急性腔隙性脑梗死患者血清C反应蛋白和白介素-8水平的变化及临床意义

目的 探讨急性腔隙性脑梗死患者血清高敏C反应蛋白(hs-CRP)、白介素-8水平(IL-8) 的变化及其在发病机制中的作用.方法 分别检测36例腔隙性脑梗死和36例脑梗死患者及36例健康对照者血清hs-CRP和IL-8含量.结果 腔梗组和脑梗组hs-CRP含量分别为(10.42±0.68)mg/L和(18.45±1.28)mg/L,均显著高于对照组的(1.28±0.47)mg/L(P<0.01),CI组hs-CRP含量亦显著高于健康对照组(P<0.01);腔梗组和脑梗组IL-8含量分别为(29.65±18.24)ng/ml和(36.57±19.01)ng/ml,显著高于对照组的(25.98±16.87)ng/ml(P<0.01).在脑梗患死者中,大面积脑梗死组(≥9ml,n=16)hs-CRP为(21.36±1.48)mg/L,显著高于小面积脑梗死组(<9ml,n=20)的(15.30±0.97)mg/l(P<0.01),2组IL-8含量分别为(38.1±19.87)ng/ml和(33.45±18.67)ng/mL,差异亦有统计学意义(P<0.01).结论 炎症过程参与了脑小血管病变;hs-CRP和IL-8水平与脑缺血程度以及脑的小血管病变范围密切相关.hs-CRP 及IL-8是预测脑梗死患者病情严重程度的重要生化指标.     

脑梗死患者血清可溶性CD40L、白介素-18水平的变化及意义

目的 探讨脑梗死患者的血清可溶性CD40L(sCD40L)、白介素-18(IL-18)水平的变化及意义.方法 采用酶联免疫吸附法测定40例腔隙性脑梗死患者(腔梗组)、40例脑梗死患者(脑梗死组)和38名正常对照者(NC组)的血清sCD40L、IL-18水平,并对脑梗死患者进行颈动脉超声检查及美国国立卫生研究院卒中量表(NIHSS)评分.结果 与正常对照组比较,腔梗组及脑梗死组血清sCD40L及IL-18显著升高(均P＜0.01);且脑梗死组显著高于腔梗组(均P＜0.01).中、重度脑梗死患者的血清sCD40L及IL-18水平显著高于正常对照组及轻度脑梗死患者(P ＜0.05 ～0.01).与内膜正常患者比较,有稳定斑块及不稳定斑块患者的血清sCD40L及IL-18水平显著升高(均P＜0.01),内膜增厚患者IL-18水平显著升高(P＜0.05).与内膜增厚患者比较,有稳定斑块患者的血清sCD40L水平和有不稳定斑块患者的血清sCD40L及IL-18水平显著升高(均P＜0.01).有不稳定斑块患者的血清sCD40L及IL-18水平显著高于有稳定斑块的患者(均P＜0.01).脑梗死患者血清sCD40L水平与IL-18水平呈正相关(r=0.729,P＜0.01).结论 脑梗死患者血清sCD40L、IL-18水平显著升高,并能反映颈动脉粥样硬化程度及脑梗死病情.     

高同型半胱氨酸血症在脑梗死氧化应激和炎症损伤机制中的作用

目的 探讨高同型半胱氨酸血症(Hhcy)在脑梗死发病机制中的作用.方法 选取急性脑梗死患者,根据血浆总同型半胱氨酸(tHcy)水平,将其分为Hhcy组和非Hhcy(Nhhcy)组,除外脑血管疾病和肝肾甲状腺疾病患者40例作为对照.分别测血浆tHcy、血清丙二醛(MDA)、白细胞介素-8(IL-8)水平,并研究其相关性.结果 病例组tHcy(μmol/L,下同)、MDA(nmol/L,下同)、IL-8(ng/ml,下同)水平分别为19.97、4.41±0.84、0.23±0.08,显著高于对照组的9.83、3.24±0.64、0.12±0.08,t值分别为8.139,8.021,7.767(均P＜0.01);病例组中Hhcy患者的tHcy、MDA、IL-8水平分别为24.40、4.70±0.76、0.25±0.07,显著高于Nhhcy患者的10.33、3.76±0.61、0.16±0.06,t值分别为13.213,6.543,6.520(P＜0.01).tHcy水平与MDA、IL-8水平具有相关性(P＜0.01).结论 Hhcy在脑梗死发病机制中的作用可能与其参与氧化应激反应和炎症损伤过程有关.     

