Complement-dependent neuroinflammation in spinal cord injury:from pathology to therapeutic implications

Spinal cord injury remains a major cause of disability in young adults,and beyond acute decompression and rehabilitation,there are no pharmacological treatments to limit the progression of injury and optimize recovery in this population.Following the thorough investigation of the complement system in triggering and propagating cerebral neuroinflammation,a similar role for complement in spinal neuroinflammation is a focus of ongoing research.In this work,we survey the current literature investigating the role of complement in spinal cord injury including the sources of complement proteins,triggers of complement activation,and role of effector functions in the pathology.We study relevant data demonstrating the different triggers of complement activation after spinal cord injury including direct binding to cellular debris,and or activation via antibody binding to damage-associated molecular patterns.Several effector functions of complement have been implicated in spinal cord injury,and we critically evaluate recent studies on the dual role of complement anaphylatoxins in spinal cord injury while emphasizing the lack of pathophysiological understanding of the role of opsonins in spinal cord injury.Following this pathophysiological review,we systematically review the different translational approaches used in preclinical models of spinal cord injury and discuss the challenges for future translation into human subjects.This review emphasizes the need for future studies to dissect the roles of different complement pathways in the pathology of spinal cord injury,to evaluate the phases of involvement of opsonins and anaphylatoxins,and to study the role of complement in white matter degeneration and regeneration using translational strategies to supplement genetic models.

Antibodies elicited by Newcastle disease virus-vectored H7N9 avian influenza vaccine are functional in activating the complement system

H7N9 subtype avian influenza virus poses a great challenge for poultry industry.Newcastle disease virus(NDV)-vectored H7N9 avian influenza vaccines(NDV_(vec)H7N9)are effective in disease control because they are protective and allow mass administration.Of note,these vaccines elicit undetectable H7N9-specific hemagglutination-inhibition(HI)but high IgG antibodies in chickens.However,the molecular basis and protective mechanism underlying this particular antibody immunity remain unclear.Herein,immunization with an NDV_(vec)H7N9 induced low anti-H7N9 HI and virus neutralization titers but high levels of hemagglutinin(HA)-binding IgG antibodies in chickens.Three residues(S150,G151 and S152)in HA of H7N9 virus were identified as the dominant epitopes recognized by the NDV_(vec)H7N9 immune serum.Passively transferred NDV_(vec)H7N9 immune serum conferred complete protection against H7N9 virus infection in chickens.The NDV_(vec)H7N9 immune serum can mediate a potent lysis of HA-expressing and H7N9 virus-infected cells and significantly suppress H7N9 virus infectivity.These activities of the serum were significantly impaired after heat-inactivation or treatment with complement inhibitor,suggesting the engagement of the complement system.Moreover,mutations in the 150-SGS-152 sites in HA resulted in significant reductions in cell lysis and virus neutralization mediated by the NDV_(vec)H7N9 immune serum,indicating the requirement of antibody-antigen binding for complement activity.Therefore,antibodies induced by the NDV_(vec)H7N9 can activate antibody-dependent complement-mediated lysis of H7N9 virus-infected cells and complement-mediated neutralization of H7N9 virus.Our findings unveiled a novel role of the complement in protection conferred by the NDV_(vec)H7N9,highlighting a potential benefit of engaging the complement system in H7N9 vaccine design.

Association of complement components with risk of colorectal cancer:A systematic review and meta-analysis

