BACKGROUND & AIMS: :This paper reevaluates the recently reported excess mortality following transurethral resection of the prostate (TURP) for benign hypertrophy as compared with traditional open resection (OPEN). We studied survival through linkage of hospital discharge data with mortality data for the entire male population of Denmark (1977-85). For a maximum of 10.5 years 38,067 prostatectomy patients were followed. Adjusting for age and health status before surgery, TURP patients were subject to significantly higher levels of mortality than OPEN patients (RR = 1.19, 95% confidence interval (1.15-1.24). The extent to which this difference is attributable to the surgical intervention itself remains an open question. The two groups of patients are quite different with regard to age and preoperative health status, and available data may not be sufficient to control such differences through statistical analysis. On the other hand, the difference in mortality persisted over calendar time, even during periods when the pattern of utilization for the two procedures changed significantly (constant RR = 1.19, adjusting for age and comorbidity). The most important causes of death among Danish TURP patients differ from the causes suggested on the basis of previously reported Canadian data. The current evidence is thus ambiguous with regard to hypothetical biologic mechanisms behind the excess mortality over TURP patients. Further investigations are needed to evaluate the safety and effectiveness of prostate surgery.

背景与目标： ：本文重新评估了最近报道的与传统的开放性切除术（OPEN）相比，经尿道前列腺良性肥大手术（TURP）后的额外死亡率。我们通过将出院数据与丹麦整个男性人口（1977-85年）的死亡率数据相联系来研究生存率。在长达10.5年的时间里，对38,067例前列腺切除术患者进行了随访。调整手术前的年龄和健康状况后，TURP患者的死亡率要比OPEN患者高得多（RR = 1.19，95％置信区间（1.15-1.24）。两组患者在年龄和术前健康状况方面都存在很大差异，可用的数据可能不足以通过统计分析来控制这种差异；另一方面，死亡率的差异在整个日历时间内仍然存在，即使在这两种方法的使用方式发生显着变化的时期（恒定RR = 1.19，已根据年龄和合并症进行了调整），丹麦TURP患者中最重要的死亡原因也不同于先前报道的加拿大所建议的原因。因此，目前的证据对于超过T的超额死亡率背后的假设生物学机制尚不明确。 URP患者。需要进一步的研究以评估前列腺手术的安全性和有效性。

BACKGROUND & AIMS: :Heart failure is one of the leading causes of mortality in the western world and encompasses a wide spectrum of cardiac pathologies. When the heart experiences extended periods of elevated workload, it undergoes hypertrophic enlargement in response to the increased demand. Cardiovascular disease, such as that caused by myocardial infarction, obesity or drug abuse promotes cardiac myocyte hypertrophy and subsequent heart failure. A number of signalling modulators in the vasculature milieu are known to regulate heart mass including those that influence gene expression, apoptosis, cytokine release and growth factor signalling. Recent evidence using genetic and cellular models of cardiac hypertrophy suggests that pathological hypertrophy can be prevented or reversed and has promoted an enormous drive in drug discovery research aiming to identify novel and specific regulators of hypertrophy. In this review we describe the molecular characteristics of cardiac hypertrophy such as the aberrant re-expression of the fetal gene program. We discuss the various molecular pathways responsible for the co-ordinated control of the hypertrophic program including: natriuretic peptides, the adrenergic system, adhesion and cytoskeletal proteins, IL-6 cytokine family, MEK-ERK1/2 signalling, histone acetylation, calcium-mediated modulation and the exciting recent discovery of the role of microRNAs in controlling cardiac hypertrophy. Characterisation of the signalling pathways leading to cardiac hypertrophy has led to a wealth of knowledge about this condition both physiological and pathological. The challenge will be translating this knowledge into potential pharmacological therapies for the treatment of cardiac pathologies.

背景与目标： ：心力衰竭是西方世界导致死亡的主要原因之一，涉及范围广泛的心脏病。当心脏长时间承受较高的工作量时，它会响应于需求增加而经历肥大性肥大。诸如由心肌梗塞，肥胖症或药物滥用引起的心血管疾病促进心脏心肌肥大和随后的心力衰竭。已知脉管系统环境中的许多信号传导调节剂可调节心脏质量，包括影响基因表达，凋亡，细胞因子释放和生长因子信号传导的那些。使用心脏肥大的遗传和细胞模型的最新证据表明，可以预防或逆转病理性肥大，并促进了旨在发现新的和特定的肥大调节剂的药物发现研究的巨大推动力。在这篇综述中，我们描述了心脏肥大的分子特征，例如胎儿基因程序的异常重新表达。我们讨论了肥大程序的协调控制的各种分子途径，包括：利钠肽，肾上腺素系统，粘附和细胞骨架蛋白，IL-6细胞因子家族，MEK-ERK1 / 2信号传导，组蛋白乙酰化，钙介导调控和最近令人振奋的microRNA在控制心脏肥大中的作用的发现。导致心脏肥大的信号传导途径的表征已导致有关这种状况的大量生理学和病理学知识。面临的挑战将是将这种知识转化为用于治疗心脏病理的潜在药理疗法。

