標(biāo)題: Titlebook: Cardiomyocytes – Active Players in Cardiac Disease; Klaus-Dieter Schlüter Book 2016 Springer International Publishing Switzerland 2016 car [打印本頁] 作者: 喜悅 時(shí)間: 2025-3-21 17:04
書目名稱Cardiomyocytes – Active Players in Cardiac Disease影響因子(影響力)
書目名稱Cardiomyocytes – Active Players in Cardiac Disease影響因子(影響力)學(xué)科排名
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書目名稱Cardiomyocytes – Active Players in Cardiac Disease網(wǎng)絡(luò)公開度學(xué)科排名
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書目名稱Cardiomyocytes – Active Players in Cardiac Disease讀者反饋學(xué)科排名
作者: 一大群 時(shí)間: 2025-3-21 20:39 作者: Counteract 時(shí)間: 2025-3-22 03:19 作者: 埋葬 時(shí)間: 2025-3-22 05:41 作者: Misnomer 時(shí)間: 2025-3-22 10:33 作者: 摻假 時(shí)間: 2025-3-22 13:27 作者: 摻假 時(shí)間: 2025-3-22 18:36 作者: drusen 時(shí)間: 2025-3-22 21:15 作者: CLAN 時(shí)間: 2025-3-23 02:02
Mechanisms of Cardiac Cell Deathtractile power of the heart. Therefore, prevention of cardiomyocyte death should be one of the major aims when thinking about cardioprotection. As cell death can take different forms that are induced by various stressors and that proceed via different pathways, it is necessary to strictly differenti作者: 放大 時(shí)間: 2025-3-23 08:44 作者: PAD416 時(shí)間: 2025-3-23 09:52 作者: Mri485 時(shí)間: 2025-3-23 16:02
Environmental Science and Engineering]. transient (CaT) decides about the strength of contraction. Increases in L-type Ca. current, SERCA activity, SR Ca. load and fractional release, IP. signalling and [Na.]. all increase CaT amplitude. Under conditions of Ca. overload, SR Ca. release also occurs spontaneously, i.e. in the absence of 作者: 前面 時(shí)間: 2025-3-23 18:31 作者: AWE 時(shí)間: 2025-3-24 00:40
https://doi.org/10.1007/978-94-010-0066-6f endogenous mechanisms that can contribute to the regulation of the myocardial contractility and illustrates the various feedback loops and signalling pathways that can be induced via corresponding modulation of the cardiac function. A detailed description of the underlying cellular and molecular m作者: Neonatal 時(shí)間: 2025-3-24 05:14
https://doi.org/10.1007/978-3-319-07055-1hormones, cytokines and neurotransmitters have been identified that trigger cardiac hypertrophy and specifically those related to the sympathetic nervous system, and the renin-angiotensin system is of importance for the transition to heart failure. An increase in the translational capacity is the ba作者: GIBE 時(shí)間: 2025-3-24 08:32
Martin Adam,Stephan Sch?ffler,Anna Brauny in particular evolved to the level that they are considered decisive in disease development. Indeed, their manipulation in vitro as well as in vivo influence cardiomyocyte function and cardiac disease outcome. Substrates subject to degradation range from single proteins (ubiquitin-proteasome pathw作者: bisphosphonate 時(shí)間: 2025-3-24 11:50 作者: adipose-tissue 時(shí)間: 2025-3-24 18:46
Ways to Study the Biology of Cardiomyocytesemodeling. Function of cardiomyocytes is mostly characterized by load-free cell shortening with remarkable reproducible results between cardiomyocytes from different species. Molecular aspects of cardiac hypertrophy can be analyzed by quantification of protein synthesis, protein degradation, and cel作者: cylinder 時(shí)間: 2025-3-24 20:25
Excitation–Contraction Coupling of Cardiomyocytes]. transient (CaT) decides about the strength of contraction. Increases in L-type Ca. current, SERCA activity, SR Ca. load and fractional release, IP. signalling and [Na.]. all increase CaT amplitude. Under conditions of Ca. overload, SR Ca. release also occurs spontaneously, i.e. in the absence of 作者: Parley 時(shí)間: 2025-3-25 01:51 作者: BRACE 時(shí)間: 2025-3-25 03:52 作者: N防腐劑 時(shí)間: 2025-3-25 08:35 作者: 協(xié)議 時(shí)間: 2025-3-25 14:08
