血瘀证的研究发展脉络与评述

主要从4个方面论述了血瘀证50年来研究进展．理论研究，着重从古今文献论述血瘀证定义和含义；客观研究，着重对生理、生化、血液流变学、免疫学、病理学和微循环等方面对血瘀证进行研究；血瘀证的动物模型研究，主要对血瘀证动物模型的建立与造模方法和途径进行研究；诊断标准研究，包括诊断标准、诊断指标的研究。并对上述内容进行了评述，并提出了展望。     

Hyperfractionated radiation therapy combined with concomitant chemotherapy for inoperable stage III non-small cell lung cancer: clinical analysis of 70 cases]

OBJECTIVE: To evaluate the effect of hyperfractionated radiation therapy and concomitant chemotherapy for inoperable stage III non-small cell lung cancer (NSCLC). METHODS: Seventy patients were randomized equally into two group. The therapy group received radiotherapy with hyperfractionated radiation therapy combined with concomitant chemotherapy, and the control group was treated with chemotherapy only. RESULT: The overall response rate, including the rate of both complete (CR) and partial responses (PR), in the therapy group was 60.0% with a CR rate of 8.6%. The overall response rate in the control group was 40.0% with a CR rate of 5.7%. The difference in overall response rate was statistically significant between the two groups (P<0.05). The median survival time, 1- and 2-years survival rate were 12.8 months, 48.6%, and 25.7%, respectively, in the hyperfractionated radiotherapy group, and 9.4 months, 34.3%, and 17.1%, respectively, in the chemotherapeutic group (P 0.031). The major toxic effects of the chemotherapy were myelosuppression and radiation esophagitis. CONCLUSION: Hyperfractionated radiation therapy plus concomitant chemotherapy with paclitaxel for inoperable stage III NSCLC improves the short-term response of the patients, but fail to raise the survival rate.     

Nuclear Factor κB and Anesthetic Preconditioning during Myocardial Ischemia-Reperfusion

Background: Volatile anesthetic preconditioning (APC) protects against myocardial ischemia-reperfusion (IR) injury, but the precise mechanisms underlying this phenomenon remain undefined. To investigate the molecular mechanism of APC in myocardial protection, the activation of nuclear factor (NF) [kappa]B and its regulated inflammatory mediators expression were examined in the current study.

Methods: Hearts from male rats were isolated, Langendorff perfused, and randomly assigned to one of three groups: (1) the control group: hearts were continuously perfused for 130 min; (2) the IR group: 30 min of equilibration, 15 min of baseline, 25 min of ischemia, 60 min of reperfusion; and (3) the APC + IR group: 30 min of equilibration, 10 min of sevoflurane exposure and a 5-min washout, 25 min of global ischemia, 60 min of reperfusion. Tissue samples were acquired at the end of reperfusion. NF-[kappa]B activity was determined by electrophoretic mobility shift assay. The NF-[kappa]B inhibitor, I[kappa]B-[alpha], was determined by Western blot analysis. Myocardial inflammatory mediators, including tumor necrosis factor [alpha], interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase, were also assessed by Western blot analysis.

Results: Nuclear factor [kappa]B-DNA binding activity was significantly increased at the end of reperfusion in rat myocardium, and cytosolic I[kappa]B-[alpha] was decreased. Supershift assay revealed the involvement of NF-[kappa]B p65 and p50 subunits. APC with sevoflurane attenuated NF-[kappa]B activation and reduced the expression of tumor necrosis factor [alpha], interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase. APC also reduced infarct size and creatine kinase release and improved myocardial left ventricular developed pressure during IR.     

关木通引起慢性间质性肾炎7例报告

目的　观察关木通所致慢性肾损伤的临床和病理改变特点。方法　本组 7例中 ,男 5例 ,女 2例。 3例服关木通汤药 ,4例服含关木通成药。分析服用时间、累积总量与肾损害首发症状及症状出现时间、肾功能和肾病理改变的关系。结果　汤药组 :服药时间平均 3 3 3个月 ,累积总量平均 82 9 3 g ,首发症状为乏力 3例 ,夜尿增多 2例 ,平均时间为 8 3个月 ,Cr平均 40 2 μmol/L。肾病理 :3例均为重度寡细胞性肾间质纤维化 ,肾小管广泛萎缩。成药组 :服药时间平均 7 5个月 ,累积总量平均 13 6g ,乏力 3例 ,夜尿增多 1例 ,恶心呕吐、头痛头晕 1例 ,平均18 8个月 ,Cr 3 62 8μmol/L。肾病理为重度寡细胞性间质纤维化和灶状纤维化各 2例 ,肾小管灶状萎缩 3例 ,广泛萎缩 1例。结论　汤药组关木通积累大 ,发病时间早 ,肾病理改变重。提示关木通所致肾损其临床表现、病理改变与服用关木通时间、剂量相关。     

1例乙酸钙不动杆菌致角膜溃疡病人的护理

不动杆菌为条件致病菌,致病力不强,一般情况下很少引起感染,但当机体抵抗力降低或正常免疫屏障被破坏时可引发疾病,确切的致病因子目前尚无定论[1].我院于2005年8月24日收治1例因乙酸钙不动杆菌所致角膜溃疡病人,经过及时、有效的治疗及精心护理,取得了较好的疗效,现将其护理总结如下.     