BACKGROUND & AIMS: STUDY OBJECTIVE:The aim was to clarify the characteristics of the phasic blood velocity pattern and their possible causes in left ventricular hypertrophy secondary to systemic hypertension. DESIGN:Measurements of blood velocities in the left anterior descending coronary artery were made with a 20 MHz Doppler catheter with a top mounted annular crystal. All patients had normal coronary arteriograms. PATIENTS:23 hypertensive patients [systolic/diastolic pressure: 181(SD 15)/100(4) mm Hg)] with left ventricular hypertrophy, and 13 atypical chest pain patients without left ventricular hypertrophy or any abnormal haemodynamic findings (normal controls) entered the study. MEASUREMENTS AND MAIN RESULTS:The left anterior descending coronary artery blood velocity waveform in pressure overloaded left ventricular hypertrophy was characterised by delayed early diastolic inflow. The diastolic rise time of coronary flow (TDR), ie, the time from the beginning of diastole to peak velocity, was higher in patients with hypertensive left ventricular hypertrophy than in normal controls, at 145(56) v 66(15) ms, p less than 0.001. In patients with hypertensive left ventricular hypertrophy, TDR correlated well with the degree of hypertrophy (r = 0.83, p less than 0.01) and also with peak left ventricular systolic pressure (r = 0.62, p less than 0.01). The coronary flow reserve, calculated from the ratio of the diastolic mean velocity after intracoronary injection of papaverine to the resting flow velocity, decreased with prolongation of TDR (r = 0.58, p less than 0.02). CONCLUSIONS:(1) Impairment of early diastolic coronary arterial inflow is the most remarkable characteristic in pressure overloaded left ventricular hypertrophy; (2) preceding systolic vascular compression and impaired left ventricular relaxation correlate with the delayed early diastolic inflow; (3) the delayed inflow is an important possible cause of the decreased coronary flow reserve in the hypertensive left ventricular hypertrophy.

背景与目标： 目的：阐明系统性高血压继发于左心室肥厚的阶段性血流速度特征及其可能原因。
设计：使用20 MHz多普勒导管和顶部安装的环形晶体对冠状动脉左前降支中的血流速度进行测量。所有患者的冠状动脉造影检查均正常。
患者：23例左室肥厚的高血压患者[收缩压/舒张压：181（SD 15）/ 100（4）mm Hg），13例非典型性胸痛患者，无左室肥厚或任何血流动力学异常（正常对照）研究。
测量和主要结果：压力超负荷左心室肥厚中左前降支冠状动脉血流波形的特征是早期舒张期迟发流入。高血压左心室肥厚患者的冠状动脉血流舒张上升时间（TDR），即从舒张开始到达到峰值速度的时间，比正常对照组长，为145（56）v 66（15）ms， p小于0.001。在患有高血压左心室肥大的患者中，TDR与肥大程度（r = 0.83，p小于0.01）以及峰值左心室收缩压（r = 0.62，p小于0.01）密切相关。由冠状动脉内注射罂粟碱后舒张平均速度与静息流速之比计算得出的冠状动脉血流储备随TDR延长而降低（r = 0.58，p小于0.02）。
结论：（1）左心室肥厚是舒张早期冠状动脉血流减少的最显着特征。 （2）收缩期前血管收缩和左心室舒张受损与舒张早期流入延迟有关。 （3）延迟流入是高血压左心室肥厚中冠状动脉血流储备减少的重要可能原因。

BACKGROUND & AIMS: :Stretch training is widely used in a variety of fitness-related capacities such as increasing joint range of motion, preventing contractures and alleviating injuries. Moreover, some researches indicate that stretch training may induce muscle hypertrophy; however, studies on the topic have been primarily relegated to animal and in vitro models. The purpose of this brief review was to evaluate whether stretch training is a viable strategy to induce muscle hypertrophy in humans. An extensive literature search was performed using PubMed/MEDLINE, SciELO and Scopus databases, using terms related to stretching and muscle hypertrophy. Only human trials that evaluated changes in measures of muscle size or architecture following training protocols that it was performed stretching exercises were selected for inclusion. Of the 10 studies identified, 3 observed some significantly positive effects of stretch training on muscle structure. Intriguingly, in these studies, the stretching was carried out with an apparatus that aided in its performance, or with an external overload. In all studies, the subjects performed stretching at their own self-determined range of motion, and no effect was observed. Of the 5 available studies that integrated stretching into a resistance training programme, 2 applied the stretching in the interset rest period and were the ones that showed enhanced muscle growth. In conclusion, passive, low-intensity stretch does not appear to confer beneficial changes in muscle size and architecture; alternatively, albeit limited evidence suggests that when stretching is done with a certain degree of tensile strain (particularly when loaded, or added between active muscle contractions) may elicit muscle hypertrophy.

背景与目标： ：伸展训练广泛用于各种与健身有关的活动中，例如增加关节的活动范围，预防挛缩和减轻伤害。此外，一些研究表明，伸展运动可能会导致肌肉肥大。但是，有关该主题的研究主要局限于动物和体外模型。这篇简短评论的目的是评估拉伸训练是否是诱导人类肌肉肥大的可行策略。使用PubMed / MEDLINE，SciELO和Scopus数据库进行了广泛的文献检索，使用了与拉伸和肌肉肥大有关的术语。只有在评估伸展运动后的训练规程后评估肌肉尺寸或结构变化的人体试验才被选为纳入研究。在确定的10项研究中，有3项观察到了拉伸训练对肌肉结构的一些显着积极影响。有趣的是，在这些研究中，使用有助于其性能的设备或外部过载进行了拉伸。在所有研究中，受试者均以自己确定的运动范围进行伸展运动，未观察到效果。在5项将伸展运动整合到阻力训练计划中的可用研究中，有2项在间歇休息期间进行了伸展运动，并显示出肌肉生长的增强。总之，被动的低强度伸展运动似乎并没有给肌肉的大小和结构带来有益的改变。另外，尽管证据有限，但当以一定程度的拉伸应变进行拉伸时（尤其是在加载时或在主动肌肉收缩之间添加拉伸时）可能会引起肌肉肥大。

