慢性荨麻疹患者外周血IL-17和IL-23的表达及临床意义

目的分析慢性荨麻疹患者外周血IL-17,IL-23的表达及临床意义。方法分析2009年1月～2013年1月在荆门市康复医院接受治疗的慢性荨麻疹患者的临床资料,并列为观察组。另纳入同期健康体检者作为对照组。结果该研究共纳入研究对象91例,其中观察组患者61例,对照组30例。观察组患者外周血IL-17及IL-23水平显著高于对照组,相比较差异具有统计学意义(P＜0.001)。Pearson相关性检验显示:观察组患者外周血IL-23与IL-17水平呈现显著正相关,差异具有统计学意义(r=0.504,P＜0.001)。经4周治疗后,观察组患者外周血IL-17水平显著降低,与治疗前比较差异具有统计学意义(65.31±18.75pg/ml vs 121.53±31.19 pg/ml,t=10.710,P＜0.001)。以治疗后IL-17水平的中位数(66.79 pg/ml)为界,将患者分为A(IL-17＜66.79 pg/ml),B(IL-17≥66.79 pg/ml)两组。Kaplan-Meier分析显示:治疗后1年,A组患者累积复发率显著低于B组,相比较差异具有统计学意义［13.79%,(4/29) vs 37.93%,(11/29)Log-rank χ2=4.344,P=0.037］。结论慢性荨麻疹患者外周血IL-17,IL-23表达升高,且可以一定程度判断预后。     

葛根素对炎症反应综合征大鼠的治疗作用

目的 建立全身炎症反应综合征(SIRS)大鼠模型,探讨葛根素治疗实验性SIRS的效果及其机制.方法 采用腹腔注射酵母多糖-石蜡悬液(ZPS)制备SD大鼠SIRS模型.通过SIRS大鼠静脉注射葛根素后动物死亡率变化,了解葛根素治疗实验性SIRS的效果.采用ELISA定量检测试剂盒了解葛根素对SIRS大鼠外周血中TNF-α、IL-6和IL-10水平的调控作用.采用单因素方差分析和χ2检验对实验数据进行统计学分析.结果 750 mg/kg和1000 mg/kg酵母多糖ZPS均可诱导大鼠发生SIRS.腹腔注射1000 mg/kg酵母多糖ZPS的大鼠死亡率为75.0%,静脉注射62.5 mg/kg葛根素后死亡率可降至16.7%(P＜0.01).大鼠腹腔注射750 mg/kg酵母多糖ZPS后24 h,外周血中TNF-α、IL-6和IL-10浓度分别为(30.87±6.81)pg/ml、(525.20±92.45)pg/ml和(1.37±0.17)ng/ml,静脉注射62.5 mg/kg葛根素后TNF-α、IL-6和IL-10浓度分别为(16.71±3.75)pg/ml、(399.30±77.87)pg/ml和(1.95±0.17)ng/ml.结论 本研究建立了稳定的SIRS大鼠模型.葛根素对实验性SIRS有良好疗效,下调促炎因子TNF-α和IL-6水平,上调抗炎因子IL-10水平可能是葛根素抗SIRS的作用机制之一.     

肝硬化合并肝源性糖尿病患者血清细胞因子水平分析

目的探讨伴乙型肝炎肝硬化的2型糖尿病血糖控制水平对血清细胞因子水平影响。方法 2010年12月至2011年12月我院肝病及内分泌科门诊或住院患者所收集病例中,合并肝硬化的肝源性糖尿病及单纯肝硬化患者各60例,检测血清IL-2、IL-4、IL-6、IL-8、IL-10、INF-γ、TNF-α水平。结果肝源性糖尿病组患者血清IL-2、TNF-α、INF-γ水平为(57.2±23.8)pg/ml、(48.2±35.1)ng/ml、(89.2±55.3)pg/ml,显著高于单纯肝硬化组的(48.5±22.1)pg/ml、(30.2±23.3)ng/ml、(58.3±37.4)pg/ml(P均<0.05);肝源性糖尿病组的IL-4、IL-8水平分别为(1.2±0.5)pg/ml、(34.4±16.7)pg/ml,显著低于单纯肝硬化组的(3.3±1.2)pg/ml、(57.1±20.8)pg/ml(P均<0.05);两组的血清IL-10、IL-6水平差异无统计学意义[(1.3±0.4)pg/mlvs.(1.5±0.5)pg/ml,(5.2±3.4)pg/mlvs.(5.5±2.8)pg/ml,P>0.05]。结论肝硬化合并肝源性糖尿病患者的细胞因子网络失衡,是肝硬化疾病进展的可能机制。     

