Guillain-Barre综合征患儿血清白介素-18、白介素-13水平的变化

目的探讨白介素(IL)-18、IL-13在Guillain-Barre综合征(GBS)患儿血清中的含量变化及意义。方法采用酶联免疫吸附法(ELISA)测定GBS患儿急性期与恢复期血清IL-18、IL-13水平,并与正常对照组比较。结果GBS患儿急性期血清IL-18[(44.87±7.53)pg/ml]与IL-13[(37.46±6.94)pg/ml]水平均明显高于恢复期[和(38.25±5.86)pg/ml、(32.14±6.89)pg/ml]和正常对照组[(32.35±4.93)pg/ml、(24.76±5.59)pg/ml](均P<0.01);且病情重者[(47.02±8.39)pg/ml、(39.46±6.72)]pg/ml]明显高于病情轻者[(41.96±5.58)pg/ml、(34.51±6.25)pg/ml](均P<0.05);GBS患者恢复期血清IL-18、IL-13水平仍高于正常对照组(均P<0.01);相关分析发现GBS病情与血清IL-18、IL-13水平呈正相关(r=0.116,0.078,均P<0.05)。结论GBS患儿血清IL-18、IL-13含量增加,其可能参与了GBS的发病机制。     

颈动脉内中膜厚度与血清白介素-6、白介素-18水平的关系

目的 探讨颈动脉内中膜厚度(IMT)与血清细胞因子白介素 (IL)-6、IL-18水平的关系. 方法选择40例短暂性脑缺血发作(TIA)患者(TIA组)、64例急性脑梗死(ACI)患者(ACI组)和30名健康对照者(正常对照组),分别测量其颈动脉IMT值,并分为IMT＜1.0 mm亚组和IMT≥1.0 mm亚组.利用液相平衡竞争放射免疫分析法(RIA)和酶联免疫吸附法(ELISA)分别测定3组的血清IL-6和IL-18水平,并对IMT与IL-6、IL-18的关系进行分析. 结果 TIA组和ACI组所有IMT≥1.0 mm患者血清IL-6、IL-18含量[TIA组分别为(141.61±27.86)pg/ml和(212.42±51.88)pg/ml;ACI组分别为(157.94±27.98)pg/ml和(224.99±59.56)pg/ml]比正常对照组[(101.41±35.56)pg/ml和165.87±29.89)pg/ml]升高(P<0.05～0.01); TIA组、ACI组IMT≥1.0 mm亚组患者血清IL-6、IL-18含量和IMT<1.0 mm亚组[TIA组分别为(141.61±27.86, 212.42±51.88)pg/ml和(108.48±35.56,170.98±29.83)pg/ml;ACI组分别为(157.94±27.98,224.99±59.56) pg/ml和(129.56±35.56,195.07±29.86)pg/ml]二者有显著差异(均P<0.05).TIA组、ACI组IMT≥1.0 mm亚组患者IMT与血清IL-18含量呈正相关(r＝0.549,P<0.01),与血清IL-6含量无相关性((r＝0.304,P＝0.057). 结论 TIA组、ACI组IMT增厚的患者血清IL-6、IL-18的水平升高;IMT的增厚与血清IL-18含量呈正相关.推测IL-6、 IL-18可能参与了动脉硬化的形成过程.     

急性脑梗死患者血清白介素-18和组织因子水平变化及其与凝血功能的关系

目的 探讨急性脑梗死(ACI)患者血清白介素(IL)-18和组织因子(TF)水平的变化及其与凝血功能关系.方法 79例ACI患者(ACI组)于入院次日、25名健康体检者(正常对照组)于体检当日早晨,分别检测血清IL-18、TF水平和凝血功能.结果 ACI组患者的血清IL-18、TF水平[(282.22±127.45)pg/ml,(2.10±1.23)ns/ml]明显高于正常对照组[(131.13±37.17)pg/ml,0.67±0.34)ng/ml](P<0.01～0.001):ACI组患者凝血功能指标中的部分凝血活酶时间及纤维蛋白原(Fib)水平显著高于正常对照组(均P<0.05);ACI组患者血清TF水平与凝血酶原时间及Fib水平呈正相关(r=0.376,r=0.473,P<0.05～0.01).结论 血清IL-18与TF水平异常增高是参与动脉粥样硬化相关性血栓形成的重要原因之一,抗凝及降纤治疗通过抑制TF水平逆转该病理过程.     

