Prognostic role of alveolar-arterial oxygen pressure difference in acute pulmonary embolism.

BACKGROUND: This study investigated the utility of the alveolar - arterial oxygen pressure difference (AaDO (2)) in predicting the short-term prognosis of acute pulmonary embolism (PE). METHODS AND RESULTS: This study retrospectively enrolled 114 consecutive patients with acute PE, diagnosed by either spiral computed tomography or high probability ventilation - perfusion lung scans. During the first 24 h of admission, all patients had initial artery blood gas collected under room air. Patient exclusion criteria were chronic lung disease, septic emboli, and moderate and low probability lung scans. Patients were assigned to 2 groups based on either 30-day death or a 30-day composite event. Receiver operating characteristic analyses was used to determine the AaDO(2) cut-off value for predicting primary and composite endpoints. Statistical analysis demonstrated significant differences in AaDO(2) between the 30-day composite endpoint group and the 30-day composite event-free survival group (p=0.012). The AaDO(2) had a strong trend between the 30-day death group and the survival group (p=0.062). The best cut-off value for AaDO(2) was 53 mmHg and using this, the positive predictive value for 30-day death was 25% and the negative predictive value was 92%. For the 30-day composite endpoint, the positive predictive value for AaDO(2) was 35%, and the negative predictive value was 84%. In this study, thrombocytopenia was also an indicator of poor prognosis for patients with acute PE. CONCLUSION: The AaDO(2) measurement is a highly useful and simple measurement for predicting short-term prognosis in patients with acute PE. It has high negative predictive value and moderate positive predictive value for 30-day death and 30-day composite event. Aggressive thrombolytic treatment strategies should be considered for patients with an initial poor prognostic parameter (ie, AaDO(2) >or=53 mmHg).     

Ketanserin降低清醒自发性高血压大鼠血压波动性的机理初探

应用计算机化清醒大鼠血流动力学测定技术，观察５－ＨＴ２受体阻滞剂Ｒｉｔａｎｓｅｒｉｎ（Ｒｉｔ）和α１受体阻滞剂哌唑嗪对清醒自发性高血压大鼠（ＳＨＲ）的血压、血压波动性（ＢＰＶ）和动脉压力感受性反射血压控制部分（ＡＢＲ－ＢＰ）的效应，旨在初步探讨兼具５－ＨＴ２受体和α１受体阻滞作用地新型抗高血压药Ｋｅｔａｎｓｅｒｉｎ降低ＢＰＶ的机制。结果表明：Ｒｉｔ对ＳＨＲ无降压作用，但侧脑室给药明显提高ＡＢＲ－Ｂ     

Effect of estradiol on accelerated atherosclerosis in rabbit heterotopic aortic allografts.

Migration and proliferation of vascular smooth muscle cells are early and major events in the formation of atherosclerotic lesions. We report on an aorta transplant model in rabbits wherein myointimal proliferation is inhibited by 17-beta-estradiol. The abdominal aortas of outbred white New Zealand rabbits were harvested and allografted to the carotid artery of the recipient. The animals, which were fed either a normal or a high-cholesterol (0.5%) diet, were killed 3 weeks later. The degree of myointimal proliferation was measured with a digitized system attached to a light microscope. The myointimal hyperplasia was expressed as the cross section area of the intima/the area of the intima + the area of the media x 100. Transmission electron micrographs were obtained for all vessels. Intimal thickening was shown mainly to consist of proliferating smooth muscle cells. The cholesterol diet resulted in significantly higher serum total cholesterol levels compared to animals on a normal diet (p < 0.0001) but did not affect serum high-density lipoprotein-cholesterol or serum triglyceride levels. The cholesterol diet was also associated with a greater but not significant amount of intimal thickening. Treatment with 17-beta-estradiol significantly decreased both serum triglyceride concentration (p < 0.05) and myointimal thickening (p < 0.01) in cholesterol-fed animals. Transmission electron microscopy showed that the endothelial cells appeared structurally normal in the estradiol-treated animals. Further, estradiol prevented the appearance of vacuolized macrophages. Thus estradiol may decrease myointimal thickening by preserving the endothelium and preventing macrophage appearance in the intima.(ABSTRACT TRUNCATED AT 250 WORDS)     

