標(biāo)題: Titlebook: Delayed Preconditioning and Adaptive Cardioprotection; G. F. Baxter,D. M. Yellon Book 1998 Springer Science+Business Media Dordrecht 1998 [打印本頁] 作者: 正當(dāng)理由 時(shí)間: 2025-3-21 18:58
書目名稱Delayed Preconditioning and Adaptive Cardioprotection影響因子(影響力)
書目名稱Delayed Preconditioning and Adaptive Cardioprotection影響因子(影響力)學(xué)科排名
書目名稱Delayed Preconditioning and Adaptive Cardioprotection網(wǎng)絡(luò)公開度
書目名稱Delayed Preconditioning and Adaptive Cardioprotection網(wǎng)絡(luò)公開度學(xué)科排名
書目名稱Delayed Preconditioning and Adaptive Cardioprotection被引頻次
書目名稱Delayed Preconditioning and Adaptive Cardioprotection被引頻次學(xué)科排名
書目名稱Delayed Preconditioning and Adaptive Cardioprotection年度引用
書目名稱Delayed Preconditioning and Adaptive Cardioprotection年度引用學(xué)科排名
書目名稱Delayed Preconditioning and Adaptive Cardioprotection讀者反饋
書目名稱Delayed Preconditioning and Adaptive Cardioprotection讀者反饋學(xué)科排名
作者: Crohns-disease 時(shí)間: 2025-3-21 21:40 作者: 精確 時(shí)間: 2025-3-22 02:38
Developments in Cardiovascular Medicinehttp://image.papertrans.cn/d/image/264941.jpg作者: cocoon 時(shí)間: 2025-3-22 05:01 作者: Perceive 時(shí)間: 2025-3-22 11:44 作者: intention 時(shí)間: 2025-3-22 13:10
?Buffer Stocks? und Aggregationsproblematikial ischemic insult and lasts 2–3 hours, and a late (or delayed) phase, which becomes apparent 12–24 hours later and lasts for 3–4 days (reviewed in references 1 and 2). These two phases have different pathophysiology and probably different mechanisms. Since the late phase lasts much longer, it may 作者: intention 時(shí)間: 2025-3-22 17:49 作者: 隨意 時(shí)間: 2025-3-22 22:43 作者: 含糊其辭 時(shí)間: 2025-3-23 04:57
https://doi.org/10.1007/978-3-663-13540-1t is the basis of adaptive modification. Adaptation involves a number of cellular and biochemical alterations including (i) changes in metabolic homeostasis and (ii) reprogramming of gene expression. Changes in metabolic pathways are generally short-lived and reversible; the consequences of reprogra作者: 手銬 時(shí)間: 2025-3-23 05:47
Gesch?ftsführung und Vertretungr promoting cell injury and death. Identifying these proteins is an important first step towards understanding the molecular mechanisms underlying the stress response. As new or elevated protein synthesis can result from increased gene expression, studies of gene transcription provide a key to ident作者: indigenous 時(shí)間: 2025-3-23 13:44
Einkommen- und K?rperschaftsteuerhe first observation that elevated temperature could trigger rapid and specific changes in chromosomal and metabolic activity of living organisms; new mRNA was synthesised within 2–3 minutes [1, 2]. During the 1970s several laboratories discovered that novel (heat shock) proteins were expressed in c作者: 甜瓜 時(shí)間: 2025-3-23 15:27
https://doi.org/10.1007/978-3-322-99076-1, heat stress [2], endotoxin [3], and cytokines [4,5]. The classic preconditioning phenomenon, in which brief, nonlethal ischaemia, rapidly increases the tolerance of the heart to subsequent lethal ischaemia, has been observed in experimental models [1] and in patients [6,7]. The mechanism of classi作者: 自由職業(yè)者 時(shí)間: 2025-3-23 21:50
Die Gemeinde und ihr Territoriumt isolation and perfusion in the Langendorff mode resulted in an enhanced post-ischaemic recovery of myocardial function (left ventricular developed pressure, + dP/dt) and an increase in catalase activity. Hearts isolated from rats which were pretreated with LPS for only 1 hour did not have an incre作者: ARCHE 時(shí)間: 2025-3-24 00:10