白介素-4 C590T基因多态性与血清白介素-4水平及动脉粥样硬化性血栓性脑梗死的关系

目的探讨白介素(IL)-4C590T基因多态性与血清IL-4水平以及动脉粥样硬化性血栓性脑梗死(ATCI)的关系。方法采用PCR-限制性片段长度多态性(PCR-RFLP)方法检测159例ATCI患者和151名健康正常对照者的IL-4C590T基因的单核苷酸多态性,用酶联免疫吸附(ELISA)法检测正常对照组的血清IL-4水平。结果正常对照组IL-4C590T基因TT型的血清IL-4水平[(31.85±5.68)pg/ml]显著高于TC型[(28.67±6.00)pg/ml]和CC型[(20.98±0.99)pg/ml],TC型又显著高于CC型(均P<0.01)。ATCI组与正常对照组IL-4C590T基因型和等位基因频率的分布差异无统计学意义(均P>0.05)。结论IL-4590T等位基因与高血清IL-4水平有关,IL-4C590T基因多态性与ATCI的发病无明显关系。     

急性期Guillain-Barr(e)综合征患者人类肿瘤坏死因子样分子1A表达与T细胞分泌γ-干扰素水平的关系

目的 探讨人类肿瘤坏死因子样分子1A(hTL1A)在急性期Guillain-Barre综合征(GBS)中表达及其与T细胞分泌γ-干扰素(IFN-γ)水平的关系.方法 ①重组人可溶性hTL1A(rhsTL1A)免疫6周龄雌性Bal b/c小鼠,用人脐带静脉内皮细胞(HUVECs)以免疫荧光染色法鉴定rhsTL1A抗血清.②鉴定rhsTL1A的生物学活性:健康捐赠者外周血单个核细胞(PBMCs)接种于96孔板,设2 μg/ml植物血凝素(PHA)、2 μg/ml PHA+25 ng/ml rhsTL1A、2 μg/ml PHA+100 ng/mlrhsTL1A、2 μg/ml PHA+400 ng/ml rhsTL1A组,~3H-TdR掺入法检测T细胞增殖.③酶联免疫吸附(ELISA)法检测急性期GBS患儿血清中IFN-γ水平.④流式细胞术检测急性期GBS患儿外周血中CD_3~+ hTL1A~+ T/CD_3~+ T细胞的百分比.⑤分离急性期GBS患儿PBMCs,给予2 μg/ml PHA和400ng/ml rhsTL1 A,培养72 h后ELISA法检测IFN-γ水平.结果 ① rhsTL1A抗血清能够识别真核细胞HUVECs表达hTL1A.②T细胞增殖实验结果显示各组刺激指数(SI)均较对照组升高,400 ng/mlrhsTL1A组的SI最大(2.65).③急性期GBS患儿血清IFN9-γ水平[(102.25±22.17)pg/ml]较对照组[(28.75±1.31)pg/ml]显著升高(t=3.309,P<0.05).④急性期GBS患儿外周血中CD_3~+TL1A~+T/CD_3~+ T细胞比例(18.22%±1.83%)较健康对照组(5.17%±0.48%)显著增高(t=6.884,P<0.01).⑤健康对照组和急性期GBS组PBMCs经2 μmg/ml PHA和400 ng/ml rhsTL1A孵育后,IFN-γ分泌量[(43.56±4.41)pg/ml、(180.64±38.39)pg/ml]均显著增高(t=4.523、2.600,P<0.01、0.05),并且急性期GBS组的IFN-γ水平显著高于健康对照组(t=3.545,P<0.05).结论 ①400 ng/ml rhsTL1A能有效促进2μg/ml PHA活化的T细胞增殖,rhsTL1A具有生物学活性.②急性期GBS患儿外周血中活化T细胞表达hTL1A增加,可通过与其受体DR_3相互结合,促进IFN-γ的分泌.     