BACKGROUND & AIMS: :Angiotensin II (Ang II) is an important bioactive peptide in the renin‑angiotensin system, and it can contribute to cell proliferation and cardiac hypertrophy. Dysfunctions in transient receptor potential canonical (TRPC) channels are involved in many types of cardiovascular diseases. The aim of the present study was to investigate the role of the TRPC channel inhibitor SKF‑96365 in cardiomyocyte hypertrophy induced by Ang II and the potential mechanisms of SKF‑96365. H9c2 cells were treated with different concentrations of Ang II. The expression levels of cardiomyocyte hypertrophy markers and TRPC channel‑related proteins were also determined. The morphology and surface area of the H9c2 cells, the expression of hypertrophic markers and TRPC channel‑related proteins and the [3H] leucine incorporation rate were detected in the Ang II‑treated H9c2 cells following treatment with the TRPC channel inhibitor SKF‑96365. The intracellular Ca2+ concentration was tested by flow cytometry. The present results suggested that the surface area of H9c2 cells treated with Ang II was significantly increased compared with untreated H9c2 cells. The fluorescence intensity of α‑actinin, the expression of hypertrophic markers and TRPC‑related proteins, the [3H] leucine incorporation rate and the intracellular Ca2+ concentration were all markedly increased in the Ang II‑treated H9c2 cells but decreased following SKF‑96365 treatment. The present results suggested that Ang II induced cardiomyocyte hypertrophy in H9c2 cells and that the TRPC pathway may be involved in this process. Therefore, SKF‑96365 can inhibit cardiomyocyte hypertrophy induced by Ang II by suppressing the TRPC pathway. The present results indicated that TRPC may be a therapeutic target for the development of novel drugs to treat cardiac hypertrophy.

背景与目标： 血管紧张素II（Ang II）是肾素-血管紧张素系统中的重要生物活性肽，可促进细胞增殖和心脏肥大。瞬态受体电位经典（TRPC）通道功能异常涉及多种类型的心血管疾病。本研究的目的是研究TRPC通道抑制剂SKF‑96365在AngⅡ诱导的心肌肥大中的作用以及SKF‑96365的潜在机制。用不同浓度的Ang II处理H9c2细胞。还确定了心肌肥大标志物和TRPC通道相关蛋白的表达水平。经TRPC通道抑制剂SKF‑96365处理后，在经Ang II处理的H9c2细胞中检测到H9c2细胞的形态和表面积，肥厚标记和TRPC通道相关蛋白的表达以及[3H]亮氨酸掺入率。通过流式细胞仪测试细胞内Ca 2浓度。本结果表明，与未处理的H9c2细胞相比，用AngⅡ处理的H9c2细胞的表面积显着增加。 Ang II处理的H9c2细胞中α-肌动蛋白的荧光强度，肥大标记和TRPC相关蛋白的表达，[3H]亮氨酸掺入率和细胞内Ca2浓度均显着增加，但经SKF‑96365处理后降低。目前的结果表明Ang II诱导了H9c2细胞中的心肌肥大，并且TRPC途径可能参与了这一过程。因此，SKF‑96365可通过抑制TRPC途径来抑制AngⅡ诱导的心肌肥大。本结果表明，TRPC可能是开发用于治疗心脏肥大的新药的治疗靶标。

BACKGROUND & AIMS: PURPOSE OF REVIEW:Given that the life expectancy and the burden of hypertension are projected to increase over the next decade, hypertensive heart disease (HHD) may be expected to play an even more central role in the pathophysiology of cardiovascular disease (CVD). A broader understanding of the features and underlying mechanisms that constitute HHD therefore is of paramount importance. RECENT FINDINGS:HHD is a condition that arises as a result of elevated blood pressure and constitutes a key underlying mechanism for cardiovascular morbidity and mortality. Historically, studies investigating HHD have primarily focused on left ventricular (LV) hypertrophy (LVH), but it is increasingly apparent that HHD encompasses a range of target-organ damage beyond LVH, including other cardiovascular structural and functional adaptations that may occur separately or concomitantly. HHD is characterized by micro- and macroscopic myocardial alterations, structural phenotypic adaptations, and functional changes that include cardiac fibrosis, and the remodeling of the atria and ventricles and the arterial system. In this review, we summarize the structural and functional alterations in the cardiac and vascular system that constitute HHD and underscore their underlying pathophysiology.