https://doi.org/10.1007/978-3-322-99003-7ns of adenosine have been appreciated for many years (see reference 1 for review). It is known that various forms of myocardial stress, including ischaemia, hypoxia or catecholamines, result in a rapid increase in extracellular levels of adenosine. This in turn results in activation of local adenosi作者: 廚師 時(shí)間: 2025-3-24 05:54 作者: GRIEF 時(shí)間: 2025-3-24 08:42 作者: Commentary 時(shí)間: 2025-3-24 14:04
https://doi.org/10.1007/978-3-642-47013-4ary endothelium determines arrhythmia severity following coronary artery occlusion and whether this plays a role in ischaemic preconditioning. In this chapter, we describe the protection against ventricular arrhythmias afforded by preconditioning, with particular emphasis on the delayed form of protection.作者: Afflict 時(shí)間: 2025-3-24 17:51 作者: 支形吊燈 時(shí)間: 2025-3-24 21:09
Book 199893, two reports heralded the recognitionof a delayed preconditioning response in the heart, now commonly knownas the `second window‘ of protection. Since then, a number of studieshave described the ability of delayed preconditioning and relatedadaptive phenomena to protect against a variety of patho作者: Mitigate 時(shí)間: 2025-3-25 02:54 作者: CAGE 時(shí)間: 2025-3-25 06:59 作者: Hiatal-Hernia 時(shí)間: 2025-3-25 08:30
?Buffer Stocks? und Aggregationsproblematikedge regarding the pathophysiology and pathogenesis of late PC against myocardial stunning and to summarise recent evidence supporting a major role of nitric oxide (NO) in the late phase of ischaemic PC (“nitric oxide hypothesis of late PC”).作者: 完成 時(shí)間: 2025-3-25 12:05
Einkommen- und K?rperschaftsteuer1–7] lead to discoveries of HSPs in all cells from bacteria to man [8], and of inducible and transient cellular protection in cells and organs as varied as heart, brain, kidney and retina, the subject of this chapter.作者: Seminar 時(shí)間: 2025-3-25 19:47 作者: CONE 時(shí)間: 2025-3-25 22:35 作者: 財(cái)主 時(shí)間: 2025-3-26 03:39 作者: DALLY 時(shí)間: 2025-3-26 07:57
Endotoxin, Monophosphoryl Lipid A and Delayed Cardioprotection,ased catalase activity or functional protection from ischaemia-reperfusion injury. These results suggested that the delayed cardioprotection produced by LPS was the result of enhanced antioxidant enzyme activity, particularly catalase.作者: GRAVE 時(shí)間: 2025-3-26 09:17
https://doi.org/10.1007/978-3-642-82936-9 7), endotoxin and its derivatives (chapter 9), and adenosine analogues (chapter 10). In this chapter, we will review the background to the discovery of delayed preconditioning, the characteristics of this phenomenon and possible mechanisms. We will concentrate particularly on the direct cytoprotect作者: AXIOM 時(shí)間: 2025-3-26 14:15
?Buffer Stocks? und Aggregationsproblematikon and leukocyte adhesion, it is likely that such a persistent impairment may have important deleterious consequences on the coronary arterial wall. Thus, coronary endothelium may be considered a major therapeutic target of anti-ischaemic treatments.作者: FLAG 時(shí)間: 2025-3-26 19:12 作者: alleviate 時(shí)間: 2025-3-26 22:53
https://doi.org/10.1007/978-3-322-99076-1hours after the initial nonlethal ischaemia. This late effect of ischaemic preconditioning was named the second window of protection [16]. Although de novo protein synthesis is not involved in the mechanism of classic preconditioning [17], the time course of the second window suggests that the synth作者: 剝皮 時(shí)間: 2025-3-27 02:06
https://doi.org/10.1007/978-3-322-99003-7 it is formed; the duration of its effects are very transient with a half-life in human blood of less than one second [3]. Thus adenosine is considered a short-term mediator that maintains the metabolic equilibrium of the heart within a time frame of seconds to minutes.作者: 詞匯表 時(shí)間: 2025-3-27 09:10
