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背景与目的抗血管生成药物是治疗恶性肿瘤的有效手段之一,美国FDA批准的药物的各期临床试验结果提示其疗效是令人惊喜的、但也必需重视不良反应、特别是心血管系统相关不良反应。本研究观察、分析恩度联合化疗之心血管系统相关不良反应的影响因素。方法观察我院2007.4-2009.2治疗的61例非小细胞肺癌（NSCLC）,每日监测血压、定时观察心电图、D-二聚体及心悸、胸闷等症状。结果各心血管系统相关不良反应从高到低的发生率依次为：心电图异常、D-二聚体异常、血小板异常、临床症状和血压异常波动。每例治疗前、后的各不良反应发生率差异均无意义,而每周期治疗前、后比较：心电图改变、临床症状和血压波动均有统计学意义（P〈0.05）;单因素logistic回归分析提示：按周期数观察,年龄对血压波动和ST-T段改变及治疗周期对血压波动均有影响（P〈0.05）;多因素logistic回归分析、排除混杂干扰因素后提示：按周期数观察,年龄对ST-T改变和血压波动有影响（P〈0.05）。结论不良反应中心电图异常最常见,高龄患者和年轻患者相比,发生心电图异常改变和血压波动的可能性大;另外,治疗周期是血压发生波动的危险因素。但治疗结束后,上述不良反应均可恢复。

R331; 简要介绍松弛素家族的成员、受体及其相关信号通路,重点回顾松弛素在心血管系统中的作用特别是其抗纤维化作用.心脏和血管是松弛素的靶器官.在临床和实验研究中,观察到松驰素在心脏病中表达上调,对机体的血流动力学和心肌肥大具有调节作用;松弛素对心肌具有一定的保护作用并可能参与心肌修复和再生,逆转心脏纤维化.进一步的研究将着重于阐明松弛素作用的确切机制,并将动物模型的研究成果应用于临床血管病的治疗.

随着透析技术的进步及医疗保险的贯彻实施，接受血液透析治疗的终末期肾病（End Stage Renal Disease，ESRD）患者越来越多，生存时间越来越长，ESRD患者的心血管系统、血液系统、骨骼疾病等躯体并发症与体征异常已引起人们的广泛关注，而ESRD患者可能出现的如神经衰弱、焦虑症、抑郁症、恐惧感等精神或神经症候群则容易被忽视。

Salvia miltiorrhiza, a traditional medical herb known as danshen, has been widely used in China to improve blood circulation, relieve blood stasis, and treat coronary heart disease. S miltiorrhiza depside salt is a novel drug recently developed at the Shanghai Institute of Materia Medica; it contains magnesium lithospermate B （MLB） and its analogs, rosmarinic acid （RA） and lithospermic acid （LA）, as active components. The drug has been used in the clinic to improve blood circulation and treat coronary heart disease. The pharma- cological effects of the depside salt from S miltiorrhiza and its components have been extensively investigated. Experimental studies have demonstrated that magnesium lithospermate B possesses a variety of biological activities, especially protective effects in the car- diovascular system such as attenuation of atherosclerosis and protection against myocardial ischemia-reperfusion injury. Rosmarinic acid and lithospermic acid also show beneficial effects on the cardiovascular system. This paper reviews the recent findings regarding the mechanisms underlying the pharmacological actions of the active components of S miltiorrhiza depside salt, based on published works and our own observations.

Background: Cumulative exposure to violence can change the regulation of epigenetic and physiological markers. Although violence has been associated with accelerated cellular aging, little is known about associations with cardiac autonomic activity. Objective: The current study aimed to investigate the relationship of exposure to community and domestic violence (CDV) with vagal activity and epigenetic aging acceleration. Methods: A total of 86 adolescents (57% female) were evaluated and interviewed at two time-points in São Gonçalo (2014-2019), a Brazilian city with high levels of violence. Exposure to CDV was assessed in both time-points. GrimAge acceleration was calculated from saliva DNA methylation using Infinium HumanMethylation450K (Illumina) collected in the first assessment. Heart rate variability (HRV) was collected during two stress tasks at the second assessment. Results: The exposure to violence witnessed or directly experienced at home and in the community increased significantly (t = 4.87, p < .01) across two-time points, and males had reported higher violence exposure (t = 2.06, p = .043). Violence at 1st assessment was significantly associated with GrimAge acceleration (B = .039, p value = .043). Violence at both assessments were associated with HRV measured during the narration of the worst trauma (traumaHRV) (B = .009, p value = .039, and B = .007, p value = .024, 1st and 2nd assessment respectively). GrimAge acceleration was significantly associated with traumaHRV (B = .043, p value = .049), and HRV measured during a 3D roller coaster video (B = .061, p value = .024). Conclusions: We found relevant evidence that experiencing violence during adolescence is associated with epigenetic aging and stress-related vagal activity. Understanding these factors during this period could contribute to the development of early interventions for health promotion. HIGHLIGHTS Higher exposure to Community and domestic violence is associated with increased GrimAge acceleration. Higher GrimAge acceleration is associated with increased stress-related vagal activity. Exposure to community and domestic violence increased significantly over time.

