金黄色葡萄球菌原发血流感染血细胞反应与预后关系探讨

目的探讨原发性金黄色葡萄球菌血流感染血细胞反应,为更好地发挥血细胞抗感染作用提供证据。方法收集南昌大学第一附属医院2008年1月-2014年12月原发性金黄色葡萄球菌血流感染患者的个人及医疗处理信息和血细胞反应指标。采用χ~2检验及二元线性Logistic回归预测各种因素与预后关系。结果共发现189例原发性金黄色葡萄球菌感染病例,其中33例因血流感染死亡。多因素分析表明,患者年龄大于65岁、MRSA感染、机械通气、中性粒细胞降低、中性粒细胞升高、血小板降低是住院期间金黄色葡萄球菌血流感染死亡的独立危险因素,其中中性粒细胞升高与血流感染死亡呈负相关。结论原发性金黄色葡萄球菌血流感染患者如果出现血细胞降低等异常时应及时采取措施调整血细胞反应值,改善患者预后。

皮肌炎合并反应性噬血细胞综合征2例并文献复习

病例1,男,15岁,因周身多发红斑,四肢肌肉酸痛5个月,发热1周入院。5个月前出现双手近端指间关节、掌指关节、肘、膝关节肿痛,局部关节伸侧出现片状红斑,甲周红斑,双上眼睑红肿;四肢乏力,下蹲、翻身困难,肌肉轻度疼痛。检查：

原发性硬化性胆管炎继发反应性噬血细胞综合征一例报告

1 临床资料患儿,女,12岁,因全身瘙痒伴皮肤巩膜黄染1个月余于2000年6月入院.门诊B超及CT检查均提示"肝内胆管扩张,左外叶占位".入院体检发现肝肋下平脐,肝上界位于右锁骨中线第5肋间,脾肋下未及.腹腔MRI诊断:肝内外胆管多发结石,阻塞性黄疸,慢性胆管炎.入院后在全麻+连续硬膜外麻醉下行左半肝切除+胆囊切除+肝胆管整形+肝胆管空肠Roux-en-Y吻合术.

异基因造血干细胞移植后并发反应性噬血细胞性淋巴组织增生症2例并文献复习

目的:提高对血液肿瘤患者异基因造血干细胞移植(allo-HSCT)后反应性噬血细胞性淋巴组织增生症(HLH)的认识,探讨恰当的治疗方案。方法:报告2例血液肿瘤患者在allo-HSCT后出现反应性HLH的临床表现、实验室检查结果以及治疗和转归特点,结合文献进行分析讨论。结果:2例患者在allo-HSCT后出现发热、血细胞减少、高甘油三酯血症、骨髓中发现噬血细胞现象和高铁蛋白血症,其中例2伴有脾大。2例患者均获益于大剂量糖皮质激素的治疗。结论:反应性HLH是一种非感染性全身炎症反应,在除外感染的情况下应用糖皮质激素疗效佳,但应注意继发性感染的预防和处理。

反应性嗜血细胞综合征临床特征分析

目的:总结反应性嗜血细胞综合征(RHS)的临床特征、实验室资料、治疗及预后。方法:分析22例诊断为RHS病人的临床特点、实验室检查和治疗方案。同时以骨髓细胞学证实发生嗜血细胞与否分组,比较2组之间的异同情况。结果:主要临床特征为高热发生率95.5%,肝脾、淋巴结肿大发生率81.8%,血液系统受累、贫血发生率72.7%,血小板减少50.0%,RHS发生时WBC(19.5±8.1)×10~9/L,血红蛋白(95.2±14.4)g/L,白蛋白(26.1±4.4)g/L,三酰甘油(3.2±2.1)mmol/L,纤维蛋白原(1.5±0.7)g/L。经骨髓细胞学明确见到嗜血现象11例,嗜血组和非嗜血组病人实验室检查各项指标阳性率差异均无统计学意义(P>0.05)。50.0%(11/22)病人经治疗后缓解出院(其中1例失访),病死10例,其中成人Still病5例,淋巴瘤1例,皮肌炎1例,抗中性粒细胞胞质抗体相关性血管炎1例,系统性红斑狼疮1例,肠系膜脂膜炎1例。呼吸衰竭是主要死因。结论:风湿性疾病导致的RHS以成人still病多见,其他RHS最常见的为淋巴瘤,该病预后差,死亡发生率较高,呼吸衰竭为主要死因。抓住实验室相关指标的动态变化有助于RHS的早期识别。激素联合环磷酰胺可控制疾病的进程。

