Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Functional electrical stimulation (FES) has been used in Brazil since 1989 to obtain functional improvement in paraplegic patients' orthostasis and locomotion. The aim of this paper is to evaluate the histochemical changes observed in the quadriceps femoris muscle following the use of FES. We studied four patients with traumatic spinal cord lesions at T4-10 level, Frankel A, all within 12-24 months postlesion. They were all submitted to FES using the following criteria: square-wave, 20-30 Hz frequency, pulses of 0.003 seconds, time of stimulation 5 seconds, resting interval 10 seconds. The stimulation was applied during 90 consecutive days, 30 minutes each time, twice daily. The interval between the stimulations was 6 hours. Quadriceps muscle biopsies were performed before and after the use of FES. We used ATPase technique for the histochemical analysis, where three different dying patterns can be observed for the three types of muscular fibres (I, IIa and IIb). The two samples from each patient were analysed measuring the fibres' diameters and their index of atrophy, and counting the total number of each type of fibre in each sample. The mean total number of fibres in each sample was 256 +/- 12.3. The results showed that the sizes of the three types of fibres were not modified with the use of FES; the number of type IIa fibres increased in a significant fashion, after using of FES.
Paraplegia 1993 Dec
PMID:Functional electrical stimulation (FES): muscle histochemical analysis. 811 69

Paraplegia may increase susceptibility to ventricular arrhythmias by altering the autonomic control of the heart. Altered cardiac autonomic control has been documented to change the expression of genes that encode cardiac Ca2+ regulatory proteins. Therefore, we tested the hypothesis that paraplegia alters cardiac electrophysiology with concomitant changes in Ca2+ regulatory proteins in a manner that increases the susceptibility to ventricular arrhythmias. To test this hypothesis, intact (n = 10) and paraplegic (n = 6) male Wistar rats were chronically instrumented to measure atrioventricular (AV) interval, sinus cycle length, sinus node recovery time (SNRT), SNRT corrected for spontaneous sinus cycle (cSNRT), Wenckebach cycle length (WCL), and the electrical stimulation threshold to induce ventricular arrhythmias. In addition, relative protein abundance and mRNA expression for sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA), phospholamban, and the Na/Ca exchanger were determined in intact (n = 8) and paraplegic (n = 8) rats. Paraplegia significantly (P < 0.05) reduced AV interval (-25%), sinus cycle length (-24%), SNRT (-28%), cSNRT (-53%), WCL (-19%), and the electrical stimulation threshold to induce ventricular arrhythmia (-48%). Paraplegia significantly increased the relative protein abundances of SERCA (45%) and the Na/Ca exchanger (40%) and decreased phospholamban levels (-28%). In contrast, only the relative mRNA expression of the Na/Ca exchanger was increased (25%) in paraplegic rats. These data demonstrate that paraplegia enhances cardiac electrophysiological properties and alters Ca2+ regulatory proteins in a manner that increases susceptibility to ventricular arrhythmias.
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PMID:Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats. 1288 Dec 14

The plasma membrane Ca2+ ATPases (PMCAs) are responsible for the clearance of Ca2+ out of cells after intracellular Ca2+ transients. Cooperating with Na+/Ca2+ exchangers (NCXs) and Ca2+ buffering proteins, PMCAs play an essential role in maintaining the long-term cellular Ca2+ homeostasis. The plasma membrane Ca2+ ATPase was first discovered in red blood cell membrane about 50 years ago, and then other PMCA isoforms and alternatively spliced variants had been identified from different tissues and different developmental stages, revealing a surprising complexity of the PMCA family. In mammals, there are four PMCA isoforms encoded by four distinct genes. Isoform 1 and 4 are found in virtually all tissues, whereas isoform 2 and 3 are primarily expressed in excitable cells such as neurons and myocytes. Perturbation of PMCAs function has been implicated in a variety of diseases and disorders, including hearing loss, ataxia, paraplegia, and infertility. Here, we would like to review the recent progresses in the study of the PMCAs and related disorders, in particular how these pathological conditions help us to gain an in-depth insight into the function of PMCAs and their contribution in the regulation of Ca2+ signaling network.
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PMID:The Plasma Membrane Calcium ATPases in Calcium Signaling Network. 2966 80