Institution
Case Western Reserve University
Education•Cleveland, Ohio, United States•
About: Case Western Reserve University is a education organization based out in Cleveland, Ohio, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 54617 authors who have published 106568 publications receiving 5071613 citations. The organization is also known as: Case & Case Western.
Topics: Population, Cancer, Health care, Medicine, Transplantation
Papers published on a yearly basis
Papers
More filters
••
TL;DR: A summary of ongoing clinical trials is provided to allow full comprehension of the range of diseases in which hMSC therapy may be beneficial and identification of gaps in knowledge about the mechanisms of action of therapeutic MSCs in disease.
Abstract: In adults, human mesenchymal stem cells (hMSCs) are found in vivo at low frequency and are defined by their capacity to differentiate into bone, cartilage, and adipose tissue, depending on the stimuli and culture conditions under which they are expanded. Although MSCs were initially hypothesized to be the panacea for regenerating tissues, MSCs appear to be more important in therapeutics to regulate the immune response invoked in settings such as tissue injury, transplantation, and autoimmunity. MSCs have been used therapeutically in clinical trials and subsequently in practice to treat graft-versus-host disease following bone marrow transplantation. Reports of successful immune modulation suggest efficacy in a wide range of autoimmune conditions, such as demyelinating neurological disease (multiple sclerosis), systemic lupus erythematosus, and Crohn's disease, among others. This review provides background information about hMSCs and also describes their putative mechanisms of action in inflammation. We pr...
750 citations
••
TL;DR: This commentary justifies the need to study more diverse populations using both empirical examples and theoretical reasoning for risk prediction of diseases across global populations.
750 citations
••
TL;DR: Fuid flow increases inversin levels in ciliated tubular epithelial cells and seems to regulate this crucial switch between Wnt signaling pathways during renal development, implying that an inhibition of canonical Wnt behavior is required for normal renal development.
Abstract: Cystic renal diseases are caused by mutations of proteins that share a unique subcellular localization: the primary cilium of tubular epithelial cells1. Mutations of the ciliary protein inversin cause nephronophthisis type II, an autosomal recessive cystic kidney disease characterized by extensive renal cysts, situs inversus and renal failure2. Here we report that inversin acts as a molecular switch between different Wnt signaling cascades. Inversin inhibits the canonical Wnt pathway by targeting cytoplasmic dishevelled (Dsh or Dvl1) for degradation; concomitantly, it is required for convergent extension movements in gastrulating Xenopus laevis embryos and elongation of animal cap explants, both regulated by noncanonical Wnt signaling. In zebrafish, the structurally related switch molecule diversin ameliorates renal cysts caused by the depletion of inversin, implying that an inhibition of canonical Wnt signaling is required for normal renal development. Fluid flow increases inversin levels in ciliated tubular epithelial cells and seems to regulate this crucial switch between Wnt signaling pathways during renal development.
749 citations
••
TL;DR: Transgenic mice have been especially useful in elucidating the physiological roles of specific sequence elements in the PEPCK-C gene promoter and in demonstrating the key role played at these sites by the isoforms of CAAT/enhancer binding protein in patterning of PEPCF gene expression during the perinatal period.
Abstract: Phosphoenolpyruvate carboxykinase (GTP) (EC 4.1.1.32) (PEPCK) is a key enzyme in the synthesis of glucose in the liver and kidney and of glyceride-glycerol in white adipose tissue and the small intestine. The gene for the cytosolic form of PEPCK (PEPCK-C) is acutely regulated by a variety of dietary and hormonal signals, which result in alteration of synthesis of the enzyme. Major factors that increase PEPCK-C gene expression include cyclic AMP, glucocorticoids, and thyroid hormone, whereas insulin inhibits this process. PEPCK-C is absent in fetal liver but appears at birth, concomitant with the capacity for gluconeogenesis. Regulatory elements that control transcription of the PEPCK-C gene in liver, kidney, and adipose tissue have been delineated, and many of the transcription factors that bind to these elements have been identified. Transgenic mice have been especially useful in elucidating the physiological roles of specific sequence elements in the PEPCK-C gene promoter and in demonstrating the key role played at these sites by the isoforms of CAAT/enhancer binding protein in patterning of PEPCK-C gene expression during the perinatal period. The PEPCK-C gene provides a model for the metabolic control of gene transcription.
749 citations
••
TL;DR: Experiments testing the self-serving bias (SSB; taking credit for personal success but blaming external factors for personal failure) have used a multitude of moderators (i.e., role, task importanc... as discussed by the authors ).
Abstract: Experiments testing the self-serving bias (SSB; taking credit for personal success but blaming external factors for personal failure) have used a multitude of moderators (i.e., role, task importanc...
747 citations
Authors
Showing all 54953 results
Name | H-index | Papers | Citations |
---|---|---|---|
Robert Langer | 281 | 2324 | 326306 |
Bert Vogelstein | 247 | 757 | 332094 |
Zhong Lin Wang | 245 | 2529 | 259003 |
John Q. Trojanowski | 226 | 1467 | 213948 |
Kenneth W. Kinzler | 215 | 640 | 243944 |
Peter Libby | 211 | 932 | 182724 |
David Baltimore | 203 | 876 | 162955 |
Carlo M. Croce | 198 | 1135 | 189007 |
Ronald Klein | 194 | 1305 | 149140 |
Eric J. Topol | 193 | 1373 | 151025 |
Paul M. Thompson | 183 | 2271 | 146736 |
Yusuke Nakamura | 179 | 2076 | 160313 |
Dennis J. Selkoe | 177 | 607 | 145825 |
David L. Kaplan | 177 | 1944 | 146082 |
Evan E. Eichler | 170 | 567 | 150409 |