过敏性紫癜患儿Th17细胞表达及意义

目的 探讨Th17细胞在儿童过敏性紫癜(henoch-schonlein purpura,HSP)免疫发病机制中的作用.方法 过敏性紫癜急性期患儿55例,采用流式细胞分析法检测外周血Th17细胞的比例,ELISA法检测血浆相关细胞因子IL-17和IL-6的水平,并进行相关性分析.同期选取20例同龄健康儿童作为对照.结果 HSP患儿外周血Th17/CD4+T细胞比例显著高于对照组[(1.91±0.78)% vs(0.52±0.24)%,(P＜0.01)];HSP患儿血浆IL-17和IL-6的水平亦明显高于对照组[IL-17:(47.4±17.6)pg/ml vs (15.6±11.2) pg/ml;IL-6:(273.8±42.4)pg/ml vs(228.7±37.4)pg/ml,(P＜0.01)].患儿血浆IL-17和IL-6的水平呈正相关(r=0.762,P＜0.01).结论 过敏性紫癜急性期患儿Th17细胞比例增加,IL-17和IL-6水平升高,提示Th17细胞可能参与了HSP的发病及其炎性反应过程.     

氧化苦参碱干预急性出血坏死性胰腺炎大鼠TNF-α mRNA和IL-1β mRNA的表达

目的 探讨氧化苦参碱(oxymatrine,OM)干预实验性急性出血坏死性胰腺炎(acute hemorrhagic necrotizing pan-creatitis,AHNP)大鼠TNF-α mRNA和IL-1βmRNA的表达.方法 以5 g/dl牛磺胆酸钠胰胆管逆行注射建立Sprague-Dewley(SD)大鼠AHNP,将SD大鼠随机分为SO组、AHNP-NS组及AHNP-OM组.检洲血清TNF-α和IL-1β含量及胰腺组织中TNF-α tuRNA和IL-1β mRNA的表达.结果 AHNP-NS组和AHNP-OM组血清TNF-α水平3 h与6 h分别为286.5±50.3pg/ml和150.3±40.7 pg/ml及500.5±45.3 pg/ml和240.5±60.3 pg/ml(P<0.05);AHNP-NS组和AHNP-OM组3 h与6 h血浆IL-1β分别为:293.8±46/3 pg/ml,388.0±44.5 pg/ml和150.2±47.5 pg/ml,182.7±30.6pg/ml(P<0.05);AHNP-OM组造模3 h与6h胰腺组织TNF-α mRNA和IL-1β mRNA的表达较AHNP-NS组显著减弱(P<0.05).结论 OM预处理能够显著减少牛磺胆酸钠SD大鼠AHNP模型炎症细胞因子IL-1β和TNF-α,从而改善胰腺炎痛变的严重程度.     

活化巨噬细胞体外分泌的源炎性细胞因子研究

目的　探讨活化巨噬细胞培养调理液内的炎性细胞因子水平及其在诱发炎性 PVR模型中的作用。方法　收集兔活化巨噬细胞培养上清调理液 ,采用双抗体夹心法 EL ISA检测试剂盒 ,检测其 TNF-α、IL - 8、IL - 6的含量 ,并进行多元回归拟合曲线分析。结果　巨噬细胞体外培养上清液中 IL - 8、TNF-α及 IL - 6的含量分别于培养后的 8、2 0、48h明显增加 (分别为 12 2 pg/ml± 31pg/ml、12 5 pg/ml± 2 2 pg/m l和 2 6 pg/ml± 4pg/ml,P<0 .0 1) ,前两种细胞因子于2 0、72 h达高峰 (分别为 192 pg/ml± 38pg/m l,15 4pg/m l± 16 pg/ml,P<0 .0 1)。IL- 6至 96 h仍呈上升状态 (2 8pg/ml±4pg/ml)。结论　注入活化巨噬细胞或其细胞培养调理液中炎源细胞因子在其启动、调控 PVR的发展中起重要作用     

