连续性血液净化对脓毒症患者促炎/抗炎免疫、内皮细胞功能及预后的影响

目的:探讨连续性血液净化(CBP)对脓毒症患者促炎/抗炎免疫、内皮细胞功能及预后的影响作用。方法:选取脓毒症患者90例,按患者自愿选择的治疗方式分为CBP组和对照组,每组各45例,2组均给予基础治疗,CBP组在此基础上加用CBP治疗72 h,比较2组患者促炎/抗炎免疫、内皮细胞功能及预后的情况。结果:治疗72 h后,CBP组患者的IL-10、Th1/Th2水平高于对照组(均P 0. 05),IL-1、TNF-α低于对照组(均P 0. 05); CBP组患者的活化蛋白C(APC)高于对照组(P 0. 05),可溶性细胞间粘附分子(s ICAM-1)、血管性假血友病因子(v WF)低于对照组(均P 0. 05); CBP组患者的平均动脉压(MAP)高于对照组(P 0. 05),血乳酸、急性生理与慢性健康状况评分(APACHEⅡ)、序贯器官衰竭评分(SOFA)、HR低于对照组(均P 0. 05)。结论:采用CBP治疗能显著降低脓毒症患者的炎症因子水平,调节免疫功能及内皮细胞功能。     

连续性血液净化对重症急性胰腺炎患者免疫内稳状态影响的临床对照研究

目的:观察连续性血液净化(CBP)治疗重症急性胰腺炎(SAP)患者的临床效果及其对免疫内稳状态的影响。方法:本文为前瞻性临床对照研究,12例男性SAP患者按随机原则分为Con组(常规治疗组,4例)和CBP治疗组(常规治疗 CBP治疗组,8例)。经72h治疗后对各组患者临床治疗效果进行比较(包括APACHE-Ⅱ评分及其它主要临床指标),同时在治疗0h、6h、12h、24h、48h和72h各时间点取血,动态观察SAP患者免疫内稳状态的变化,主要包括采用抗体芯片技术检测各组患者血浆细胞因子表达谱、Th1(促炎)/Th2(抗炎)细胞因子比例的变化,并观察治疗过程中单核细胞功能(HLA-DR表达)和单核细胞数目的变化。结果:(1)临床治疗效果比较:经72h治疗后,CBP组患者病情显著改善,血淀粉酶水平明显下降,肾功能恢复正常(P<0.05)。而Con组患者除血淀粉酶水平较治疗前有一定程度下降外,患者病情并无明显缓解,肾功能以及动脉血气等指标方面也无明显改善(P>0.05)。(2)免疫内稳状态指标的比较:除IL-4外,两组患者血浆中其它各种细胞因子水平均明显高于健康人群(P<0.05)。经72h治疗后,CBP组患者血IFN-γ,IL-1,IL-2和IL-5,IL-10,IL-13水平较治疗前明显降低(P<0.05);而血肿瘤坏死因子α(TNF-α)和IL-6水平虽较治疗前亦降低,但差异不具有统计学意义(P>0.05),IL-4水平则始终无明显变化。比值比提示经CBP治疗后SAP患者体内Th2类抗炎细胞因子IL-13、IL-10相对于Th1类促炎细胞因子IL-1、TNF-α水平下降显著。而且,经CBP治疗后,患者外周血单核细胞HLA-DR表达和单核细胞数目均较治疗前明显上升(P<0.05)。结论:CBP治疗除能快速有效改善SAP患者病情,纠正体内酸碱紊乱、清除体内代谢毒素外,还能清除体内过多生成的促炎和抗炎细胞因子,改善患者单核细胞抗原呈递能力,重建机体免疫系统内环境稳态,疗效明显优于传统疗法。经CBP治疗后SAP患者体内Th2类抗炎细胞因子IL-13、IL-10相对于Th1类促炎细胞因子IL-1、TNF-α水平下降显著,有利于改善患者体内的免疫抑制状态。     