格林-巴利综合征患者血浆肿瘤坏死因子-α和白介素-2的检测及意义

目的　探讨肿瘤坏死因子 α(TNF α)和白介素 2 (IL 2 )在格林 巴利综合征 (GBS)发病机制中的作用。方法　应用ELISA双抗体夹心法 ,检测 31例GBS患者血浆TNF α和IL 2浓度。结果　 31例GBS患者TNF α和IL 2浓度明显高于对照组 (P <0 .0 0 1) ,且与临床分级显著相关 (P <0 .0 5)。 16例接受糖皮质激素治疗 ,病情好转的恢复期患者TNF α和IL 2浓度相应下降至正常或接近正常。结论　本组结果提示 ,TNF α和IL 2可能直接和间接参与周围神经脱髓鞘的病理损害 ,在GBS的发病机制中起着重要用。     

抗CD40配体单克隆抗体干预重症肌无力的研究

目的研究抗CD40配体单克隆抗体(CD40LmcAb)干预重症肌无力(MG)患者外周血单个核细胞(PBMC)的效果并探讨其机制。方法MG患者25例和健康对照组16名,分离培养外周血单个核细胞,分别用植物血凝素(PHA)和美洲商陆原(PWM)进行刺激,并用CD40LmcAb进行干预。PHA刺激组培养后收集上清检测γ干扰素(IFN γ)和白细胞介素4 (IL 4);PWM刺激组培养后收集上清检测抗乙酰胆碱受体抗体(AchRab)和抗突触前膜受体抗体(PsmRab)。比较MG患者两组中CD40LmcAb干预与否的差异并与健康对照组比较。结果MG患者PBMC体外诱生AchRab(0 32±0 11)、PsmRab(0 28±0 11)、IFN γ[ (36 24±10 47)pg/ml]和IL 4水平[ (263 08±35 95)pg/ml]对比健康对照组显著增高[分别为(0 10±0 02), (0 15±0 03), (17 56±2 94)pg/ml和(190 00±6 50)pg/ml,P<0 01),CD40LmcAb干预后MG组的上述四项指标均基本降至健康对照组水平(P>0 05)。结论CD40LmcAb在体外能有效干预MG患者PBMC诱生AchRab、PsmRab、IFN γ和IL 4的水平。     

拜阿司匹灵对脑梗死患者血浆血小板4因子的影响

目的观察脑梗死患者用拜阿司匹灵治疗前、后血浆血小板4因子(PF4)的变化。方法70例脑梗死患者被随机分为不用拜阿司匹灵组(n=40)和服用拜阿司匹灵组(100mg/次,睡前服用,n=30),其他治疗两组间无差异。用酶标免疫测定法测定二组治疗前、治疗后7d及30例正常对照组血浆PF4的含量。结果急性脑梗死不用拜阿司匹灵组的患者血浆PF4治疗前为15.12±6.32ng/ml,治疗后为9.83±4.93ng/ml,治疗后PF4的明显下降(P<0.01),但显著高于正常对照组(6.50±2.70ng/ml,P<0.01);服用拜阿司匹灵组的患者血浆PF4治疗前为15.48±3.16ng/ml,治疗7d后为7.66±1.47ng/ml,较治疗前明显下降(P<0.01),也明显低于不用拜阿司匹灵组的患者(P<0.01),但仍高于正常对照组(6.50±2.70ng/ml,P<0.05)。结论拜阿司匹灵能降低脑梗死患者血浆PF4含量水平,抑制血小板活性。     