豚鼠内耳磁微粒栓塞缺血模型初探

OBJECTIVE: To set up an inner ear ischemic model in guinea pig with ferromagnetic embolism. METHODS: A magnet was fitted in the external auditory canal and carbonyl iron filings (1%, 1 ml/kg) was injected into jugular, then the inner ear vessels were obstructed by ferromagnetic spheres. Cochlear blood flow (CBF) and number of red blood cells in the stria vessels were used to detect the model's ischemia of cochleae. The slice of temple bone and basal membrane stained by silver nitrate were used for inner ear's histopathological observations. RESULTS: The iron spheres were amassed in the one and two-day-later's model of inner ear vessels, which resulted in embolism. The number of red blood cells in the stria vessels decreased and then recovered to normal level after 4 days, but the CBF decreased to 50% +/- 10% of basic level immediately and recovered to 99% +/- 41% 4 days later. Scattered lesion of out hair cell cilium could be seen in cochleae in eight-day-later's model, and degenerations in different degree were found in vascular stria. CONCLUSION: The methods of inner ear ischemic model with ferromagnetic embolism could be practical and the decrease of CBF was reversible, so it may be an ideal model for studying some ischemic inner ear diseases and evaluating the effects of therapeutic drugs.     

PRENATAL DIAGNOSIS Ⅰ. EARLY DIAGNOSIS OF OPEN NEURAL TUBE DEFECTS BY QUALITATIVE ACETYLCHOLINESTERASE ISOENZYME IN AMNIOTIC FLUID

The measurement of amniotic fluid (AF) acetylcholinesterase isoenzyme (AChEI) is a relatively new method for early diagnosis of open neural tube defects (NTDs). As quantitative methods are of unproven reliability at present, the authors used a high resolving power qualitative method-vertical slab polyaerylamide gel electrophoresis. The benefits of this technique are: simplicity of operation, accuracy, unsophisticated equipment, and easily available reagents. Combined results of 9 NTDs studies revealed that samples from early pregnancy gave more accurate results than those from late pregnancy.     

Monokines produced by macrophages stimulate the growth of osteoblasts

We have previously reported that the J774A.1 macrophage-like tumor cell line produces two potent monokines which stimulate the growth of osteoblasts and chondrocytes. These growth factors, which have an affinity for heparin-agarose, have been termed HEP I (a 30 Kd PDGF-like molecule) and HEP II (an approximately 20 Kd molecule), respectively, based on their elution profile. Unlike HEP I, HEP II does not stimulate the growth of fibroblasts. Extensive biological and chromatographic studies disclosed that HEP II appears to be a unique bone cell mitogen unlike any known growth factor, including the FGFs, IL-1s, and TNFs, EGF, IGF-I and -II, TGF-beta, beta 2 microglobulin, G-CSF, CSF-1 and GM-CSF. To characterize more fully the effects of the macrophage-derived monokines on osteoblast growth and function, clones were derived from calvaria explant cultures. Two clones, SDFRC-2.05 and SDFRC-3, were developed and found to exhibit osteoblastic characteristics, including high levels of alkaline phosphatase, synthesis of type I but not type III collagen, and an increased intracellular cAMP production in response to PTH. The SDFRC-3 cells exhibited a polygonal morphology like that of the explant-derived cells while SDFRC-2.05 cells exhibited a more fibroblastic morphology. When tested on the explant cultures and clones, HEP I and HEP II were found to stimulate DNA synthesis and increase protein per culture, but decreased alkaline phosphatase activity. Clone SDFRC-3 was found to be more responsive to HEP II than clone SDFRC-2.05. Both monokines were found to be more potent mitogens for bone cells than TGF-beta. HEP II, but not HEP I or TGF-beta, induced a transformation of bone cells from a polygonal to a fibroblastic morphology, suggesting the induction of migration prior to proliferation. Thus, macrophages may be responsible not only for bone repair but also for ensuring the linkage of bone formation to resorption during physiological remodeling.