背景与目标： 审查目的：鉴于预期寿命和高血压负担将在未来十年内增加，因此，高血压心脏病（HHD）有望在心血管疾病（CVD）的病理生理学中发挥更加重要的作用。因此，对构成HHD的特征和基本机制的更广泛的理解至关重要。
最近的发现：HHD是由于血压升高而引起的疾病，并构成心血管疾病发病率和死亡率的关键潜在机制。从历史上看，研究HHD的研究主要集中在左心室肥大（LVH），但是越来越明显的是，HHD涵盖了LVH以外的一系列靶器官损害，包括可能单独或同时发生的其他心血管结构和功能适应性改变。 HHD的特征是微观和宏观的心肌改变，结构表型适应以及包括心脏纤维化，心房和心室以及动脉系统重塑在内的功能改变。在这篇综述中，我们总结了构成HHD的心脏和血管系统的结构和功能改变，并强调了其潜在的病理生理学。

BACKGROUND & AIMS: OBJECTIVE:In this review, we critically evaluate studies directly comparing the effects of plyometric vs. resistance training on skeletal muscle hypertrophy. METHODS:We conducted electronic searches of PubMed/MEDLINE, Scopus, SPORTDiscus, and Web of Science to find studies that explored the effects of plyometric vs. resistance training on muscle hypertrophy. RESULTS:Eight relevant studies were included in the review. Six studies compared the effects of plyometric vs. resistance training on muscle hypertrophy, while 2 studies explored the effects of combining plyometric and resistance training vs. isolated resistance training on acute anabolic signaling or muscle hypertrophy. Based on the results of these studies, we conclude that plyometric and resistance training may produce similar effects on whole muscle hypertrophy for the muscle groups of the lower extremities. Therefore, it seems that plyometric training has a greater potential for inducing increases in muscle size than previously thought. Despite the findings observed at the whole muscle level, the evidence for the effects of plyometric training on hypertrophy on the muscle fiber level is currently limited for drawing inferences. Compared to isolated resistance training, combining plyometric and resistance exercise does not seem to produce additive effects on anabolic signaling or muscle growth; however, this area requires future study. The limitations of the current body of evidence are that the findings are specific to (a) musculature of the lower extremities, (b) short-term training interventions that lasted up to 12 weeks, and (c) previously untrained or recreationally active participants. CONCLUSION:This review highlights that plyometric and resistance training interventions may produce similar effects on whole muscle hypertrophy, at least for the muscle groups of the lower extremities, in untrained and recreationally trained individuals, and over short-term (i.e., ≤12 weeks) intervention periods.

背景与目标： 目的：在这篇综述中，我们严格地评估了研究，直接比较了腹肌训练与阻力训练对骨骼肌肥大的影响。
方法：我们对PubMed / MEDLINE，Scopus，SPORTDiscus和Web of Science进行了电子搜索，以找到探索测厚与阻力训练对肌肉肥大的影响的研究。
结果：八项相关研究被纳入该评价。六项研究比较了体能测量和阻力训练对肌肉肥大的影响，而两项研究探讨了综合体能训练和阻力训练与孤立抵抗训练相结合对急性合成代谢信号或肌肉肥大的影响。根据这些研究的结果，我们得出结论，进行体力训练和阻力训练可能会对下肢的肌肉群的全肌肉肥大产生相似的影响。因此，似乎比以前认为的，体能训练具有更大的潜力来引起肌肉尺寸的增加。尽管在整个肌肉水平上都观察到了发现，但目前进行推论训练对肥大对肌肉纤维水平的影响的证据仍然有限。与孤立的阻力训练相比，将体能测验和阻力训练相结合似乎不会对合成代谢信号或肌肉生长产生累加作用。但是，这个领域需要进一步研究。当前证据的局限性在于，这些发现特定于（a）下肢的肌肉组织，（b）持续长达12周的短期训练干预措施，以及（c）以前未经训练或积极参加运动的参与者。
结论：这篇综述强调了，体力训练和阻力训练干预可能会对全肌肉肥大产生类似的影响，至少对于下肢的肌肉群，未经训练和接受过娱乐训练的个体以及短期（即≤12周）都可能产生类似的影响干预期。

BACKGROUND & AIMS: :Right ventricular (RV) pressure overload causes right ventricular hypertrophy in several types of pulmonary and congenital heart diseases. The associated cardiac dysfunction has generally been attributed to alterations in RV function. However, due to global neurohormonal adaptations and mechanical ventricular interaction left ventricular (LV) function could be affected as well.Therefore,LV function, RV function and their interaction were studied in rats with monocrotaline (MCT)-induced RV hypertrophy and control rats. MCT (30 mg/kg) was used to induce pulmonary hypertension, which resulted, after 28 days, in marked RV hypertrophy (RV-weight: control 220 +/- 15,MCT 437 +/- 34mg,p < 0.05). In Langendorff-perfused hearts with balloons inserted in both the LV and the RV, the diastolic pressure-volume relations showed increased stiffness, and relaxation was prolonged in the LV and RV in the MCT group compared to controls. In the MCT group, developed pressures were increased only in the RV. An increase of LV volume increased RV diastolic pressure to a similar extent in both groups. However, an increase in RV volume did not affect LV diastolic pressure in controls, but significantly increased LV diastolic pressure in the MCT group. LV and RV developed pressure-volume relations were not affected. Calculated circumferential end-diastolic wall stresses (sigma) were larger in the MCT group (LV-sigma: 0.55 +/- 0.02, RV-sigma: 1.94 +/- 0.30 kN/m(2), both p< 0.05 to control) compared to controls (LV-sigma: 0.34 +/- 0.06,RV-sigma: 1.23 +/- 0.46 kN/m2). In the MCT group, collagen content was increased in the LV, septum and RV compared to controls. In conclusion, structural changes of the RV and LV result in depressed LV diastolic function during RV hypertrophy.