脑梗死患者外周血淋巴细胞PPARγ mRNA表达变化及其与血清IL-6相关性

目的探讨脑梗死患者过氧化小体增殖剂激活型受体γ(PPARγ)mRNA表达变化及其与血清IL-6水平的相关性。方法序贯收集2002年7月至2003年1月在我院神经内科就诊的、发病3 d以内的、符合试验入选标准的脑梗死患者32例,同时收集相匹配的同期体检者30例作为对照。用RT-PCR法测定两组对象空腹周围血淋巴细胞PPARγ mRNA表达情况,放免法测定血清IL-6水平。结果脑梗死患者和正常对照组PPARγ mRNA表达值分别为0.24±0.05和0.84±0.07,差异有显著意义(P<0.01);脑梗死患者血清IL-6浓度为(352.1±31.7)pg／ml,正常对照组为(135.4±18.3)pg／ml,差异有显著意义(P<0.01);脑梗死患者PPARγmRNA表达和血清IL-6水平呈负相关,相关系数为-0.432,P=0.014。结论发病3 d内脑梗死患者周围血淋巴细胞PPARγmRNA表达下调,并与血清IL-6水平呈负相关,提示:PPARγ可能参与脑缺血病理过程。     

氯氮平所致脂质代谢异常与白介素6及其受体的关系

目的：了解氯氮平所致脂质代谢异常与白介素6及其受体活性的关系。方法；采用自身对照研究，比较30例精神分裂症患氯氮平治疗前和6 周后胆 固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL）、低密度脂蛋白胆固醇（LDL）、载脂蛋白A1（APOA1）、载脂蛋白B（APOB）、白介素6（IL－6）及其受体（sIL-6R)水平的差异。结果：治疗后TC、TG、ApoB、IL－6及sIL-6R水平明显升高，其差异有显性意义（P＜0．05）；TC与sIL-6R呈正相关（P＜0．01）；TG与IL－6呈正相关（P＜0．05），与sIL-6R呈正相关（P＜0．01）；ApoB水平与IL－6及sIL-6R均无相关性。结论：氯氮平对白介素6及其受体活性的影响可能是脂质代谢异常的原因之一。     

Meta-analysis of the IL23R and IL12B polymorphisms in multiple sclerosis

Purpose: Polymorphisms in the genes encoding interleukin-23 receptor (IL23R) and the p40 subunit of IL-12/23 (IL12B) have been implicated in multiple sclerosis (MS) risk. However, results of different studies are inconsistent. Our aim was to perform a meta-analysis on this topic. Methods: We assessed two variants (rs10889677 and rs7517847) of IL23R and the A1188C polymorphism (rs3212227) of IL12B. Electronic databases (PubMed, Web of Science and Scopus) were searched for eligible studies published until September 2014. Odds ratio (OR) and 95% confidence interval (95% CI) were used to investigate the strength of association in dominant, recessive, homozygote and allelic comparison models. Results: Seven case–control studies with 2250 MS patients and 2320 controls were included in this meta-analysis. The pooled results showed no association of rs10889677 and rs7517847 with MS risk in any of the genetic models. Although the pooled analysis showed an association between rs3212227 and MS in all study subjects in dominant (OR = 0.81, 95% CI: 0.66–0.99, P_h = 0.480, P_z = 0.044) and allelic comparison (OR = 0.84, 95% CI: 0.72–0.98, P_h = 0.967, P_z = 0.030) models, subgroup analysis based on ethnicity did not suggest an association between rs3212227 and MS risk in Caucasians in any of the genetic models, and there was no association between rs3212227 and MS risk in an Asian group. Conclusions: The IL23R polymorphisms rs10889677, rs7517847, and the IL12B polymorphism rs3212227 are not associated with MS risk.     