大肠杆菌在体外快速激活系统血液固有免疫反应中红细胞CD59、淋巴细胞CD4、CD8表达量的性质及意义

目的:探讨CD4、CD8以及CD59分子在系统血液快速固有免疫反应中的作用性质与意义。方法:采用大肠杆菌在体外快速激活全血细胞固有免疫反应的研究体系:实验组0.2mL灭活大肠杆菌(3×108/mL),加0.2mL全血细胞悬液加0.3mL新鲜血浆,对照组用生理盐水0.2mL取代大肠杆菌悬液,2管放37℃水浴1h后,用直接免疫荧光流式细胞仪法测定红细胞CD59,淋巴细胞CD4和CD8分子表达量变化。结果:全血实验组红细胞CD59,淋巴细胞CD4和CD8分子表达量明显高于全血对照组各测定值(P<0.05)。结论:红细胞CD59与淋巴细胞CD4和CD8分子共同参与了快速固有免疫反应,红细胞CD59,淋巴细胞CD4和CD8分子同属固有免疫分子,此免疫网络关系属于系统免疫学研究范畴,这一新的认识值得深入研究。

日本血吸虫毛蚴对钉螺的钻穿及在螺体内的分布和移行

采自安徽贵池的钉螺每粒感染 50只湖南株日本血吸虫毛蚴后的组织学观察说明 :毛蚴钻穿钉螺有从螺鳃部、头足部的表皮以及实质组织 (外套膜、触角和阴茎 )等三方面途径 ,其中以前二者尤为重要 ;毛蚴进入螺鳃丝后直接进入血液循环系统。从头足表皮进入的毛蚴 ,除了少数在钻穿部位附近滞留外 ,多数继续向头足部深层的肌肉和窦状组织间隙移行 ,以前头足窦、直肠和消化道外的组织间隙以及肾脏为主要的移行部位 ;从外套膜、触角、阴茎等部位进入的毛蚴不表现明显的组织间移行 ;至于毛蚴能否从消化道部位入侵 ,需进一步观察。螺宿主对吸虫幼虫期的血细胞反应主要是在毛蚴入侵早期以及子胞蚴逸离母胞蚴的早期 ,表明螺宿主血细胞反应可能具有对幼虫发育期的特异性。

Arsenic trioxide inhibites transgenic tumor necrosis factor-α promoter activity in vascular smooth muscle cells and THP-1 monocytes in vitro

Aim This study was to evaluate the effect of arsenic trioxide （As2O3） on the transgenic TNF-α promoter activity in cultured vascular smooth muscle cells （VSMCs） and THP-1 monocytes. Methods Human TNF-α promoter was constructed by reporter gene system and was transiently transfected into VSMCs and THP-1 in vitro. The promoter activity was tested by luciferase activity with or without LPS and Ang Ⅱ stimulation, before and after different dosage of As2O3 treatment. Results 1. TNF-α promoter effectively expressed in VSMCs and THP-1 compared with CMV promoter （58.3% and 80.9%, respectively）. Both LPS and Ang Ⅱ significantly up-regulated TNF-α promoter activity （P〈0.05）. 2. As2O3 significantly inhibited, both intact and LPS/Ang Ⅱ stimulated promoter activity, in a dose dependent manner （P〈0.05）, and in both cell type. Conclusion These results manifested that, the inhibition effect of As2O3 on the activity of human TNF-α promoter indicated its potential inhibition on pro-inflammatory cytokine genes expression at transcriptional level and its potential anti-inflammatory property in the cardiovascular system.

