Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Lecture”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,297 records · Page 72Linked to original sources
PubMed2006

Protecting the myocardial cell during coronary revascularization. The William W. L. Glenn Lecture.

BACKGROUND: Using the ischemic myocardial cell as a paradigm, competitive coronary revascularization technologies will be analyzed for their potential in causing additional myocardial cell damage during the course of therapeutic procedures. METHODS AND RESULTS: Percutaneous coronary intervention (PCI) using balloon and/or stent (bare metal or coated) approaches may be associated with myonecrosis related to atherosclerotic debris plugging the downstream coronary microcirculation as well as ischemia/reperfusion injury associated with revascularization of occluded coronary vessels. The placement of distal mechanical devices and filters during the course of PCI has not been successful in ameliorating this problem. Coronary revascularization using coronary artery bypass grafting (CABG) similarly may be associated with myocardial stunning and cell necrosis associated with ischemia/reperfusion injury. Surgically induced myocardial ischemia secondary to aortic cross clamping, results from the attenuation or cessation of coronary blood flow such that oxygen delivery to the myocardium is insufficient to meet basal myocardial requirements to preserve cellular membrane stability and viability. Recovery involves: (1) resumption of normal oxidative metabolism and the restoration of myocardial energy reserves; (2) reversal of ischemia induced cell swelling and loss of membrane ion gradients and the adenine nucleotide pool; (3) repair of damaged cell organelles such as the mitochondria and the sarcoplasmic reticulum. Despite meticulous adherence to presently known principles of surgical myocardial protection using advanced cardioplegic technologies, some patients require inotropic support and/or mechanical assist devices postoperatively, when none was required preoperatively. CONCLUSIONS: Which method of coronary revascularization causes the least amount of myocardial cell injury and is associated with superior long-term outcomes remains an area of increasing controversy.

Angioplasty, Balloon, Coronary↗
PubMed2001

Oxygen radicals in cerebral ischemia: the 2001 Willis lecture.

The sequential univalent reduction of oxygen generates superoxide, hydrogen peroxide, and hydroxyl radical. The generation of hydroxyl radical is dependent on catalysis by ferrous iron. In addition, superoxide and nitric oxide produce peroxynitrite, which spontaneously generates hydroxyl radical independently of iron-mediated catalysis. These agents have a variety of cellular actions, which render them suitable candidates as mediators of tissue destruction and cellular death. In the intact brain, superoxide and its derivatives cause vasodilation, mediated by opening of potassium channels, altered vascular reactivity, breakdown of the blood-brain barrier, and focal destructive endothelial lesions. These abnormalities are also seen in early reperfusion following brain ischemia. During reperfusion there is a marked transient increase in superoxide production. Vasodilation, abnormal vascular reactivity, and blood-brain barrier breakdown are inhibited by eliminating superoxide. Superoxide production during reperfusion may be initiated by glutamate via activation of alpha-amino-3-hydroxy-5-methylisoxasolepropionic acid (AMPA) receptors. These experimental findings have important implications for human cerebral ischemia. Agents directed at eliminating oxygen radicals must be administered before or in the early stages of reperfusion following ischemia. The therapeutic window appears to be narrow and limited to, at most, a few hours. The inhibition of AMPA receptors may be a promising approach to inhibit the production of oxygen radicals during ischemia-reperfusion of the brain.

Animals↗
PubMed2026

2025 Donald Seldin Lecture: Leveraging Diverse Population Genomics and Multiomics Integration for Gene Discovery of Cardiovascular and Kidney Diseases.

This review discusses the implications of frameworks leveraging genetic admixture and multiomics data for advancing gene discovery in cardiovascular and kidney disease research. By broadening gene discovery efforts to additional populations that have a disproportionately high risk of disease and leveraging genetic diversity in admixed populations, studies can identify population-enriched risk variants that traditionally have been missed in genome-wide association studies. The use of multiomics approaches, including the transcriptome, proteome, and metabolome, advances a mechanistic understanding of disease beyond associations. As single-cell omics technologies continue to improve, their integration into gene discovery may help uncover cell-type-specific regulatory pathways and more precise biological contexts. The full potential of these approaches depends on sustained investment in diverse, well-characterized omics data sets, methodological innovation in multiancestry statistical approaches, and interdisciplinary collaboration bridging genomics, epidemiology, and clinical medicine. These efforts will need to be translated into clinically actionable insights, including ancestry-informed risk stratification and targeted therapeutics, to improve outcomes for cardiovascular and kidney diseases.

Humans↗
PubMed2006

Iron induced oxidative damage as a potential factor in age-related macular degeneration: the Cogan Lecture.

Iron is a potent generator of oxidative damage whose levels increase with age, potentially exacerbating age-related diseases. Several lines of evidence suggest that iron accumulation may be a factor in age-related macular degeneration (AMD). AMD retinas have more iron within the photoreceptors, RPE, and drusen than do age-matched control retinas. Accelerated AMD-like maculopathy develops in patients with retinal iron overload from the hereditary disease aceruloplasminemia. Mice with retinal iron overload resulting from knockout of ceruloplasmin and its homologue hephaestin exhibit retinal degeneration with some features of AMD, including subretinal neovascularization, accumulation of RPE lipofuscin and sub-RPE deposits, and RPE/photoreceptor death. Increased understanding of the mechanisms of retinal iron homeostasis may help in the development of therapies to prevent iron overload. For example, herein it is shown that one regulator of systemic iron homeostasis, HFE, is expressed in the RPE. Thus, patients with the common disease hereditary hemochromatosis, which is often caused by an HFE mutation, may have retinal iron overload predisposing to AMD. Preliminary data suggest that iron chelation can reduce RPE iron overload in mice and protect them from degeneration, suggesting that iron-binding drugs may one day prove useful in reducing RPE oxidative stress and decreasing the risk of AMD progression.

Animals↗
PubMedDate not supplied

Rhoads Lecture. Heat and life: the ongoing scientific odyssey.

The source of body heat has fascinated philosophers and scientists for millennia. Resting heat production is a major component of human energy requirements in health and disease. This review traces through mankind's attempts to understand the nature of resting heat production in humans and animals and its relationships to body mass and composition. Far from being fully understood, the study of heat production is an area of intense research interest bridging the gap between modern biology and physics.

Body Weight↗