白细胞的

Objective To investigate the clinical features, causes of blindness and diagnosis of Vogt Koyanagi Harada syndrome Methods The data of 157 patients with VKH syndrome were reviewed and analyzed Patients were carefully examined with slit lamp, ophthalmoscope, three mirror lens, fundus fluorescein angiography, indocyanine green angiography and HLA typing Results Headache was noted in 73 5% of these patients Simultaneous involvement of both eyes occurred in 80 8% of these patients Chroiditis,papilledema and edema of the retina adjacent to the optic nerve were noted in 100% of these patients in the posterior uveitis stage, whereas recurrent granulomatous anterior uveitis (98 4%),"sunset glow" fundus (95 8%) and Dalen Fuchs nodules (71 2%) were the common ocular findings in the recurrent anterior uveitis stage The common causes of blindness were papillitis, exudative retinal detachment and complicated cataract in the posterior uveitis stage, anterior uveal involvement stage and its recurrent stage Poliosis (36 3%) and alopecia (35 0%) were the most common extraocular findings Early irregular patches of fluorescence, followed by localized hyperfluorescent spots were the typical findings of FFA Dilation of choroidal vessels and leakage of ICG from the choroidal vessels were the common ICGA findings The prevalence of HLA DR4 and HLA DRw53 in patients (54 9% and 71 8% respectively) was significantly higher than that in controls (14 7% and 38 2% respectively) Conclusions VKH syndrome is characterized by chroiditis, papillitis or neuroretinitis in the posterior uveitis stage, followed by a generalized uveitis with a typical recurrent granulomatous anterior uveitis Extraocular findings and relevant examinations including FFA, ICGA and HLA typing are helpful to the diagnosis of VKH syndrome

目的探讨Vogt-Koyanagi-Harada综合征患者的临床特征、盲目原因及诊断等有关问题。方法对在1996年1月至2000年12月间就诊资料完整的157例VKH综合征患者进行回顾性分析，并对裂隙灯、眼底镜、三面镜、荧光素眼底血管造影(fundus fluorescein angiography，FFA)、吲哚青绿血管造影(indocyanine green angiography，ICGA)及人类白细胞抗原分型等检查结果进行分析。结果 VKH综合征最常见的前驱症状为头痛(102例，73.5%)，双眼同时患病118例(80.8%)；后葡萄膜炎期眼部主要表现为脉络膜炎、视乳头及附近视网膜水肿(100.0%)；前葡萄膜炎反复发作期眼部表现为复发性肉芽肿性前葡萄膜炎(128例，98.4%)、晚霞状眼底改变(95.8%)及Dalen-Fuchs结节(71.2%)；后葡萄膜炎期、前葡萄膜受累期及前葡萄膜炎反复发作期导致盲目的主要原因分别为视乳头炎、视网膜脱离及并发性白内障；毛发变白(36.3%)及脱发(35.0%)是最常见的眼外表现；炎症活动期FFA典型表现为斑驳状高荧光，ICGA发现脉络膜血管扩张、通透性增高等改变；VKH综合征患者HLA-DR4及HLA-DRw53的阳性率(54.9%及71.8%)显著高于正常对照组(14.7%及38.2%)。结论 VKH综合征患者在后葡萄膜炎期眼部典型表现为双侧脉络膜炎、视乳头炎或神经视网膜炎，随后出现以反复发作的肉芽肿性前葡萄膜炎为特征的全葡萄膜炎。眼外症状及相关的辅助检查包括FFA、ICGA 及HLA分型等有助于VKH综合征的诊断。

As the body response for the trauma, the adipose tissues as blood serum behavior in the wounded tissue were suffered mobilization. At the same time, the ectogenesis fat tissue entranced blood circulation. As the result of hemodynamics alteration, there were blood platelet and erythrocyte and leucocytes and lipid granules collecting on the surface of these lipid droplets. The volumes of these lipid droplets were enlargement. These lipid droplets were changed to fat embolus by the promotion of coagulation and fibrin deposition intra-blood vessel.

现代医学理论认为，外伤后组织存留的血清状态的脂肪组织受到动员，同时，损伤部位的血管外源性脂肪进入血循环，而创伤引起的机体反应使血液动力学发生改变，血小板、红细胞、白细胞及血脂乳化不稳定所析出的脂质颗粒等，均可聚集于以上脂滴的表面，使之体积增大，加之组织凝血活化酶的释放，促使血管内凝血，纤维蛋白沉积的发生，从而形成脂肪栓子，导致脂肪栓塞。

Parthenolide is extract from feverfew, it's main component is sesquiterpene, it is commanly used in west country and is mainly used to therapy skin infection, rheumatic disorder, migraine. But recent research indicate that parthenolide can regulate many pathway of signal in the cell, inhibit the cyclooxygenase, TNF-α, interleukin-1 expression induced by lipopolysaccharide in macrophage, inhibit the iNOS expression in human monocyt, inhibit the activity of NF-κB in Hela cell, inhibit the growth of tumor cell and can relieve the myocardial ischemical reperfusion injury and so on. But the invention research about the effection of parthenolide on the VSMC is very rare in the world, so we do some research about the effection of inhibition of parthenpolide on the proliferation of VSMC and the signal transduction mechanism.