标本兼治红斑狼疮

红斑性狼疮（LE）是一种全身性、慢性进行性、反复发作和缓解的自身免疫性疾病,男女发病之比约为1:20,而女性中以16～30岁发病率最高。发病原因目前还不十分清楚,可能由于先天遗传因素加上病毒感染、日晒、药物、内分泌或其他因素,引起自身组织损伤及细胞突变,形成了自身抗原（DNA）。这种自身抗原和病人自己身体中的抗体（IgH）结合,沉积在皮肤、血管、内脏中,再有补体（C3）的参与,引起人体中的血细胞反应。根据自身免疫病变的程度和部位不同。

Immortalization of human umbilical vein endothelial cells with telomerase reverse transcriptase and simian virus 40 large T antigen

Objective: To establish normally conditionally-immortalized human umbilical vein endothelial cells (HUVECs) by ectopic expression of the human telomerase catalytic enzyme (hTERT) and simian virus 40 large T (SV40 LT) antigen. Methods:Primary HUVECs were transfected with recombinant retrovirus containing hTERT or SV40 LT respectively. Subsequently drug resistant cell clones were screened and expanded for further studies. Endothelial cell biomarkers were confirmed by examination.Results: The morphological phenotype of the transfected cells was similar to the non-transfected cells. Von Willebrand factor,hTERT and SV40 LT could be detected in transfected HUVECs. Moreover, higher telomerase activity in transfected cells was maintained for over 50 population doublings compared with only low level of endogenous telomerase transiently at early population doublings in primary HUVECs. When exposed to TNF-α (tumor necrosis factor-α), the expression of E-selectin in transfected cells was significantly up-regulated, but no alteration of endothelial lipase was found. Conclusion: Ectopic coexpression of hTERT and SV40 LT can effectively immortalize HUVECs without tumorigenicity in vitro. Immortalized HUVECs may be an ideal target of further molecular function studies.

人禽流感概述

2003年12月，H5N1型禽流感病毒在越南、日本和韩国爆发，到2004年2月，该病毒已在亚洲广泛蔓延并带来了巨大损失。H5N1是球型RNA病毒，禽类间可通过呼吸系统、眼分泌物和粪便传播，也可传染人类甚至导致死亡。H5N1感染者的特征是反应性噬血细胞综合征、细支气管炎症、支气管上皮坏死和机化、弥漫性肺泡病变和间质纤维化。血清白细胞介素-2受体、白细胞介素-6和γ干扰素亦可增高。发病机理可能是病毒在呼吸道的增殖触发了高细胞因子血症和反应性噬血细胞综合征。临床表现和普通流感相似，与重症疾病有关的危险因素包括年龄较大、住院过迟、肺炎、白细胞降低及淋巴细胞减少等。可用H1试验、ELISA试验和RT-PCR以及序列分析法检测病毒。治疗方法和普通流感相同，包括支持疗法和应用金刚烷胺。

The serum levels of MMP-9, sICAM-1, CRP and WBC increased in patients with acute coronary syndrome

