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PubMed2002

Keynote lecture: perspective of infection control and prevention in hospitals-importance of antisepsis.

Since the end of the 20th century, precautions of hospital infection have been re-evaluated with rationalization. Evidence-based precautions are proposed to be discussed. Problems of hospital infection in the early 21st century are highlighted as follows: (1) infections in compromised patients; (2) emergence of resistant bacteria; (3) terminal infection; (4) bloodborne virus infection; (5) neonatal infections; (6) emerging and re-emerging diseases. In the near future, it will be possible to lower the hospital infection rate by increasing medical in place of surgical treatments, the development of low invasive surgeries and/or progress of immunotherapy instead of chemotherapy. Strategies for hospital infection control and prevention in the early 21st century are based on evidence-based precautions, effective organization, accurate surveillance, compliance of precautions, risk management, outcome evaluation and feedback, economical evaluation, sterility assurance and peer review for these strategies.

Antisepsis↗
PubMed1997

Plastination in the neurosciences. Keynote lecture.

Plastination is a unique technique of tissue preservation developed by Dr. Gunther von Hagens in Heidelberg, Germany, in 1978. In this process, water and lipids in biological tissues are replaced by curable polymers which are subsequently hardened, resulting in dry, odorless and durable specimens. In neuroanatomy silicone and polyester resins are used. Silicone rubber is used for whole brains and brain dissections resulting in natural looking specimens. Polyester resin is used for brain slices resulting in an excellent distinction between gray and white matter. The silicone S 10 standard technique and the polyester P 35 technique are described in detail. The advantages of plastinated specimens in neuroanatomy teaching and research are discussed.

Brain↗
PubMed2006

Oxidative stress and vascular disease: 2005 Duff lecture.

There is compelling evidence that oxidative stress plays a key role in the pathophysiology of several major cardiovascular diseases. In atherosclerosis, hypertension, stroke, diabetes, and heart failure, expression of superoxide is increased in blood vessels, and endothelial vasomotor function is impaired, presumably caused in large part by inactivation of nitric oxide by superoxide. Endothelial dysfunction is predictive of cardiovascular risk, and probably plays a key role in the pathophysiology of atherosclerosis and its complications. In preliminary studies in hypercholesterolemic mice and in older humans, we have found high levels of superoxide in the aortic valve, as well as aorta. We speculate that superoxide, in addition to playing a key role in atherogenesis, may play a key role in signaling that leads to calcific aortic valvular stenosis. Antioxidant enzymes, especially the three isoforms of superoxide dismutase (SOD), modulate basal levels of superoxide and protect against vasomotor dysfunction. A common gene variant of extracellular SOD (ecSOD) is associated with increased risk of ischemic heart disease. We have made recombinant adenoviruses to examine cardiovascular effects of ecSOD and its heparin-binding domain. This approach might be used to study the almost 500 other proteins with a heparin-binding domain. Finally, several key unanswered questions in relation to oxidative stress and atherosclerosis are raised, and proposed as fruitful areas of research.

Animals↗
PubMed2001

2000 George Lyman Duff Memorial Lecture: atherosclerosis is a liver disease of the heart.

The production of apolipoprotein B (apoB)-containing lipoproteins by the liver is regulated by a complex series of processes involving apoB being cotranslationally translocated across the endoplasmic reticulum and assembled into a lipoprotein particle. The translocation of apoB across the endoplasmic reticulum is facilitated by the intraluminal chaperone, microsomal triglyceride transfer protein (MTP). MTP facilitates the translocation and folding of apoB, as well as the addition of lipid to lipid-binding domains (which consist of amphipathic beta sheets and alpha helices). In the absence of MTP or sufficient lipid, apoB exhibits translocation arrest. Thus, apoB translation, translocation, and assembly with lipids to form a core-containing lipoprotein particle occur as concerted processes. Abrogation of >/=1 of these processes diverts apoB into a degradation pathway that is dependent on conjugation with ubiquitin and proteolysis by the proteasome. The nascent core-containing lipoprotein particle that forms within the lumen of the endoplasmic reticulum can be "enlarged" to form a mature very low density lipoprotein particle. Additional studies show that the assembly and secretion of apoB-containing lipoproteins are linked to the cholesterol/bile acid synthetic pathway controlled by cholesterol 7alpha-hydroxylase. Studies in cultured cells and transgenic mice indicate that the expression of cholesterol 7alpha-hydroxylase indirectly regulates the expression of lipogenic enzymes through changes in the cellular content of mature sterol response element binding proteins. Oxysterols and bile acids may also act via the ligand-activated nuclear receptors LXR and FXR to link the metabolic pathways controlling energy balance and lipid metabolism to nutritional state.