BACKGROUND Complement components could contribute to the tumor microenvironment and the systemic immune response.Nevertheless,their role in colorectal cancer(CRC)remains a contentious subject.AIM To elucidate the relationship between complement components and CRC risk and clinical characteristics.METHODS Searches were conducted in PubMed,the Cochrane Library,and the China National Knowledge Infrastructure database until June 1,2023.We included cohort studies encompassing participants aged≥18 years,investigating the association between complement components and CRC.The studies were of moderate quality or above,as determined by the Agency for Healthcare Research and Quality.The meta-analysis employed fixed-effects or random-effects models based on the I^(2)test,utilizing risk ratio(RR)and their corresponding 95%confidence interval(CI)for outcomes.Sensitivity and subgroup analyses were performed to validate the robustness of the collective estimates and identify the source of heterogeneity.RESULTS Data from 15 studies,comprising 1631 participants that met the inclusion criteria,were included in the meta-analysis.Our findings indicated that protein levels of cluster of differentiation 46(CD46)(RR=3.66,95%CI:1.75-7.64,P<0.001),CD59(RR=2.86,95%CI:1.36-6.01,P=0.005),and component 1(C1)(RR=5.88,95%CI:1.75-19.73,P=0.004)and serum levels of C3(standardized mean difference=1.82,95%CI:0.06-3.58,P=0.040)were significantly elevated in patients with CRC compared to healthy controls.Strong expression of CD55 or CD59 was associated with a higher incidence of lymph node metastasis,whereas strong CD46 expression correlated with a higher incidence of tumor differentiation compared to low CD46 expression(P<0.05 for all).Although specific pooled results demonstrated notable heterogeneity,subgroup analyses pointed to regional differences as the primary source of inconsistency among the studies.CONCLUSION Our analysis underscores that increased levels of specific complement components are associated with a heightened risk of CRC,emphasizing the potential significance of monitoring elevated complement component levels.

Complement factor Ⅰ knockdown inhibits colon cancer development by affecting Wnt/β-catenin/c-Myc signaling pathway and glycolysis

BACKGROUND Colon cancer(CC)occurrence and progression are considerably influenced by the tumor microenvironment.However,the exact underlying regulatory mechanisms remain unclear.AIM To investigate immune infiltration-related differentially expressed genes(DEGs)in CC and specifically explored the role and potential molecular mechanisms of complement factor I(CFI).METHODS Immune infiltration-associated DEGs were screened for CC using bioinformatics.Quantitative reverse transcription polymerase chain reaction was used to examine hub DEGs expression in the CC cell lines.Stable CFI-knockdown HT29 and HCT116 cell lines were constructed,and the diverse roles of CFI in vitro were assessed using CCK-8,5-ethynyl-2’-deoxyuridine,wound healing,and transwell assays.Hematoxylin and eosin staining and immunohistochemistry staining were employed to evaluate the influence of CFI on the tumorigenesis of CC xenograft models constructed using BALB/c male nude mice.Key proteins associated with glycolysis and the Wnt pathway were measured using western blotting.RESULTS Six key immune infiltration-related DEGs were screened,among which the expression of CFI,complement factor B,lymphoid enhancer binding factor 1,and SRY-related high-mobility-group box 4 was upregulated,whereas that of fatty acid-binding protein 1,and bone morphogenic protein-2 was downregulated.Furthermore,CFI could be used as a diagnostic biomarker for CC.Functionally,CFI silencing inhibited CC cell proliferation,migration,invasion,and tumor growth.Mechanistically,CFI knockdown downregulated the expression of key glycolysis-related proteins(glucose transporter type 1,hexokinase 2,lactate dehydrogenase A,and pyruvate kinase M2)and the Wnt pathway-related proteins(β-catenin and c-Myc).Further investigation indicated that CFI knockdown inhibited glycolysis in CC by blocking the Wnt/β-catenin/c-Myc pathway.CONCLUSION The findings of the present study demonstrate that CFI plays a crucial role in CC development by influencing glycolysis and the Wnt/β-catenin/c-Myc pathway,indicating that it could serve as a promising target for therapeutic intervention in CC.

Repetitive traumatic brain injury–induced complement C1–related inflammation impairs long-term hippocampal neurogenesis

Repetitive traumatic brain injury impacts adult neurogenesis in the hippocampal dentate gyrus,leading to long-term cognitive impairment.However,the mechanism underlying this neurogenesis impairment remains unknown.In this study,we established a male mouse model of repetitive traumatic brain injury and performed long-term evaluation of neurogenesis of the hippocampal dentate gyrus after repetitive traumatic brain injury.Our results showed that repetitive traumatic brain injury inhibited neural stem cell proliferation and development,delayed neuronal maturation,and reduced the complexity of neuronal dendrites and spines.Mice with repetitive traumatic brain injuryalso showed deficits in spatial memory retrieval.Moreover,following repetitive traumatic brain injury,neuroinflammation was enhanced in the neurogenesis microenvironment where C1q levels were increased,C1q binding protein levels were decreased,and canonical Wnt/β-catenin signaling was downregulated.An inhibitor of C1 reversed the long-term impairment of neurogenesis induced by repetitive traumatic brain injury and improved neurological function.These findings suggest that repetitive traumatic brain injury–induced C1-related inflammation impairs long-term neurogenesis in the dentate gyrus and contributes to spatial memory retrieval dysfunction.

