803 research outputs found
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The autonomic nervous system and renal physiology
Research in resistant hypertension has again focused on autonomic nervous system denervation – 50 years after it had been stopped due to postural hypotension and availability of newer drugs. These (ganglionic blockers) drugs have all been similarly stopped, due to postural hypotension and yet newer antihypertensive agents. Recent demonstration of the feasibility of limited regional transcatheter sympathetic denervation has excited clinicians due to potential therapeutic implications. Standard use of ambulatory blood pressure recording equipment may alter our understanding of the diagnosis, potential treatment strategies, and health care outcomes – when faced with patients whose office blood pressure remains in the hypertensive range – while under treatment with three antihypertensive drugs at the highest tolerable doses, plus a diuretic. We review herein clinical relationships between autonomic function, resistant hypertension, current treatment strategies, and reflect upon the possibility of changes in our approach to resistant hypertension
Der Umgang mit chronisch kranken Dialysepatienten aus der Sicht des Pflegepersonals
Die Arbeit beschäftigt sich mit dem Umgang mit chronisch kranken Dialysepatienten aus der Sicht des Pflegepersonals
Referenzen und Impulse: vom Nutzen empirischer Weiterbildungsdaten in der Praxis
Was kann die Weiterbildungspraxis mit empirischen Daten über den Bereich der Weiterbildung praktisch anfangen? Der Autor, kaufmännischer Leiter eines Volkshochschul-Zweckverbandes, zeigt im Betrag das praktische Potenzial empirischer Bildungsforschung auf. Die erhobenen Daten dienen als Vergleichsgrößen für lokale Kennzahlen und können helfen, Entwicklungsfelder zu identifizieren und zu untermauern. Er erläutert dies an den Beispielen des Milieumarketings und der Kursleiterqualifizierungen
A Variational Loop Shrinking Analogy for Handle and Tunnel Detection and {Reeb} Graph Construction on Surfaces
The humble loop shrinking property played a central role in the inception of modern topology but it has been eclipsed by more abstract algebraic formalism. This is particularly true in the context of detecting relevant non-contractible loops on surfaces where elaborate homological and/or graph theoretical constructs are favored in algorithmic solutions. In this work, we devise a variational analogy to the loop shrinking property and show that it yields a simple, intuitive, yet powerful solution allowing a streamlined treatment of the problem of handle and tunnel loop detection. Our formalization tracks the evolution of a diffusion front randomly initiated on a single location on the surface. Capitalizing on a diffuse interface representation combined with a set of rules for concurrent front interactions, we develop a dynamic data structure for tracking the evolution on the surface encoded as a sparse matrix which serves for performing both diffusion numerics and loop detection and acts as the workhorse of our fully parallel implementation. The substantiated results suggest our approach outperforms state of the art and robustly copes with highly detailed geometric models. As a byproduct, our approach can be used to construct Reeb graphs by diffusion thus avoiding commonly encountered issues when using Morse functions
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Diabetic Microvascular Complications: Possible Targets for Improved Macrovascular Outcomes
The results of recent outcome trials challenge hypotheses that tight control of both glycohemoglobin and blood pressure diminishes macrovascular events and survival among type 2 diabetic patients. Relevant questions exist regarding the adequacy of glycohemoglobin alone as a measure of diabetes control. Are we ignoring mechanisms of vasculotoxicity (profibrosis, altered angiogenesis, hypertrophy, hyperplasia, and endothelial injury) inherent in current antihyperglycemic medications? Is the polypharmacy for lowering cholesterol, triglyceride, glucose, and systolic blood pressure producing drug interactions that are too complex to be clinically identified? We review angiotensin-aldosterone mechanisms of tissue injury that magnify microvascular damage caused by hyperglycemia and hypertension. Many studies describe interruption of these mechanisms, without hemodynamic consequence, in the preservation of function in type 1 diabetes. Possible interactions between the renin-angiotensin-aldosterone system and physiologic glycemic control (through pulsatile insulin release) suggest opportunities for further clinical investigation
Novel cell death program leads to neutrophil extracellular traps
Neutrophil extracellular traps (NETs) are extracellular structures composed of chromatin and granule proteins that bind and kill microorganisms. We show that upon stimulation, the nuclei of neutrophils lose their shape, and the eu- and heterochromatin homogenize. Later, the nuclear envelope and the granule membranes disintegrate, allowing the mixing of NET components. Finally, the NETs are released as the cell membrane breaks. This cell death process is distinct from apoptosis and necrosis and depends on the generation of reactive oxygen species (ROS) by NADPH oxidase. Patients with chronic granulomatous disease carry mutations in NADPH oxidase and cannot activate this cell-death pathway or make NETs. This novel ROS-dependent death allows neutrophils to fulfill their antimicrobial function, even beyond their lifespan
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Do biologic markers predict cardiovascular end points in diabetic end-stage renal disease? A prospective longitudinal study
Background: Diabetic patients on hemodialysis are at high risk of death from cardiovascular disease, and research has suggested that various biologic markers of inflammation, oxidative stress and hemostasis may give added value to clinical information for predicting cardiovascular event (CVE)-free survival. This information could be particularly important in evaluating this population for renal transplant, given the scarcity of organs. We hypothesized that in diabetic patients undergoing renal replacement therapy (RRT) these biologic markers would prove useful in predicting event-free follow-up in a prospective study. Methods: One hundred and fifty diabetic (76 type 1, 74 type 2) and 27 non-diabetic stable RRT patients were followed for 0.04–13.69 years for CVE (myocardial infarction, coronary arterial intervention, peripheral arterial bypass or amputation, cerebrovascular accident or carotid artery intervention), cardiac and all-cause mortality. Measured biologic markers of inflammation included the following: Il-6, C reactive protein, fibrinogen; of hemostasis: fibrinogen, plasminogen activator inhibitor (PAI), fibrinolytic activity, von Willebrand factor VII (vWF), platelet-selectin, viscosity and of oxidative stress: advanced glycated end products and antibody to oxidized low-density lipoprotein. For each, upper versus lower tertiles were compared for duration of event-free follow-up. Results: Cardiovascular events prior to study entry occurred in 51.3% of DM1, 54.0% of DM2 and 25.9% of DM0 patients. Subsequent cardiovascular events were noted in 31.6% of DM1, 45.9% of DM2 and 11.1% of DM0 patients. All mean levels of biologic markers at baseline were abnormal (P < 0.05). Conclusions: In this RRT population, all biologic marker levels except PAI did not improve clinical prediction of events
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