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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4.
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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.
L. Maximilian Buja Victor J. Ferrans Barry J. Maron 《The American journal of pathology》1974,74(3):613-648
Junctional structures formed by two parts of the plasma membrane of the same cardiac muscle cell were observed in ventricular myocardium of: a) patients with neoplasms, aortic valvular disease or idiopathic hypertrophic subaortic stenosis and b) dogs subjected to prolonged normothermic anoxic cardiac arrest. Most of these structures had features of desmosomes; other, more complex structures had components with features of desmosomes, fasciae adherentes and nexuses, and, therefore, resembled intercalated discs. These intracytoplasmic junctions were localized to: a) the peripheral cytoplasm at the sides or ends of cells, b) narrow invaginations of plasma membranes, c) narrow zones of deep, broad plasmalemmal invaginations and d) narrow branches of T tubules. In patients with idiopathic hypertrophic subaortic stenosis or aortic valvular disease and in the dogs subjected to anoxic cardiac arrest, intracytoplasmic junctions were observed in hypertrophied or degenerated muscle cells which were located in areas of fibrosis and which showed loss of contact with adjacent cells. In patients with neoplasms, intracyto-plasmic junctions were found in degenerated cells which were located in areas of interstitial edema and which also showed loss of contact with adjacent cells. Our observations suggest that remodeling of cell surfaces following loss of intercellular contact is the most likely mechanism of formation of intracytoplasmic junctions. 相似文献
10.
A Mukherjee T M Wong G Templeton L M Buja J T Willerson 《The American journal of physiology》1979,237(2):H224-H238
Oxidative phosphorylation of isolated canine myocardial mitochondria has been evaluated after exposure to different concentrations of phosphate (5--50 mM), lactate ion in excess (5--40 mM, pH 7.4), calcium (50--270 nmol/mg protein), to lactic acidosis (pH 6.3), and to mitochondrial protein dilution (in vitro volume expansion) for 10 min to 8 h. The influence of phosphate and lactate ion addition, lactic acidosis, and in vitro volume expansion on mitochondrial function were studied in the isolation medium (0.18 M KCl, 0.5% BSA (bovine serum albumin), with or without Tris-EDTA, pH 7.4) prior to evaluation of mitochondrial function in the assay medium (0.25 M sucrose, 10 mM Tris-HCl, and 10 mM inorganic phosphate, pH 7.4). The effect of calcium addition was assessed in the assay medium. The results of these studies demonstrate that each of these interventions detrimentally alters mitochondrial oxidative phosphorylative ability. The most severe mitochondrial functional impairment resulted from phosphate or calcium addition. The detrimental effect of phosphate and in vitro volume expansion was partially corrected by the addition of cytochrome c. 相似文献