Benjamin Lee Predmore

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Dept of Surgery, Div of Cardiothoracic Surgery, Emory University School of Medicine and The Carlyle Fraser Heart Center, Atlanta, GA; Dept of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan; Medicinal Chemistry Division, NAN Laboratorios, Monterrey, Mexico; Dept of Biology, Lakehead University, Thunder Bay, Ontario, Canada; Div of(More)
SIGNIFICANCE An abundance of experimental evidence suggests that hydrogen sulfide (H(2)S) plays a prominent role in physiology and pathophysiology. Many targets exist for H(2)S therapy. The molecular targets of H(2)S include proteins, enzymes, transcription factors, and membrane ion channels. RECENT ADVANCES Novel H(2)S precursors are being synthesized(More)
BACKGROUND Cystathionine γ-lyase (CSE) produces H2S via enzymatic conversion of L-cysteine and plays a critical role in cardiovascular homeostasis. We investigated the effects of genetic modulation of CSE and exogenous H2S therapy in the setting of pressure overload-induced heart failure. METHODS AND RESULTS Transverse aortic constriction was performed in(More)
Hydrogen sulfide acts as an environmental toxin across a range of concentrations and as a cellular signaling molecule at very low concentrations. Despite its toxicity, many animals, including the mudflat polychaete Glycera dibranchiata, are periodically or continuously exposed to sulfide in their environment. We tested the hypothesis that a broad range of(More)
OBJECTIVES This paper examined whether nebivolol protects the heart via nitric oxide (NO) synthase and NO-dependent signaling in an in vivo model of acute myocardial infarction. BACKGROUND Beta(3)-adrenergic receptor (AR) activation promotes endothelial nitric oxide synthase (eNOS) activity and NO bioavailability. We hypothesized that specific beta(3)-AR(More)
Diallyl trisulfide (DATS), a polysulfide constituent found in garlic oil, is capable of the release of hydrogen sulfide (H(2)S). H(2)S is a known cardioprotective agent that protects the heart via antioxidant, antiapoptotic, anti-inflammatory, and mitochondrial actions. Here, we investigated DATS as a stable donor of H(2)S during myocardial(More)
OBJECTIVE β(2)-adrenoreceptor activation has been shown to protect cardiac myocytes from cell death. We hypothesized that acute β(2)-adrenoreceptor stimulation, using arformoterol (ARF), would attenuate myocardial ischemia/reperfusion (R) injury via NO synthase activation and cause a subsequent increase in NO bioavailability. METHODS AND RESULTS Male(More)
OBJECTIVE Humanin (HN), an endogenous antiapoptotic peptide, has previously been shown to protect against Alzheimer's disease and a variety of cellular insults. We evaluated the effects of a potent analog of HN (HNG) in an in vivo murine model of myocardial ischemia and reperfusion. METHODS AND RESULTS Male C57BL6/J mice (8 to 10 week old) were subjected(More)
Hydrogen sulfide (H(2)S) and nitric oxide (NO) are both gasotransmitters that can elicit synergistic vasodilatory responses in the in the cardiovascular system, but the mechanisms behind this synergy are unclear. In the current study we investigated the molecular mechanisms through which H(2)S regulates endothelial NO production. Initial studies were(More)
Coronary artery disease is a major cause of morbidity and mortality in the Western world. Acute myocardial infarction, resulting from coronary artery atherosclerosis, is a serious and often fatal consequence of coronary artery disease, resulting in cell death in the myocardium. Pre- and post-conditioning of the myocardium are two treatment strategies that(More)