Different serum levels of IgG and complements and recurrence rates in IgG4-positive and negative lacrimal gland benign lymphoepithelial lesion

·AIM:To analyze the differences in immune indicators and prognosis between Ig G4-positive and negative lacrimal gland benign lymphoepithelial lesion(LGBLEL).·METHODS:This was a single-center retrospective clinical study including 105 cases of Ig G4-positive LGBLEL and 41 cases of Ig G4-negative LGBLEL.Basic information,related indicators of peripheral venous blood samples using immunoscattering turbidimetry,treatment(partial surgical excision and glucocorticoid therapy)and prognosis(recurrence and death)were collected.Survival curves for recurrence were created using the Kaplan-Meier analysis.Univariate analysis and multivariate regression analysis were used to analyze prognostic factors.·RESULTS:The mean age was 50.10±14.23y and 44.76±11.43y(P=0.033)in Ig G4-positive and negative group respectively.The serum C3 and C4 was lower in Ig G4-positive group(P=0.005,P=0.002),while the serum Ig G and Ig G2 was higher in Ig G4-positive group(P=0.000 and P=0.008).Twenty-one cases had recurrence in Ig G4-positive group and 3 cases recurrence in Ig G4-negative group.The 5-year recurrence-free cumulative percentages of Ig G4-positive group was 81.85%,and 83.46%in the Ig G-negative group(P=0.216).The history of preoperative glucocorticoid therapy,serum C4,Ig G1 and Ig G2 were the factors affecting recurrence in Ig G4-positive group,while serum C4,and Ig G1 were the factors affecting recurrence of LGBLEL.·CONCLUSION:Serum C4 and Ig G1 are the factors affecting recurrence of LGBLEL,while the Ig G4 does not affect recurrence of LGBLEL.

Association of C-reactive protein and complement factor H gene polymorphisms with risk of lupus nephritis in Chinese population

BACKGROUND Complement overactivation is a major driver of lupus nephritis(LN).Impaired interactions of C-reactive protein(CRP)with complement factor H(CFH)have been shown as a pathogenic mechanism that contributes to the overactivation of complement in LN.However,genetic variations of neither CRP nor CFH show consistent influences on the risk of LN.AIM To examine whether genetic variations of CRP and CFH in combination can improve the risk stratification in Chinese population.METHODS We genotyped six CRP single nucleotide polymorphisms(SNPs)(rs1205,rs3093062,rs2794521,rs1800947,rs3093077,and rs1130864)and three CFH SNPs(rs482934,rs1061170,and rs1061147)in 270 LN patients and 303 healthy subjects.RESULTS No linkage was found among CRP and CFH SNPs,indicating lack of genetic interactions between the two genes.Moreover,CRP and CFH SNPs,neither individually nor in combination,are associated with the risk or clinical manifestations of LN.Given the unambiguous pathogenic roles of the two genes.CONCLUSION These findings suggest that the biological effects of most genetic variations of CRP and CFH on their expressions or activities are not sufficient to influence the disease course of LN.