胎儿肝、脾、肾中凝血因子Ⅷ:C与vWF的研究

凝血因子Ⅷ(FⅧ)由vWF和FⅧ:C组成。FⅧ:C的合成部位至今尚未确认。本文检测了16～22周胎龄胎儿肝、脾、肾及肾小球组织中Ⅷ:C活性及vWF:Ag含量后,发现肾中Ⅷ:C活性较高(1.679±1.588 U/ml),尤其是肾小球中高达46.313±40.651U/ml,脾中次之(0.372±0.462 U/ml),肝中最低(0.021±0.029U/ml)。将3种组织细胞培养后,发现仍以肾中Ⅷ:C活性最高。由此提示,肾可能是Ⅷ:C的合成部位。同时检测三器官中vWF:Ag,发现含量极微。这些组织中Ⅷ:C与vWF的关系有待研究。     

Chemical constituents of Isodon albopilosus (C.Y. Wu et H.W. Li) Hara]

Five compounds have been isolated from the stems and leaves of Isodon albopilosus. On the basis of spectroscopic and chemical data, they were identified as macrocalyxin C, stearic acid, beta-sitosterol, ursolic acid and beta-sitosterol-beta-D-glucoside, respectively.     

不同压力下人脐带静脉的形态变化

运用扫描电镜和光镜观察了人脐带静脉的形态结构及其在0～8.0kPa 压力下的变化.脐静脉结构类似中等动脉.内皮细胞和内弹力膜的形态随实验压力增大而改变.6.7～7.3kPa是脐静脉内膜的临界破坏压,5.3～6.7kPa 是制备脐静脉作为管道移植材料的最佳压力.     

Fluorescence in situ hybridization analysis of chromosome 12p in paraffin-embedded tissue is useful for establishing germ cell origin of metastatic tumors.

The over-representation of chromosome 12p sequences is crucial for the development of invasive testicular germ cell tumors. Testicular cancer patients may have metastatic tumors of diverse histologic types, including adenocarcinoma, undifferentiated carcinoma, sarcoma, or other malignancies that lack features of germ cell tumors. We sought to investigate the possible germ cell origin of such tumors using interphase fluorescence in situ hybridization. In all, 10 metastatic malignant somatic-type tumors from patients with histories of testicular cancer, as well as one malignant somatic-type tumor from a patient with primary mediastinal germ cell tumor were studied and included: adenocarcinoma (five cases), poorly differentiated carcinoma (one), sarcoma (four), and neuroendocrine carcinoma (one). The tumors were analyzed using fluorescence in situ hybridization using 12p spectrum green and 12 centromeric spectrum orange probes in paraffin sections. The patients ranged in age from 27 to 55 years (mean, 43). Colon and lung cancers from patients without germ cell tumors were used as controls. Adequate signals were observed in all tumors. Gain of chromosome 12p was seen in six tumors. None of the control tumors showed 12p amplification. Fluorescence in situ hybridization for 12p amplification in routinely processed surgical specimens is a useful adjuvant diagnostic tool in confirming the germ cell origin of metastatic tumors having the histologic appearance of somatic-type neoplasms.     

Polymorphisms in ADAM33 are associated with allergic rhinitis due to Japanese cedar pollen

BACKGROUND: A recent report provided evidence that a disintegrin and metalloprotease domain 33 (ADAM33), a member of the ADAM family, is a novel susceptibility gene in asthma linked to bronchial hyper-responsiveness. However, there has been no investigation of the genetic role of ADAM33 variants in nasal allergy. OBJECTIVE: The purpose of this study was to test the association between ADAM33 polymorphisms and Japanese cedar pollinosis (JCPsis), a most common seasonal allergic rhinitis in Japan. METHODS: We conducted a case-control association study among a Japanese population, involving 95 adult individuals with JCPsis and 95 normal healthy controls. A total of 22 single-nucleotide polymorphisms (SNPs) in ADAM33 were genotyped using PCR-based molecular methods. RESULTS: Six SNPs of ADAM33 gene, three in introns (7575G/A, 9073G/A and 12540C/T) and three in the coding region (10918G/C, 12433T/C and 12462C/T), were strongly associated with JCPsis (P = 0.0002-0.022 for absolute allele frequencies) and most of the SNPs were in linkage disequilibrium with each other. A higher frequency of the common alleles of these SNPs was noted for the subjects with JCPsis in comparison with healthy controls. We also identified a haplotype associated with the disease susceptibility. In addition, associations were found between ADAM33 polymorphisms and various cedar pollinosis phenotypes including clinical severity, eosinophil counts in nasal secretion and allergen-specific IgE levels in sera, but not total serum IgE levels. CONCLUSION: These results indicate that polymorphisms in the ADAM33 gene are associated with susceptibility to allergic rhinitis due to Japanese cedar pollen, but the functional relationship still needs clarification.