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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
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Three structurally related compounds, 4-acetoxy-3-acetoxy-methyl-acetophenone(AAMAP), 1-[4'- hydroxy-3'-hydroxy-methylphenyl]-2-[benzyl-t-butylamino]ethanone hydrochloride (HHBEH) and 1-[4'-hydroxy-3'-hydroxymethyl-phenyl]-2-[benzyl-t-butylamino]ethanol (HHBE), gave positive dose-related mutagenic responsesin the Ames test when Salmonella typhimurium strain TA100 wasused as the test organism. Strain TA100 carries the hisG46 allele,which is revertable by base changes, together with plasmid pKM101,which encodes mucAB genes that are analogous to umuDC, the chromosomalSOS-repair genes of Escherichia coli K-12. None of the compoundswas mutagenic in Ames strain TA1535, which is the plasmid-freederivative of strain TA100. Only AAMAP, and that at only thehighest concentration tested, was mutagenic in strain TA98,which detects frameshift mutations and carries plasmid pKM101.No compound was significantly mutagenic in strain TA1538, whichis the plasmid-free derivative of strain TA98. When the threecompounds were tested for the induction of sister-chromatidexchanges (SCEs) in Chinese hamster cells, the two more potentmutagens, AAMAP and HHBEH were found to increase SCEs, whereasHHBE did not give a significant response at any concentrationtested. Ames test data showing plasmid pKM101-dependent mutagenesisare therefore, at least for these compounds, relevant indicatorsof eukaryotic genotoxicity.
Parts of this paper were communicated to the Science Group atthe 123rd British Pharmaceutical Conference, Jersey, 1986. 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