补体C3水平对冻融胚胎移植妊娠结局的早期预测价值

目的探讨补体C3对冻融胚胎移植(F-ET)妊娠结局的早期预测价值。方法前瞻性收集378个F-ET周期相关资料,依据补体C3预测F-ET妊娠结局的最佳截断值分为A组(补体C3≤1.05)120个周期;B组(补体C3>1.05)258个周期,比较两组结局。分析B组补体C3预测F-ET自然流产的最佳截断值。结果年龄是F-ET妊娠成功的危险因素(P<0.05);补体C3和胚胎类型是F-ET妊娠成功的保护因素(P<0.05)。补体C3对F-ET妊娠结局的受试者工作特征曲线(ROC)曲线下面积为0.702,最佳截断值为1.05 g/L,其预测临床妊娠灵敏度为87.60%、特异度为52.00%。B组临床妊娠率(67.05%)和胚胎着床率(52.75%)明显高于A组,差异有统计学意义(P<0.05)。补体C3早期预测F-ET后自然流产最佳截断值为1.32 g/L,ROC曲线下面积为0.760,灵敏度为69.00%、特异度为81.20%。结论补体C3对早期预测F-ET妊娠结局有一定的临床意义,当补体C3超过1.32 g/L可能会导致自然流产率升高。

来氟米特联合环磷酰胺对狼疮性肾炎患者血清白蛋白及补体C3水平的影响

目的探讨狼疮性肾炎(LN)患者应用来氟米特联合环磷酰胺治疗的临床效果。方法选择2019年4月至2021年4月九江市第一人民医院收治的84例LN患者作为研究对象,采用随机数字表法将其分为观察组(42例)及对照组(42例)。两组均予以泼尼松治疗,观察组同时给予环磷酰胺加用来氟米特治疗,对照组同时给予环磷酰胺治疗。两组均持续用药6个月。比较两组的临床疗效、肾功能指标、血清白蛋白和补体C3水平,并记录不良反应发生情况。结果观察组的治疗总有效率高于对照组,差异有统计学意义(P<0.05);观察组治疗后的血尿素氮(BUN)、血肌酐(SCr)、24 h尿蛋白量水平均低于对照组,血清白蛋白、补体C3水平均高于对照组,差异有统计学意义(P<0.05);两组的不良反应总发生率比较,差异无统计学意义(P>0.05)。结论来氟米特联合环磷酰胺治疗LN效果显著,可有效提高血清白蛋白和补体C3水平,促进肾功能恢复,减轻肾功能损害,缓解临床症状,稳定病情,值得推广应用。

重症肌无力的免疫靶向治疗进展

重症肌无力(myasthenia gravis,MG)是由神经肌肉接头处的特异性自身抗体引起的自身免疫性疾病。MG的传统免疫治疗药物包括糖皮质激素、免疫抑制剂、静脉注射免疫球蛋白等。虽然这些免疫抑制剂对大多数MG患者有效,但所带来的不良反应或并发症仍为MG治疗中的难题。此外,非特异性免疫抑制剂通常起效较慢,且存在骨髓抑制、增加感染及肿瘤发生的风险。随着多种新型靶向生物制剂的涌现,MG的治疗进入分子免疫时代,为患者和临床医生提供了更多的治疗选择。本文重点综述了分别作用于MG病理生理过程中不同靶点的3类新型生物制剂,包括B细胞耗竭剂、末端补体C5抑制剂以及新生儿Fc受体(FcRn)抑制剂等。与传统的免疫制剂相比,此类靶向药物在MG治疗中的副作用更少,起效更快,而且具有潜在的长期持续疾病缓解能力。

血清主导的及肾小球沉积的IgG亚型和补体分子对肾小球疾病作用的研究进展

肾小球疾病患者血清主导的、肾小球沉积的IgG亚型和补体分子对疾病发生发展及其预后发挥重大作用。系统性红斑狼疮引起的狼疮肾炎患者,血清和肾小球中的IgG亚型以IgG1和IgG3为主,肾小球常见补体C1q和C3沉积,补体活化以经典途径为主,起病较急,病情较重,预后较差,补体C3、C4降低均反映疾病活动;原发性膜性肾病患者,血清和肾小球中的IgG亚型以IgG4为主,肾小球常见补体C3、C4d沉积,补体活化以凝集素途径为主,起病较慢,病情较轻,预后较好,血清特异性抗磷脂酶A2受体抗体滴度升高反映病情活动。其他肾小球疾病如IgA肾病、抗中性粒细胞胞浆抗体相关小血管炎肾损伤等,血清及肾小球IgG亚型、补体分子也有较多研究报道,而感染性、代谢性、肿瘤相关肾小球疾病,相关研究报道较少,对疾病的诊断、鉴别诊断以及预后的评估价值有待进一步探讨。

