抑郁症患者血清 Galectin-3、Netrin-1、IL-33水平与其认知功能损害的关系

目的 探讨抑郁症患者血清半乳糖凝集素-3(Galectin-3)、神经轴突导向因子-1(Netrin-1)、白介素-33(IL-33)水平表达,分析其与患者认知功能损害的关系.方法 选取2016年1月至2019年12月我科收治的抑郁症患者130例作为研究对象(抑郁症组).同期,另选取我院体检健康志愿者100例(对照组).采用酶联免疫吸附法检测两组血清Galectin-3、Netrin-1、IL-33水平.采用智力状态检查量表(MMSE)评估患者认知功能受损程度.采用多因素Logistic回归分析影响抑郁症患者认知功能损害的危险因素.结果 抑郁症组血清Galectin-3、IL-33水平高于对照组,血清Netrin-1低于对照组,差异有统计学意义(P＜0.05).认知障碍组血清Galectin-3、Netrin-1、IL-33、HAMD-17评分和MMSE评分与认知正常组血清Galectin-3、Netrin-1、IL-33、HAMD-17评分和MMSE评分相比,差异有统计学意义(P＜0.05).多因素Logistic回归分析显示,血清Galectin-3、IL-33、HAMD-17评分升高和血清Netrin-1降低是影响抑郁症患者认知功能损害的独立危险因素(P＜0.05).ROC曲线结果显示,血清Galectin-3、Netrin-1、IL-33及三者联合检测预测患者认知功能损害的AUC分别为0.801、0.788、0.843和0.910.结论 抑郁症患者血清GaIectin-3、IL-33水平升高及Netrin-1水平降低,与患者认知功能损害密切相关,联合检测血清Galectin-3、Netrin-1、IL-33对抑郁症患者认知功能损害的预测价值更高,从而有助于尽早进行预防.     

血清YKL-40及sLOX-1水平与急性缺血性脑梗死患者短期预后的相关性研究

目的 探讨血清甲壳质酶蛋白-40(YKL-40)及可溶性凝集素样氧化型低密度脂蛋白受体-1(sLOX-1)水平与急性缺血性脑梗死患者短期预后的相关性.方法 收集2017年6月至2020年6月我院诊治的急性缺血性脑梗死患者168例,依据患者脑梗死体积分为大梗死组(n = 36)、中梗死组(n = 77)、小梗死组(n= 55),依据患者神经功能缺损程度分为轻度组(n = 36)、中度组(n = 70)、重度组(n = 62),依据患者发病后3个月预后不同分为死亡组(n= 17)、未死亡组(n= 151).比较各组一般资料和血清YKL-40、sLOX-1水平,并对急性缺血性脑梗死患者血清YKL-40、sLOX-1水平与短期预后的关系进行相关性分析.结果 大梗死组血清YKL-40、sLOX-1水平较中梗死组、小梗死组明显升高,神经功能缺损程度较中梗死组和小梗死组明显加重(P＜0.05),而中梗死组较小梗死组亦明显加重(P＜0.05).重度组、中度组、轻度组血清YKL-40、sLOX-1水平依次明显降低,组间两两比较差异有统计学意义(P＜0.05).死亡组脑梗死体积、神经功能损伤程度、血清YKL-40、sLOX-1水平较未死亡组明显提高(P＜0.05);脑梗死体积、神经功能受损程度、YKL-40、sLOX-1是急性缺血性脑梗死患者短期预后的危险因素(P＜0.05).Spearman参数相关性分析提示血清YKL-40,sLOX-1水平与急性缺血性脑梗死短期随访死亡率呈明显的正相关(r = 0.613、0.592,PP＜0.05).结论 急性缺血性脑梗死患者血清YKL-40及sLOX-1水平呈明显增高趋势,其表达水平与急性缺血性脑梗死患者短期预后存在明显的相关性,可作为急性缺血性脑梗死患者短期预后评估的有效标志物.     

急性缺血性脑卒中患者血清Occludin表达水平及其临床意义

目的 探讨急性缺血性脑卒中(AIS)患者血清闭合蛋白(Occludin)表达水平及其临床意义.方法 选取我院2019年1月至2020年12月收治的207例AIS患者为AIS组,另选取同期68例体检健康者为对照组.收集患者临床资料,酶联免疫吸附法测定血清Occludin水平.比较不同病情严重程度AIS患者血清Occludin水平,Spearman相关性分析AIS患者血清Occludin水平与NIHSS评分的相关性.分析血清Occludin水平与出血转化的关系,多因素Logistics回归分析AIS患者预后不良影响因素,ROC曲线分析血清Occludin水平与AIS发生、出血转化、预后的关系.结果 AIS组血清Occludin水平明显高于对照组(P<0.05).重度缺损组血清Occludin水平明显高于中、轻度缺损组,中度缺损组血清Occludin水平明显高于轻度缺损组(P<0.05).血清Occludin水平与NIHSS评分呈正相关(rs=0.512,P<0.05).出血转化组血清Occludin水平明显高于非出血转化组(P<0.05).高血清Occludin水平(OR=2.121,95％CI:1.457～3.086)为AIS患者预后不良独立危险因素(P<0.05).血清Occludin水平预测AIS发生、出血转化、预后不良的曲线下面积为0.856、0.770、0.857.结论 AIS患者血清水平明显升高,与病情严重程度密切相关,可作为AIS发生、出血转化、预后不良的预测指标.     

