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| 1 | Contractile apparatus dysfunction early in the pathophysiology of diabetic cardiomyopathy显示文摘Diabetes mellitus significantly increases the risk of cardiovascular disease and heart failure in patients.Independent of hypertension and coronary artery disease,diabetes is associated with a specific cardiomyopathy,known as diabetic cardiomyopathy(DCM).Four decades of research in experimental animal models and advances in clinical imaging techniques suggest that DCM is a progressive disease,beginning early after the onset of type 1 and type 2 diabetes,ahead of left ventricular remodeling and overt diastolic dysfunction.Although the molecular pathogenesis of early DCM still remains largely unclear,activation of protein kinase C appears to be central in driving the oxidative stress dependent and independent pathways in the development of contractile dysfunction.Multiple subcellular alterations to the cardiomyocyte are now being highlighted as critical events in the early changes to the rate of force development,relaxation and stability under pathophysiological stresses.These changes include perturbed calcium handling,suppressed activity of aerobic energy producing enzymes,altered transcriptional and posttranslational modification of membrane and sarcomeric cytoskeletal proteins,reduced actin-myosin cross-bridge cycling and dynamics,and changed myofilament calcium sensitivity.In this review,we will present and discuss novel aspects of the molecular pathogenesis of early DCM,with a special focus on the sarcomeric contractile apparatus. | Mark T Waddingham Amanda J Edgley Hirotsugu Tsuchimochi Darren J Kelly Mikiyasu Shirai James T Pearson | 2015 | World Journal of Diabetes2015，6，7： | 10 |
| 2 | Protein C Deficiency:A Case Re-view显示文摘 | Kelly A Pearson G D | 2011 | Neonatal Netw2011，30，3： | 1 |
| 3 | Myeloid progenitor cells lacking p53exhibit delayed up-regulation of Puma and prolonged survival after cytokine deprivation显示文摘 | Jabbour A M Daunt C P Green B D Vogel S Gordon L Lee R S Silke N Pearson R B Vandenberg C J Kelly P N Nutt S L Strasser A Borner C Ekert P G | 2010 | Blood2010，115，2： | 1 |
| 4 | Colning and characterization of a cDNA encoding the collagen-binding stress protein HSP47 in zebrafish显示文摘 | Pearson DS Kulyk WM Kelly GM | 1996 | DNA Cell Biol1996，15，3： | 1 |
| 5 | Cloning and character- ization of a cDNA encoding the collagen - binding stress protein hsp47 in zebrafish 显示文摘 | Pearson DS Kulyk WM Kelly GM | 1996 | DNA Cell Biol1996，15，3： | 1 |
| 6 | Loss of CDKN 2A expression is a frequent event in primary invasive melanoma and correlates with sensitivity to the CDK 4/6 inhibitor PD 0332991 in melanoma cell lines显示文摘 | Richard J. Young Kelly Waldeck Claire Martin Jung H. Foo Donald P. Cameron Laura Kirby Hongdo Do Catherine Mitchell Carleen Cullinane Wendy Liu Stephen B. Fox Ken Dutton‐Regester Nicholas K. Hayward Nicholas Jene Alexander Dobrovic Richard B. Pearson Jame | 2014 | Pigment Cell Melanoma Res2014，，4： | 1 |
| 7 | Perron-Frobenius theorem for nonnegative tensors显示文摘 | Chang K C Pearson Kelly Zhang Tan | 2008 | Communal Math Science2008，6，14： | 1 |
| 8 | Cloning and characterization of a eDNA encoding the collagen-binding stress protein hsp47 in zebrafish显示文摘 | PEARSON D S KULYK W M KELLY G M | 1996 | DNA Cell Biol1996，15，3： | 1 |
| 9 | Maximal number of distinct H-eigenpairs for a two-dimensional real tensor显示文摘基于 J 介绍的概括典型多项式。在概括典型多项式精明[J。符号的 Comput, 1990, 9 (3 ) :241250 ] ,它是立即的为任何 m 顺序 n 维的真实张肌,不同 H 特征值的数字小于等于 n (m1 ) n1。然而,一般来说不同 Heigenvectors 的最大的数字上没有已知的界限。我们为任何 m 证明那 2, m 顺序 2-dimensional 张肌 A 存在以便 A 有 2 (m 1 ) 不同 H-eigenpairs。我们与六不同 H 特征值以及六不同 H 特徵向量给 4 顺序 2-dimensional 张肌的例子。我们证明为更高的顺序张肌的 eigenpairs 的结构比一个矩阵的更加复杂。而且,我们在某些条件下面介绍弱对称的张肌,叫的 p 对称的张肌,和表演的一个新班, p 对称将有效地为给定的二维的张肌减少不同 H 特徵向量的最大的数字。最后,我们提供给定的 4 顺序 2-dimensional nonnegative 的 H 特徵向量的一个完全的分类 p 对称的张肌。另外,我们从拥有六 pairwise 给阻止给定的 4 顺序 2-dimensional nonnegative 的足够的条件无法缩减的弱对称的张肌不同 H 特徵向量。 | Kelly J. PEARSON Tan ZHANG | 2013 | Frontiers of Mathematics in China2013，8，1： | 0 |
| 10 | 感觉性多发性神经病的诊断和治疗显示文摘感觉性多发性周围神经病是由感觉性周围神经功能障碍引起的一组异质性疾病,包括常见的糖尿病神经病变及其他少见的类型。由于潜在病因和受累神经纤维类型不同,该疾病的临床症状、起病缓急、病程、严重程度和发病率各不相同。细小的有髓和无髓神经纤维受累主要导致神经病理性疼痛,而粗大的有髓感觉传入神经受累则引起深感觉障碍和共济失调。感觉性多发性神经病的病因包括代谢、中毒、感染、炎症、自身免疫和遗传。特发性感觉性多发神经病也很常见,但属于排除性诊断。辅助检查包括神经传导速度、周围神经组织病理检查、自主神经功能检查以及血清学检查和脑脊液化验。治疗方法取决于潜在的病因,包括控制危险因素、免疫治疗、对症治疗和基因治疗(如最新研发的针对转甲蛋白相关家族性淀粉样周围神经病的RNA干扰和反义寡核苷酸治疗)。然而,在大多数情况下仍缺乏病因治疗,以对症和支持治疗为主。未来仍需对感觉性多发性神经病潜在的病理生理学机制进行更多研究,以推动该病的治疗进展。 | Kelly Graham Gwathmey Kathleen T Pearson 钱敏(译) 李佳(译) 陈琳(校) 关鸿志(校) | 2021 | 英国医学杂志中文版2021，24，8： | 0 |
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