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Ivor J. Benjamin
Researcher at Medical College of Wisconsin
Publications - 139
Citations - 12734
Ivor J. Benjamin is an academic researcher from Medical College of Wisconsin. The author has contributed to research in topics: Heat shock protein & HSF1. The author has an hindex of 51, co-authored 135 publications receiving 11973 citations. Previous affiliations of Ivor J. Benjamin include Memorial Sloan Kettering Cancer Center & University of Utah.
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Journal ArticleDOI
Diabetes and cardiovascular disease : A statement for healthcare professionals from the American heart association
Scott M. Grundy,Ivor J. Benjamin,Gregory L. Burke,Alan Chait,Robert H. Eckel,Barbara V. Howard,William E. Mitch,Sidney C. Smith,James R. Sowers +8 more
TL;DR: The most prevalent form of diabetes mellitus is type 2 diabetes as discussed by the authors, which typically makes its appearance later in life and is associated with other cardiovascular risk factors: dyslipidemia, hypertension, and prothrombotic factors.
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Stress (Heat Shock) Proteins: Molecular Chaperones in Cardiovascular Biology and Disease
TL;DR: The regulation and function of HSP chaperones and their clinical significance in conditions such as cardiac hypertrophy, vascular wall injury, cardiac surgery, ischemic preconditioning, aging, and, conceivably, mutations in genes encoding contractile proteins and ion channels are discussed.
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HSF1 is required for extra-embryonic development, postnatal growth and protection during inflammatory responses in mice
Xianzhong Xiao,Xiaoxia Zuo,Alberta A. Davis,D. Randy McMillan,Bishop B. Curry,James A. Richardson,Ivor J. Benjamin +6 more
TL;DR: Direct causal effects for the HSF1 transactivator in regulating critical physiological events during extra‐embryonic development and under pathological conditions such as sepsis to modulate pro‐inflammatory responses are established, indicating that these pathways have clinical importance as therapeutic targets in humans.
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Targeted Disruption of Heat Shock Transcription Factor 1 Abolishes Thermotolerance and Protection against Heat-inducible Apoptosis
TL;DR: It is concluded that 1) constitutive and inducibly expressed HSPs exhibit distinct physiological functions for cellular maintenance and adaptation, respectively, and 2) other mammalian HSFs or distinct evolutionarily conserved stress response pathways do not compensate for HSF1 in the physiological response to heat shock.
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Human αB-Crystallin Mutation Causes Oxido-Reductive Stress and Protein Aggregation Cardiomyopathy in Mice
Namakkal S. Rajasekaran,Patrice Connell,Elisabeth S. Christians,Liang-Jun Yan,Ryan P. Taylor,András Orosz,Xiu Q. Zhang,Tamara J. Stevenson,Ronald M Peshock,Jane A. Leopold,William H. Barry,Joseph Loscalzo,Shannon J. Odelberg,Ivor J. Benjamin,Ivor J. Benjamin +14 more
TL;DR: It is demonstrated that dysregulation of G6PD activity is necessary and sufficient for maladaptive reductive stress and suggest a novel therapeutic target for abrogating R120GCryAB cardiomyopathy and heart failure in humans.