高血压合并急性缺血性脑卒中患者血清Gal-3水平与预后的关系

目的 探究血清半乳糖凝集素-3(galectin-3,Gal-3)水平与高血压合并急性缺血性脑卒中患者预后的关系.方法选取2019年3月至2020年2月我院就诊的120例高血压合并急性缺血性脑卒中患者,设为观察组,同时选取同期60例高血压无合并缺血性脑卒中患者作为高血压组,选取60名体健志愿者作为对照组.观察组患者入组后根据美国国立卫生研究院卒中量表(national institute of health stroke scale,NIHSS),将其分为轻症组,中症组,重症组.治疗90 d后进行相关随访,根据mRS评分(改良Rankin量表,modified rankin scale,mRS)将患者分为预后良好组与预后不良组.采用酶联免疫吸附试验(ELISA)检测各组患者血清Gal-3表达水平,分析血清Gal-3表达水平与患者病情严重程度及预后的关系,绘制受试者工作特征曲线(ROC)分析血清Gal-3表达水平对高血压合并急性缺血性脑卒中患者的预后价值.结果治疗前观察组患者血清Gal-3表达水平显著高于高血压组及对照组患者,差异具有统计学意义(P<0.05),且观察组患者血清GAL-3水平随病症严重程度而显著上升,组间差异具有统计学意义;预后良好组患者血清Gal-3水平显著低于预后不良组患者,差异具有统计学意义(P<0.05);血清Gal-3相关性分析结果如下,血清Gal-3表达水平与NIHSS评分及mRS评分呈正相关(r分别为0.675、0.525,P<0.05),血清Gal-3表达水平ROC曲线下面积(AUC)分别为0.789,其诊断灵敏度、特异性分别为74.95％、72.77％.结论血清Gal-3水平与高血压合并急性缺血性脑卒中患者疾病严重程度与预后结果呈正相关,可作为该病严重程度诊断及预后评价指标.     

急性缺血性脑卒中患者血清血小板膜糖蛋白水平的变化及对预后的评估价值

目的 分析急性缺血性脑卒中患者入院时血清血小板膜糖蛋白-血小板活化因子-1(PAF-1)水平与疾病严重程度和患者90d临床预后的关系,为疾病早期诊断和预后评估提供敏感的生化指标.方法 选择2019年3月至2020年9月入我院初次确诊急性缺血性脑卒中患者共102例,采用改良Rankin量表(MRS)评分评估观察组出院后90d神经预后,并以此分为良好组(共81例,MRS评分0～2分)和较差组(共21例,MRS评分3～6分).另选同期门诊体检的80名健康人员作为对照组.分析患者入院血清PAF-1水平与美国国立卫生研究院卒中量表(NIHSS)评分的相关性;比较两组临床资料以及相关生化指标和入院PAF-1水平的差异.采用多因素Logistic回归分析筛选观察组90d预后的主要影响因素,采用受试者工作曲线(ROC)分析入院PAF-1水平预测90 d预后的效能.结果 缺血性脑卒中组血清PAF-1水平高于对照组(P<0.01).患者入院血清PAF-1水平与NIHSS评分呈现较好的正相关性(r=0.812,P=0.008).治疗90d预后良好组的PAF-1水平、NIHSS评分和梗死体积明显小于较差组(P<0.05).多因素Logistic回归分析显示,入院PAF-1水平和NIHSS评分是90d预后的主要影响因素(P<0.05).ROC分析显示,入院PAF-1水平截断值为9.5ng/mL预测90d预后不良的AUC为0.867,灵敏度为80.5％,特异性为73.6％.结论 急性缺血性脑卒中患者血清PAF-1水平升高与疾病发生以及90 d预后有紧密联系,可作为临床早期诊断脑卒中和判断短期预后的重要生化指标.     