基于改进互补品序贯拍卖模型的建设用地指标定价机制

在引入用地指标与土地间相互依存特征前提下,本文改进了传统的互补品序贯拍卖模型,以期提出具有针对性的用地指标定价方法。研究表明,建设用地指标的成交价格受竞标人数和土地闲置费用的影响。竞标人指标报价随竞标人数递增而降低,但随土地闲置费递增而递增。进一步分析表明,适当提高土地闲置费用及资质审核要求可最大程度显化指标核心价值,激发农民退出闲置宅基地的积极性,提高农村用地的使用效率。研究为盘活农村闲置土地资产,实现可持续化发展给予了一定的理论参考。

遗传性血管性水肿急诊科诊疗路径

遗传性血管性水肿(hereditary angioedema,HAE)是一种常染色体显性遗传病,以反复发作的皮肤和黏膜水肿为特征。水肿可出现在任何部位,最致命的为喉水肿,引发窒息,危及生命。若水肿累及消化道黏膜,可引起腹痛、呕吐等症状,易误诊为急腹症。颜面、躯干及四肢等皮肤水肿也严重影响患者生活质量。为提高急诊科医生的识别及处理能力,本专业组特编写此诊疗路径。路径除对HAE的发病机制、临床表现等进行介绍外,还汇总了既往在中国已经发表的急诊科病例,以便广大医生更好的理解疾病,并绘制诊疗路径图,为临床实践提供参考依据。

土壤学互融互补混合式智慧教学模式改革成效

土壤学是理论系统性高和应用实践性强的重要专业基础课。探索基于网络信息技术的土壤学线上线下混合式教学的新型模式,对于全面推进新时代一流专业建设及一流专业人才培养至关重要。综合应用文献查阅法、问卷调查法和经验总结法,以优化教学内容和变革教学策略为途径,构建土壤学“互融互补混合式智慧教学模式”。这一新型教学模式包含“思政元素、专业应用、学科前沿、行业发展”的四元融合知识体系、“课前-课中-课后”三环渐进混合式智慧教学方式、“一、二课堂互补,现实虚拟互补”的二维互补实践创新能力培养体系。模式实施以来有力地提升土壤学“一流课程”“思政示范课”建设质效,以及富有“三农”情怀、能“识土-辨土-用土-改土”的新农科复合型高级人才质量,为其他传统专业课改革提供借鉴。

全可再生能源多能互补系统优化配置与运行探索

在机组100%为全可再生能源的多能互补系统的基础上,通过部分市网供电及“隔墙售电”消纳改进其容量配置和调度优化模型并通过LINGO求解,考察市网供电和“隔墙售电”对系统经济性和碳排放参数的影响。结果表明:随着隔墙售电的电价增长,系统的运行费用及蓄电池的容量随之下降,在售电电价增至0.33元/kWh后蓄电池单元容量趋于稳定;在售电电价达到0.37元/kWh后系统不再因电价的上升而引起系统运行策略的改变;园区多能互补系统相比不参与“隔墙售电”的传统系统,系统年总费用降低25.9%,年运行成本降低37.8%,碳排放强度由76.9 kgCO_(2)/(m^(2)·a)降至52.3 kgCO_(2)/(m^(2)·a)。