背景与目标： ：右心室（RV）压力超负荷会导致多种肺和先天性心脏病的右心室肥大。相关的心脏功能障碍通常归因于RV功能的改变。然而，由于整体的神经激素适应和机械性的心室相互作用，左心室（LV）功能也可能受到影响。因此，在MCA诱发的RV中，左室功能，RV功能及其相互作用受到了研究。 MCT（30 mg / kg）用于诱发肺动脉高压，在28天后导致明显的RV肥大（RV重量：对照组220 / -15，MCT 437 /-34mg，p <0.05）。与对照相比，在MCT组中，在LV和RV均插入有气球的Langendorff灌注心脏中，舒张压-容积关系显示出增加的刚度，并且LV和RV的舒张时间延长。在MCT组中，仅RV出现的压力增加。两组左室容积的增加使右室舒张压增加到相似的程度。但是，RV体积的增加并未影响对照组的左室舒​​张压，但在MCT组中却显着增加了左室舒张压。左室和右室发展的压力-体积关系不受影响。与MCT组相比，计算得出的舒张末期壁舒张末期壁应力（sigma）更大（LV-sigma：0.55 /-0.02，RV-sigma：1.94 /-0.30 kN / m（2），与对照相比均p <0.05）控件（LV-sigma：0.34 /-0.06，RV-sigma：1.23 /-0.46 kN / m2）。在MCT组中，与对照组相比，LV，隔膜和RV中的胶原蛋白含量增加。总之，RV和LV的结构变化会导致RV肥大期间LV舒张功能降低。

BACKGROUND & AIMS: :Hypertrophy in capillary malformation (CM) may be present at birth or manifest itself later in life. To gain insight into the pathology of hypertrophic CM, we investigated a series of 11 excisional biopsies of hypertrophic lips.All biopsies showed dilated thin-walled microvessels in the superficial dermis without a neural component. However, large multinodular conglomerates of thick-walled vessels with a substantial increase in nerve fibers were found in the deeper parts of the lesions. These veins extended deep into the facial musculature. Hypertrophy in CM is caused by venous malformation underlying the CM. So CM associated with hypertrophy should be considered as Capillary Venous malformations.

背景与目标： ：毛细血管畸形（CM）的肥大可能在出生时就出现，或者在以后的生活中表现出来。为了深入了解肥厚性CM的病理，我们对11例肥厚性双唇切除活检进行了一系列研究。所有活检均显示浅层真皮中的扩张性薄壁微血管无神经成分。但是，在病变的较深部分发现了厚壁血管的大型多结节性结块，其中神经纤维显着增加。这些静脉深入面部肌肉组织。 CM肥大是由CM下方的静脉畸形引起的。因此，与肥大相关的CM应被认为是毛细血管静脉畸形。

BACKGROUND & AIMS: AIM:To address to what extent hypertrophy and hyperplasia contribute to liver mass restoration after major tissue loss. METHODS:The ability of the liver to regenerate is remarkable on both clinical and biological grounds. Basic mechanisms underlying this process have been intensively investigated. However, it is still debated to what extent hypertrophy and hyperplasia contribute to liver mass restoration after major tissue loss. We addressed this issue using a genetically tagged system. We were able to follow the fate of single transplanted hepatocytes during the regenerative response elicited by 2/3 partial surgical hepatectomy (PH) in rats. Clusters of transplanted cells were 3D reconstructed and their size distribution was evaluated over time after PH. RESULTS:Liver size and liver DNA content were largely recovered 10 d post-PH, as expected (e.g., total DNA/liver/100 g b.w. was 6.37 ± 0.21 before PH and returned to 6.10 ± 0.36 10 d after PH). Data indicated that about 2/3 of the original residual hepatocytes entered S-phase in response to PH. Analysis of cluster size distribution at 24, 48, 96 h and 10 d after PH revealed that about half of the remnant hepatocytes completed at least 2 cell cycles. Average size of hepatocytes increased at 24 h (248.50 μm2 ± 7.82 μm2, P = 0.0015), but returned to control values throughout the regenerative process (up to 10 d post-PH, 197.9 μm2 ± 6.44 μm2, P = 0.11). A sizeable fraction of the remnant hepatocyte population does not participate actively in tissue mass restoration. CONCLUSION:Hyperplasia stands as the major mechanism contributing to liver mass restoration after PH, with hypertrophy playing a transient role in the process.

背景与目标： 目的：探讨肥大和增生在主要组织丢失后在多大程度上有助于肝脏肿块的恢复。
方法：无论从临床还是生物学的角度来看，肝脏的再生能力都很显着。深入研究了此过程的基本机制。然而，仍存在争议，在主要组织丢失后，肥大和增生在多大程度上有助于肝块的恢复。我们使用基因标记的系统解决了这个问题。在2/3部分外科手术肝切除术（PH）引起的再生反应过程中，我们能够追踪单个移植肝细胞的命运。 PH移植后，将移植的细胞簇进行3D重建，并评估其大小分布。
结果：在PH后10 d，肝脏大小和肝脏DNA含量在很大程度上恢复了（如在PH前的总DNA /肝脏/ 100 g b.w.为6.37±0.21，而在PH后10 d恢复至6.10±0.36）。数据表明，约有2/3的原始残余肝细胞响应PH而进入S期。 PH后24、48、96 h和10 d的簇大小分布分析表明，大约一半的残留肝细胞完成了至少2个细胞周期。肝细胞的平均大小在24 h时增加（248.50μm2±7.82μm2，P = 0.0015），但在整个再生过程中恢复到对照值（PH后长达10 d，197.9μm2±6.44μm2，P = 0.11）。相当一部分肝细胞残余不能积极参与组织块的恢复。
结论：增生是造成PH后肝脏肿块恢复的主要机制，肥大在此过程中起暂时作用。