Objective：To evaluate the association of the peripheral levels of the defined inflammatory markers with different types of acute coronary syndrome （ACS） and stable angina, and the role inflammation played in the pathogenesis of ACS. Methods ：For understanding the variation of serum concentrations of matrix metalloproteinase-9 （MMP-9）, soluble intercellular adhesion molecule-1 （sICAM-1） ,C-reactive protein （CRP）, and white blood cell count （WBC） and their association with ACS, 90 patients with coronary heart disease （CHD） and 30 healthy volunteers were recruited. The enrolled people were assigned into four equal groups, including acute myocardial infarction （AMI） group, unstable angina pectoris（UAP） group, stable angina pectoris（SAP） group and healthy control group. The serum levels of MMP-9 and sICAM-1 were measured with ELISA kits, CRP were measured with im munoturbidimetric assay, and WBC number were assessed all before any treatment was administrated. Results： （1）The serum levels of MMP-9 ,sICAM-1 ,CRP and WBC in the patients with ACS were significantly higher than those in the control group （P 〈 0.01 ）. （2）Compared with control group, patients with SAP only had higher serum level of sICAM-1 （P 〈 0.01 ）. While the levels of MMP-9, CRP, and WBC had no significant difference between them （P 〉 0.05 all）. （3）Significant positive correlation between the serum levels of MMP-9 and sICAM-1 and CRP and WBC all were observed in the patients with ACS （P 〈 0.05）. Conclusion： The elevation of serum concentrations of inflammatory markers including MMP-9, slCAM-1, CRP and WBC were associated with initiation and progression of ACS, and they may help predicting cardiovascular events.

Acute liver failure caused by drug-induced hypersensitivity syndrome associated with hyperferritinemia

Drug-induced hypersensitivity syndrome(DIHS) is a severe reaction usually characterized by fever,rash,and multiorgan failure,occurring 2-6 wk after drug introduction.It is an immune-mediated reaction involving macrophage and T-lymphocyte activation and cytokine release.A 54-year-old woman was diagnosed with rheumatic arthritis and initiated salazosulfapyridine by mouth.About 10 d later,she had a high fever,skin rash and liver dysfunction.She was admitted to hospital and diagnosed with a drug eruption.She was treated with oral prednisolone 30 mg/d;however,she developed high fever again and her blood tests showed acute liver failure and cytopenia associated with hyperferritinemia.She was diagnosed with acute liver failure and hemophagocytosis caused by DIHS.She was transferred to the Department of Medicine and Bioregulatory Science,Kyushu University,where she was treated with arterial steroid injection therapy.Following this treatment,her liver function improved and serum ferritin immediately decreased.We hypothesized that an immune-mediated reaction in DIHS may have generated over-activation of macrophages and T-lymphocytes,followed by a cytokine storm that affected various organs.The measurement of serum ferritin might be a useful marker of the severity of DIHS.

Comparing irinotecan/cisplatin with etoposide/cisplatin in patients with ED-SCLC: A meta-analysis of efficacy and toxicity

Objective： Irinotecan in combination with cisplatin for extensive-stage disease small-ceU lung cancer （ED-SCLC） patients has gained wide interest. Varying results for this treatment underpin the need for a synthesis of evidence. Methods： We conducted a literature-based meta-analysis to quantify the magnitude of the benefit comparing irinotecan in combination with cisplatin （IP） with etoposide in combination with cisplatin （EP） in ED-SCLC patients. The primary outcome was overall survival （OS） and progression-free survival （PFS）; secondary outcomes included overall response rate, 1- and 2-year survival rates, disease control rate and toxicity. Results： Four trials including 1,541 patients were identified in the analysis. No positive results （P〈0.05） were seen： OS （HR=0.85, CI95%=0.71-1.01; P=-0.08） with high heterogeneity （Chi2=7.76, dr=-3 [P=-0.05]; I2=61%）, PFS （HR=0.91, CI95%=0.74-1.28; P=-0.36） with high heterogeneity （Chi2=11.96, df=3 [P=-0.008]; I2=75%）, overall response rate（OR=1.16; CI95%=0.79-1.70; P=0.45）, disease control rate （OR=1.01; CI95%=0.74-1.38; P=0.95）, 1-year survival rate （OR = 1.30; CI95%=0.98-1.72; P=0.07） and 2-year survival rate （OR=1.97; CI95%=0.95-4.09; P=-0.07）. Fewer patients who received IP suffered severe hematologic toxicities （grade≥3）, such as neutropenia, thrombocytopenia and leucopenia. However, severe non-hematologic toxicities （grade≥3）, such as diarrhea, nausea, vomiting, fatigue, anorexia, and dehydration, were more common among patients who received IP. Conclusion： IP does not lengthen the overall survival or progression-free survival compared with EP in patients with ED-SCLC Fewer patients receiving IP had grade ≥ 3 hematological toxicities of nentropenia, leucopenia and thrombocytopenia, but more had grade≥3 diarrhea, nausea, vomiting, fatigue, anorexia and dehydration.