Gas6在免疫性血小板减少症患者中表达增高及临床意义

目的探究Gas6在免疫性血小板减少症(ITP)患者中的表达情况及其临床意义。方法以2013年10月~2015年12月于上海长海医院血液科确诊的35例ITP患者外周血作为实验组,以同期体检的35例健康个体外周血作为对照组,两组样本分离血浆后以酶联免疫吸附法(ELISA)检测Gas6,IFN-α,IL-4,IFN-γ和IL-17蛋白表达水平,组间比较采用两独立样本t检验,对Gas6与IFN-α等细胞因子的关系进行Pearson相关性分析。结果 Gas6在实验组与对照组的表达水平为27.28±7.56ng/ml vs 20.51±5.39ng/ml(t=4.314,P0.0001);IFN-γ在实验组与对照组的表达水平为221.67±57.64 pg/ml vs 45.32±16.79 pg/ml(t=17.38,P0.0001);IL-4在实验组与对照组的表达水平为113.86±26.48 pg/ml vs 49.87±14.98 pg/ml(t=12.44,P0.0001);IL-17在实验组与对照组的表达水平为168.96±47.88 pg/ml vs109.56±28.97 pg/ml(t=6.28,P0.0001);IFN-α在实验组与对照组的表达水平为34.83±8.12 pg/ml vs 29.89±5.76pg/ml(t=2.936,P=0.0045),差异均具有统计学意义(P0.05)。Pearson相关性分析显示Gas6与IL-17,IL-4,IFN-γ呈正相关(r=0.564,0.486,0.449,P均0.05),差异具有统计学意义,与IFN-α不具有相关性。结论 Gas6可能通过影响Th细胞亚群细胞因子的分泌参与了ITP致病过程,是临床上治疗和预测该病的潜在靶位点。     

慢性乙型肝炎患者外周血Th17细胞和IL-17检测及其临床意义

目的观察慢性乙型肝炎(CHB)患者外周血Th17细胞表达频率和白细胞介素(IL)17浓度并探讨其临床意义。方法细胞内因子染色法结合流式细胞术检测20例CHB患者、6例慢加急性肝衰竭(ACLF)患者和19例健康对照(HC)组外周血Th17细胞表达频率,酶联免疫吸附法检测血浆IL-17浓度,分析Th17细胞表达频率和IL-17浓度与HBV DNA载量以及谷丙转氨酶(ALT)、凝血酶原活动度(PTA)、总胆红素(TB)水平之间的相关性。结果 CHB和ACLF患者Th17细胞表达频率为(3.34±1.79)%和(3.89±1.67)%,均高于健康对照组(2.01±0.78)%,CHB患者Th17细胞表达频率与ALT呈正相关(r=0.6188,P=0.0062)。CHB和ACLF患者血浆IL-17浓度[(168.8±53.86)pg/ml和(185.5±63.66)pg/ml]均低于健康对照[(260.8±100.30)pg/ml],CHB患者IL-17浓度与PTA负相关(r=-0.5803,P=0.0073),ACLF患者IL-17浓度与HBV DNA水平负相关(r=-0.8605,P=0.0278)。结论 CHB患...     

