University of Louisville

About: University of Louisville is a education organization based out in Louisville, Kentucky, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 24600 authors who have published 49248 publications receiving 1573346 citations. The organization is also known as: UofL.

Preventing Plant Blindness

Abstract: Editor: Randy Moore, Biology Department, University of Louisville, Louisville, KY 40292, Phone: (502) 852-6490, E-mail: randy.moore@louisville.edu Managing Editor: Christine Chantry Associate Editor: Kris Collum Publisher: Wayne W. Carley Editorial Staff: Kay Acevedo, Carmen Altamirano, Cheryl Merrill ABT Produiction Office: 11250 Roger Bacon Drive, #19, Reston, VA 20190-5202, Phone: (703) 471-1134, Fax: (703) 435-5582, E-mail: NABTer@aol.com, Web site: www.nabt.org

Reversal of Severe Heart Failure With a Continuous-Flow Left Ventricular Assist Device and Pharmacological Therapy A Prospective Study

Abstract: Background—We have previously shown that a specific combination of drug therapy and left ventricular assist device unloading results in significant myocardial recovery, sufficient to allow pump removal, in two thirds of patients with dilated cardiomyopathy receiving a Heartmate I pulsatile device However, this protocol has not been used with nonpulsatile devices Methods and Results—We report the results of a prospective study of 20 patients who received a combination of angiotensin-converting enzymes, β-blockers, angiotensin II inhibitors, and aldosterone antagonists followed by the β2-agonist clenbuterol and were regularly tested (echocardiograms, exercise tests, catheterizations) with the pump at low speed Before left ventricular assist device insertion, patient age was 352±126 years (16 male patients), patients were on 20±09 inotropes, 7 (35) had an intra-aortic balloon pump, 2 were hemofiltered, 2 were ventilated, 3 had a prior Levitronix device, and 1 had extracorporeal membrane oxygenation C

Cytokine-Induced Modulation of Cardiac Function

Abstract: Cytokines act in an autocrine and/or paracrine fashion to induce a diverse variety of biological responses. Several cardiac diseases are associated with cytokine activation, and such activation significantly influences several physiologic parameters, including cardiac mechanical function. This review summarizes the current concepts regarding the modulation of myocardial function by cytokines and provides rationale for the sometimes-conflicting results in the literature regarding underlying mechanisms and patterns of dysfunction. Although traditionally considered cardiodepressant mediators, contractile responses are complex and bimodal, with an early response (within minutes) of variable direction, stimulatory or depressant, depending on the ambient physiologic milieu and relative contributions of the underlying signaling pathways that are activated. These pathways include sphingomyelinase-, nitric oxide (NO)-, and phospholipase A2-dependent signaling with resultant combined effects on contraction and the Ca 2+ transient. This is subsequently followed by a profoundly cardiodepressant late response lasting hours to days, depending on the production of secondary mediators and the combined influence of NO generated from inducible NO synthase, reactive oxygen species, and alterations in β-adrenergic receptor signaling. The interrelationships between these pathways and the time-dependence of their activation are important considerations in the evaluation of cytokine-dependent dysfunction during both acute cardiac injury and chronic cardiac pathologies.

The effect of cigarette smoking and smoking cessation on spinal fusion.

Abstract: Study Design. The effect of cigarette smoking and smoking cessation on spinal fusion was studied in a retrospective review of 357 patients who had undergone instrumented spinal fusion. Objective: To document the widely assumed but unreported benefit of cigarette smoking cessation on fusion rate and clinical outcome after spinal fusion surgery. Background Data. Cigarette smoking has been shown to inhibit lumbar spinal fusion and to adversely effect outcome in treatment of lumbar spinal disorders. Prior reports have compared smokers and nonsmokers, as opposed to comparing smokers and quitters. Methods. This study retrospectively identified 357 patients who underwent a posterior instrumented fusion at either L4-L5 or L4-S1 between 1992 and 1996. Analysis of the medical record and follow-up telephone surveys were conducted. Clinical outcome and fusion status was analyzed in relation to preoperative and postoperative smoking parameters. Results. In this study, the nonunion rate was 14.2% for nonsmokers and 26.5% for patients who continued to smoke after surgery (P< 0.05). Patients who quit smoking after surgery for longer than 6 months had a nonunion rate of 17.1%. The nonunion rate was not significantly affected by either the quantity that a patient smoked before surgery or the duration of preoperative smoking abatement. Return-to-work was achieved in 71% of nonsmokers, 53% of nonquitters, and 75% of patients who quit smoking for more than 6 months after surgery. Discussion. These results validate the hypothetical assumption that postoperative smoking, cessation helps to reverse the impact of cigarette smoking on outcome after spinal fusion.