Suppression of angiotensin Ⅱ stimulated responses in aortic vascular smooth muscle cells of experimental cirrhotic rats

Functional responses to angiotensin Ⅱ (AT-Ⅱ) were determined in aortic vascular smooth muscle cells (VSMCs) from experimental cirrhotic rats. Our data showed that AT-Ⅱ-stimulated extracellular acidification rate (ECAR), which was measured by Cytosensor microphysiometry, was significantly reduced in the aortic VSMCs from the cirrhotic rats as compared to those from the control animals. The ability of AT-Ⅱ to promote formation of inositol phosphates, the second messenger produced by the activation of Gq-coupled receptors, was also considerably suppressed in the cirrhotic VSMCs. Furthermore, the maximal p42/44 MAPK phosphorylation stimulated by AT-Ⅱ was significantly reduced in the cirrhotic VSMCs in contrast to that in the normal VSMCs. Taken together, our data clearly demonstrated that the functional responses to AT-Ⅱ was severely suppressed in aortic VSMCs in cirrhosis, indicating the impairment of general Gq-coupled receptor signaling and subsequent biological function in the cirrhotic VSMCs.

Noradrenaline as a putative neurotransmitter mediating hypotension-induced Fos-like immunoreactivity inthe supraoptic nucleus of the rat

Hemorrhage or hypotension induces extensive Foslike immunoreactivity in the magnocellular neurosecretory cells in the supraoptic nucleus of the hypothalamus in rat, especially in the vasopressin neurons. The present study was to explore the neurotransmitter mediating this effect. Microinfusion of the alpha-adrenergic blocker into the supraoptic nucleus reduced the hypotension-induced Fos, whereas beta-antagonist did not affect it significantly. Alpha1- and alpha2-antagonist, prazosin and yohimbine,both reduced the Fos-positive cell counts. However, the effective dosage of yohimbine was much larger. Alpha1-agonist, methoxamine, induced abundant Fos-like immnnoreactivity in the vasopressin cells in this nucleus,while beta-and alpha2-agonist did not elicit such effect.Administration of the noradrenergic re-uptake inhibitor,desipramine, to this nucleus to locally accumulate the spontaneously released noradrenaline from the nerve terminals also induced Fos expression, mostly in the vasopressin cells.

The Influence of IFN-α on Blood Plasmacytoid Dendritic Cell in Chronic Myeloid Leukaemia

OBJECTIVE To study the mechanism of IFN on CML.METHODS Samples of 15 CML patients and 10 healthy controlswere studied. The flow cytometry was performed to identifycirculating pDCs. The concentration of IFN-α in serum and that inthe supernatant of peripheral blood mononuclear cells (PBMCs)cultured after stimulation with CpG ODN2216 were examinedboth in CML patients and in the healthy controlsRESULTS There was significant reduction in the numberof circulating pDCs, serum concentration of IFN-α and thecapacity of IFN-α producing PBMCs in CML patients comparedwith those in healthy control individuals (P < 0.001). After theactive treatment with IFN-α and hydroxyurea, the quantity andfunction of pDCs were increased in stabilized patients, especiallythe function of pDCs in 2 patients achieving major cytogeneticresponse (MCR). The proportion and function of pDCs and theserum levels of IFN were inversely correlated with both WBC andage of the patients with CML, and positively correlated with thestate of the illness.CONCLUSION CML patients had a reduced number anddysfunction of circulating pDCs. The active treatment with IFN inCML patients may be related to the restoration of pDCs.