BACKGROUND & AIMS: Background & objectives:Inferior turbinate hypertrophy (ITH) is a common condition causing nasal obstruction. This study was undertaken to compare the efficacy of potassium titanyl phosphate (KTP) laser and diode laser in the reduction of the turbinate size. Methods:This randomized controlled trial included 209 patients with ITH. Pre-operative symptoms were assessed based on the Nasal Obstruction Symptom Evaluation (NOSE) score. Diagnostic nasal endoscopy was done to rule out other nasal sinuses. Nasal mucociliary clearance was measured by saccharin transit time (STT). Postoperatively, the NOSE score, STT and complications were assessed at days one and two, at one week, one month and three months. Results:Of the 209 patients analyzed at day one, the median NOSE score was 50 in the diode group and 40 in the KTP group, and at three months, 15 in the diode group and five in the KTP group. KTP laser showed a 93 per cent improvement in the NOSE score as compared to 77 per cent improvement shown by diode laser group. Among the intra-operative complications, of the 104 patients in the diode group, 6.73 per cent had burning sensation and 91.43 per cent had bleeding, and of 105 patients in the KTP group, 54.29 per cent had burning sensation and 36.54 per cent had bleeding. Among the post-operative complications in the KTP group, 32 and 34 per cent had bloody nasal discharge on days one and two, compared to 12 and 14 per cent in diode group. Crusting was present in 61 and 49 per cent on days one and two in KTP group as compared to 9 and 15 per cent in diode group, respectively. In the KTP group 30 per cent had synechiae as compared to 10 per cent in diode group. Interpretation & conclusions:KTP laser was more efficacious than diode laser in improving the NOSE scores but with slightly increased rate of complications in early post-operative period. Both the lasers impaired the mucociliary clearance mechanism of the nose till three months of post-operative follow up.

背景与目标： 背景与目的：下鼻甲肥大（ITH）是导致鼻塞的常见病。进行这项研究以比较磷酸钛氧钾（KTP）激光和二极管激光在减小鼻甲大小方面的功效。
方法：该随机对照试验包括209例ITH患者。根据鼻塞症状评估（NOSE）评分评估术前症状。进行了诊断性鼻内窥镜检查以排除其他鼻窦。鼻粘膜纤毛清除率通过糖精转运时间（STT）测量。术后第1天和第2天，第1周，第1个月和第3个月评估NOSE评分，STT和并发症。
结果：在第一天分析的209例患者中，二极管组的NOSE中位数为50，KTP组为40，三个月时，二极管组为15，KTP组为5。 KTP激光器的NOSE得分提高了93％，而二极管激光器组则提高了77％。在术中并发症中，二极体组104例患者中，烧灼感为6.73％，出血为91.43％，KTP组的105例患者中，烧灼感为54.29％，出血为36.54％ 。在KTP组的术后并发症中，分别在第一天和第二天有32％和34％的人流鼻血，而二极管组则分别为12％和14％。 KTP组第1天和第2天的结壳率分别为61％和49％，而二极管组的结壳率分别为9％和15％。在KTP组中，有30％的人患有粘连症，而在二极管组中则为10％。
解释与结论：KTP激光在改善NOSE评分方面比二极管激光更有效，但术后早期的并发症发生率略有增加。两种激光都削弱了鼻子的粘膜纤毛清除机制，直到术后三个月随访为止。

BACKGROUND & AIMS: :Transition from compensated to decompensated left ventricular hypertrophy (LVH) is accompanied by functional and structural changes. Here, the aim was to evaluate dystrophin expression in murine models and human subjects with LVH by transverse aortic constriction (TAC) and aortic stenosis (AS), respectively. We determined whether doxycycline (Doxy) prevented dystrophin expression and myocardial stiffness in mice. Additionally, ventricular function recovery was evaluated in patients 1 year after surgery. Mice were subjected to TAC and monitored for 3 weeks. A second group received Doxy treatment after TAC. Patients with AS were stratified by normal left ventricular end-diastolic wall stress (LVEDWS) and high LVEDWS, and groups were compared. In mice, LVH decreased inotropism and increased myocardial stiffness associated with a dystrophin breakdown and a decreased mitochondrial O2 uptake (MitoMVO2). These alterations were attenuated by Doxy. Patients with high LVEDWS showed similar results to those observed in mice. A correlation between dystrophin and myocardial stiffness was observed in both mice and humans. Systolic function at 1 year post-surgery was only recovered in the normal-LVEDWS group. In summary, mice and humans present diastolic dysfunction associated with dystrophin degradation. The recovery of ventricular function was observed only in patients with normal LVEDWS and without dystrophin degradation. In mice, Doxy improved MitoMVO2. Based on our results it is concluded that the LVH with high LVEDWS is associated to a degradation of dystrophin and increase of myocardial stiffness. At least in a murine model these alterations were attenuated after the administration of a matrix metalloprotease inhibitor.