溃疡性结肠炎患者血清促炎因子与抗炎因子的表达及其关系

目的 探讨溃疡性结肠炎（UC）患者血清促炎因子与抗炎因子的表达及其关系.方法 选择69例UC患者（UC组）,根据病情程度分为轻、中、重度,根据病理分级分为Ⅰ、Ⅱ、Ⅲ级;另选健康体检者60例作为对照组.采用ELISA法检测其血清TNF-α、IL-1β、IL-4和IL-13表达.结果 UC组血清TNF-α和IL-1β表达明显高于对照组,且随病情程度和病理分级升高而显著升高（P均＜0.05）;IL-4和IL-13表达明显低于对照组,且随病情程度和病理分级升高而显著降低（P均＜0.05）;UC组的血清TNF-α与IL-4、IL-13,以及IL-13与IL-4、IL-13均呈明显负相关（P均＜0.05）.结论 在UC发生、发展过程中,促炎因子与抗炎因子的动态平衡发生紊乱,促炎因子过度表达,且二者表达有密切关系.     

老年血管性痴呆患者外周血辅助性T细胞水平变化及临床意义

目的观察老年血管性痴呆患者外周血辅助性T（Th）细胞水平变化并探讨其临床意义。 方法选取徐州市第一人民医院老年医学科自2019年2月至2020年1月收治的96例老年血管性痴呆患者为疾病组,并于同时间段招募92名老年健康志愿者作为健康组,利用流式细胞术检测外周血Th1、Th2、Th17比例,利用酶联免疫吸附试验检测上述细胞因子（IL-2、TNF-α、IL-17、IL-4、IL-10）水平。对比2组患者外周血Th1、Th2、Th17比例及细胞因子水平,并分析比较疾病组不同认知功能障碍程度患者外周血Th1、Th2、Th17比例、细胞因子水平及治疗前后日常生活活动能力（ADL）评分。疾病组均予以常规治疗,随访6个月,统计预后情况,分析外周血Th1、Th2、Th17比例与预后不良的关系。 结果疾病组外周血Th1、Th17比例及细胞因子水平均高于健康组,且重度认知功能障碍患者均高于轻度认知功能障碍患者,差异均具有统计学意义（P<0.05）。疾病组外周血Th2比例及细胞因子水平低于健康组,且重度认知功能障碍患者低于轻度认知功能障碍患者,差异均具有统计学意义（P<0.05）。治疗前后疾病组重度认知功能障碍患者ADL评分低于轻度认知功能障碍患者,同组患者治疗后ADL评分较治疗前提高,差异均具有统计学意义（P<0.05）。疾病组外周血Th1、Th17比例及细胞因子IL-2、TNF-α、IL-17水平均与ADL评分呈负相关（P<0.05）,外周血Th2比例及细胞因子IL-4、IL-10水平均与ADL评分呈正相关（P<0.05）。疾病组预后不良发生率为29.17%,且高龄、重度认知功能障碍、抽烟、酗酒、外周血Th1和Th17比例是疾病组预后不良的危险因素（P<0.05）,外周血Th2比例、治疗依从是其保护因素（P<0.05）。 结论老年血管性痴呆患者外周血Th1、Th17比例及细胞因子水平偏高,而Th2比例及细胞因子水平偏低,且与认知功能障碍程度、预后均有关。     