半乳糖凝集素3与急性缺血性脑卒中的相关性研究

目的 探讨半乳糖凝集素3(galectin-3,gal-3)与急性缺血性脑卒中的关系及临床意义.方法 选择急性缺血性脑卒中患者165例为患者组,同期健康体检中心无脑卒中病史的健康体检者100名为对照组,采用酶联免疫吸附法(ELISA)检测gal-3;行头颅核磁共振检查计算脑梗死体积大小,按美国国立卫生研究所中风量表(NIHSS评分)进行神经功能缺损程度评估.结果 对照组血清gal-3水平(5.18±1.56μg/L)与患者组(14.57±3.35 μg/L)差异有统计学意义(t=23.517,P＜0.01);gal-3水平随脑梗死体积增加而呈递增趋势,差异有统计学意义(F=130.86,P＜0.01).Spearman相关分析显示,脑梗死体积与血清gal-3水平正相关(rs =0.927,P＜0.01);gal-3水平随神经缺损程度增加而呈递增趋势,差异有统计学意义(F=126.53,P＜0.01).Spearman相关分析显示,神经缺损程度与血清gal-3水平正相关(rs =0.872,P＜0.01).结论 急性缺血性脑卒中患者gal-3水平显著升高,其升高程度与脑梗死体积、神经功能缺损程度相关.     

缺血性脑卒中患者血清MMP-9、Hs-CRP与脑梗死体积及神经功能缺损的关系

目的:观察急性缺血性脑卒中患者血清基质金属蛋白酶-9(Matrix metalloproteinase-9,MMP-9)、超敏C反应蛋白(High-sensitive C-reactive protein,Hs-CRP)的水平变化,并探讨其与脑梗死体积及神经功能缺损的关系。方法:选择急性缺血性脑卒中患者120例为观察对象,采用酶联免疫法(ELISA)测定MMP-9、Hs-CRP水平与同期健康体检者72例对照。将缺血性脑卒中患者按梗死体积分为小梗死组(<5 cm3),中梗死组(5～15 cm3),大梗死组(>15 cm3);根据神经功能缺损程度评分分为轻度损伤组(0～15分),中度损伤组(16～30分),重度损伤组(31～45分),比较不同梗死体积和损伤程度时MMP-9、Hs-CRP水平的变化,并进行MMP-9与Hs-CRP之间的直线相关和回归分析。结果:①急性缺血性脑卒中患者MMP-9、Hs-CRP水平明显高于对照组;②脑梗死体积越大,缺血性脑卒中患者血清中MMP-9、Hs-CRP水平越高;③神经功能缺损程度越重,缺血性脑卒中患者血清中MMP-9、Hs-CRP水平越高;④直线与相关回归分析表明MMP-9、Hs-CRP呈显著正相关。结论:①血清MMP-9、Hs-CRP水平升高与缺血性卒中密切相关;②MMP-9、Hs-CRP水平可能反映急性缺血性卒中病情的严重程度;③MMP-9与Hs-CRP互相影响以促进脑卒中的发生、发展。     

血清尿酸水平与急性缺血性中风患者预后的关系

目的探讨血清尿酸(UA)水平与急性缺血性中风(IS)患者预后的关系.方法观察450例IS患者入院(13.5±11.2)h的血清UA水平,同时测定血糖(GLU)、甘油三酯(TG)、胆固醇(CHO)、肌酐(Cr)、红细胞比容(Hct)和血沉(ESR).并根据患者出院时神经功能恢复程度将其分为两组:轻度组(n=287)和中重度组(n=163).结果IS患者入院时血清UA水平轻度组明显高于中重度组(P＜0.01).经多因素Logistic回归分析,OR=1.14,OR 95%CI为1.00～1.26.结论血清UA水平升高可能是急性缺血性中风患者预后良好的独立预示因素之一.提示急性缺血性中风与氧化损害有关.     

HBV相关慢加急性肝衰竭患者血清Clusterin、S1P水平变化及临床意义

目的 探讨HBV相关慢加急性肝衰竭(HBV-ACLF)患者血清簇集蛋白(Clusterin)、1-磷酸鞘氨醇(S1P)水平变化及临床意义.方法 选取2017年6月至2020年6月我科收治的HBV-ACLF患者115例(观察组).同期,另选取我院体检健康志愿者100例(对照组).采用酶联免疫吸附法检测各组血清Clusterin、S1P水平.根据HBV-ACLF患者入院后30 d的临床结局,将其分为死亡组(n=36)和生存组(n=79),收集患者临床资料包括年龄、性别、慢性基础疾病、ALT、AST、MELD评分等.采用多因素Logistic回归分析影响HBV-ACLF患者预后的危险因素;绘制ROC曲线分析血清Clusterin、S1P对HBV-ACLF患者不良预后的预测价值.结果 观察组血清Clusterin、S1P水平与对照组相比,差异有统计学意义(P<0.05).死亡组血清Clusterin、S1P水平明显低于生存组,差异有统计学意义(P<0.05).Pearson相关性分析显示,血清Clusterin、S1P分别与MELD评分呈负相关(P<0.05).多因素Logistic回归分析结果显示,血清Clusterin、S1P降低是HBV-ACLF患者预后不良的重要危险因素(P<0.05).血清Clusterin、S1P及二者联合检测预测HBV-ACLF患者不良预后的AUC分别为0.812、0.830、0.900.结论 HBV-ACLF患者血清Clusterin、S1P水平明显降低,其水平降低与患者死亡率增加密切相关,联合检测血清Clusterin、S1P在预测HBV-ACLF患者短期预后方面具有一定参考价值.     

