血浆NT-proBNP水平与冠心病严重程度和预后的相关性分析

目的 分析血浆氨基末端B型脑钠肽前体(N-terminal B-type natriuretic peptide precursor,NT-proBNP)与冠心病严重程度及预后的相关性.方法 收集医院2015年1月至2017年6月收治的200例冠心病患者的临床资料,选择同期来医院体检的50例正常健康人作为对照组,入院后均测定NT-proBNP水平,比较冠心病患者与正常健康人NT-proBNP水平的差异及不同病情严重程度、不同预后冠心病患者血浆NT-proBNP水平的差异,分析血浆NT-proBNP水平与冠心病严重程度及预后的关系.结果 对照组NT-proBNP水平低于冠心病患者(P＜0.05),急性心肌梗死(acute myocardial infarction,AMI)、不稳定型心绞痛(unstable angina,UAP)患者NT-proBNP水平明显高于稳定型心绞痛(stable angina pectoris,SAP)患者(P＜0.05),AMI患者血浆NT-proBNP水平又高于UAP患者(P＜0.05);狭窄程度为Ⅱ～Ⅳ级患者血浆NT-proBNP水平高于Ⅰ级患者(P＜0.05),Ⅲ～Ⅳ级患者血浆NT-proBNP水平又高于Ⅱ级(P＜0.05),Ⅳ级患者血浆NT-proBNP水平又高于Ⅲ级患者,比较差异均有统计学意义(P＜＜0.05);主要不良心脏事件(major adverse cardiac events,MACE)组患者血浆NT-proBNP水平明显高于无MACE组,比较差异有统计学意义(P＜0.05);冠心病狭窄程度、MACE事件发生率与血浆NT-proBNP水平呈正相关(r=0.721、0.896,P均＜0.05).结论 冠心病患者血浆NT-proBNP水平明显升高,且随冠心病严重程度的上升,血浆NT-proBNP水平升高,且其水平升高通常提示不良预后.     

血清新蝶呤与冠状动脉斑块形态的关系的临床研究

目的 探讨冠心病患者新蝶呤与冠状动脉斑块形态的关系.方法 86例冠心病患者分为急性心肌梗死(AMI)组21例,不稳定型心绞痛(UAP)组35例,稳定型心绞痛(SAP)组30例,均经冠状动脉造影(CAG)确诊,30例CAG结果正常者为对照组.采用酶联免疫吸附法(ELISA)测定其新蝶呤水平,分析与冠状动脉斑块形态的关系.结果 新蝶呤浓度在AMI和UAP组中均高于SAP(P＜0.01);但在AMI组与UAP组,SAP和对照组之间差异无统计学意义(P＞0.05).新蝶呤浓度在Ⅱ型斑块组中高Ⅰ型、Ⅲ型斑块组(P＜0.05).结论 新蝶呤参与动脉硬化粥样斑块的发生发展过程,可作为预测斑块稳定性的标志物.     

冠心病患者发病早期血清超敏C反应蛋白和血脂四项水平变化

目的:回顾性分析96例冠心病患者发病48h内血清超敏C-反应蛋白(hs-CRP)和血脂四项的检测结果。方法:96例冠心病患者分为急性心肌梗死组(AMI组,n=41)、不稳定型心绞痛组(UAP组,n=35)和稳定型心绞痛组(SAP组,n=20)组,另选30例体检健康者作为对照组。采用免疫散射比浊法测定各组血清hs-CRP水平,采用酶法测定各组血脂水平,包括总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)和高密度脂蛋白(HDL)。统计分析冠心病各组间各指标水平差异。结果:冠心病各组与对照组hs-CRP水平差异有统计学意义(P0.05),AMI组、UAP组、SAP组血清hs-CRP水平均明显高于对照组(P0.01),AMI组hs-CRP明显高于UAP组和SAP组(P0.01),UAP组又明显高于SAP组(P0.05);冠心病各组与对照组TG、HDL水平差异亦有统计学意义(P0.01),AMI组、UAP组和SAP组TG水平显著高于对照组(P0.05),AMI组HDL水平显著低于对照组(P0.05)。结论:不同分层冠心病患者,其血清hs-CRP和血脂四项在发病早期的变化不同,AMI患者以hs-CRP和TG升高以及HDL降低最明显。     