重型肝炎患者外周血3项水平变化及临床意义

目的通过检测重型肝炎患者外周血单核细胞Toll样受体(TLRs)和血清肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL-10)的水平变化,探讨其临床意义。方法采用荧光定量聚合酶链反应(PCR)检测慢性乙型肝炎组20例、重型肝炎早期组17例、重型肝炎中晚期组9例患者及健康对照组18例外周血单个核细胞TLRs mRNA的表达;采用酶联免疫吸附试验检测血浆TNF-α、IL-10水平。结果 TLRs mRNA慢性乙型肝炎组、重型肝炎早期组、重型肝炎中晚期组TLRs mRNA均高于健康对照组,差异有统计学意义(P<0.05),重型肝炎中晚期组低于早期组。血清TNF-α及IL-10水平随病情加重逐渐升高,IL-10在慢性乙型肝炎组与重型肝炎早期组比较,差异无统计学意义(P>0.05)。结论 IL-10持续上升可能导致单核细胞免疫缺陷,与不良预后有关。     

动脉粥样硬化性缺血性脑血管病患者外周血 TNF-α，IL-6，IL-8 和 WBC 水平与慢性失眠症 PSQI 的相关性研究

目的　分析动脉粥样硬化性缺血性脑血管病患者外周血肿瘤坏死因子 α（TNF-α）、白介素 -6（IL-6）、白介素 -8（IL-8）和白细胞（WBC）水平与慢性失眠症匹兹堡睡眠质量批数（PSQI）的相关性。方法　将 103 例动脉粥样硬化性缺血性脑血管病患者 (2019 年 1~12 月收治 ) 分为不伴失眠症组 (PSQI 评分≤ 10 分,共 66 例 ) 和伴失眠症组(PSQI 评分 >10 分,共 37 例 )。不伴失眠症组和伴失眠症组均未经治疗行外周血 TNF-α,IL-6,IL-8 和 WBC 检测,分析两组的外周血 TNF-α,IL-6,IL-8,WBC 和 PSQI 评分差异,采用 Pearson 秩相关法分析外周血 TNF-α,IL-6,IL-8和 WBC 与 PSQI 评分之间的相关性。结果　伴失眠症组的 TNF-α(26.49±4.82 nmol/L),IL-6(16.92±3.44 pg/ml),IL-8(21.45±3.87 pg/ml) 和 PSQI(16.74±2.25 分 ) 高于不伴失眠症组 (22.19±4.64 nmol/L,13.62±3.03 pg/ml,17.91±3.14pg/ml 和 6.91±1.93 分 ),伴失眠症组的 WBC[(6.41±1.28)×10 9 /L] 低于不伴失眠症组 [(8.76±1.46)×10 9 /L],经 t 检验分析差异均具有统计学意义 (t=4.450~9.098,均 P<0.05)。外周血 TNF-α,IL-6 和 IL-8 水平均与 PSQI 呈正相关,经Pearson 秩相关法分析 (r =0.874 3~ 0.933 9,P <0.05);外周血 WBC 水平与 PSQI 呈负相关,经 Pearson 秩相关法分析 (r= - 0.843 0,P=0.000)。结论　动脉粥样硬化性缺血性脑血管病并发慢性失眠症患者具有明显的炎症反应和白细胞浸润,且炎症反应、白细胞浸润的程度越高,并发慢性失眠症的程度越严重。     

Migraine and genetic and acquired vasculopathies

It is remarkable that migraine is a prominent part of the phenotype of several genetic vasculopathies, including cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL), retinal vasculopathy with cerebral leukodystrophy (RVCL) and hereditary infantile hemiparessis, retinal arteriolar tortuosity and leukoencephalopahty (HIHRATL). The mechanisms by which these genetic vasculopathies give rise to migraine are still unclear. Common genetic susceptibility, increased susceptibility to cortical spreading depression (CSD) and vascular endothelial dysfunction are among the possible explanations. The relation between migraine and acquired vasculopathies such as ischaemic stroke and coronary heart disease has long been established, further supporting a role of the (cerebral) blood vessels in migraine. This review focuses on genetic and acquired vasculopathies associated with migraine. We speculate how genetic and acquired vascular mechanisms might be involved in migraine.     