Apolipoproteins↗
PubMed2005

Corcoran Lecture. Cardiovascular genomics and oxidative stress.

The majority of modifiable cardiovascular risk factors are complex, polygenic, or at least oligogenic traits, with genetic and environmental determinants playing important roles in disease risk and its phenotypic expression. The Human Genome Project and subsequent mouse and rat genome data have provided powerful tools to commence the dissection of genetic determinants of hypertension and other cardiovascular risk factors. Despite several new methodologies such as genome-wide scans, genome-wide gene expression profiling, and proteomic screens, it is fair to say that the progress of genetic studies designed as nonhypothesis driven has been relatively slow. On the other hand, several interesting candidate pathways have been identified, where investigators allowed for hypothesis-driven functional studies. One example of such pathway is vascular oxidative stress with its extensive network of genes and proteins, many with proven contributions to cardiovascular disease. Therefore, in parallel to genome-wide or proteome-wide studies, it will be constructive to pursue "pathwayomics" defined here as functional studies of a candidate pathway for disease pathogenesis.

Animals↗
PubMed1997

Arthus C. Corcoran Memorial Lecture. Influence of nitric oxide and angiotensin II on renal involvement in hypertension.

Remarkable advances have been made with prolonged antihypertensive therapy in reversing cardiovascular morbidity and mortality. Deaths from stroke have been reduced by 70% and from coronary heart disease by 35%. In contrast, endstage renal disease resulting from hypertension continues to increase. The explanations for this seeming paradox remain unresolved even though experimental models have demonstrated that certain antihypertensive agents may have beneficial renal and intrarenal hemodynamic effects; but reversal of the intrarenal pathological lesions have not been shown to improve. This discussion summarizes recent studies from our laboratory in aged (73- and 85-week-old) spontaneously hypertensive rats (SHR) with naturally occurring end-stage renal disease and in a model of aged SHR employing nitric oxide inhibition in younger, adult (20-week-old) SHR. Our findings demonstrated that the systemic and whole renal hemodynamics, intrarenal glomerular dynamics, proteinuria, and renal pathological lesions can be prevented or reversed with angiotensin-converting enzyme inhibition therapy but not with hydrochlorothiazide (at similar levels of arterial pressure reduction). The implications and possible mechanisms involved in the development of both naturally occurring and nitric oxide-exacerbated SHR are multifactorial, involving the endothelial nitric oxide system and its interaction with angiotensin II (and possibly bradykinin) among other factors. Moreover, these pathophysiological cellular mechanisms may be shared by the aging process as well as in naturally occurring spontaneous hypertension in the rat and, perhaps, in humans with essential hypertension. Thus, antihypertensive therapy seems to be specific in its ability to prevent and even reverse the pathophysiological derangements of renal involvement in hypertension. Thus, prevention and reversal of end-stage renal disease do not seem to require greater reduction of arterial pressure than with other target-organ involvement. However, they do require specific inhibition of the arteriolar and glomerular lesions produced by the disease.

Aging↗
PubMed1997

Theodore Cooper Memorial Lecture. A mouse view of hypertension.

Essential hypertension probably results from combinations of genetic variations, not necessarily the same in all afflicted persons, which individually may not cause sufficient deviation from normality to be significantly harmful. Genes contributing to hypertension are being sought by analytic experiments aimed at identifying candidate genes associated or segregating with the phenotype in humans and animals and by synthetic experiments in which changes are made in candidate genes in animals and their effects on blood pressure are determined. We have used gene targeting to vary the amounts of angiotensinogen and angiotensin-converting enzyme (ACE) synthesized from their genes (Agt and Ace). These "gene titration" experiments establish that changes in Agt gene expression cause changes in the blood pressures of mice. Surprisingly, quantitative changes in Ace gene expression over a threefold range do not affect blood pressures. Computer simulations with a simple version of the renin-angiotensin system predict that changes in Agt function alter the steady state levels of both angiotensin I (Ang I) and angiotensin II (Ang II). In contrast, modest changes in Ace function alter Ang I levels considerably but scarcely affect Ang II levels. Simulations over the ranges of ACE levels that can be achieved with ACE inhibitors predict that Ang II levels will decrease only when Ang I levels have plateaued. Comparisons of the computer simulations with our genetic experiments and with prior work of others using wide dose ranges of ACE inhibitor show a satisfactory agreement and help reconcile the apparent contradictions between the genetic and pharmacological experiments.

Animals↗