妊娠期糖尿病患者血清Xenin-25、CTRP12水平及对妊娠结局的影响

目的分析妊娠期糖尿病(GDM)患者血清神经降压素相关肽(Xenin-25)、C1q肿瘤坏死因子相关蛋白12(CTRP12)与妊娠结局的关系。方法选取2021年2月—2022年2月川北医学院附属医院生殖医学科诊治的GDM患者92例为GDM组,再根据是否发生不良妊娠结局,分为预后不良亚组(n=34)和预后良好亚组(n=58)。以同期健康妊娠妇女50例为正常妊娠组。采用酶联免疫吸附法检测血清Xenin-25、CTRP12水平;Pearson相关性分析血清Xenin-25、CTRP12与糖代谢指标的相关性;多因素Logistic回归分析影响GDM患者不良妊娠结局的因素;受试者工作特征曲线评价血清Xenin-25、CTRP12对妊娠结局的预测价值。结果GDM组血清Xenin-25、CTRP12低于正常妊娠组,而空腹血糖(FPG)、糖化血红蛋白(HbA_(1c))、空腹胰岛素(FINS)及稳态模型评估的胰岛素抵抗指数(HOMA-IR)水平均高于正常妊娠组(t/P=16.046/<0.001,22.114/<0.001,11.510/<0.001,13.666/<0.001,12.101/<0.001,14.413/<0.001);GDM组血清Xenin-25、CTRP12表达与FPG、FINS、HbA_(1c)及HOMA-IR呈显著负相关(Xenin-25:r/P=-0.665/<0.001,-0.598/<0.001,-0.567/<0.001,-0.702/<0.001;CTRP12:r/P=-0.579/<0.001,-0.622/<0.001,-0.667/<0.001,-0.725/<0.001);预后不良亚组血清Xenin-25、CTRP12低于预后良好亚组,HOMA-IR高于预后良好亚组(t/P=6.783/<0.001,17.997/<0.001,15.146/<0.001);血清CTRP12升高、Xenin-25升高是影响GDM患者不良妊娠结局的独立保护因素[OR(95%CI)=0.646(0.499~0.837),0.619(0.465~0.824)],HOMA-IR升高是危险因素[OR(95%CI)=1.353(1.110~1.649)]。血清Xenin-25、CTRP12及二者联合预测GDM患者不良妊娠结局的AUC分别为0.828、0.815、0.870,二者联合优于各自单独预测效能(Z=4.113、4.327,P=0.003、0.001)。结论GDM孕妇血清Xenin-25、CTRP12水平降低,均参与GDM的疾病过程,二者联合对GDM患者不良妊娠结局具有较高的评估价值。

靶向补体的IgA肾病治疗进展

越来越多的证据表明,补体系统活化在IgA肾病发病和进展中起重要作用。近年来,一些靶向补体成分的新药开发,为IgA肾病的治疗提供了新的措施。针对补体成分C3、B因子、D因子、C5、C5a受体等的药物,已经进入治疗IgA肾病的临床试验。本文对靶向补体的IgA肾病治疗进展进行综述。

ST段抬高型心肌梗死患者血清转化生长因子11、补体C1q/肿瘤坏死因子相关蛋白5的表达及临床意义

目的 探讨转化生长因子11(transforming growth factor 11,GDF11)、补体C1q/肿瘤坏死因子相关蛋白5(complement C1q/tumor necrosis factor-related protein 5,CTRP5)在ST段抬高型心肌梗死(ST-segment elevation myocardial infarction,STEMI)患者血清中的表达及诊断价值。方法 选取2019年3月到2021年2月石家庄市第三医院收治的60例STEMI患者为心肌梗死组,另选取同期健康体检者50名为对照组。检测两组受试者血清GDF11、CTRP5的表达水平。采用Pearson相关性分析对STEMI患者血清中GDF11和CTRP5表达水平及二者与高密度脂蛋白胆固醇(high-density lipoprotein cholesterol,HDL-C)、血糖(blood glucose,GLU)、白细胞计数(white blood cell count,WBC)、中性粒细胞计数(neutrophil count,NEUT)、单核细胞计数(monocyte count,MONO)及超敏C反应蛋白(hypersensitive C reactive protein,hs-CRP)、高敏心肌肌钙蛋白T(high-sensitivity cardiac troponin T,hs-cTnT)、肌酸激酶同工酶(creatine kinase isoenzymes,CK-MB)浓度及预后不良事件的相关性进行分析。采用受试者工作特征曲线(receiver operating characteristic curve,ROC)分析血清中GDF11和CTRP5对STEMI患者的诊断价值。结果 心肌梗死组患者的血清GDF11(1.42±0.35 vs. 0.99±0.18,t=7.860,P<0.05)和CTRP5(1.49±0.43 vs. 1.01±0.22,t=7.148,P<0.05)表达水平高于对照组,差异有统计学意义。相关性分析结果显示,心肌梗死组血清GDF11和CTRP5表达水平呈正相关(r=0.550,P<0.05),GDF11和CTRP5表达水平与HDL-C呈负相关(r=-0.548,-0.592,P<0.05),与GLU(r=0.447,0.534,P<0.05)、WBC(r=0.653,0.502,P<0.05)、NEUT(r=0.562,0.578,P<0.05)、MONO(r=0.439,0.423,P<0.05)、hs-CRP(r=0.513,0.542,P<0.05)、hs-cTnT(r=0.513,0.524,P<0.05)、CK-MB(r=0.630,0.417,P<0.05)及预后不良事件(r=0.557,0.529,P<0.05)呈正相关。GDF11和CTRP5联合诊断STEMI的ROC曲线下面积大于GDF11、CTRP5单独诊断(Z=2.424、2.507,P<0.05)。结论 GDF11和CTRP5在STEMI患者血清中表达水平升高,两者联合对STEMI具有较高的诊断价值。