Fibrinogen and fibrin structure and functions

Fibrinogen molecules are comprised of two sets of disulfide-bridged Aalpha-, Bbeta-, and gamma-chains. Each molecule contains two outer D domains connected to a central E domain by a coiled-coil segment. Fibrin is formed after thrombin cleavage of fibrinopeptide A (FPA) from fibrinogen Aalpha-chains, thus initiating fibrin polymerization. Double-stranded fibrils form through end-to-middle domain (D:E) associations, and concomitant lateral fibril associations and branching create a clot network. Fibrin assembly facilitates intermolecular antiparallel C-terminal alignment of gamma-chain pairs, which are then covalently 'cross-linked' by factor XIII ('plasma protransglutaminase') or XIIIa to form 'gamma-dimers'. In addition to its primary role of providing scaffolding for the intravascular thrombus and also accounting for important clot viscoelastic properties, fibrin(ogen) participates in other biologic functions involving unique binding sites, some of which become exposed as a consequence of fibrin formation. This review provides details about fibrinogen and fibrin structure, and correlates this information with biological functions that include: (i) suppression of plasma factor XIII-mediated cross-linking activity in blood by binding the factor XIII A2B2 complex. (ii) Non-substrate thrombin binding to fibrin, termed antithrombin I (AT-I), which down-regulates thrombin generation in clotting blood. (iii) Tissue-type plasminogen activator (tPA)-stimulated plasminogen activation by fibrin that results from formation of a ternary tPA-plasminogen-fibrin complex. Binding of inhibitors such as alpha2-antiplasmin, plasminogen activator inhibitor-2, lipoprotein(a), or histidine-rich glycoprotein, impairs plasminogen activation. (iv) Enhanced interactions with the extracellular matrix by binding of fibronectin to fibrin(ogen). (v) Molecular and cellular interactions of fibrin beta15-42. This sequence binds to heparin and mediates platelet and endothelial cell spreading, fibroblast proliferation, and capillary tube formation. Interactions between beta15-42 and vascular endothelial (VE)-cadherin, an endothelial cell receptor, also promote capillary tube formation and angiogenesis. These activities are enhanced by binding of growth factors like fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), and cytokines like interleukin (IL)-1. (vi) Fibrinogen binding to the platelet alpha(IIb)beta3 receptor, which is important for incorporating platelets into a developing thrombus. (vii) Leukocyte binding to fibrin(ogen) via integrin alpha(M)beta2 (Mac-1), which is a high affinity receptor on stimulated monocytes and neutrophils.     

Telemedicine and teleradiology technologies and applications

Summary. Telemedicine and teleradiology hold the key for improving future health care delivery. In this paper we first review current communication and computer technologies used in telemedicine and teleradiology. Five examples in teleradiology applications are given including hospital-integrated picture archiving and communication systems, tele-neuro-imaging, telemammography, university consortium teleradiology service, and teleradiology for second opinion. Parameters important to teleradiology applications like costs, image quality, system reliability, and turn around time are considered. Data security is discussed, including patient confidentiality and image authenticity-which will be a major issue in future teleradiology applications.     

创伤高血糖与感染和MODS早期诊断和干预

本文详细介绍了创伤后血糖应激适度理论,以及高血糖与感染和多器官功能不全综合征的关系;提出涉及胰岛B细胞功能不全的MODS实验诊断新方案和极化液个体化干预新措施,可早期发现创伤MODS、降低感染率及MODS发生率和病死率。     

腹膜后纤维化与肾积水发生关系的临床研究

目的：探讨腹膜后纤维化（RPF）导致肾积水的原因及诊治经验。方法：回顾分析2004年1月—2010年12月24例腹膜后纤维化致肾积水患者的诊治资料。结果：（1）RPF患者常见首发症状为腰背痛或腹痛（69.2%）;（2）红细胞沉降率（ESR）增快和血清IgG4升高最常见。超声检查仅提示上尿路积水。RPF的静脉肾盂造影（IVP）和CT尿路成像（CTU）表现具有特征性。IVP肾盂输尿管显影不良时,CTU能较清晰的显示上尿路影像。CT扫描发现腹膜后软组织肿块9例（37.5%）,优于超声检查;（3）输尿管松解和腹腔化手术治疗22例;行肾切除术1例;行输尿管置双J管术1例。最终确诊为继发性RPF8例,其中4例为术前诊断,3例为术中腹膜后软组织肿块冷冻活检证实,1例为术后病理证实;（4）特发性RPF手术后肾积水均获长期缓解,而继发性RPF的预后取决于原发疾病及其治疗方案。结论：影像学检查是诊断RPF的重要手段,CTU优于超声检查和IVP。输尿管松解和腹腔化手术可以使特发性RPF输尿管梗阻得到长期的缓解,术中对肿块进行冷冻活检有助于鉴别特发性和继发性RPF,及时调整治疗方案。     