促红细胞生成素联合参附注射液对慢性心力衰竭合并贫血患者血清炎性因子水平和心功能的影响

目的探讨促红细胞生成素联合参附注射液对慢性心力衰竭(CHF)合并贫血患者血清炎性因子水平和心功能的影响。方法选取2015年7月—2016年6月三门峡市中心医院收治的CHF合并贫血患者76例,随机分为对照组和观察组,每组38例。在常规治疗基础上,对照组患者给予促红细胞生成素,而观察组患者给予促红细胞生成素联合参附注射液;两组患者均连续治疗两周。比较两组患者治疗前后血清血红蛋白(Hb)、游离脂肪酸(FFA)、炎性因子[包括白介素6(IL-6)、肿瘤坏死因子α(TNF-α)]水平及心功能指标[包括左心室射血分数(LVEF)、左心室舒张末期内径(LVEDD)、左心室舒张末期容积(LVEDV)、左心室收缩末期容积(LVESV)]。结果治疗前两组患者血清Hb、FFA水平比较,差异无统计学意义(P>0.05);治疗后观察组患者血清Hb水平高于对照组,血清FFA水平低于对照组(P<0.05);治疗后两组患者血清Hb水平均高于治疗前,血清FFA水平均低于治疗前(P<0.05)。治疗前两组患者血清IL-6、TNF-α水平比较,差异无统计学意义(P>0.05);治疗后观察组患者血清IL-6、TNF-α水平低于对照组(P<0.05);治疗后两组患者血清IL-6、TNF-α水平均低于治疗前(P<0.05)。治疗前两组患者LVEF、LVEDD、LVEDV、LVESV比较,差异无统计学意义(P>0.05);治疗后观察组患者LVEF高于对照组,LVEDD、LVEDV、LVESV小于对照组(P<0.05);治疗后两组患者LVEF均高于治疗前,LVEDD、LVEDV、LVESV均小于治疗前(P<0.05)。结论促红细胞生成素联合参附注射液可有效纠正CHF合并贫血患者贫血状态,降低血清炎性因子水平并改善患者心功能。     

急性胰腺炎患者致炎与抗炎因子的变化及生长抑素的调节作用

目的:探讨急性胰腺炎患者血浆中致炎因子肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)和抗炎因子转化细胞生长因子-β(TGF-β)、白介素-10(IL-10)的变化、意义及生长抑素的调节作用。方法:急性胰腺炎48例,随机分成生长抑素治疗组和常规治疗组,分别在治疗前(入院时)、治疗后8 h和第2、3、4 d清晨空腹抽肘静脉血3 ml,测定TNF-α、IL-6、TGF-β和IL-10,并设对照组。结果:TNF-α和IL-6各监测点均比对照组显著升高(P<0.05,P<0.01),高峰在入院时。TGF-β和IL-10入院后8 h以后各监测点均比对照组显著升高(P<0.05,P<0.01);第2天达高峰。生长素抑素治疗组TNT-α、IL-6、和TGF-β、IL-10含量治疗后8 h明显低于常规治疗组。治疗后各观察点持续降低(P<0.05,P<0.01)。结论:急性胰腺炎患者血中致炎因子与抗炎因子均升高,机体免疫功能紊乱。生长抑素对致炎因子与抗炎因子的升高有抑制作用。     

丹皮酚软膏对老年性皮肤瘙痒症免疫偏移的影响

目的探讨丹皮酚软膏对老年性皮肤瘙痒症患者Th1、Th2免疫偏移的影响。方法收集2009年1月至2011年12月于该院就诊的泛发型老年性皮肤瘙痒症患者80例,40例为基础治疗组,仅口服氯雷他定;40例为试验组,在口服氯雷他定的基础上,外用丹皮酚软膏。同期收集40例健康老年人作为对照组。采集各组患者治疗前后及健康志愿者的血液标本,ELISA法检测细胞因子IFN-γ、IL-2、TNF-α、IL-4、IL-5、IL-10的表达水平。结果老年性皮肤瘙痒症患者IFN-γ、IL-2、TNF-α等Th1细胞因子的表达均高于健康对照组(P<0.05);而IL-4、IL-5、IL-10等Th2细胞因子的表达均低于健康对照组(P<0.05);治疗后与治疗前比较,口服氯雷他定组患者IFN-γ、IL-2、TNF-α等Th1细胞因子无明显变化(P>0.05),IL-4、IL-5、IL-10等Th2细胞因子的表达高于治疗前(P<0.05);外用丹皮酚组患者IFN-γ、IL-2、TNF-α等Th1细胞因子低于治疗前(P<0.05),IL-4、IL-5、IL-10等Th2细胞因子的表达高于治疗前(P<0.05)。结论老年性皮肤瘙痒症患者存在不同程度的Th1/Th2免疫偏移,表现为Th1型细胞因子功能亢进,Th2型细胞因子功能降低;丹皮酚能纠正此免疫偏移状态。     

