黄柏及中成药中小檗碱和巴马亭的高效液相色谱法测定

本文以正相高效液相色谱法,用窗口图解技术对色谱条件进行了优化。对黄柏及其中成药中的有效成分——小檗碱、巴马亭的提取、测定条件、标准曲线进行了研究。并对两种含黄柏的中成药样品进行了分析。其中小檗碱的回收率均在97%以上,巴马亭的回收率均在96%以上。     

Indium-111 labeled platelet deposition following transfemoral angiography

The incidence of thromboembolitic events in patients undergoing transfemoral angiography was examined using indium-111 labeled platelets. Twenty-seven patients received approximately 300 muCi of autologous labeled platelets at least 3 hours before angiography and were scanned with a gamma camera immediately before and after angiography. All patients were free of clinically obvious complications in the 1-2 day period after angiography. Our results showed evidence of platelet deposition at 21 sites other than the puncture site in 12 (44%) patients. Most platelet deposition (54%) occurred along the region between the puncture site and the aortic bifurcation; 24% occurred at sites not traversed by the catheter. At the puncture site itself, there was substantial platelet uptake in 44% of patients. This study indicates the need for further work in determining the most suitable catheter material and in assessing the efficacy of other measures such as anticoagulant or antiplatelet therapy.     

老年大鼠松质骨骨重建的组织形态计量学研究

目的：研究老年大鼠及在促骨合成药前列腺素E2（PGE2）作用下松质骨骨重建和骨建造的形态计量学改变，探讨动物骨重建形态学新参数测量方法及其意义。方法：50只20月龄雄性Wistar大鼠随机分成5组，年龄对照组（基础组、10d和30d年龄对照组），PGE2给药组（分别10d和30d给予3mg/kg/d处理组）。用体内双荧光标记，不脱钙组织切片，粘合线（cement line）染色，骨组织形态计量学方法，测定骨重建和骨建造参数。结果：20月龄雄性大鼠胫骨近端松质骨的形成表面大多数为骨重建单位（占63．3％），少部分为骨建造单位（占26．7％）；PGE2用药后骨重建单位增加1．5倍，骨建造单位增加4倍，比值倒置，成骨细胞10d时明显增多。说明PGE2通过刺激成骨细胞骨合成而介民导骨建造性骨增加和骨重建性骨量增加，并以前为主。结论：老年雄性大鼠 松质骨以骨重建活动为主，仍有骨建造活动。PGE2主要通过刺激成骨细胞骨建造而增加骨量。     

Incidence and mortality of venous thrombosis: a population-based study

Background: Estimates of the incidence of venous thrombosis (VT) vary, and data on mortality are limited. Objectives: We estimated the incidence and mortality of a first VT event in a general population. Methods: From the residents of Nord‐Trøndelag county in Norway aged 20 years and older (n = 94 194), we identified all cases with an objectively verified diagnosis of VT that occurred between 1995 and 2001. Patients and diagnosis characteristics were retrieved from medical records. Results: Seven hundred and forty patients were identified with a first diagnosis of VT during 516 405 person‐years of follow‐up. The incidence rate for all first VT events was 1.43 per 1000 person‐years [95% confidence interval (CI): 1.33–1.54], that for deep‐vein thrombosis (DVT) was 0.93 per 1000 person‐years (95% CI: 0.85–1.02), and that for pulmonary embolism (PE) was 0.50 per 1000 person‐years (95% CI: 0.44–0.56). The incidence rates increased exponentially with age, and were slightly higher in women than in men. The 30‐day case‐fatality rate was higher in patients with PE than in those with DVT [9.7% vs. 4.6%, risk ratio 2.1 (95% CI: 1.2–3.7)]; it was also higher in patients with cancer than in patients without cancer [19.1% vs. 3.6%, risk ratio 3.8 (95% CI 1.6–9.2)]. The risk of dying was highest in the first months subsequent to the VT, after which it gradually approached the mortality rate in the general population. Conclusions: This study provides estimates of incidence and mortality of a first VT event in the general population.     

