瘦素与妇产科疾病的关系及临床意义

瘦素(Leptin)是1994年Zhang等首先克隆并发现的一种由ob／ob基因编码．分子量为16000的蛋白类激素,是肥胖基因的表达产物．由脂肪组织分泌的一种神经内分泌激素,通过内分泌、旁分泌及自分泌方式作用于下丘脑、胰腺或脂肪等肌体多种组织上的特异性受体,使其在调节饮食、体重、能量代谢及性生活过程中发挥着重要作用。     

瘦素与类风湿关节炎

瘦素是脂肪细胞分泌的肽类激素,在能量营养代谢方面起着重要调节作用。越来越多的证据表明,瘦素既作为激素又作为免疫因子在神经内分泌免疫网络中起着重要调节作用,是营养状况、能量代谢、神经内分泌免疫相互影响、相互作用的重要中介物。其含量消长与多种自身免疫病的发生、发展有密切联系,可能在免疫系统中具有双向调节作用。因此瘦素作为新型免疫介质在炎症及免疫应答中发挥作用受到关注。现就瘦素在自身免疫病及类风湿性关节炎中的作用作一概述。     

脂联素与自身免疫性疾病

脂肪细胞分泌的各种脂肪因子如脂联素、瘦素、抵抗素等参与机体众多的生理过程,包括调节糖代谢、脂代谢、造血、炎症、补体激活、血栓形成等.脂联素是脂肪细胞专一分泌的多功能激素蛋白,在免疫病理和炎症过程中发挥重要作用.随着人们对自身免疫性疾病发病机制的不断深入研究,脂联素在自身免疫性疾病发生发展中的作用备受关注,本文就脂联素在自身免疫性疾病中的研究进展进行综述.     

瘦素和急性心肌梗死

急性心肌梗死(AMI)的发病与肥胖、高血脂、高血压、高血糖及胰岛素抵抗(即X综合征)密切相关。近年研究发现[1] ,瘦素与AMI的发生和发展有一定关系。1　瘦素、瘦素受体和瘦素抵抗1 1　瘦素　1994年Zhang等[2 ] 首次发现瘦素,它是脂肪细胞分泌的一种肽类激素。他们采用定位克隆技术,克隆出小鼠的肥胖基因(ob -gene)在白色脂肪组织中的特异表达产物—瘦素。瘦素是由16 7个氨基酸残基组成,可通过血脑屏障,与下丘脑特异性受体结合发挥作用,通过抑制食欲、减少能量摄取、增加能量消耗和抑制脂肪合成调节机体脂肪代谢。瘦素生成和分泌受以下因…     

苦参素对兔实验性左房纤维化的影响

目的:观察苦参素对实验性兔心房颤动左房纤维化心肌组织基质金属蛋白酶抑制因子-1(TIMP-1)和Ⅲ型前胶原(PCⅢ),Ⅳ型胶原(CⅣ)表达的影响.探讨苦参素对心房颤动左房纤维化的干预作用及可能的机制.方法:通过建立肺静脉源性房颤心肌纤维化动物模型,同时用苦参素进行干预,用免疫组织化学方法和放射免疫法检测心肌组织中TIMP-1和PCⅢ、CⅣ的表达,并作网状纤维及HE染色,观察心肌胶原及组织病理学变化.结果:苦参素防治组的心肌胶原表达量显著低于模型组,且苦参素防治组TIMP-1表达量较模型组显著下降(P<0.05).结论:苦参素具有抗心肌纤维化作用,其机制可能是通过抑制TIMP-1、PCⅢ和CⅣ的合成而实现.     

瘦素与肥胖的关系

1　前言瘦素 (Leptin ,LP)是由脂肪细胞分泌的一种肽类激素[1] 。瘦素被认为是一种饱食信号 ,可以通过刺激饱食中枢而降低摄食。LP主要是由白色脂肪组织分泌的 ,且只有在成熟的脂肪细胞中才有表达。LP原形由 16 7个氨基酸组成 ,在分泌入血过程中去除由 2 1个氨基酸组成的N—端信号肽 ,形成成熟的LP。其相对分子量为 16KD ,具有强亲水性 ,以单体形式存在于血浆中 ,通常血液浓度约为 10 - 9g/ml。其半衰期为 (9.4± 3.0 )min。瘦素是一种蛋白质类内分泌因子 ,其作用必然是通过靶细胞膜上的受体及相应的信号转导体系而实现。瘦素受体广泛…     