血浆IL-35水平评价冠心病及其与冠脉Gensini积分和LVEF的相关性

目的 探讨白细胞介素35(interleukin-35,IL-35)评价冠心病及其与Gensini积分和左心室射血分数(left ventricular ejection fraction,LVEF)的相关性.方法 选取2014年1月至2015年12月经冠状动脉造影术(CAG)确诊为冠心病的患者90例,按临床分型,其中稳定型心绞痛(SAP) 25例,不稳定型心绞痛(UAP) 33例,急性心肌梗死(AMI) 32例;选择同期CAG结果提示冠状动脉管腔直径狭窄率＜50％的患者50例为对照组.采用酶联免疫法检测血浆IL-35水平,比较冠心病患者与对照组之间的差异.结果 与对照组比较,SAP、UAP和AMI组的IL-35水平、冠脉Gensini积分差异均具有统计学意义(P＜0.05);与对照组比较,UAP组的左心室射血分数差异无统计学意义(P＞0.05),SAP、AMI组的左心室射血分数差异有统计学意义(P＜0.05).IL-35水平与冠脉Gensini积分不相关(r=0.28,P＞0.05),但与LVEF呈正相关性(r =0.41,P＜0.01).结论 IL-35水平与冠心病密切相关,可作为CHD评价和预后的指标.     

血浆cTnI、CK-MB及BNP水平在急性胸痛患者中的变化及临床意义

目的探究血浆心肌肌钙蛋白I(cTnI)、肌酸激酶同工酶(CK-MB)、脑钠肽(BNP)水平在急性胸痛患者中的变化及临床意义。方法选择2016年1月至2019年1月我院收治的以急性胸痛为首发症状的患者作为研究对象,其中急性心肌梗死(AMI)患者59例,不稳定心绞痛(UAP)患者42例,稳定型心绞痛(SAP)患者38例,另39例患者经检查冠脉未见明显异常,纳入对照组。收集患者临床资料,采用GRACE评分工具进行危险分级,测定血浆cTnI、CK-MB及BNP水平。结果SAP、UAP、AMI组患者高脂血症患病率显著高于对照组(P<0.05),左心射血分数(LVEF)显著低于对照组(P<0.05),血浆cTnI、CK-MB、BNP水平高于对照组(P<0.05);ROC曲线示,血浆cTnI、CK-MB、BNP指标诊断心源性胸痛的曲线下面积分别为0.834、0.792、0.892,各指标联合诊断的曲线下面积为0.935;随着危险程度的升高,血浆cTnI、CK-MB、BNP水平升高(P<0.05);Pearson相关性分析示,血浆cTnI、CK-MB、BNP与LVEF呈负相关(P<0.05),与冠脉病变支数、GRACE评分呈正相关(P<0.05)。结论心源性胸痛患者可出现血浆cTnI、CK-MB、BNP等水平的升高,且升高幅度与病情严重程度相关,临床上可将其作为诊断高危性缺血性疾病的参考指标。     

血清腱糖蛋白-C、hs-CRP与急性冠脉综合症的相关性分析

目的 通过观察血清腱糖蛋白-C(TN-C)和高敏C反应蛋白(hs-CRP)在不同类型急性冠状动脉综合征患者血中表达水平,探讨二者与不同类型冠脉综合征的相关性.方法 总共入组诊断为急性冠脉综合症的患者90例,进一步分为两组:急性心肌梗死(AMI)组(n=48),不稳定性心绞痛(UAP)组(n=42),以及另入组稳定性心绞痛60例稳定心绞痛(SAP)组,及健康体检者55例为对照组.采用酶联免疫吸附试验(ELISA法)、放射免疫法分别测定血清TN-C和hs-CRP水平,并在各组间进行比较.结果 AMI组和UAP组TN-C表达水平明显高于SAP组、对照组,差异有统计学意义(P＜0.05);SAP组TN-C水平高于对照组但差异无统计学意义(P＞0.05).AMI组、UAP组和SAP组hs-CRP水平明显高于对照组,差异有统计学意义(均P＜0.05),而AMI组和UAP组hs-CRP较SAP相比差异无统计学意义(均P＞0.05).结论 TN-C、hs-CRP在ACS患者血清中升高,TN-C可作为急性冠状动脉综合征斑块稳定性病变严重程度的预测因子.     