脂多糖诱导鼠脑中的白细胞介素—6基因表达

目的 分子水平研究正常鼠脑内的白细胞介素－６（ＩＬ－６）分布和诱导水平。方法 脂多糖（ＬＰＳ）１００ｕｇ／ｋｇ,ｉｐ,不同时间,用ＰＴ－ＲＣＲ对鼠脑的６个不同区域,进行ＩＬ－６信使核糖核酸（ｍＲＮＡ）半定量分析。结果 ＩＬ－６ｍＲＮＡ表达由高到低依次为海马,下丘脑,脑干,小鼠,丘脑和皮层。除皮层表达高峰在６小时外,其余在４小时。结论 ＬＰＳ诱导的ＩＬ－６ｍＲＮＡ在正常鼠脑的不同部位表达曲线不同。     

IL18R1基因多态性与中国汉族精神分裂症的关联性分析

目的:探讨IL18受体IL18R1基因多态性与中国汉族精神分裂症的关系。方法:采用病例对照研究方法,选取1 174例精神分裂症患者(病例组)与1 120名正常健康对照者(对照组),利用连接酶检测-聚合酶链反应(LDR-PCR)方法对IL18R1基因多态位点rs1035130进行基因分型,观察其等位基因及基因型与精神分裂症发病风险的关系。结果:rs1035130的基因型与等位基因频率在病例组与正常对照组中的分布差异无统计学意义(P0.05)。结论:IL18R1基因rs1035130多态性可能与中国汉族精神分裂症无关。     

IL6-174G > C genetic polymorphism influences antidepressant treatment outcome

Background: Major depressive disorder is a condition associated with dysregulated cytokine levels; among these, IL6. Furthermore, genetic variations within cytokine genes have been proposed to predict antidepressant treatment outcome.

Objectives: This study aims to evaluate the role of IL6-174G?>?C and IL6R D358A A?>?C functional polymorphisms in antidepressant treatment phenotypes, specifically remission, relapse, and treatment resistant depression (TRD).

Methods: The referred polymorphisms were genotyped in 80 MDD patients followed at Hospital Magalhães Lemos, Portugal, within a period of 27 months.

Results: It was found that patients carrying IL6-174 GC genotype present a protection towards the development of TRD (OR?=?0.242; 95% CI?=?0.068–0.869; p?=?.038), when compared with GG genotype. Additionally, carriers of IL6-174?CC genotype remit earlier than patients with IL6-174 GG/GC genotypes, with a median time to remission of 6 weeks for CC carriers and 15 weeks for GG or GC carriers (p?=?.030, Log-rank test). No association was found between IL6R D358A genetic polymorphism and any of the treatment phenotypes evaluated.

Conclusions: The IL6-174G?>?C polymorphism influences antidepressant treatment outcome in this sub-set of MDD patients, providing a putative mechanistic link for the dysregulated IL-6 levels described in the literature in patients with TRD.     

A genetic link between CXCR5 and IL2RA gene polymorphisms and susceptibility to multiple sclerosis

ABSTRACT

Objectives: Multiple sclerosis (MS) is a T-cell-mediated disease of the central nervous system that develops in individuals possessing a complex susceptibility trait. We explored relationship between gene polymorphisms in MS.

Methods: To identify the associations of CXCR5 and IL2RA gene polymorphisms with susceptibility to MS, we recruited 263 MS patients from the Han nationality and 138 from the Hui nationality as MS group and 284 healthy volunteers from the Han nationality and 156 from the Hui nationality as controls. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was employed to test gene polymorphisms of IL2RA (rs2104286 and rs12722489). Sequenom MassARRAY system was applied to analyze genotyping of CXCR5 (rs3922).

Results: The genotypes and allele frequency distributions at the loci of IL2RA rs2104286 and rs12722489 showed significant differences between the MS and control groups. The gene polymorphisms at the loci of IL2RA rs2104286 and rs12722489 may increase the onset risk of MS. IL2RA-rs2104286 showed a positive relationship with CXCR5-rs3922. The same relationship was also observed between IL2RA-rs12722489 and CXCR5-rs3922. The genotypes and allele frequencies of loci of rs2104286 and rs12722489 were significantly different in MS clinical subtypes and severity (EDSS score). Additionally, CAC and TGC haplotype at rs3922-rs12722489-rs2104286 may reduce the risk of MS, while CGT and TGT haplotypes increase the risk.