https://doi.org/10.1007/978-3-031-28844-9ossibility that angina heralding MI may represent the clinical correlate of ischaemic preconditioning is extremely appealing because of its inherent cardioprotective action. Therefore, this chapter will review the concept that angina pectoris before MI may exert a protective role, through an adaptiv作者: Freeze 時(shí)間: 2025-3-27 12:20 作者: 鋼筆記下懲罰 時(shí)間: 2025-3-27 15:16 作者: 鞭打 時(shí)間: 2025-3-27 20:49
Delayed Preconditioning Against Lethal Ischaemic Injury, 7), endotoxin and its derivatives (chapter 9), and adenosine analogues (chapter 10). In this chapter, we will review the background to the discovery of delayed preconditioning, the characteristics of this phenomenon and possible mechanisms. We will concentrate particularly on the direct cytoprotect作者: Fermentation 時(shí)間: 2025-3-28 01:58 作者: Aerate 時(shí)間: 2025-3-28 05:51
Changes in Cardiac Gene Expression After Ischaemia and Reperfusion, or surgery, and to understand the adaptive processes that may protect myocardial function. Few studies of gene transcription have, however, been conducted using human tissue, due to the limitations of working with living subjects. As a result, our understanding of the transcriptional response of my作者: 現(xiàn)存 時(shí)間: 2025-3-28 06:31
, Role of Manganese Superoxide Dismutase in Delayed Preconditioning,hours after the initial nonlethal ischaemia. This late effect of ischaemic preconditioning was named the second window of protection [16]. Although de novo protein synthesis is not involved in the mechanism of classic preconditioning [17], the time course of the second window suggests that the synth作者: conceal 時(shí)間: 2025-3-28 11:06 作者: 腐蝕 時(shí)間: 2025-3-28 16:39 作者: Silent-Ischemia 時(shí)間: 2025-3-28 19:54 作者: MORPH 時(shí)間: 2025-3-29 00:39
Delayed Preconditioning Against Lethal Ischaemic Injury,g transient sublethal periods of ischaemia [1, 2]. These two studies initiated an area of research on ischaemic preconditioning of myocardium which has developed considerably in the last five years. This form of preconditioning, known variously as "delayed preconditioning", "late preconditioning", t作者: recede 時(shí)間: 2025-3-29 03:09
, Role of Nitric Oxide as Trigger and Mediator,ial ischemic insult and lasts 2–3 hours, and a late (or delayed) phase, which becomes apparent 12–24 hours later and lasts for 3–4 days (reviewed in references 1 and 2). These two phases have different pathophysiology and probably different mechanisms. Since the late phase lasts much longer, it may 作者: 子女 時(shí)間: 2025-3-29 10:11
Delayed Preconditioning Against Endothelial Dysfunction, of platelet and leukocyte function. Numerous experimental and clinical data suggest that these essential physiological functions of the endothelium are altered in various pathophysiological situations, such as hypertension, hypercholesterolaemia or diabetes. Such dysfunction can be characterised by作者: Carcinogenesis 時(shí)間: 2025-3-29 13:12 作者: 受人支配 時(shí)間: 2025-3-29 17:40
Intracellular Signalling Mechanisms in Myocardial Adaptation to Ischaemia,t is the basis of adaptive modification. Adaptation involves a number of cellular and biochemical alterations including (i) changes in metabolic homeostasis and (ii) reprogramming of gene expression. Changes in metabolic pathways are generally short-lived and reversible; the consequences of reprogra作者: Obstreperous 時(shí)間: 2025-3-29 21:31
Changes in Cardiac Gene Expression After Ischaemia and Reperfusion,r promoting cell injury and death. Identifying these proteins is an important first step towards understanding the molecular mechanisms underlying the stress response. As new or elevated protein synthesis can result from increased gene expression, studies of gene transcription provide a key to ident