外周血miR-494及Let-7e在诊断急性缺血性脑卒中患者中的临床价值

目的：通过检测急性缺血性脑卒中患者与正常对照组外周血中miR-494及Let-7e的表达水平,探讨其与急性缺血性脑卒中的关系。方法：收集67例急性缺血性脑卒中患者及50例非卒中正常健康人群,采用实时荧光定量PCR法(Quantitative Real-time PCR,QRT-PCR)检测血浆中miR-494及Let-7e表达水平,比较两组外周血中表达水平的差异。并对miR-494及Let-7e行ROC曲线分析,分析其对急性缺血性脑卒中的诊断价值。进一步将急性缺血性脑卒中患者分为预后不佳组(MRS 3-6)和预后良好组(MRS0-2),分析其在两组之间的差异。结果：急性缺血性脑卒中患者外周血中的miR-494(1.71±1.14)及Let-7e(1.43±0.93)的表达水平较正常对照组外周血明显升高(P<0.05)。miR-494及Let-7eROC曲线下面积分别为0.777、0.756。预后不良组的miR-494(2.04±0.11 vs.1.46±0.05)及Let-7e(1.68±0.61 vs.1.24±0.27)表达水平均较预后良好组显著升高,两组之间有统计学差异(P<0.05)。结论：miR-494及Let-7e可能与急性缺血性脑卒中相关,对急性缺血性脑卒中患者的临床诊断和预后判断具有潜在的应用价值。     

Pain and Effusion and Quadriceps Activation and Strength

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

• Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
• The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
• To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.

Quadriceps weakness is a common consequence of traumatic knee joint injury^1,2 and chronic degenerative knee joint conditions.^3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.⁵ The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,⁶ biomechanical deficits,⁷ and possibly reinjury.⁵ Furthermore, researchers^8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,^10–12 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al^13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators¹⁵ have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,⁷ produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,^16–18 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.⁵ The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.¹⁹ Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.^16–18 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.²⁰ Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.     

即早基因c-fos与脑血管病及学习记忆

即早基因c-fos是广泛存在于原核细胞和真核细胞的高度保守基因.在正常情况下,c-fos基因参与细胞生长、分化、信息传递、学习和记忆等生理过程,而在病理情况下c-fos基因表达及调控变化与多种疾病的发生和发展有关.C-fos在中枢神经系统的某些部位可有基础水平的表达,但表达很低,当受到如脑缺血、脑出血、痫性发作、应激等刺激后,其在数十分钟内做出反应,在对外界刺激-转录耦联的信忠传递过程中起着核内第三信使的重要作用.     

Opportunities and challenges in the prevention and control of cancer and other chronic diseases: children's diet and nutrition and weight and physical activity

OBJECTIVE: The purpose of this article is to review the role of behavioral research in disease prevention and control, with a particular emphasis on lifestyle- and behavior-related cancer and chronic disease risk factors--specifically, relationships among diet and nutrition and weight and physical activity with adult cancer, and tracking developmental origins of these health-promoting and health-compromising behaviors from childhood into adulthood. METHOD: After reviewing the background of the field of cancer prevention and control and establishing plausibility for the role of child health behavior in adult cancer risk, studies selected from the pediatric published literature are reviewed. Articles were retrieved, selected, and summarized to illustrate that results from separate but related fields of study are combinable to yield insights into the prevention and control of cancer and other chronic diseases in adulthood through the conduct of nonintervention and intervention research with children in clinical, public health, and other contexts. RESULTS: As illustrated by the evidence presented in this review, there are numerous reasons (biological, psychological, and social), opportunities (school and community, health care, and family settings), and approaches (nonintervention and intervention) to understand and impact behavior change in children's diet and nutrition and weight and physical activity. CONCLUSIONS: Further development and evaluation of behavioral science intervention protocols conducted with children are necessary to understand the efficacy of these approaches and their public health impact on proximal and distal cancer, cancer-related, and chronic disease outcomes before diffusion. It is clear that more attention should be paid to early life and early developmental phases in cancer prevention.