探讨儿童慢性顽固性咳嗽与支原体感染的关系及临床治疗观察

目的探讨儿童慢性顽固性咳嗽与肺炎支原体（MP）感染的关系及临床疗效观察。方法采用回顾性研究方法对于现将2005年3月至2008年3月在我院的55例确诊慢性顽固性咳嗽患儿,主要表现为肺炎支原体感染为临床特点进行分析,并进一步临床治疗研究。结果①临床特点：在55例确诊慢性咳嗽的患儿中,以慢性顽固性咳嗽为主要症状。58％（32／55）的病例无肺部体征;②外周血：85％（47／55）的病例外周血变化不大,WBC（4—10）×10 9／L之间,嗜酸性粒细胞增多;③特别检查：47．27％（26／55）肺炎支原体IgM（MP—IgM）抗体阳性,83．64％（46／55）PeR技术检测肺炎支原体特异性DNA;④X光报告为多种形式。结论肺炎支原体（MP）感染是引起儿童慢性顽固性咳嗽的病因之一,对儿童慢性咳嗽,特别是顽固性咳嗽的诊治中应更加重视。     

Acetaminophen and acetylcysteine dose and duration: Past,present and future

Abstract

Acetylcysteine has been utilized successfully in the treatment of acetaminophen overdose since the 1970s. Although prospective trials as to efficacy and safety of acetylcysteine were conducted, there were no randomized controlled trials. This commentary addresses the reasons for this, and the background to choice of dose of acetylcysteine utilized in the oral and IV dosing regimens. Nomograms to predict possible hepatotoxicity based upon time of ingestion of acetaminophen were developed from a relatively arbitrary definition of toxicity as an aspartate aminotransferase/alanine aminotransferase (ALT/AST) greater than 1000 IU/L. While these have proved generally useful, patients still continue to develop hepatic damage after acetaminophen overdose, particularly if they present late after ingestion. The optimum management of these patients remains unclear, and one area of uncertainty is the dose and duration of acetylcysteine in various circumstances. This article discusses the issues that need to be elucidated to better target changes in acetylcysteine dose. The potential for measurements of other markers to improve treatment selection is the subject of further research.     

VEGF和NSE在良恶性嗜铬细胞瘤中的表达及意义

目的探讨肿瘤标志物血管内皮生长因子（VEGF）和神经元特异性烯醇化酶（NSE）在良、恶性嗜铬细胞瘤组织中的表达,分析其可能的临床价值及病理学意义,为临床鉴别良、恶性嗜铬细胞瘤提供辅助依据。方法应用免疫组化（SP法）检测16例恶性嗜铬细胞瘤、18例良性嗜铬细胞瘤及17例正常肾上腺髓质组织中细胞因子VEGF和NSE表达情况,显微镜下判断组织切片的染色结果。结果①恶性嗜铬细胞瘤VEGF表达明显强于正常肾上腺髓质和良性嗜铬细胞瘤（P〈0.01）。良性肿瘤和正常肾上腺髓质的VEGF表达差异无统计学意义（P〉0.05）。恶性嗜铬细胞瘤强阳性率明显高于良性嗜铬细胞瘤（P〈0.01）。②良、恶性嗜铬细胞瘤NSE表达差异有统计学意义（P〈0.05）,良性嗜铬细胞瘤NSE的表达高于正常肾上腺髓质的NSE表达（P〈0.05）。恶性嗜铬细胞瘤强阳性率高于良性嗜铬细胞瘤（P〈0.05）。③VEGF和NSE共同阳性表达在良、恶性嗜铬细胞瘤之间差异有统计学意义（P=〈0.01）。结论临床上检测VEGF和NSE可能为鉴别良、恶性嗜铬细胞瘤提供辅助依据,共同检测VEGF和NSE可能提高良、恶性嗜铬细胞瘤鉴别的敏感性。