2型糖尿病患者脂肪细胞功能分析

目的 研究2型糖尿病(T2DM)患者糖耐量试验中脂肪细胞分泌功能.方法 通过T2DM组、对照组葡萄糖耐量样本,观察脂肪细胞分泌脂联素、瘦素、抵抗素,胰腺β细胞分泌胰岛素的动态变化,分析T2DM患者脂肪细胞和胰腺β细胞在葡萄糖耐量试验中的分泌功能变化.结果 葡萄糖耐量过程中,T2DM患者脂联素、瘦素、抵抗素、胰岛素餐后分泌下降(P＜0.05).结论 脂肪细胞分泌缺陷与β细胞分泌缺陷相关,细胞膜转运障碍导致细胞功能障碍,机体多细胞功能障碍与T2DM发病机制密切相关.     

Leptin对大鼠肥厚心肌细胞L-型钙离子通道的影响

Lepfin主要是由白色脂肪细胞分泌的蛋白质类激素，除促进脂肪代谢外，还对多种心血管疾病有保护作用，如可加速心肌重塑等。心肌细胞L-型钙离子通道是重要的离子电流之一，在心肌动作电位形成和机械收缩活动中起作用。因此，本研究通过给予肥厚心肌细胞不同浓度Lepfin处理，观察其对L-型钙离子通道的影响。     

可溶性瘦素受体与疾病关联性的研究进展

瘦素是脂肪组织分泌的激素,由肥胖基因（obese gene,ob）编码,具有抑制食欲、调节能量代谢、神经内分泌、生长、生殖和免疫反应等多种功能.瘦素通过结合瘦素受体发挥其广泛的生理作用.瘦素可通过与下丘脑的受体结合从而降低食欲和增加能量消耗;还可通过与外周组织受体结合而影响一系列机体代谢过程.瘦素在血液循环中以游离型和结合型两种形式存在,其游离型具有生物活性.现知道,可溶性瘦素受体（soluble leptin receptor,sOB-R）是人体血液循环中最主要的瘦素结合蛋白[1],它们从细胞表面瘦素受体的胞外区水解脱落产生,调节瘦素的生物利用度及其生理功能.越来越多的临床研究显示,在不同的生理及病理情况下,如1型糖尿病、肥胖等患者中,血浆sOB-R的水平不同.因此,sOB-R可能通过增强或减弱瘦素的信号功能,从而在疾病的发生发展中起重要的调节作用.本文就近年来临床研究中有关血浆sOB-R与疾病的关联研究的相关进展作一综述.     

生物活性肽与高血压性心肌肥大

高血压患者持续血压增高,尤其是夜间持续升高,对左心室肥大的发生发展起着重要的作用。高血压导致心肌肥大的因素可分为机械性和化学性刺激两大类,其化学刺激指心脏的自分泌、旁分泌和内分泌系统所分泌的生物活性物质,在心肌肥大的发生、发展中起到重要作用,研究其具体经过对指导心血管疾病的康复具有重要的理论和实践意义。     

102例社区房颤病例的临床回顾分析

目的 为提高社区全科医生对房颤患者的处理水平。方法 采取回顾分析法对社区102例房颤患者的临床资料及患者进行分析和回访。结果 房颤诱发因素多为劳累受凉、情绪激动和其它疾病发生等等。有基础心脏疾病者发生房颤率占87．26％，快速房颤用西地兰的有效率为96％，本组资料的房颤并发栓塞的发生率占9．8％。结论 应加强易患人群的健康宣传，和心血管疾病的预防工作，避免房颤的诱发因素，西地兰是治疗快速房颤的首选药，胺碘酮也作为社区转复房颤心律的常用药，可用于伴预激征治疗的首选用药，尤其以小剂量的口服对预防复发，毒副作用小，中医中药在慢性房颤的治疗中亦有一定疗效，社区医生要重视对房颤病人并发栓塞的预防。     

超声心动图在房颤诊治中的临床价值

目的 评价超声心动图在房颤病因诊断、治疗选择方面的临床价值。方法 对临床确诊的200例房颤患者的临床和超声心动图资料进行回顾性分析。结果 房颤药物转复成功率与左房大小、房颤持续时间、是否合并器质性心脏病变密切相关。结论 超声心动图在房颤患者的病因诊断、指导治疗、判断预后等方面能提供重要临床信息。     

Prevention of atrial fibrillation following cardiac surgery: basis for a novel therapeutic strategy based on non-hypoxic myocardial preconditioning