小白菊内酯(parthenolide，又名Sesquiterpene lactone)是艾叶菊属黑叶母菊的提取物，主要成分是倍半萜烯内酯，西方国家较为常用，主要用于治疗皮肤感染、风湿病和偏头痛，但近年来发现小白菊内酯能调控细胞内多种信号途径，如抑制巨噬细胞中脂多糖诱导的Cox，肿瘤坏死因子α和白细胞介素-1的表达，能抑制人单核细胞中iNOS的表达，能抑制Hela细胞中NF-κB的活性，抑制肿瘤细胞的生长，同时能减轻心肌缺血再灌注损伤等，但小白菊内酯在VSMC中的干预研究目前国内外非常罕见，为了确切评价小白菊内酯对血管平滑肌细胞增殖的抑制作用及相关的信号转导机制，我们进行了一些研究。

So it is assumed that the E-box might be associated with the enhancement of transcription activity.Here, the LTRs of WH17 ,DLA-25,DLA-118 and LTR with single mutation in the E-box motif were separately cloned into pCAT-Basic vector resulting in a series of recombinant plasmids containing CAT reporter under the control of different versions of LTRs.

通过对EIAV分离株WH17的LTR与L株、DA和DLA株的LTR序列进行比较，发现其在在U3-R结合处多一个E-box基序，推测该基序的变化可能会起到促进转录作用，为此将EIAV强毒株(DLA-25)、驴白细胞弱毒株(DLA-118)、EIAV分离株WH17以及U3-R结合处的E-box基序点突变的LTR分别克隆到pCAT3-basic质粒中的报告基因氯霉素乙酰转移酶的上游，获得一系列受不同LTR控制的CAT表达质粒。

Aside from pancreatic enzymes activiation and autodigestive process, recent investigations have established that the upregulation of inflammatory mediator are believed to be the critical steps in the progression of mild pancreatitis to severe pancreatitis. Tumor necrosis factor-, ThyomboxaneA2 ,ProstaglandinsI2 are all important inflammatory mediator. TNF-( is one of cytokines. It is important to the over-production of ICAM-1,VCAM-1, TXA2 andPGI2. The ICAM-1 and VCAM-1 mediate both leukocytes adhesion and migration through the endothelium into tissues to connect with injuried target cells. The TXA2 and PGI2 are the production of arachidonic acid. They are responsible for the tissue ischaemia.

肿瘤坏死因子（Tumor necrosis factor-， TNF-、血栓素A2（ThyomboxaneA2，TXA2），前列环素（ProstaglandinsI2，PGI2）均是炎症反应中重要的炎性介质，其中肿瘤坏死因子-是非常重要的细胞因子之一，它由活化的单核细胞产生，在细胞间黏附分子（Intercellular adhesion molecule-1，ICAM-1）及血管细胞黏附分子(Vascular cell adhesion molecule-1，VCAM-1的表达、血栓素A2及前列环素过量生成方面起着重要的作用，前两者是介导白细胞与内皮细胞黏附，迁移于组织并与受损的靶细胞相结合的主要媒介，是炎症反应中的重要介质，后两者是花生四烯酸的代谢产物，亦是重要的炎性介质，参与构成血液循环障碍。

Leucocytic differentiation antigen 40 sign-al access participates in regulation of inflammatory reaction accommodation of major cell component (vascular endothelial cell、vascular smooth muscle cell and macrophage), it is playing critical role in AS process, participates ather-osclerotic occurrence and development ,reside in atherosclerotic plaque cell thro-ugh CD40-CD40L interaction, induce activate by itself , express and secrete profit to happen immune response、inflammatory reaction、hemagglutination t-hrombogenic proteo-cytokine.