Adenosine Monophosphate-activated Protein Kinase （AMPK）, a serine/threonine kinase and a member of the Snfl/AMPK protein kinase family, consists of three protein subunits that together make a functional enzyme. AMPK, which is expressed in a number of tissues, including the liver, brain, and skeletal muscle, is allosterically activated by a rise in the AMP： ATP ratio （ie in a low ATP or energy depleted state）. The net effect of AMPK activation is to halt energy consuming （anabolic） pathways but to promote energy conserving （catabolic） cellular pathways. AMPK has therefore often been dubbed the ＂metabolic master switch＂. AMPK also plays a critical physiological role in the cardiovascular system, increasing evidence suggest that AMPK might also function as a sensor by responding to oxidative stress. Mostly importantly, AMPK modulates endogenous antioxidant gene expression and/or suppress the production of oxidants. AMPK promotes cardiovascular homeostasis by ensuring an optimum redox balance on the heart and vascular tissues. Dysfunctional AMPK is thought to underlie several cardiovascular pathologies. Here we review this kinase from its structure and discovery to current knowledge of its adaptive and maladaptive role in the cardiovascular system.

microRNAs (miRNAs) are a class of conserved, short, non-coding RNAs that have important and potent capacities to regulate gene expression at the posttranscriptional level. In the past several years, the aberrant expressions of miRNAs in the cardiovascular system have been widely reported, and the crucial roles of some special miRNAs in heart development and pathophysiology of various cardiovascular diseases have been gradually recognized. Recently, it was discovered that miRNAs are presented in peripheral circulation abundantly and stably. This has raised the possibility of using circulating miRNAs as biomarkers for diseases. Furthermore, some studies demonstrated that circulating miRNAs may serve as novel extracellular communicators of cell-cell communication. These discoveries not only reveal the functions of circulating miRNAs in cardiovascular system but also inform the development of miRNAs therapeutic strategies. In this review, we discuss the potential roles of circulating miRNAs in a variety of cardiovascular diseases from biomarkers to therapeutic targets to clearly understand the roles of circulating miRNAs in cardiovascular system.

Intermedin（IMD）or adrenomedullin 2 is a novel peptide related to the calcitonin gene-related peptide（CGRP）family.Via calcitonin receptor-like receptor/receptor activity modifying proteins,the common receptor complexes of CGRP,IMD exerts a wide range of biological effects,especially regulation of cardiovascular homeostasis.Proteolytic processing of a larger IMD precursor yields a series of biologically active C-terminal fragments,IMD1–53,IMD1–47 and IMD8–47.IMD and its receptors are present in the cardiovascular system,and IMD is present at low levels in plasma.In the cardiovascular system,IMD has multiple functions such as regulation of blood pressure and cardiac function,pro-angiogenesis,endothelial barrier function protection,anti-oxidative stress,and anti-endoplasmic reticulum stress.IMD participates widely in the pathogenesis of atherosclerosis,hypertension,pulmonary arterial hypertension and vascular calcification.It is a vascular regulatory factor of homeostasis and a vital endogenous protective factor against vascular diseases.

AbstractThe human cardiovascular system is a closed-loop and complex vascular network with multi-scaled heterogeneous hemodynamic phenomena. Here, we give a selective review of recent progress in macro-hemodynamic modeling, with a focus on geometrical multi-scale modeling of the vascular network, micro-hemodynamic modeling of microcirculation, as well as blood cellular, subcellular, endothelial biomechanics, and their interaction with arterial vessel mechanics. We describe in detail the methodology of hemodynamic modeling and its potential applications in cardiovascular research and clinical practice. In addition, we present major topics for future study: recent progress of patient-specific hemodynamic modeling in clinical applications, micro-hemodynamic modeling in capillaries and blood cells, and the importance and potential of the multi-scale hemodynamic modeling.Graphical AbstractHere we give a selective review of recent progress in macro-hemodynamic modeling, with a focus on geometrical multi-scale modeling of the vascular network, micro-hemodynamic modeling of microcirculation, as well as blood cellular, subcellular, endothelial biomechanics, and their interaction with arterial vessel mechanics. We describe in detail the methodology of hemodynamic modeling and its potential applications in cardiovascular research and clinical practice. In addition, we present major topics for future study: recent progress of patient-specific hemodynamic modeling in clinical applications, micro-hemodynamic modeling in capillaries and blood cells, and the importance and potential of the multi-scale hemodynamic modeling.

The renin-angiotensin system（RAS）regulates vascular tone and plays a critical role in vascular remodeling,which is the result of a complex interplay of alterations in vascular tone and structure.Inhibition of the RAS has led to important pharmacological tools to prevent and treat vascular diseases such as hypertension,diabetic vasculopathy and atherosclerosis.Angiotensin converting enzyme 2（ACE2）was recently identified as a multifunctional monocarboxypeptidase responsible for the conversion of angiotensin（Ang）II to Ang-（1-7）.The ACE2/Ang-（1-7）signaling has been shown to prevent cellular proliferation,pathological hypertrophy,oxidative stress and vascular fibrosis.Thus,the ACE2/Ang-（1-7）signaling is deemed to be beneficial to the cardiovascular system as a negative regulator of the RAS.The addition of the ACE2/Ang-（1-7）signaling to the complexities of the RAS may lead to the development of novel therapeutics for the treatment of hypertension and other vascular diseases.The present review considers recent findings regarding the ACE2/Ang-（1-7）signaling and focuses on its regulatory roles in processes related to proliferation,inflammation,vascular fibrosis and remodeling,providing proof of principle for the potential use of ACE2 as a novel therapy for vascular disorders related to vascular remodeling.