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排序方式: 共有1159条查询结果,搜索用时 15 毫秒
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Carel Bron Michel Wensing Jo LM Franssen Rob AB Oostendorp 《BMC musculoskeletal disorders》2007,8(1):107
Background
Shoulder disorders are a common health problem in western societies. Several treatment protocols have been developed for the clinical management of persons with shoulder pain. However available evidence does not support any protocol as being superior over others. Systematic reviews provide some evidence that certain physical therapy interventions (i.e. supervised exercises and mobilisation) are effective in particular shoulder disorders (i.e. rotator cuff disorders, mixed shoulder disorders and adhesive capsulitis), but there is an ongoing need for high quality trials of physical therapy interventions. Usually, physical therapy consists of active exercises intended to strengthen the shoulder muscles as stabilizers of the glenohumeral joint or perform mobilisations to improve restricted mobility of the glenohumeral or adjacent joints (shoulder girdle). It is generally accepted that a-traumatic shoulder problems are the result of impingement of the subacromial structures, such as the bursa or rotator cuff tendons. Myofascial trigger points (MTrPs) in shoulder muscles may also lead to a complex of symptoms that are often seen in patients diagnosed with subacromial impingement or rotator cuff tendinopathy. Little is known about the treatment of MTrPs in patients with shoulder disorders. 相似文献3.
Canine myocardial reperfusion injury: protection by a free radical scavenger, N-2-mercaptopropionyl glycine 总被引:5,自引:0,他引:5
S E Mitsos J C Fantone K P Gallagher K M Walden P J Simpson G D Abrams M A Schork B R Lucchesi 《Journal of cardiovascular pharmacology》1986,8(5):978-988
Oxygen-derived free radicals and their metabolites may contribute to the extension of irreversible cellular injury, which occurs on reperfusion of the previously ischemic myocardium. Therefore, therapy directed against the toxic effects of reactive oxygen species may provide protection to the ischemic myocardium, which undergoes subsequent reperfusion. We evaluated the effectiveness of N-2-mercaptopropionyl glycine (MPG), a free radical scavenger, to limit the extent of irreversible injury resulting from 90 min of ischemia followed by 6 h of reperfusion in a canine model of myocardial infarction. In three groups of dogs, MPG (20 mg/kg) was administered as a constant infusion into the left atrium. Group I received MPG for 2 h, starting 15 min before occlusion of the left circumflex coronary artery and ending 15 min after reperfusion. Group II received MPG for 1 h, starting 15 min before reperfusion. Group III received MPG for 1 h beginning 45 min after reperfusion. Each group was compared with its respective saline control group. Infarct size was reduced by 35% in Group I (32.2 +/- 5.1% vs. 47.7 +/- 3.4% of the area at risk, p less than 0.05) and Group II (31.4 +/- 3.6% vs. 47.5 +/- 5.1% of the area at risk, p less than 0.025) in comparison with the saline treated control animals. In contrast, in Group III infarct size did not differ significantly from the saline-treated control group (45.9 +/- 3.3% vs. 47.7 +/- 3.5% of the area at risk). The percent of left ventricle at risk did not differ among the groups. The beneficial effects of MPG could not be explained on the basis of hemodynamic differences. In addition, MPG did not influence regional myocardial blood flow. In vitro studies indicated that MPG effectively scavanges O2- generated by the hypoxanthine-xanthine oxidase reaction, as well as by PMA-activated polymorphonuclear leukocytes. Based on these observations, we propose that MPG exerts its beneficial effects by protecting against free radical-mediated damage during the early phase of reperfusion. 相似文献
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Andres A; Morales JM; Praga M; Campo C; Lahera V; Garcia-Robles R; Rodicio JL; Ruilope LM 《Nephrology, dialysis, transplantation》1997,12(7):1437-1440
BACKGROUND: Cyclosporin has been shown to facilitate renal vasoconstriction
and to have an antinatriuretic effect. The existence of an interference of
cyclosporin with the vasodilating properties of endothelium mediated by
nitric oxide production could mediate these effects. On the other hand, the
infusion of the nitric oxide precursor L-arginine has been shown to induce
renal vasodilatation and to facilitate natriuresis in normal volunteers. We
have investigated the renal effects of the administration of an infusion of
L-arginine in renal transplant patients chronically treated with
cyclosporin. To facilitate the analysis of the data the effects of the
administration of a similar dose of cyclosporin on renal function during
the infusion of a vehicle were also investigated during the administration
of a vehicle of L-arginine. DESIGN: Ten male renal transplant patients,
chronically treated with cyclosporin and with a stable renal function were
studied during 2 consecutive days after the administration of the usual
morning dose of cyclosporin. The first day they received an intravenous
infusion of vehicle and the second the infusion of graded doses of
L-arginine (50, 100, 150 mg/kg/h) during 3 consecutive h. RESULTS: The
first day, after cyclosporin administration a significant fall (P <
0.01) was observed in natriuresis and kaliuresis in the absence of changes
in renal plasma flow and glomerular filtration rate. After the
administration of L-arginine significant (P < 0.01) increases of renal
plasma flow, glomerular filtration rate, and natriuresis were seen. The
increase in blood levels of cyclosporin after its administration did not
differ between days 1 and 2. CONCLUSION: These results indicate that
L-arginine facilitates renal vasodilatation and natriuresis in renal
transplant patients. Furthermore, the observed increase in sodium excretion
could indicate that L-arginine counteracts the antinatriuretic effect of
cyclosporin.