腹腔镜结肠癌根治术对老年结肠癌患者的炎性因子、血清应激指标及免疫功能的影响

目的探究腹腔镜结肠癌根治术治疗老年结肠癌患者的疗效,分析其对机体炎性因子、血清应激指标及免疫功能的影响。方法选取2016年9月-2018年6月保定市第二医院收治的60例结肠癌老年患者的临床资料,根据手术方式不同分为2组:对照组(n=30)、观察组(n=30),观察组患者予以腹腔镜结肠癌根治术治疗,对照组患者予以开腹根治术治疗,对比2组患者炎性因子、血清应激指标及免疫功能情况。结果术后观察组的CRP、IL-17、TNF-α、去甲肾上腺素、肾上腺素与皮质醇水平均明显低于对照组(P<0.05),而观察组的CD8⁺、CD4⁺及NK细胞水平均明显高于对照组(P<0.05)。结论腹腔镜结肠癌根治术治疗效果与开腹手术无明显差异,但炎症反应较低,机体应激反应较小,对免疫功能影响较小,微创及美容优势显著,具有一定的临床应用价值。     

Graves病患者甲状腺131I转化率与Th1/Th2细胞因子偏移率的相关性研究

目的探讨Th1/Th2细胞因子偏移对格雷夫斯病（Craves disease,GD）碘转化率之间的相关性。方法选诊断为GD要求¹³¹Ⅰ治疗的60例患者和30例健康对照者,分别测定IL-2代表Th1细胞因子,IL-6代表Th2细胞因子。结果 IL-6在GD组明显高于对照组（P<0.01）;IL-2水平明显低于对照组（P<0.01）。IL-2、IL-6及IL-2/IL-6与甲状腺碘转换率均无明显相关性（P>0.05）。结论 GD患者的Th1/Th2细胞亚群失衡以偏向Th2为主;Th1/Th2细胞的偏移与甲状腺的碘转化率无相关性。     

左乙拉西坦治疗老年癫痫的疗效及对患者脑电图和炎性因子的影响

目的 探讨左乙拉西坦治疗老年癫痫的疗效及对患者脑电图和炎性因子的影响。方法 选择老年癫痫患者80例，依据随机表法分为治疗组与对照组各40例。对照组口服卡马西平治疗，治疗组在卡马西平基础上结合左乙拉西坦片治疗。两组治疗疗程24 w。统计两组治疗24 w总有效率；比较两组治疗前后脑电图频段功率、癫痫发作次数、智力评估情况、炎性因子变化。结果 治疗组总有效率显著高于对照组(P<0.05)。两组治疗后脑电图α和β频段显著高于治疗前，而δ和θ频段显著低于治疗前(P<0.05);治疗组治疗后脑电图α和β频段显著高于对照组，而δ和θ频段显著低于对照组(P<0.05)。两组治疗后癫痫发作次数显著低于治疗前(P<0.05),且治疗组显著低于对照组(P<0.05)。两组治疗后操作智商、语言智商和总智商评分显著高于治疗前(P<0.05),且治疗组显著高于对照组(P<0.05)。两组治疗后血清白细胞介素(IL)-1β、IL-2和肿瘤坏死因子(TNF)-α水平显著低于治疗前(P<0.05),且治疗组显著低于对照组(P<0.05)。结论 左乙拉西坦治疗老年癫痫...     