老年卒中后抑郁患者血清细胞因子的研究

目的 探讨老年卒中后抑郁患者(PSD)血清细胞因子白细胞介素-1β(II-1β)、白细胞介素-6(IL-6)以及肿瘤坏死因子(TNF-α)的水平.方法 采用酶联免疫吸附法检测PSD组(36例)及卒中后无抑郁患者(对照组;32例)的血清IL-1β、IL-6及TNF-α水平,并以汉密尔顿抑郁量表(HAMD)评分将PSD组分为轻度组(8～16分;9例)、中度组(17～23分;17例)及重度组(≥24分;10例),比较各组血清IL-1β、IL-6及TNF-α水平的差异.结果 (1)PSD组血清IL-1β[(35.2±4.2)ng/L]、IL-6[(11.3±4.3)ng/L]及TNF-α[(32.4±6.9)ng/L]水平,均高于对照组[分别为(18.1±3.3)ng/L、(6.1±1.9)ng/L及(21.6±4.8)ng/L;P＜0.01];(2)卒中后重度抑郁组血清IL-1β[(41.8±3.2)ng/L]、IL-6[(17.5±5.7)ng/L]及,TNF-α[(38.8±5.8)ng/L]水平,均高于轻度抑郁组[分别为(29.1±2.3)ng/L、(6.6 ±1.7)ng/L及(25.9 ±3.3)ng/L;P＜0.05]、中度抑郁组[分别为(34.6±2.6)ng/L、(10.2 ±3.5)ng/L及(32.1±3.6)ng/L;P＜0.05],中度抑郁组亦高于轻度抑郁组(P＜0.05);(3)血清IL-1β(r=0.637)、IL-6(r=0.698)、TNF-α(r=0.722)水平均与抑郁的严重程度显著相关(P＜0.01).结论 IL-1β、IL-6及TNF-α可能在卒中后抑郁的发生发展中起重要作用.     

丹参素预处理对脑梗死大鼠血浆纤溶激活系统的影响

目的 观察丹参素预处理对脑梗死大鼠血浆纤溶激活系统的影响.方法 40只雄性大鼠,随机分为假手术组、脑梗死对照组、低剂量[5 mg/(kg·d)]丹参素组和高剂量[10 mg/(kg·d)]丹参素组,每组10只.应用自体血栓注入,制成大鼠脑梗死模型;用ELISA方法 检测血浆中组织型纤溶酶原激活物(t-PA)及其抑制物(PAI-I)含量;RT-PCR测定大鼠脑组织中t-PA mRNA及其PAI-I mRNA表达的变化.结果 与脑梗死对照组[(2.65±0.43)ng/ml]比较,低剂量及高剂最丹参素组t-PA含量[(3.29±0.13)ng/ml、(6.37±0.19)ng/ml]明显升高(均P＜0.01),两丹参素组之间差异亦有统计学意义(P＜0.0I);与脑梗死对照组比较,低剂量丹参素组PAI-I含量[(2.65±0.40)ng/ml]降低(P＜0.05),高剂量丹参素组PAI-I含量[(1.98±0.32)ng/ml]明显降低(P＜0.01),两丹参素组之间差异亦有统计学意义(P＜0.01);与脑梗死对照组比较,低剂量及高剂量丹参素组t-PA mRNA表达[灰度值分别为(0.37±0.14)、(0.46±0.12)]均明显升高(均P＜0.01),两丹参素组之间差异亦有统计学意义(P＜0.01);与脑梗死对照组比较,低剂量及高剂量丹参素组PAI-I mRNA表达[灰度值分别为(0.54±0.12)、(0.36±0.07)]均明显降低(均P＜0.01),两丹参素组之间差异亦有统计学意义(P＜0.01).结论 丹参素可以改善脑梗死大鼠纤溶功能,并且有剂量依赖性.     