冠心病患者血浆OLAB、BNP和CRP水平变化分析

检测冠心病患者血浆OLAB、BNP和CRP水平变化, 探讨冠心病发病机制及不稳定性心绞痛(UAP)治疗前后对其影响.用RIA和ELISA法对124例冠心病患者和30名对照者血浆中的OLAB、BNP和CRP水平变化及相关性进行研究, 同时对48例UAP经皮冠状动脉形成术(PTCA)治疗前、后对上述三项指标的变化进行分析; 结果表明冠心病患者与对照组比较BNP水平有显著性差异(P＜0.01),尤其是AMI和UAP组比SAP组升高更明显; CRP水平比对照组明显增高(P＜0.05),特别是不稳定性心绞痛和AMI组升高明显(P＜0.05);AMI组血浆OLAB水平明显高于正常和其他两组, OLAB、BNP和CRP三项在UAP组中治疗前后比较差异显著(P＜0.01).总之,OLAB、BNP和CRP参与了冠心病的发病过程, 并可预测心肌梗死患者远期心功能恢复的情况, UAP组经PTCA支架术后, 三项指标均明显降低, 可作为疗效观察的一个重要参数, OLAB参与了冠状动脉粥样硬化的全过程及AMI的发病始末.     

APN、CD62P、hs-CRP在冠心病病程发展中的作用

目的:探讨在冠状动脉粥样硬化发展中脂联素(adipomectin,APN)、CD62P、hs-CRP的作用.方法:检测60例稳定型心绞痛患者(stable angina pectoris,SAP组)、58例不稳定型心绞痛(unstable angina pectoris,SAP组),50例急性心肌梗死患者(AMI组)及...     

冠心病患者血清超敏C反应蛋白、肌钙蛋白、血脂水平的变化及临床意义

目的 探究冠心病患者血清超敏C反应蛋白（hs-CRP）、肌钙蛋白Ⅰ（cTnⅠ）、血脂水平的变化及临床意义。方法 选择2017年2月~2019年2月我院收治的80例冠心病患者作为研究对象,根据疾病类型分为稳定型心绞痛（SAP）组35例、急性心肌梗死（AMI）组20例及不稳定性心绞痛（UAP）组25例,另选取同期在我院进行体检的50例健康者作为对照组,比较四组hs-CRP、cTnⅠ、血脂水平（TC、TG、HDL-C、LDL-C）。结果 SAP、UAP、AMI组hs-CRP、cTnⅠ高于对照组,AMI组hs-CRP、cTnⅠ高于SAP组、UAP、SAP组hs-CRP、cTnⅠ高于SAP组,差异有统计学意义（P＜0.05）。SAP、UAP、AMI组TC、TG、LDL-C高于对照组,HDL-C低于对照组,差异有统计学意义（P＜0.05）;UAP、AMI组TC、TG、LDL-C低于SAP组,HDL-C高于SAP组,差异有统计学意义（P＜0.05）。结论 冠心病患者检测血清hs-CRP、cTnⅠ、血脂水平可有效预防疾病,对判断病情及评估预后有重要的临床意义。     

胰岛素样生长因子-1与急性冠脉综合症的关系

目的 探讨胰岛素样生长因子-1(IGF-1)与急性冠脉综合症的关系.方法 采用酶联免疫吸附法(ELIsA)分别对急性心肌梗死(AMI),不稳定型心绞痛(UAP),稳定型心绞痛(SAP)患者及正常对照组,进行血清IGF-1水平测定.结果 AMI和UAP组中IGF-1明显高于SAP和对照组(P＜0.01).SAP组IGF-1明显低于对照组(P＜0.01).结论 IGF-1参与动脉硬化粥样斑块的发生发展过程.可作为预测斑块稳定性的标志物.     

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.