Conclusion: The gene polymorphisms at the loci of IL2RA rs2104286 and rs12722489 are closely associated with susceptibility to MS in the Han and Hui nationalities.     

Bovine anterior pituitary progenitor cell line expresses interleukin (IL)-18 and IL-18 receptor

In the anterior pituitary gland, inflammatory mediators regulate cell function through an immuno-endocrine pathway. Recent studies have shown that undifferentiated stem cells act as immunomodulators. These studies prompted us to establish a progenitor cell line from the bovine anterior pituitary gland and to detail its function. First, we localised interleukin (IL)-18 by immunohistochemistry to the marginal cell layer of Rathke's pouch that is assumed to embody a stem/progenitor cell compartment of the postnatal pituitary gland. A cloned anterior pituitary-derived cell line from the bovine anterior pituitary gland was established from single cell clone by the limiting dilution method and was designated as bovine anterior pituitary-derived cell line (BAPC)-1. BAPC-1 cells constantly expressed mRNAs for IL-18 and IL-18 receptor, and grew steadily and rapidly in the medium containing epidermal growth factor and basic fibroblast growth factor. The cell line also expressed the mRNAs for the stem/progenitor cell- related factors such as Nanog, Oct-4, Ptch1, Nestin, Notch1, Hes1, Lrp and Fzd4, and the mRNAs for embryonic pituitary-related factors, such as Lhx3, PitX1 and Pit-1. The nuclei of BAPC-1 were immunostained positively for Pit-1, Hes1 and beta-catenin antibodies. Furthermore, BAPC-1 cells expressed mRNAs for cytokine such as IL-1alpha, IL-6, IL-7, IL-12 and IL-15. Stimulation of BAPC-1 cells with IL-18 increased expression of mRNAs for IL-1alpha, IL-6, IL-1beta and IL-8. At day 6 in culture, BAPC-1 cells also express growth hormone mRNA. These results strongly suggest that BAPC-1 is a stem/progenitor cell line and modulates the immuno-endocrine function of the anterior pituitary cells through its cytokine production.     

IL1β- and LPS-induced serotonin secretion is increased in EC cells derived from Crohn's disease

Abstract Gut mucosal enterochromaffin (EC) cells are regarded as key regulators of intestinal motility and fluid secretion via secretion of serotonin (5HT), are increased in numbers in mucosal inflammation and located in close proximity to immune cells. We examined whether interleukin (IL)1β and Escherichia coli lipopolysaccharide (LPS) induced EC cell 5HT release through Toll‐like/IL‐1 (TIL) receptor activation, nuclear factor kappa B (NFκB) and mitogen‐activated protein kinase (MAPK) phosphorylation and evaluated whether somatostatin could inhibit this phenomenon. Pure (>98%) human intestinal EC cells were isolated by fluorescent activated cell sorting from preparations of normal (n = 5) and Crohn’s colitis (n = 6) mucosa. 5HT release was measured (ELISA), and NFκB and ERK phosphorylation quantitated (ELISA) in response to IL1β and LPS. 5HT secretion was increased by both E. coli LPS (EC₅₀ = 5 ng mL^?1) and IL1β (EC₅₀ = 0.05 pmol L^?1) >2‐fold (P < 0.05) in Crohn’s EC cells compared with normal EC cells. Secretion was reversible by the TLR4 antagonist, E. coli K12 LPS (IC₅₀ = 12 ng mL^?1) and the IL1β receptor antagonist (ILRA; IC₅₀ = 3.4 ng mL^?1). IL1β caused significant (P < 0.05) NFκB and MAPK phosphorylation (40–55%). The somatostatin analogue, lanreotide inhibited IL1β‐stimulated secretion in Crohn’s (IC₅₀ = 0.61 nmol L^?1) and normal EC cells (IC₅₀ = 1.8 nmol L^?1). Interleukins (IL1β) and bacterial products (E. coli LPS) stimulated 5HT secretion from Crohn’s EC cells via TIL receptor activation (TLR4 and IL1β). Immune‐mediated alterations in EC cell secretion of 5HT may represent a component of the pathogenesis of abnormal bowel function in Crohn’s disease. Inhibition of EC cell‐mediated 5HT secretion may be an alternative therapeutic strategy in the amelioration of inflammatory bowel disease symptomatology.     