Atrial fibrillation is the most common complication of cardiac surgical procedures performed with cardiopulmonary bypass. It contributes to increased hospital length of stay and treatment costs. At present, preventive strategies offer only suboptimal benefits, despite improvements in anesthesia, surgical technique, and medical therapy. The pathogenesis of postoperative atrial fibrillation is considered to be multifactorial. However oxidative stress is a major contributory factor representing the unavoidable consequences of ischemia/reperfusion cycle occurring in this setting. Considerable evidence suggests the involvement of reactive oxygen species (ROS) in the pathogenic mechanism of this arrhythmia. Interestingly, the deleterious consequences of high ROS exposure, such as inflammation, cell death (apoptosis/necrosis) or fibrosis, may be abrogated by a myocardial preconditioning process caused by previous exposure to moderate ROS concentration known to trigger survival response mechanisms. The latter condition may be created by n-3 PUFA supplementation that could give rise to an adaptive response characterized by increased expression of myocardial antioxidant enzymes and/or anti-apoptotic pathways. In addition, a further reinforcement of myocardial antioxidant defenses could be obtained through vitamins C and E supplementation, an intervention also known to diminish enzymatic ROS production. Based on this paradigm, this review presents clinical and experimental evidence supporting the pathophysiological and molecular basis for a novel therapeutic approach aimed to diminish the incidence of postoperative atrial fibrillation through a non-hypoxic preconditioning plus a reinforcement of the antioxidant defense system in the myocardial tissue.     

Catheter ablation for atrial fibrillation: mechanism-based curative treatment

The considerable cumulative morbidity and mortality burden resulting from atrial fibrillation has prompted renewed efforts to seek curative and widely applicable therapies. Currently used drugs are not only frequently ineffective at eliminating fibrillation, but may actually be life threatening. Extensive surgery involving both atria has shown that atrial fibrillation can be eliminated in most, if not all, patients, but at a significant cost. The recent discovery of the pivotal role that myocardial extensions into the pulmonary veins play in the initiation, and probably also the maintenance, of atrial fibrillation, has provided a relatively limited target conducive to catheter-based interventions. In experienced hands, paroxysmal atrial fibrillation can be eliminated in more than 85% of patients by a percutaneous intervention lasting less than 3 h with an attendant nonlethal complication risk of 1 to 2%. Thromboembolic complications and pulmonary vein stenosis are the principal complications that may result from this treatment, but their incidence is decreasing. Success rates in patients with persistent or permanent atrial fibrillation are lower, and it is anticipated that increased understanding of the underlying mechanisms will allow doctors to identify those subsets with the greatest potential for benefit from percutaneous catheter-based interventions. Such progress may allow doctors to extend the benefits of eliminating atrial fibrillation to the widest possible range of patients with this recalcitrant disorder.     

Catheter ablation for atrial fibrillation: mechanism-based curative treatment

The considerable cumulative morbidity and mortality burden resulting from atrial fibrillation has prompted renewed efforts to seek curative and widely applicable therapies. Currently used drugs are not only frequently ineffective at eliminating fibrillation, but may actually be life threatening. Extensive surgery involving both atria has shown that atrial fibrillation can be eliminated in most, if not all, patients, but at a significant cost. The recent discovery of the pivotal role that myocardial extensions into the pulmonary veins play in the initiation, and probably also the maintenance, of atrial fibrillation, has provided a relatively limited target conducive to catheter-based interventions. In experienced hands, paroxysmal atrial fibrillation can be eliminated in more than 85% of patients by a percutaneous intervention lasting less than 3 h with an attendant nonlethal complication risk of 1 to 2%. Thromboembolic complications and pulmonary vein stenosis are the principal complications that may result from this treatment, but their incidence is decreasing. Success rates in patients with persistent or permanent atrial fibrillation are lower, and it is anticipated that increased understanding of the underlying mechanisms will allow doctors to identify those subsets with the greatest potential for benefit from percutaneous catheter-based interventions. Such progress may allow doctors to extend the benefits of eliminating atrial fibrillation to the widest possible range of patients with this recalcitrant disorder.     

Atrial fibrillation, elevated troponin, ischemic stroke and adverse outcomes: understanding the connection

Cardiac troponin is widely used for the diagnosis of acute myocardial infarction. In addition to this indication, the elevation of troponin has been found to play a prognostic role in ischemic stroke. It is hypothesized that approximately 15–20 % of all ischemic strokes are associated with atrial fibrillation and that these events are more often fatal. Recent studies have demonstrated that troponin elevation can also be used as a prognosticator in patients with atrial fibrillation and for risk stratification to predict which patients are more prone to stroke or other thromboembolic events. Therefore, troponin appears to play a pivotal role in the overlap of atrial fibrillation and ischemic stroke and the subsequent development of an adverse outcome. The different aspects of this association will be addressed and novel explanations will be proposed to better clarify the underlying mechanisms.     