TNF-α hs-CRP LDL-c与老年急性脑梗死的相关性研究

目的研究肿瘤坏死因子(TNF-α)、血清超敏C反应蛋白(Chs-CRP)、低密度脂蛋白(LDL-c)与老年急性脑梗死的相关性。方法选取我院2013-03—2015-10收治的老年急性脑梗死患者62例设为观察组,选取同的健康体检者56例设为健康对照组。检测2组受试者TNF-α、hs-CRP、LDL-c水平,分析TNF-α、hs-CRP、LDL-c水平与老年急性脑梗死的相关性。结果观察组TNF-α(2.24±0.37)ng/L、hs-CRP(10.38±1.27)mg/L、LDL-c(3.75±0.42)mmol/L,均显著高于健康对照组的(1.23±0.14)ng/L、(2.86±0.43)mg/L、(2.06±0.23)mmol/L,差异均有统计学意义(P0.05);中型脑梗死和重型脑梗死患者的TNF-α、hs-CRP、LDL-c水平显著高于轻型脑梗死患者(P0.05),重型脑梗死患者TNF-α、hs-CRP、LDL-c水平显著高于中型脑梗死患者(P0.05)。结论老年急性脑梗死患者血清TNF-α、hs-CRP、LDL-c水平与病情严重程度呈正相关,TNF-α、hs-CRP、LDL-c指标的检测对老年急性脑梗死患者病情的评估具有较高的临床价值。     

无症状脑梗死患者血清高敏C反应蛋白和肿瘤坏死因子-α水平的变化及其临床意义

目的：探讨无症状脑梗死（SCI）患者血清高敏C反应蛋白（hs-CRP）、肿瘤坏死因子-α（TNF-α）水平的变化及其在发病机制中的作用。方法：分别检测40例SCI、40例脑梗死（CI）患者、40例健康对照者血清hs-CRP和TNF-α含量。结果：SCI组和cI组hs—CRP含量分别为（8．86±0．96）和（16．32±1．88）mg／L，均显著高于对照组的（1．69±0．56）mg／L（P〈0．01），CI组hs—CRP含量亦显著高于SCI组（P〈0．05）；SCI组和CI组TNF-α含量分别为（1．92±0．73）和（2．56±0．91）ng／mL，显著高于对照组的（1．13±0．42）ng／mL（P〈0．01），CI组TNF-α含量亦显著高于SCI组（P〈0．05）。在SCI患者中，梗死灶数〉2个组（n=19）hs-CRP为（9．45±0．97）mg／L，显著高于梗死灶数≤2个组（n=17）的（7．21±0．75）mg／L（P〈0．01），两组TNF-α含量分别为（1．97±0．83）和（1．66±0．56）ng／mL，无显著差异。血压测定值越高，腔隙性梗死灶数量越多，未服降压药者梗死灶数量显著多于正规降压治疗者（P〈0．05）。结论：炎症过程参与了脑小血管病变；hs—CRP和TNF-α水平与脑缺血程度、神经功能缺损程度以及脑的小血管病变范围密切相关。高血压是腔隙性SCI最常见的病因，未降压治疗的重度高血压更易引起多发性腔隙性脑梗死。从预防再发的角度看，对SCI应尽早采取积极有效的治疗措施，高血压患者应尽早正规服用降压药。     