对QT离散度实质的探讨

为探讨ＱＴ离散度（ＱＴｄ）的真实意义，观察１３９例急性心肌梗死（ＡＭＩ，ＡＭＩ组）及１０９例正常人（对照组）的最长ＱＴ间期（ＱＴｍａｘ）、校正ＱＴｍａｘ（ＱＴｃｍａｘ）及ＱＴｄ的变化。结果：①ＡＭＩ组的ＱＴｍａｘ、ＱＴｃｍａｘ和ＱＴｄ均显著高于对照组（分别为４２２．６０±３０．５１ｍｓｖｓ３８２．４６±２３．４０ｍｓ、４６０．２１±２８．９６ｍｓｖｓ３８８．５１±２０．１５ｍｓ、５９．８０±２８．４０ｍｓｖｓ３９．４３±１２．２１ｍｓ，Ｐ均＜０．００１）。②ＡＭＩ组中发生严重室性心律失常（ＶＡ）患者（１１４例）的ＱＴｍａｘ、ＱＴｃｍａｘ、ＱＴｄ与无ＶＡ的患者（２５例）相比，均有显著差异（分别为４４８．５８±３３．４０ｍｓｖｓ４１６．１０±３５．３０ｍｓ、４８１．４３±３５．１７ｍｓｖｓ４３９．６０±２７．１０ｍｓ、６６．９０±２０．７２ｍｓｖｓ４８．３２±２３．６１ｍｓ，Ｐ均＜０．００１）。认为ＡＭＩ时ＱＴｄ系Ｔ向量环在不同导联上的“投影”差异所引起的，其异常的本质是ＱＴ间期延长     

Aberrant expression in multiple components of the transforming growth factor-β1-induced Smad signaling pathway during 7,12-dimethylbenz[a]anthracene-induced hamster buccal-pouch squamous-cell carcinogenesis

Transforming growth factor (TGF)-β1 signaling controls a plethora of cellular processes including tumorigenesis. The TGF-β1 ligand initiates signaling by binding to TGF-βreceptor II (TβRII) and allowing heterodimerization with TGF-βreceptor I (TβRI); thus, TβRI is phosphorylated by TβRII. After phosphorylation, Smad2 and Smad3 heterodimerize with Smad4, and this complex migrates to the nucleus to regulate the expression of specific target genes. However, Smad7 interrupts above signal transduction by preventing phosphorylation of Smad2 or Smad3. The objective of this study was to examine the TGF-β1-induced Smad signaling pathway during 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal-pouch squamous-cell carcinogenesis. Fifty 6-week-old male Syrian golden hamsters were divided into three experimental and two control groups (10 animals in each). Both pouches of each animal in the experimental groups were painted with 0.5% DMBA solution, and both pouches of each animal of one of the control groups were similarly treated with mineral oil; the other control group remained untreated throughout the experiment. Animals from three experimental groups were sacrificed at the end of 3rd, 9th, and 14th-weeks after DMBA treatment, respectively, and animals from two control groups were all sacrificed at 14th-weeks after the treatment. Immunohistochemical staining for TGF-β1, TβRI, TβRII, Smad2-4 and Smad7 were performed. RESULTS: A significant increase in the expression of Smad7 and significant decreases in the expression of TβRII, Smad 2, Smad3 and Smad4 were noted during hamster buccal-pouch carcinogenesis induced by DMBA. Our findings indicate that a disruption in TGF-β1-induced Smad signaling occurs as a result of aberrant expression of multiple components in the TGF-β1 signaling pathway during DMBA-induced hamster buccal-pouch carcinogenesis, leading to loss of TGF-β1 growth-suppressive effects on transformed pouch keratinocytes.     

Persistent and relapsing babesiosis in immunocompromised patients.

BACKGROUND: Human babesiosis is a tickborne malaria-like illness that generally resolves without complication after administration of atovaquone and azithromycin or clindamycin and quinine. Although patients experiencing babesiosis that is unresponsive to standard antimicrobial therapy have been described, the pathogenesis, clinical course, and optimal treatment regimen of such cases remain uncertain. METHODS: We compared the immunologic status, clinical course, and treatment of 14 case patients who experienced morbidity or death after persistence of Babesia microti infection, despite repeated courses of antibabesial treatment, with those of 46 control subjects whose infection resolved after a single course of standard therapy. This retrospective case-control study was performed in southern New England, New York, and Wisconsin. RESULTS: All case patients were immunosuppressed at the time of acute babesiosis, compared with <10% of the control subjects. Most case patients experienced B cell lymphoma and were asplenic or had received rituximab before babesial illness. The case patients were more likely than control subjects to experience complications, and 3 died. Resolution of persistent infection occurred in 11 patients after 2-10 courses of therapy, including administration of a final antimicrobial regimen for at least 2 weeks after babesia were no longer seen on blood smear. CONCLUSIONS: Immunocompromised people who are infected by B. microti are at risk of persistent relapsing illness. Such patients generally require antibabesial treatment for >or=6 weeks to achieve cure, including 2 weeks after parasites are no longer detected on blood smear.