背景与目标： 从代偿性向代偿性失衡的左心室肥大（LVH）的转变伴随着功能和结构的变化。在这里，目的是通过横向主动脉缩窄（TAC）和主动脉狭窄（AS）评估鼠模型和LVH人体受试者中的肌营养不良蛋白表达。我们确定强力霉素（Doxy）是否能预防小鼠中的肌营养不良蛋白表达和心肌僵硬。此外，术后1年评估患者的心室功能恢复。对小鼠进行TAC并监测3周。第二组在TAC后接受Doxy治疗。 AS患者按正常左心室舒张末期壁应力（LVEDWS）和高LVEDWS进行分层，并比较各组。在小鼠中，LVH降低了肌力，并增加了肌营养不良蛋白的分解和线粒体O2摄取（MitoMVO2）的减少，从而增加了心肌的硬度。这些改变被Doxy减弱了。 LVEDWS高的患者显示的结果与小鼠观察到的结果相似。在小鼠和人类中都观察到肌营养不良蛋白与心肌硬度之间的相关性。术后1年的收缩功能仅在正常LVEDWS组中得以恢复。总之，小鼠和人类表现出与肌营养不良蛋白降解相关的舒张功能障碍。仅在LVEDWS正常且无肌营养不良蛋白降解的患者中观察到心室功能的恢复。在小鼠中，Doxy改善了MitoMVO2。根据我们的结果，可以得出结论，LVEDWS高的LVH与肌营养不良蛋白的降解和心肌硬度的增加有关。至少在鼠模型中，在施用基质金属蛋白酶抑制剂后，这些改变被减弱了。

BACKGROUND & AIMS: :Increasing evidence suggests that a mismatch between angiogenesis and myocardial growth contributes to the transition from adaptive cardiac hypertrophy to heart failure following pressure overload. Syndecan-4 is a transmembrane proteoglycan that binds to growth factors and extracellular matrix proteins and is critical in focal adhesion formation. However, its effects on coronary angiogenesis during pressure overload-induced heart failure have not been studied. Here, we hypothesize that syndecan-4 modulates cardiac remodeling in response to pressure overload through its ability to regulate adaptive angiogenesis. Syndecan-4 knockout (syndecan-4 KO) and wild-type (WT) mice were subjected to pressure overload induced by transverse aortic constriction (TAC). Syndecan-4 KO mice exhibited reduced capillary density, attenuated cardiomyocyte size, and worsened left ventricular cardiac function after TAC surgery compared with WT mice. Moreover, syndecan-4 KO mice showed a significant decrease in protein kinase C alpha expression. Our data suggest that syndecan-4 is essential for the compensated hypertrophy and the maintenance of cardiac function during the process of heart failure following pressure overload.

背景与目标： ：越来越多的证据表明，在压力超负荷后，血管新生与心肌生长之间的不匹配会导致从适应性心脏肥大向心力衰竭的转变。 Syndecan-4是一种跨膜蛋白聚糖，可与生长因子和细胞外基质蛋白结合，对形成粘着斑至关重要。然而，尚未研究其在压力超负荷引起的心力衰竭期间对冠状血管生成的影响。在这里，我们假设syndecan-4通过调节适应性血管新生的能力来调节心脏重塑，以应对压力超负荷。 Syndecan-4基因敲除（syndecan-4 KO）和野生型（WT）小鼠受到横动脉主动脉缩窄（TAC）诱导的压力超负荷。与WT小鼠相比，在TAC手术后，Syndecan-4 KO小鼠的毛细血管密度降低，心肌细胞大小减少和左心室心脏功能恶化。此外，syndecan-4 KO小鼠显示蛋白激酶Cα表达明显降低。我们的数据表明，在压力超负荷后心力衰竭过程中，syndecan-4对于代偿性肥大和维持心功能至关重要。

BACKGROUND & AIMS: BACKGROUND AND AIM:Secreted frizzled-related protein 2 (sFRP2) has been reported to be involved in cardiovascular diseases. However, its role in cardiac hypertrophy induced by pressure overload is still elusive. We aimed to examine the role of sFRP2 in the development of cardiac hypertrophy in vivo and in vitro. METHODS AND RESULTS:Following cardiac hypertrophy stimulated by aortic banding (AB), the expression of sFRP2 was downregulated in the hypertrophic ventricle. Adeno-associated virus 9 (AAV9) was injected through the tail vein to overexpress sFRP2 in the mouse myocardium. Overexpression of sFRP2 alleviated cardiomyocyte hypertrophy and interstitial fibrosis, as identified by the reduced cardiomyocyte cross-sectional area, heart weight/body weight ratio, and left ventricular (LV) collagen ratio. Additionally, sFRP2 decreased cardiomyocyte apoptosis induced by pressure overload. Western blot showed that sFRP2 prevented the expression of active β-catenin. The Wnt/β-catenin agonist LiCl (1 mmol/kg) abolished the inhibitory effects of sFRP2 on cardiac hypertrophy and apoptosis, as evidenced by the increased cross-sectional area and LV collagen ratio and the deterioration of echocardiographic data. CONCLUSION:Our study indicated that decreased sFRP2 levels were observed in failing mouse hearts. Overexpression of sFRP2 attenuated myocyte hypertrophy and interstitial fibrosis induced by hypertrophic stimuli by inhibiting the Wnt/β-catenin pathway. We revealed that sFRP2 may be a promising therapeutic target for the development of cardiac remodeling.