不同炎症反应在脑梗死与短暂性脑缺血发作患者中表达及意义研究

目的探讨不同炎症因子在脑梗死与短暂性脑缺血发作患者的表达情况。方法选取64例短暂性脑缺血发作患者(TIA组)、58例脑梗死患者(CI组)以及50例健康人员(NC组),分析并统计3组受试对象炎症因子表达情况。结果 CI组MMP-9(83.14±9.27)μg/L、NF-κB(36.88±6.27)%、IL-33(71.63±4.83)ng/m L及hs-CRP(12.57±1.29)mg/L,TIA组分别为(29.17±4.54)μg/L、NF-κB(31.20±5.97)%、IL-33(104.59±8.27)ng/m L及hs-CRP(6.23±1.04)mg/L,两组间比较差异具有统计学意义(P=0.026、P=0.032、P=0.025和P=0.009)。Logistic回归分析显示,TC、MMP-9、IL-33及hs-CRP为CI的独立危险因素。TC、hs-CRP为TIA的独立危险因素。MMP-9+IL-33+hs-CRP预测CI发生的AUC为0.859(95%CI:0.751~0.911),显著高于MMP-9(AUC为0.711,95%CI:0.649~0.824)、IL-33(AUC为0.698,95%CI:0.659~0.855)和hs-CRP(AUC为0.705,95%CI:0.671~0.848)的诊断效能(Z=9.267、11.553和10.234,均P=0.000)。结论脑梗死、短暂性脑缺血发作患者存在炎症因子表达差异,MMP-9、IL-33及hsCRP联合检测对CI具有较高的诊断价值。     

脑梗死后癫(癎)患者血清细胞因子水平的改变

目的 研究脑梗死后癫(癎)患者血清细胞因子水平的改变.方法 应用放射免疫法检测87例脑梗死后癫癎患者(脑梗死癫(癎)组)和75名健康体检者(正常对照组)的血清肿瘤坏死因子α(TNF-α),白细胞介素(IL)-2和IL-6水平.结果 脑梗死癫(癎)组血清TNF-α[(2.5±0.57)ng/L]、IL-2[(9.0 4-0.83)ns/L]及IL-6[(97.5±3.1)ng/L]水平明显高于正常对照组[TNF-α(0.89 4-0.36)ng/L,IL-2(4.3±1.5)ng/L,IL-6(13.3 4-11.1)ng/L](均P＜0.01).结论 脑梗死后癫(癎)患者的血清细胞因子TNF-α、IL-2及IL-6水平显著升高,提示细胞因子可能在脑梗死后癫(癎)的发病中起重要作用.     

进展性脑梗死患者血清超敏C反应蛋白水平的变化及其临床意义

目的探讨进展性脑梗死患者血清超敏C反应蛋白(hs-CRP)水平的变化及其临床意义。方法检测63例脑梗死患者(25例进展性脑梗死、38例完全性脑梗死)和73名健康对照者(正常对照组)的血清hs-CRP含量。结果脑梗死患者的血清hs-CRP水平[(5.69±3.78)mg/L]明显高于正常对照组[(0.85±0.47)mg/L](P<0.01);进展性脑梗死组血清hs-CRP水平[(7.55±4.25)mg/L]明显高于完全性脑梗死组[(4.52±2.96)mg/L](P<0.01)。结论脑梗死患者血清hs-CRP水平明显升高,进展性脑梗死患者较完全性脑梗死患者血清hs-CRP水平升高更明显;提示hs-CRP参与了脑梗死的发生与发展过程。     

Presence and severity of anorexia and bulimia among male and female Omani and non-Omani adolescents

OBJECTIVE: The population of Oman is a heterogeneous mix of nationalities providing a natural setting for studying the cross-cultural differences in the presence and severity of eating disorders as well as an opportunity for evaluating the performance of measurement instruments for these disorders. METHOD: Disordered eating screening instruments (the Eating Attitude Test and the Bulimic Investigatory Test) were administered to Omani teenagers, non-Omani teenagers, and Omani adults. RESULTS: On the Eating Attitude Test, 33% of Omani teenagers (29.4% females and 36.4% males) and 9% of non-Omani teenagers (7.5% of males and 10.6% females) showed a propensity for anorexic-like behavior. On the Bulimic Investigatory Test, 12.3% of Omani teenagers showed a propensity for binge eating or bulimia (13.7% females and 10.9% males). Among the non-Omani teenagers, 18.4% showed a tendency toward bulimia, with females showing a slightly greater tendency than males. In contrast, barely 2% of Omani adults showed either a presence of or a severity of disorderly behavior with food. CONCLUSION: Omani teenagers scored significantly higher than other ethnic groups and Omani adults. This finding is discussed in the light of emerging evidence from many parts of the world suggesting that cultural transition, compounded by demographic constraints, plays a significant role in abnormal eating attitudes.     