Interleukin-10 (IL10) and tumor necrosis factor alpha (TNF) gene polymorphisms in Parkinson's disease patients

Recent studies revealed that inflammatory processes might play an important role in the pathogenesis of Parkinson's disease (PD). We hypothesized that genetically determined differences in the immune response, especially in anti- and pro-inflammatory cytokines production might influence the risk for the development and/or onset of sporadic PD. In the present study, we investigated the genetic polymorphisms of the IL10 (−1082 and −519) and TNF (−308) genes in relation to the risk of PD, and their associations with age of PD onset in a group of 316 patients, divided into two subgroups: Group 1: patients with early onset PD (EOPD), i.e. before 50 years of age (102 patients), and group 2: patients with onset of PD after 50 years of age comprising 214 subjects. Control samples were obtained from 300 randomly selected healthy individuals from the same geographical region with no signs of Parkinsonism as evaluated by a neurologist. PCR–RFLP methods were used for genotyping. No statistically significant differences between PD patients and controls were found in the frequency of a single locus of IL10 promoter. We found TNF −308A allele significantly more frequent in EOPD patients compared to the controls (p = 0.007). The overrepresentation of the A allele was reflected by a significant increase in AA homozygous individuals in EOPD patients compared to the controls (p = 0.0021). The results from our study revealed that the TNF −308AA genotype might increase the risk of early onset of PD.     

短暂性脑缺血发作与IL6、IL8和IL10的关系

目的探讨IL6、IL8及IL10和短暂性脑缺血发作(TIA)患者颈动脉斑块稳定性与疾病预后的关系。方法根据颈动脉CTA检查将TIA患者分为不稳定性斑块组和稳定性斑块组,比较两组患者血清IL6、IL8及IL10水平的差异;检测健康对照组血清IL6、IL8及IL10水平,并与TIA患者组比较;根据TIA患者的预后分为痊愈组、反复发作组、进展为脑梗死组,比较三组患者间血清IL6、IL8及IL10水平的差异。结果不稳定性斑块组患者血清IL6、IL8水平明显高于稳定性斑块组,血清IL10水平低于稳定性斑块组。TIA患者血清IL6、IL8及IL10水平均高于健康对照组。进展为脑梗死组、反复发作组患者的血清IL6、IL8及IL10水平均高于痊愈组。结论血清IL6、IL8水平与颈动脉斑块的稳定性呈负相关,而血清IL10水平与颈动脉斑块的稳定性呈正相关。血清IL6、IL8及IL10水平高的TIA患者易进展为脑梗死。     

脑胶质瘤患者围术期血清脑脊液MMP及IL指标变化的研究

目的分析脑胶质瘤患者围术期血清、脑脊液MMP及IL指标的变化情况。方法选取2011-06—2015-04于本院进行手术治疗的37例脑胶质瘤患者为观察组,同时期进行健康体检的37例健康人群为对照组,观察2组术前及术后12h、24h、36h、48h及72h时和对照组的血清及脑脊液MMP及IL指标水平。结果观察组术前与术后12h、24h、36h及48h的血清及脑脊液MMP水平高于对照组,术前与术后12h、24h、36h、48h及72h的血清及脑脊液IL水平均高于对照组,观察组术后12h、24h、36h、48h及72h的血清及脑脊液MMP指标均低于术前,术后24h、36h、48h及72h的血清及脑脊液IL指标均高于术前,差异均有统计学意义(P0.05)。结论脑胶质瘤患者围术期血清及脑脊液MMP及IL指标的变化较为明显,应注意对其变化的监测,以为疾病的治疗干预提供依据。