大剂量阿托伐他汀联合双联抗血小板对急性脑梗死患者C3aR1的影响及颈动脉斑块的超声研究

目的探讨大剂量阿托伐他汀联合双联抗血小板对急性脑梗死患者补体激活3a受体1(C3aR1)及颈动脉斑块的影响。方法回顾性分析保定市第一中心医院诊治的129例急性脑梗死患者的一般资料,分为大剂量组65例,常规剂量组64例。常规剂量组接受常规剂量阿托伐他汀联合双联抗血小板治疗,大剂量组接受大剂量阿托伐他汀联合双联抗血小板治疗,比较2组患者颈动脉斑块面积、颈动脉内膜中层厚度(IMT)、NIHSS评分、生活自理量表(ADL)评分、超敏C反应蛋白(hs-CRP)、血脂、C3aR1及不良反应发生率。结果治疗后大剂量组甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、总胆固醇(TC)水平较常规剂量组低,高密度脂蛋白胆固醇(HDL-C)水平较常规剂量组高(P<0.05)。治疗后,大剂量组hs-CRP、C3aR1水平较常规剂量组低(P<0.05),颈动脉斑块面积较常规剂量组小,IMT较常规剂量组薄(P<0.05)。治疗后,大剂量组NIHSS评分较常规剂量组低,ADL评分较常规剂量组高(P<0.05)。2组治疗期间不良反应发生率比较(13.85%比9.38%)差异无统计学意义(χ^(2)=0.627,P=0.428)。结论大剂量阿托伐他汀联合双联抗血小板治疗可改善急性脑梗死患者的血脂水平,减轻炎症反应和神经损伤,降低C3aR1水平,减小颈动脉斑块面积,疗效确切,安全性高。

急性脑梗死患者血清CFH、VASH-1表达与病情、疾病转归的关系

目的分析急性脑梗死患者血清补体H因子(CFH)、血管生成抑制蛋白-1(VASH-1)表达与病情、疾病转归的关系。方法选择96例急性脑梗死患者为研究组,根据美国国立卫生院卒中量表(NIHSS)评分分为轻度组、中度组、重度组,按疾病转归分为恶化组、转归组。另选取同期体检健康者80例为对照组。比较各组血清CFH、VASH-1水平。采用ROC评估血清CFH、VASH-1对急性脑梗死患者疾病转归的诊断价值,Logistic回归分析影响疾病转归的因素。结果血清CFH水平研究组<对照组,重度组<中度组<轻度组,恶化组<转归组;血清VASH-1水平研究组>对照组,重度组>中度组>轻度组,恶化组>转归组(P<0.05)。血清CFH、VASH-1及二者联合评估急性脑梗死疾病转归的AUC分别为0.830、0.866、0.915。血清低CFH、高VASH-1及高NHISS评分为急性脑梗死患者疾病转归的危险因素(P<0.05)。结论急性脑梗死患者血清CFH、VASH-1水平与病情、疾病转归有关,可作为评估急性脑梗死患者疾病转归的可靠生物学标志物。