抗癌及癌化学预防药物的研究:3-α-酮醛香豆素衍生物的合成及其抗致突活性与结构间的关系

α-酮醛及其衍生物在抗病毒、抗肿瘤方面有一定活性。我们合成了18个新的3-α-酮醛香豆素衍生物,研究该类化合物的质谱裂解方式与氢核磁共振谱的特征峰。体外药理筛选发现其中部分化合物有不同程度的抗致突活性,对其构效关系进行了分析,并提出了这类化合物产生抗致突活性的可能亚结构。     

Osteochondroma of the rib: an unusual cause of haemothorax.

The case is described of a 36 year old woman who presented with a large left sided haemothorax. A thoracic computed tomographic (CT) scan suggested there was a bony outgrowth arising from the fourth rib. This was resected surgically and found to be an osteochondroma which was surrounded by blood clot. No definite site of bleeding was identified, but it is thought that the tumour may have traumatised the lung, the pericardiacophrenic artery, or the superior pulmonary vein, resulting in life threatening haemorrhage.     

Angiotensin II Receptor Blockade in Syrian Hamster (T0-2) Cardiomyopathy Does Not Affect Microscopic Cardiac Material Properties: Implications for Mechanisms of Tissue Remodeling

This study delineates the role of angiotensin II type I (AT1) receptor in the remodeling of Syrian cardiomyopathic hamsters. Twelve cardiomyopathic (T0-2) hamsters received L-158,809 treatment ad libitum in their drinking water (27 μg/ml) and 9 cardiomyopathic and 9 normal F1-B hamsters received tap water from 1 to 4 months of age. Although pharmacologically effective with regard to complete suppression of the blood pressure response to angiotensin II infusion, L-158,809 did not diminish the progression or severity of cardiomyopathy. Heart weight/100 g body weight and left ventricular wall thickness adjusted for body weight of both L-158,809 and cardiomyopathic control hamsters did not differ and exceeded those of F1-B controls (p < 0.05). Myocardial material properties (e.g., stiffness and density) of cardiomyopathic hamsters treated with L-158,809 were not affected. Thus, the progression of fibrosis, calcification, and necrosis in T0-2 cardiomyopathic hamsters was not sensitive to AT1 receptor blockade. This revised version was published online in July 2006 with corrections to the Cover Date.     

A flow cytometric method for identifying Marek's disease virus pp38 expression in lymphocyte subpopulations

Identification of Marek's disease virus-infected lymphocytes is essential for a full understanding of the pathogenesis of Marek's disease. This paper describes the development of a simple, quantitative and reproducible flow cytometric technique for the identification of the phenotype of Marek's disease virus-infected lymphocytes. The method is based upon the detection of the Marek's disease virus-specific phosphoprotein pp38, in saponin-permeabilized lymphocytes, using the monoclonal antibody BDI, and the identification of the phenotype of pp38(+) lymphocytes using monoclonal antibodies against lymphocyte surface markers. pp38 expression in the spleen was demonstrated in the cytolytic phase of infection. The mean proportion of pp38(+) lymphocytes at 4 days post-infection was 0.43%. Of these, 95% were B lymphocytes, while only 4% were T lymphocytes (both CD4(+) and CD8(+)). The potential of the technique for the investigation of the cytolytic phase of Marek's disease is discussed.     

Post transfusion septicaemia 1980-1989: importance of donor arm cleansing.

AIMS: To determine the prevalence of Pseudomonas fluorescens on the arms of blood donors, and to elucidate one possible cause for its predominance (60% of cases during 1980-89) in exogenous post transfusion septicaemia (PTS). METHODS: Skin swabs were taken from the arms of 782 blood donors and cultured on to heated blood agar. After incubation, Oxidase reagent and the Gram stain were used to select non-fermentative Gram negative rods, which were then subcultured and identified using the Analytical Profile System (API) 20 NE system. RESULTS: Non-fermentative Gram negative rods were found on the arms of 11.7% of donors, Pseudomonas spp on 1.0%, and Ps fluorescens on the arms of 0.3% of donors. CONCLUSIONS: This evidence emphasises the absolute requirement for efficient skin cleansing of blood donors' arms to minimise the risk of exogenous PTS.