相似文献
8.
Does altered biomechanics cause marrow edema? 总被引:21,自引:0,他引:21
9.
J J Lynch A C Uprichard J W Frye E M Driscoll J M Kitzen B R Lucchesi 《Journal of cardiovascular pharmacology》1989,14(4):585-597
The effects of milrinone and pimobendan upon the initiation of programmed ventricular stimulation-induced ventricular tachycardia (VT) and the incidence of lethal ischemic ventricular arrhythmias were assessed in conscious dogs with recent anterior myocardial infarctions. Based upon the results of previous studies, the animals which were entered into this investigation were nonresponsive to baseline programmed stimulation and, therefore, considered to be at "low risk" toward the development of subsequent lethal ischemic arrhythmias. Milrinone (200 micrograms/kg/h continuous i.v. infusion) and pimobendan (300 micrograms/kg i.v.) were administered in dosing regimens shown to produce equivalent and sustained increases in left ventricular (LV) + dP/dt. At the time of repeat electrophysiologic testing, 9 of 9 pimobendan-, 9 of 10 milrinone-, and 12 of 12 concurrent vehicle-treated animals remained nonresponsive to programmed ventricular stimulation. Compared to a total control population of 39 "low risk" postinfarction dogs; however, both milrinone and pimobendan administration increased the incidence of sudden ventricular fibrillation occurring in response to the development of acute posterolateral ischemia (milrinone 4 of 10 [40%] and pimobendan 4 of 10 [40%] versus "low risk" control population 4 of 39 [10.3%]; p = 0.038). The incidence of ischemic mortality at 24 h after the development of posterolateral myocardial ischemia was increased in the milrinone-treated group (6 of 10 [60%]) compared to the "low risk" control population (6 of 39 [15.2%]; p = 0.007), whereas the incidence of 24-h ischemic mortality in the pimobendan-treated group (4 of 10 [40%]) was only of borderline statistical significance when compared to that of the "low risk" control population (p = 0.083). Milrinone, but not pimobendan, delayed the onset of acute posterolateral myocardial ischemia in the postinfarction dogs. The predominant electrophysiologic effects of both milrinone and pimobendan were decreases in ventricular refractoriness in both non-infarct (NZ) and in infarct zones (IZ), as well as reductions in electrocardiographic QTc or QT intervals. These findings suggest that with both positive inotropic agents, including milrinone which may possess protective antithrombotic action, sudden death may be increased via a reduction in ventricular refractoriness in the ischemically injured heart. The enhanced susceptibility toward the development of ischemic ventricular arrhythmias in the presence of the inotropic interventions is not predicted by programmed ventricular stimulation testing prior to the ischemic event. 相似文献
10.
Positional cloning of the gene for X-linked retinitis pigmentosa 3: homology with the guanine-nucleotide-exchange factor RCC1 总被引:6,自引:7,他引:6
Roepman R; van Duijnhoven G; Rosenberg T; Pinckers AJ; Bleeker-Wagemakers LM; Bergen AA; Post J; Beck A; Reinhardt R; Ropers HH; Cremers FP; Berger W 《Human molecular genetics》1996,5(7):1035-1041
The gene for retinitis pigmentosa 3 (RP3), the most frequent form of X-
linked RP (XLRP), has been mapped previously to a chromosome interval of
less than 1000 kbp between the DXS1110 marker and the OTC locus at
Xp21.1-p11.4. Employing a novel technique, YAC Representation Hybridization
(YRH)', we have recently identified a small XLRP associated microdeletion
in this interval, as well as several putative exons including the 3' end of
a gene that was truncated by the deletion. cDNA library screening and
sequencing of a cosmid centromeric to the deletion has now enabled us to
identify numerous additional exons and to detect several point mutations in
patients with XLRP. The predicted gene product shows homology to RCC1, the
guanine-nucleotide- exchange factor (GEF) of the Ras-like GTPase Ran. Our
findings suggest that we have cloned the long-sought RP3 gene, and that it
may encode the GEF of a retina-specific GTP-binding protein.
相似文献