A型肉毒毒素轻链基因的克隆及其结构分析

以献报道的A型肉毒毒素基因全序列为标准,设计并合成一对引物,自肉毒梭菌基因组中扩增出肉毒毒素轻链基因片段,并将扩增产物与pGEM—T载体在体外连接,构建测序重组质粒,进行测序和基因结构分析。PCR扩增获得了产物为1 364bp的DNA片段,测序结果与DNA数据库对照检索分析证明,此基因片段与GenBank中的A型肉毒毒素LC基因的一致性达99．9％以上,可以认为克隆的基因为A型肉毒毒素LC基因。     

Analysis of large-scale gene expression data.

DNA microarray technology has resulted in the generation of large complex data sets, such that the bottleneck in biological investigation has shifted from data generation, to data analysis. This review discusses some of the algorithms and tools for the analysis and organisation of microarray expression data, including clustering methods, partitioning methods, and methods for correlating expression data to other biological data.     

卤虫染色体倍性组成的研究

本文报道了我国4个地理品系卤虫的染色体倍性组成及卵径分布,分析了卤虫染色体的非整倍性,讨论了卤虫种的分布。 天津卤虫有2倍体(2n=42),占33.3％和5倍体,占16.2％;染色体数的波动为21—108;卵径为262±17μm。 海南卤虫有2倍体(2n=42),占8％;4倍体,占17.7％;5倍体,占18.3％;染色体数的波动为16—111;卵径为285±15μm。 新疆卤虫有2倍体(2n=42),占39.2％;染色体数的波动为17—106;卵径为269±15μm。 山西卤虫有2倍体(2n=42),占45.1％,染色体数的波动为17—84;卵径为234±13μm。     

Diagnosis of Gilbert's Syndrome: Role of Reduced Caloric Intake Test

Reduction in caloric intake to 400 a day for 72 hours resulted in a significant increase in the plasma bilirubin concentration in patients with Gilbert''s syndrome and in normal subjects. This was due to an increase in unconjugated pigment. There was no significant increase in the bilirubin concentration in patients with liver disease or haemolytic anaemia.The increase in unconjugated bilirubin was signficantly greater in Gilbert''s syndrome than in normals but only when the initial bilirubin concentration was raised. It was usually seen within 24 hours of reducing the caloric intake. An increase of 100% or more suggests that unconjugated hyperbilirubinaemia is due to Gilbert''s syndrome. In the normal subjects the unconjugated bilirubin level did not exceed 1·0 mg/100 ml.The increase in unconjugated bilirubin concentration on reducing the caloric intake may be due to decreased hepatic bilirubin uridine diphosphate glucuronyl transferase activity, which was shown to be present in seven rats starved for 72 hours. The effect of a 400 calorie diet for 24 hours on the unconjugated bilirubin level may distinguish Gilbert''s syndrome from other causes of unconjugated hyperbilirubinaemia.     

Hepatic reactions associated with ketoconazole in the United Kingdom.

Ketoconazole was introduced in the United Kingdom in 1981. By November 1984 the Committee on Safety of Medicines had received 82 reports of possible hepatotoxicity associated with the drug, including five deaths. An analysis of the 75 cases that had been adequately followed up suggested that 16, including three deaths, were probably related to treatment with the drug. Of the remainder, 48 were possibly related to treatment, five were unlikely to be so, and six were unclassifiable. The mean age of patients in the 16 probable cases was 57.9, with hepatotoxicity being more common in women. The average duration of treatment before the onset of jaundice was 61 days. None of these well validated cases occurred within the first 10 days after treatment. The results of serum liver function tests suggested hepatocellular injury in 10 (63%); the rest showed a mixed pattern. In contrast, the results of histological examination of the liver often showed evidence of cholestasis. The characteristics of the 48 patients in the possible cases were similar. Allergic manifestations such as rash and eosinophilia were rare. Hepatitis was usually reversible when treatment was stopped, with the results of liver function tests returning to normal after an average of 3.1 months. In two of the three deaths probably associated with ketoconazole treatment the drug had been continued after the onset of jaundice and other symptoms of hepatitis. Clinical and biochemical monitoring at regular intervals for evidence of hepatitis is advised during long term treatment with ketoconazole to prevent possible serious hepatic injury.