白细胞分化抗原40 (CD40)信号通路参与了动脉粥样硬化斑块内主要细胞成分(血管内皮细胞、血管平滑肌细胞以及巨噬细胞)炎症反应的调节，其在AS进程中扮演着关键性的角色，参与了动脉粥样硬化的发生和发展；存在于AS斑块内的细胞通过CD40-CD40L相互作用，导致自身活化，表达和分泌了有利于免疫应答发生、炎症反应、血凝和血栓形成的蛋白质细胞因子，如激活在AS斑块中的关键性细胞成分如黏附分子、炎症因子、基质金属蛋白酶等的产生，导致斑块的不稳定和破裂，而最终导致粥样硬化斑块病变的恶化。

Topotecan is an effective agent for SCLC when used as monotherapy or in combined treatment, but myelosuppression such as leucopenia and thrombopenia was relatively severe. Although it has been recommended as a second-line agent for recurrence of sensitive SCLC, more clinical trials are needed to define its role in first-line treatment.

拓扑替康治疗小细胞肺癌有确切临床疗效，无论是单药还是与其他药物的联合用药均具有与当前一线经典方案相当的疗效，但具有相对高的致白细胞和血小板下降的骨髓毒性，已被认为是治疗化疗敏感的小细胞肺癌患者复发的二线推荐药物，但是作为一线用药仍然需要更多的实践来证实。

Meta-analyses showed that the response rate of TP (topotecan + cisplatin) regimen had no significant difference compared with EP regimen (etoposide + cisplatin) with OR 0.83 and 95%CI 0.63 to 1.09, but myelo-suppression such as leucopenia and thrombopenia was more severe with TP regimen; the response rate of monotherapy with topotecan was similar with that of CE (carboplatin + etoposide) regimen with OR 0.59 and 95%CI 0.22 to 1.60; the response rate of TEP (topotecan + etoposide + cisplatin) regimen was comparable with that of EP regimen with OR 1.37 and 95%CI 0.82 to –2.28, but myelosuppression and anemia were more severe with TEP regimen; the response rate with OR 0.97 and 95％CI 0.60 to –1.57, median time to progression with WMD –2.32 and 95％CI –5.72 to 1.09 and median survival time with WMD –1.65 and 95％CI –7.13 to 3.83 of IV topotecan were similar to those of oral topotecan, while neutropenia was more severe with IV topotecan.

Meta分析结果表明，TP 方案与EP方案的反应率相似 [OR 0.83， 95%CI (0.63，1.09)]，但具有相对高的致血小板下降的骨髓毒性；单药拓朴替康与CE方案的反应率相似 [OR 0.59， 95%CI (0.22，1.60)]；TEP方案（拓扑替康＋足叶乙甙＋顺铂）与EP方案的反应率相似 [OR 1.37， 95%CI (0.82，2.28)]，TEP方案致化疗后重度白细胞下降、重度血小板下降、重度血红蛋白下降均高于EP方案；口服拓扑替康与静脉滴注拓扑替康的化疗后反应率 [OR 0.97， 95％CI (0.60，1.57)]、中位疾病进展期 [WMD –2.32， 95％CI (–5.72， 1.09)]、中位生存期 [WMD –1.65， 95％CI (–7.13，3.83)] 相似，口服拓扑替康化疗后重度中性粒细胞下降明显低于静脉滴注拓扑替康。

For the first time, we found that the EHFV propagated in HUVEC has a potentiating stimulation to ET-1 and PGI〓 secretion , which may be respensible for the increased plasma ET -1 level and PGI〓 concentration in patients with EHF during the early phase of the disease.

我们的研究结果提示，HUVEC对EHFV敏感，EHFV感染未引起HUVEC的细胞病变，但可抑制HUVEC的增殖，这有可能改变EC的基因调节，或低调，如Ⅷ R：Ag合成障碍，引起止血功能异常；或高调，如主要组织相容性复合物Ⅱ型抗原、干扰素β和内皮细胞白细胞粘附因子的表达增加，增强EC的炎症反应。

However, the cytotox-ic dugs cant selectively kill the cancer cells without any side -effects, the decrease of peripheral blood WBC for myleosuppression caused by cytotoxic dugs contribute to the limitation of regular chemotherapy. Evidence was provided that cisplatin and cyclophosphamide used for ovarian cancer caused apoptosis in several in vivo tumors. For the reasons above, in our study, we detected the apoptosis of total peripheral blood WBC in patients with ovarian cancers before and after chemotherapy.

然而，由于化疗药物的非选择性组织杀伤引起的骨髓抑制而导致的末梢血白细胞减少，已经成为限制化疗剂量和按期进行规范性化疗的重要障碍，研究已证实卵巢癌的常规化疗方案中的顺铂及环磷酰胺能在多种肿瘤组织中诱导凋亡。

This one mode pays close attention to network credence foundation of the businessman very much.

这一模式非常关注商人的网络信用基础。

Cell morphology of bacterial ghost of Pasteurella multocida was observed by scanning electron microscopy and inactivation ratio was estimated by CFU analysi.

扫描电镜观察多杀性巴氏杆菌细菌幽灵和菌落形成单位评价遗传灭活率。