Physical and Sexual Abuse and Neglect and Eating Disorder Symptoms

For eating-disordered patients with a history of post-traumatic stress, childhood abuse and neglect, and dissociative disorder, eating behavior symptoms may function as a rational response to unmetabolized traumatic experiences. This paper will review trauma-based theory, dissociation, abreactive, and ego-states therapy as they apply to eating disorder patients.     

Efficacy and Effectiveness of Child and Adolescent Psychotherapy and Pharmacotherapy

Decades of intervention research have produced a rich body of evidence on the effects of psychotherapies and pharmacotherapies with children and adolescents. Here we summarize and critique that evidence. We review findings bearing on the efficacy of psychosocial treatments and medications under controlled experimental conditions. We also report evidence, where available, on the effectiveness of both classes of treatment with clinically referred youth treated in real-world clinical contexts. In general, the large body of evidence on efficacy contrasts sharply with the small base of evidence on effectiveness. Addressing this gap through an enriched research agenda could contribute importantly to linking scientific inquiry and clinical practice—to the benefit of both ventures. This is one element of a multifaceted agenda for future research and for synthesis of research, which will require the interplay of multiple disciplines related to child and adolescent mental health.     

Physical and Sexual Abuse and Neglect and Eating Disorder Symptoms

Abstract

For eating-disordered patients with a history of post-traumatic stress, childhood abuse and neglect, and dissociative disorder, eating behavior symptoms may function as a rational response to unmetabolized traumatic experiences. This paper will review trauma-based theory, dissociation, abreactive, and ego-states therapy as they apply to eating disorder patients.     

Antidepressants and cytokines--clinical and experimental studies

Clinical and experimental studies indicate that stress and depression are associated with the up-regulation of the immune system, including increased production of pro-inflammatory cytokines. When administered to patients or laboratory animals, some of these cytokines induce typical symptoms of depression. It is known that cytokines modulate brain neurotransmission and the activity of the hypothalamic-pituitary-adrenal axis, both of which are disturbed in depression. This review summarizes in vivo, ex vivo and in vitro clinical and experimental studies of the effect of antidepressants on cytokine production. In vitro culture and animal studies in particular suggest that antidepressants of several classes decrease the production of pro-inflammatory cytokines and shift the pro/anti-inflammatory cytokine balance towards the latter. Some studies suggest that immunological disturbances, including changes in cytokine levels, are not shared by all depressive patients, which means that only in certain groups of patients may the immunomodulatory action of antidepressants play a significant role in producing the therapeutic effect.     

Anger and depression--theoretical and clinical considerations

The Freudian idea of inhibited anger being central to the pathogenesis of depression has been one of the cornerstones of psychiatric thinking. The aim of this article is to review the literature on psychotherapy theory and the relevant research with regard to the association of anger and depression, and to discuss clinical implications in treating depressive patients. Choice of research articles was based on systematic search of databases. Psychotherapy theories are mostly found in books not included in databases. Literature on psychotherapy theory was selectively chosen. Over-control, under-control and mixtures of the two may be present in depression, indicating problems in anger regulation. The links between anger and depression form a complex network. When treating patients with depression, explicit or implicit dealing with anger often seems to be helpful. In clinical reality, the relative amounts of elicitation of anger experience and training in expressive control needed by depressive patients may vary between different types of patients, different phases of depressive disorder, and different phases of therapy.