Left atrium and the imaging of atrial fibrosis: catch it if you can!

Atrial fibrillation is a sustained arrhythmia commonly encountered in clinical practice. It has a high prevalence among the elderly and contributes significantly to the global socio‐economic burden. Among many risk factors predisposing to atrial fibrillation is left atrial remodelling and wall fibrosis. Frequently, pathological left atrial wall remodelling and fibrosis results in low atrial compliance and elastance significantly increase the risk of developing permanent atrial fibrillation. We reviewed all literature which employs imaging and left atrial fibrosis and we present all available imaging modalities. Current imaging tools may play a role in the detection of atrial fibrosis, hence providing valuable information for risk stratification and management of patients with atrial fibrillation.     

螺内酯对老年心房颤动患者血清Ⅰ型胶原代谢的影响

目的 通过测定老年心房颤动(房颤)患者使用螺内酯治疗前后血清醛固酮、Ⅰ型前胶原羧基端肽(PICP)及Ⅰ型胶原羧基端交联肽(CITP)水平的变化,探讨螺内酯减轻心房纤维化的可能机制.方法 选择房颤患者67例和条件相匹配的窦性心律患者30例,并将房颤患者随机分为常规治疗组(33例)及螺内酯(20mg/d)治疗组(34例),治疗6个月,用放射免疫法测定治疗前后血清醛固酮、PICP及CITP水平.另选对照组为30例,无房颤发作史,心电图及24小时动态心电图为窦性心律,一般资料匹配.结果 房颤组血清PICP、CITP、醛固酮浓度及左房大小均显著高于对照组(P＜0.01).房颤组血清醛固酮与左房大小呈正相关( r=0.302,P＜0.05)、血清PICP浓度与左房大小呈正相关( r=0.369,P＜0.01),螺内酯治疗组与常规治疗组治疗后血清醛固酮、PICP水平与治疗前相比均下降,但螺内酯治疗组下降更明显,治疗后两组血清醛固酮及PICP水平比较差异具有统计学意义(P＜0.01).结论 螺内酯通过降低房颤患者血清醛固酮、PICP水平,从而减轻心房纤维化,延缓房颤的发生发展.     

心脏磁共振成像在高血压性心脏病左心室评价中的研究进展

高血压性心脏病是全球范围最常见的慢性疾病之一,以左心室结构及功能变化为特征性表现,主要包括心脏舒张功能障碍,左心室肥厚及弥漫性心肌纤维化。心脏磁共振成像作为一种无创性影像学检查方法,在心血管疾病诊疗中发挥着重要作用。作者就心脏磁共振成像在评价高血压性心脏病的左心室心功能、心脏重塑、心肌纤维化、心外膜脂肪组织及预后评估的研究进展进行综述。     

Heart failure complicated by atrial fibrillation: mechanistic,prognostic, and therapeutic implications

Atrial fibrillation and congestive heart failure are two distinct clinical entities that are responsible for significant morbidity and mortality in the Western world. Hypertension, coronary artery disease, and nonischemic cardiomyopathy represent the most prevalent underlying pathologies of both diseases, implying a coincidence of both in many patients. The prevalence of atrial fibrillation with a progressive degree of congestive heart failure is increasing, as judged by New York Heart Association functional class. Moreover, the presence of congestive heart failure has been identified as one of the most powerful independent predictors of atrial fibrillation, with a sixfold increase in relative risk of its development. On the other hand, atrial fibrillation can cause or significantly aggravate symptoms of congestive heart failure in previously asymptomatic or well-compensated patients. In some patients, symptomatic dilated cardiomyopathy may develop over time entirely due to atrial fibrillation with rapid ventricular rates. Upon restoration of sinus rhythm, this type of "tachymyopathy" has been shown to be often reversible. Recent investigations of the physiologic and structural changes of the atrial myocardium ("electrical and structural remodeling") have shown that neurohumoral activation, fibrosis, and apoptosis are demonstrable with both diseases. On the other hand, experimental data suggest that the substrates of atrial fibrillation in congestive heart failure are different from those of pure atrial tachycardia-related forms of atrial fibrillation. This review highlights the clinical and pathophysiologic similarities and differences of atrial fibrillation and congestive heart failure relevant to the understanding, treatment, and prevention of these diseases in the population at risk.