Protein Degradation in Cardiomyocytes: Target Proteins and Clinical Consequencesy in particular evolved to the level that they are considered decisive in disease development. Indeed, their manipulation in vitro as well as in vivo influence cardiomyocyte function and cardiac disease outcome. Substrates subject to degradation range from single proteins (ubiquitin-proteasome pathw作者: 推延 時(shí)間: 2025-3-25 18:48 作者: certitude 時(shí)間: 2025-3-25 23:30 作者: exostosis 時(shí)間: 2025-3-26 00:58 作者: aggravate 時(shí)間: 2025-3-26 06:17 作者: 笨重 時(shí)間: 2025-3-26 11:01 作者: Militia 時(shí)間: 2025-3-26 16:31 作者: PLUMP 時(shí)間: 2025-3-26 20:32 作者: BILK 時(shí)間: 2025-3-26 22:55 作者: semiskilled 時(shí)間: 2025-3-27 04:08
Tursun Ibrayev,Batyrbek Badjanov,Marina Lifour chambers (two atria, two ventricles) that have distinct differentiation during embryonic development and either derives from the first heart field, the second heart field, or the cardiac neural crest. Interestingly, at least cardiomyocytes lose their ability to proliferate early after birth in 作者: 致敬 時(shí)間: 2025-3-27 08:17 作者: concubine 時(shí)間: 2025-3-27 11:22 作者: hegemony 時(shí)間: 2025-3-27 14:56
https://doi.org/10.1007/978-94-010-0066-6system. The heart has to carry out this task 24 h a day without interruption. Over this period, it beats about 115,000 times, transporting about 8000 l of blood through both heart chambers. To be able to achieve this throughput, specific demands are placed on the heart: the contraction and relaxatio作者: AWRY 時(shí)間: 2025-3-27 18:15
https://doi.org/10.1007/978-3-319-07055-1e large majority of mammalian cardiomyocytes lose the ability to cytokinesis shortly after birth, this is the most important process by which the heart muscle mass can be adapted to increased mechanical stress. Cardiac hypertrophy is a physiological process during adolescence in which the total hear作者: 擺動(dòng) 時(shí)間: 2025-3-28 00:24 作者: Conflict 時(shí)間: 2025-3-28 03:43
Hans-Peter Steinbacher,Philipp Althalerer certain signaling mechanisms and cellular adaptation to cardiomyocytes. Ischemia itself induces metabolic and structural changes to cardiomyocytes that are prone to reperfusion-induced stress, i.e., by inducing plasmalemmal fragility. Reperfusion restores immediately energy resources, but due to 作者: 熱心助人 時(shí)間: 2025-3-28 08:41
Michael Felderer,Johannes Keckeistractile power of the heart. Therefore, prevention of cardiomyocyte death should be one of the major aims when thinking about cardioprotection. As cell death can take different forms that are induced by various stressors and that proceed via different pathways, it is necessary to strictly differenti作者: Rebate 時(shí)間: 2025-3-28 13:43
Michael Felderer,Johannes Keckeisng molecules (RNS). However, under certain conditions the balance between formation of oxygen radicals and degradation of them is severely affected resulting in oxidative stress that significantly contributes to cardiac dysfunction. In this chapter key molecules that trigger ROS and RNS formation in作者: Ptsd429 時(shí)間: 2025-3-28 15:28 作者: 托運(yùn) 時(shí)間: 2025-3-28 20:02
http://image.papertrans.cn/c/image/221877.jpg作者: 古代 時(shí)間: 2025-3-29 01:06
Michael Felderer,Johannes Keckeisior of mitochondrial function. Therefore, ROS and RNS couples mitochondrial function to key regulatory processes of cardiomyocytes, such as force generation and growth control, despite their genuine function in energy metabolism.作者: 等待 時(shí)間: 2025-3-29 04:51
Oxidative Stress and Nitrosative Stressior of mitochondrial function. Therefore, ROS and RNS couples mitochondrial function to key regulatory processes of cardiomyocytes, such as force generation and growth control, despite their genuine function in energy metabolism.作者: VEN 時(shí)間: 2025-3-29 10:35
depict regeneration capacities and possibilities of cardiacThis book summarizes ourcurrent understanding about the biology and patho-biology of cardiomyocytes anddepicts common techniques for the study of these cells. Thebook is divided into two parts; the first part provides insight into role andf作者: 惡意 時(shí)間: 2025-3-29 13:18
