综合征者.此综合征为肿瘤患者的一种复合症状,该症状不能用肿瘤本身或肿瘤转移来解释.现按主要受累系统的几种综合征简介如下,以加强临床医师对卵巢肿瘤合并副肿瘤性综合征特点的认识,减少误诊、误治。     

Effects of cerulenin on the endogenous fatty acid synthetic activity in squamous cell carcinoma of the oral cavity.

PURPOSES: Inhibition of cerulenin on the endogenous fatty acid synthetic activities of oral squamous cell carcinoma (OSCC) and normal oral mucosa was assayed. METHODS: Squamous cell carcinoma and normal oral mucosa were collected fresh from surgical specimens. The collected tissues were minced in RPMI 1640 and divided into 3 groups: cerulenin treated, dimethylsulfoxide treated, and control. The tissues were incubated in [1(2)-(14)C]acetic acid, sodium salt for the last 2.5 hours of the treatment at 37 degrees C in 5% CO(2). After labeling, total lipids were extracted and counted for (14)C by scintillation counting. RESULTS: Endogenous fatty acid synthetic activities of oral squamous cell caranoma in the cerulenin-treated group decreased by 19% at 1 hour, 64% at 2 hours, and 87% at 4 hours; remained nearly unchanged in the dimethylsulfoxide-treated group; and increased slightly in the control group. The oral mucosa tissues were only mildly affected by cerulenin in fatty acid synthesis. CONCLUSIONS: Cerulenin significantly inhibits fatty acid synthetic activity in squamous cell carcinoma and only mildly affected the oral mucosa, indicating that the fatty acid synthetic pathway may be exploited as a target for developing anticancer drugs.     

中西医联合治疗单纯疱疹性角膜炎的疗效观察

目的 :探讨单纯疱疹性角膜炎是中西医联合用药的治疗方法。方法 :本组 10 0例 ( 10 6只眼 )单纯疱疹性角膜炎患者应用抗病毒药物联合清热解毒中药的疗效观察。结果 :本组病例治疗后总有效率 82 .0 8%。结论 :中西医联合治疗措施是我们对单纯疱疹性角膜炎治疗的一项新的探讨。     

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.     

Protein ubiquitination in postsynaptic densities after transient cerebral ischemia.

The mechanisms underlying neurologic deficits and delayed neuronal death after ischemia are not fully understood. In the present study, we report that transient cerebral ischemia induces accumulation of ubiquitinated proteins (ubi-proteins) in postsynaptic densities (PSDs). By immunoelectron microscopy, we demonstrated that ubi-proteins were highly accumulated in PSD structures after ischemia. On Western blots, ubi-proteins were markedly increased in purified PSDs at 30 minutes of reperfusion, and the increase persisted until cell death in the CA1 region after ischemia. In the resistant DG area, however, the changes were transient and significantly less pronounced. Deposition of ubi-proteins in PSDs after ischemia correlates well with PSD structural damage in the CA1 region as viewed by electron microscopy. These results suggest that the ubiquitin-proteasome system fails to repair and remove damaged proteins in PSDs. The changes may demolish synaptic neurotransmission, contribute to neurologic deficits, and eventually lead to delayed neuronal death after transient cerebral ischemia.