儿童腺样体肥大致肺动脉高压3例并右心导管检查分析

目的：分析近年来收治的肺高血压合并腺样体肥大致睡眠呼吸暂停综合症病例的临床资料,为临床诊治提供经验。方法：对武汉亚洲心脏病医院自2012年至2014年收治的肺高血压病例的临床资料及随访结果进行回顾性分析,其中3例为腺样体肥大致睡眠呼吸暂停综合症并肺高血压。结果：3例右心导管结果mPAP 33.33±10.06mmHg,PVR1015±606.66(dyn.s.cm-5),经治疗后复查活动能力均明显改善,心功能改善。结论：腺样体肥大致肺高血压行病因治疗联合靶向药物波生坦口服安全有效。     

Effects of glutathione-S-transferase M1, T1, and P1 on childhood lung function growth

The effects of glutathione-S-transferase (GST) M1, GSTT1, and GSTP1 genotypes on lung function growth were investigated in 1,940 children enrolled in the Children's Health Study as fourth graders (aged 8-11 years) in two cohorts during 1993 and 1996 and were followed annually over a 4-year period. Genotypes for GSTM1 and GSTT1 and GSTP1 codon 105 variants (ile105 and val105) were determined using DNA from buccal cell specimens. We used two-level regression models to estimate the effects of GSTM1, GSTT1, and GSTP1 genotypes on the adjusted annual average lung function growth. GSTM1 null was associated with deficits in annual growth rates for FVC (-0.21%; 95% confidence interval [CI], -0.40, -0.03) and FEV(1) (-0.27%; 95% CI, -0.50, -0.04). Children who were homozygous for the GSTP1 val105 allele had slower lung function growth (FVC -0.35%; 95% CI, -0.62, -0.07; and FEV(1) -0.34%; 95% CI, -0.68, 0.00) than children with one or more ile105 alleles. Children with asthma who were homozygous for the GSTP1 val105 allele had substantially larger deficits in FVC, FEV(1), and maximal mid-expiratory flow than children without asthma. The deficits in FVC and FEV(1) growth associated with both GSTM1 null and the GSTP1 val105 allele were largest and were statistically significant in non-Hispanic white children. We conclude that GSTM1 and GSTP1 genotypes are associated with lung function growth in school children.     

Expression, regulation, and function of IGF-1, IGF-1R, and IGF-1 binding proteins in blood vessels

The vascular insulin-like growth factor (IGF)-1 system includes the IGFs, the IGF-1 receptor (IGF-1R), and multiple binding proteins. This growth factor system exerts multiple physiologic effects on the vasculature through both endocrine and autocrine/paracrine mechanisms. The effects of IGF-1 are mediated principally through the IGF-1R but are modulated by complex interactions with multiple IGF binding proteins that themselves are regulated by phosphorylation, proteolysis, polymerization, and cell or matrix association. During the last decade, a significant body of evidence has accumulated, indicating that expression of the components of the IGF system are regulated by multiple factors, including growth factors, cytokines, lipoproteins, reactive oxygen species, and hemodynamic forces. In addition, cross-talk between the IGF system and other growth factors and integrin receptors has been demonstrated. There is accumulating evidence of a role for IGF-1 in multiple vascular pathologies, including atherosclerosis, hypertension, restenosis, angiogenesis, and diabetic vascular disease. This review will discuss the regulation of expression of IGF-1, IGF-1R, and IGF binding proteins in the vasculature and summarize evidence implicating involvement of this system in vascular diseases.     