背景与目标： 背景与目的：据报道，卷曲的相关蛋白2（sFRP2）与心血管疾病有关。然而，它在由压力超负荷引起的心脏肥大中的作用仍然难以捉摸。我们旨在研究sFRP2在体内和体外心脏肥大发展中的作用。
方法和结果：在主动脉束带（AB）刺激的心肌肥大之后，sFRP2的表达在肥厚性心室中被下调。通过尾静脉注射腺相关病毒9（AAV9）以在小鼠心肌中过表达sFRP2。 sFRP2的过表达减轻了心肌肥大和间质纤维化，这通过减少的心肌细胞横截面积，心脏重量/体重比和左心室（LV）胶原蛋白比来确定。另外，sFRP2减少了压力超负荷引起的心肌细胞凋亡。 Western印迹表明，sFRP2阻止了活性β-catenin的表达。 Wnt /β-catenin激动剂LiCl（1 mmol / kg）取消了sFRP2对心脏肥大和细胞凋亡的抑制作用，这一点由横截面积和LV胶原比例的增加以及超声心动图数据的恶化所证明。
结论：我们的研究表明在衰竭的小鼠心脏中观察到sFRP2水平降低。 sFRP2的过表达通过抑制Wnt /β-catenin途径减弱了肥厚性刺激诱导的心肌肥大和间质纤维化。我们发现，sFRP2可能是心脏重塑发展的有希望的治疗靶标。

BACKGROUND & AIMS: OBJECTIVE:In patients with type 2 diabetes, left ventricular hypertrophy (LVH) predicts cardiovascular events, and the prevention of LVH is cardioprotective. We sought to compare the effect of ACE versus non-ACE inhibitor therapy on incident electrocardiographic (ECG) evidence of LVH (ECG-LVH). RESEARCH DESIGN AND METHODS:This prespecified study compared the incidence of ECG-LVH by Sokolow-Lyon and Cornell voltage criteria in 816 hypertensive type 2 diabetic patients of the Bergamo Nephrologic Diabetes Complications Trial (BENEDICT), who had no ECG-LVH at baseline and were randomly assigned to at least 3 years of blinded ACE inhibition with trandolapril (2 mg/day) or to non-ACE inhibitor therapy. Treatment was titrated to systolic/diastolic blood pressure <130/80 mmHg. ECG readings were centralized and blinded to treatment. RESULTS:Baseline characteristics of the two groups were similar. Over a median (interquartile range) follow-up of 36 (24-48) months, 13 of the 423 patients (3.1%) receiving trandolapril compared with 31 of the 376 patients (8.2%) receiving non-ACE inhibitor therapy developed ECG-LVH (hazard ratio [HR] 0.34 [95% CI 0.18-0.65], P = 0.0012 unadjusted, and 0.35 [0.18-0.68], P = 0.0018 adjusted for predefined baseline covariates). The HR was significant even after adjustment for follow-up blood pressure and blood pressure reduction versus baseline. Compared with baseline, both Sokolow-Lyon and Cornell voltages significantly decreased with trandolapril but did not change with non-ACE inhibitor therapy. CONCLUSIONS:ACE inhibition has a specific protective effect against the development of ECG-LVH that is additional to its blood pressure-lowering effect. Because ECG-LVH is a strong cardiovascular risk factor in people with hypertension and diabetes, early ACE inhibition may be cardioprotective in this population.

背景与目标： 目的：在2型糖尿病患者中，左心室肥大（LVH）可以预测心血管事件，对LVH的预防具有心脏保护作用。我们试图比较ACE与非ACE抑制剂治疗对LVH的入射心电图（ECG）证据（ECG-LVH）的影响。
研究设计和方法：这项预先设定的研究比较了816例Bergamo肾病糖尿病并发症试验（BENEDICT）的高血压2型糖尿病患者的Sokolow-Lyon和Cornell电压标准对ECG-LVH的发生率，他们在基线和基线时均没有ECG-LVH随机分配至少3年使用trandolapril（2 mg /天）的ACE盲治疗或非ACE抑制剂治疗。将治疗滴定至收缩压/舒张压<130/80 mmHg。心电图读数集中并且对治疗不知情。
结果：两组的基线特征相似。在36（24-48）个月的中位（四分位间距）随访中，接受trandolapril治疗的423例患者中有13例（3.1％）接受了非ACE抑制剂治疗的376例患者（8.2％）中的31例发展了ECG- LVH（危险比[HR] 0.34 [95％CI 0.18-0.65]，未调整P = 0.0012，0.35 [0.18-0.68]，对于预定义的基线协变量已调整P = 0.0018）。即使在调整了后续血压和相对于基线的血压降低后，HR仍显着。与基线相比，使用trandolapril的Sokolow-Lyon和Cornell电压均显着降低，但使用非ACE抑制剂治疗则无变化。
结论：ACE抑制对ECG-LVH的发展具有特定的保护作用，这是其降低血压的作用。由于ECG-LVH在高血压和糖尿病患者中是很强的心血管危险因素，因此早期ACE抑制可能对该人群具有心脏保护作用。