The renal vasodilatory effect of prostaglandins is ameliorated in isolated-perfused kidneys of endotoxemic mice [0.03%]
内毒素血症小鼠分离灌流肾脏的前列腺素肾血管扩张效应被缓解
Manuel Meurer,Katharina Ebert,Frank Schweda et al.
Manuel Meurer et al.
Endotoxemia-related acute kidney injury (AKI) is associated with increased formation of prostaglandins, which may serve as a compensatory mechanism to maintain renal function. We hypothesized that an increase of renal EP2 or EP4 receptors a...
NaPi-IIa interacting partners and their (un)known functional roles [0.03%]
NaPi-IIa 相互作用蛋白及其已知和未知的功能角色
Nati Hernando
Nati Hernando
The sorting and stabilization of proteins at specific subcellular domains depend upon the formation of networks build up by specific protein-protein interactions. In addition, protein networks also ensure the specificity of many regulatory ...
Mechanisms and regulation of epithelial phosphate transport in ruminants: approaches in comparative physiology [0.03%]
反刍动物上皮磷酸盐转运的机制及其调节：比较生理学研究方法
Alexandra S Muscher-Banse,Gerhard Breves
Alexandra S Muscher-Banse
Ruminants have a unique utilization of phosphate (Pi) based on the so-called endogenous Pi recycling to guarantee adequate Pi supply for ruminal microbial growth and for buffering short-chain fatty acids. Large amounts of Pi enter the gastr...
GTS-21 attenuates loss of body mass, muscle mass, and function in rats having systemic inflammation with and without disuse atrophy [0.03%]
GTS-21减轻全身炎症伴有和不伴废用性萎缩的大鼠体重、肌肉量和功能的丢失
Stefan J Schaller,Michio Nagashima,Martin Schönfelder et al.
Stefan J Schaller et al.
Muscle changes of critical illness are attributed to systemic inflammatory responses and disuse atrophy. GTS-21 (3-(2,4-dimethoxy-benzylidene)anabaseine), also known as DMBX-A) is a synthetic derivative of the natural product anabaseine tha...
Long-term endurance running activity causes pulmonary changes depending on the receptor for advanced glycation end-products [0.03%]
长期耐力跑步引起的肺部变化依赖于晚期糖基化终产物受体
Samiya Al-Robaiy,Anke Kindermann,Susanne Wodischeck et al.
Samiya Al-Robaiy et al.
The receptor for advanced glycation end-products (RAGE) is an immunoglobulin superfamily cell adhesion molecule predominantly expressed in the lung, but its pulmonary importance is incompletely understood. Since RAGE alters the respiratory ...
Mitochondrial junctions with cellular organelles: Ca2+ signalling perspective [0.03%]
线粒体与细胞器连接的钙离子信号学观点
Alexei V Tepikin
Alexei V Tepikin
Cellular organelles form multiple junctional complexes with one another and the emerging research area dealing with such structures and their functions is undergoing explosive growth. A new research journal named "Contact" has been recently...
Looking on the "brite" side exercise-induced browning of white adipose tissue [0.03%]
从“亮”面看运动诱导的白色脂肪组织褐变现象
Logan K Townsend,David C Wright
Logan K Townsend
The need for effective and convenient ways of combatting obesity has created great interest in brown adipose tissue (BAT). However, because adult humans have relatively little amounts of BAT, the possibility of browning white adipose tissue...
Telmisartan prevents diet-induced obesity and preserves leptin transport across the blood-brain barrier in high-fat diet-fed mice [0.03%]
替米沙坦可预防高脂饮食喂养的小鼠出现饮食诱导的肥胖并能保持高脂饮食喂养小鼠中瘦素运送到脑内的过程
Franziska Schuster,Gianna Huber,Ines Stölting et al.
Franziska Schuster et al.
Obesity is a global health problem and treatment options are still insufficient. When chronically treated with the angiotensin II receptor blocker telmisartan (TEL), rodents do not develop diet-induced obesity (DIO). However, the underlying...
Correction to: Cardiospecific deletion of αE-catenin leads to heart failure and lethality in mice [0.03%]
Correction to：小鼠αE-连环素心脏特异性缺失导致心力衰竭和致死性
Volodymyr V Balatskyi,Larysa L Macewicz,Ana-Maria Gan et al.
Volodymyr V Balatskyi et al.
The original version of this article unfortunately contained a mistake. The published paper presented an incorrect version of Table 1. The corrected Table is given here.
Maksymilian Prondzynski,Giulia Mearini,Lucie Carrier
Maksymilian Prondzynski
Hypertrophic cardiomyopathy (HCM) is an inherited myocardial disease with an estimated prevalence of 1:200 caused by mutations in sarcomeric proteins. It is associated with hypertrophy of the left ventricle, increased interstitial fibrosis,...