利用烟囱技术治疗主动脉弓部分支血管受累Stanford B型主动脉夹层23例临床分析

【摘要】 目的 探讨烟囱技术治疗主动脉弓部分支血管受累Stanford B型主动脉夹层的临床效果,为临床治疗提供参考。方法 对我院2013年9月至2016年10月治疗主动脉弓部分支血管受累的Stanford B型主动脉夹层23例的临床资料、手术方法、随访结果行回顾性分析。结果23例患者中1例烟囱支架闭塞;1例术后死亡;1例逆剥形成A型夹层;5例术后Ⅰ型内漏;无脊髓缺血导致截瘫,无远端支架贴附不良,无支架远端相关并发症,无支架移位,无脑梗及脏器缺血等并发症。结论 对于主动脉弓分支血管受累的Stanford B型主动脉夹层采用烟囱技术扩大了腔内治疗的适应症,提高手术成功率,将复杂的手术简单化,使患者受益于这一有效的治疗手段,获得了满意的临床疗效。     

MIP-1alpha, MIP-1beta, RANTES, and ATAC/lymphotactin function together with IFN-gamma as type 1 cytokines

We analyzed for the first time the expression of chemokines in subpopulations of the murine immune system at the single-cell level. We demonstrate in vitro and in a model of murine listeriosis that macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, regulated on activation normal T cell expressed and secreted (RANTES), and activation-induced, T cell-derived, and chemokine-related cytokine (ATAC)/lymphotactin are cosecreted to a high degree with IFN-gamma by activated individual natural killer (NK), CD8(+) T, and CD4(+) T helper 1 (Th1) cells. Functionally, ATAC and the CC chemokines cooperate with IFN-gamma in the up-regulation of CD40, IL-12, and tumor necrosis factor-alpha, molecules playing a central role in the effector phase of macrophages. Our data indicate that (i) MIP-1alpha, MIP-1beta, RANTES, and ATAC are not only chemoattractants but also coactivators of macrophages, (ii) MIP-1alpha, MIP-1beta, RANTES, and ATAC constitute together with IFN-gamma a group of "type 1 cytokines," and (iii) these cytokines act together as a functional unit that is used by NK cells in the innate phase and then "handed over" to CD8(+) T cells in the antigen-specific phase of the immune defense, thus bridging the two components of a Th1 immune reaction.     

DJ-1 is critical for mitochondrial function and rescues PINK1 loss of function

Mutations or deletions in PARKIN/PARK2, PINK1/PARK6, and DJ-1/PARK7 lead to autosomal recessive parkinsonism. In Drosophila, deletions in parkin and pink1 result in swollen and dysfunctional mitochondria in energy-demanding tissues. The relationship between DJ-1 and mitochondria, however, remains unclear. We now report that Drosophila and mouse mutants in DJ-1 show compromised mitochondrial function with age. Flies deleted for DJ-1 manifest similar defects as pink1 and parkin mutants: male sterility, shortened lifespan, and reduced climbing ability. We further found poorly coupled mitochondria in vitro and reduced ATP levels in fly and mouse DJ-1 mutants. Surprisingly, up-regulation of DJ-1 can ameliorate pink1, but not parkin, mutants in Drosophila; cysteine C104 (analogous to C106 in human) is critical for this rescue, implicating the oxidative functions of DJ-1 in this property. These results suggest that DJ-1 is important for proper mitochondrial function and acts downstream of, or in parallel to, pink1. These findings link DJ-1, pink1, and parkin to mitochondrial integrity and provide the foundation for therapeutics that link bioenergetics and parkinsonism.     

beta(1)-Adrenergic receptor function, autoimmunity, and pathogenesis of dilated cardiomyopathy

Dilated cardiomyopathy (DCM) is a heart disease characterized by progressive depression of cardiac function and left ventricular dilatation of unknown etiology in the absence of coronary artery disease. Genetic causes and cardiotoxic substances account for about one third of the DCM cases, but the etiology of the remaining 60% to 70% is still unclear. Over the past two decades, evidence has accumulated continuously that functionally active antibodies or autoantibodies targeting cardiac beta(1)-adrenergic receptors (anti-beta(1)-AR antibodies) may play an important role in the initiation and/or clinical course of DCM. Recent experiments in rats indicate that such antibodies can actually cause DCM. This article reviews current knowledge and recent experimental and clinical findings focusing on the role of the beta(1)-adrenergic receptor as a self-antigen in the pathogenesis of DCM.