[Successfully treated open heart stab injury. Case report].
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Biomedical subjects
Publications and source records attributed to G Engel.
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The majority of research on distal radius fractures consists of retrospective, descriptive studies of patients with unstable fractures requiring fixation. The purpose of this investigation was to report on impairments in flexibility, grip strength, and motor control and on the presence of swelling and atrophy immediately after cast immobilization of closed reductions of simple distal radius fractures. Sixteen adult subjects from Kaiser Permanente Medical Center, San Francisco, entered the study, and 13 completed it. At the initial evaluation, upper extremity ranges of motion, grip strength, forearm circumferences, two-point discrimination, and motor reaction times were measured on the uninvolved side. The same measurements were taken on the affected side within 48 hours after cast removal. All but one subject worked throughout the casting period. There were significant postcasting impairments in forearm rotation (40% deficit in pronation and supination); wrist flexion, extension, and radial and ulnar deviation (50% reduction in all motions); grip strength (-32 kg, or approximately 24% of the strength of the unaffected side); and forearm circumference (-1.1 cm) and wrist circumference (+1.5 cm). Patients complained of awkwardness of the involved hand. These measured impairments immediately after immobilization of simple radius fractures were greater than the reported impairments in patients after reduction of radius fractures with fixation 6 to 27 months after injury. To prevent long-term disability and recover flexibility, strength, and function, patients with simple distal radius fractures should be referred to a hand, occupational, or physical therapist for evaluation, education, and treatment after immobilization. Longitudinal studies are needed to quantify long-term functional recovery with regard to the type of fracture and the degree of impairment measured immediately after casting.
We describe a new class of drugs that selectively block serotonin M-receptors on peripheral neurones. Because of their high affinity, some of these drugs are the most potent of any pharmacological class yet reported. They have allowed the identification of three M-receptor subtypes, one of which is responsible for mediating the painful effects of serotonin in humans.
AIM: The successful operative stabilization of the shoulder joint is a demanding surgical procedure. The causality of shoulder instability is complex with in some cases multiple lesions in different anatomical structures. The surgeon has to understand the complexity of factors causing instability in order to be therapeutically successful. The aim of the study was to document the intraoperative pathology in revision instability surgery. METHOD: 46 patients with recurrent postoperative instability were included (8 female, 38 male, follow-up > 12 months). After diagnostic arthroscopy an open revision surgery was performed in all cases. RESULTS: In 19 cases (40%) an insufficient surgical procedure was performed (inadequate capsular shift with worn out labral tissue). Selection of an incorrect surgical technique was the reason for revision in 12 patients (25%). Anamnestically 5 patients reported a re-injury, whereas objectively only one patient described an adequate trauma. The most frequent finding was an open rotator interval (persisting Foramen Weitbrecht), which was seen in 22 cases (46%). CONCLUSION: A stable range of motion of the shoulder is achieved by a variety of different factors, which leads in most instances to a combination of pathological changes in case of a dislocated shoulder. To understand the contributing factors of an instable shoulder joint is a necessity to carry out a successful surgical procedure.
The complex between urokinase-type plasminogen activator (uPA) and its inhibitor PAI-1 (plasminogen activator inhibitor 1) has been prognostically evaluated in patients with breast cancer. The concentrations of uPA antigen, PAI-1 antigen and the uPA/PAI-1 complex were analysed in extracts from breast cancer tumours from 233 patients (median follow-up of patients: 71months). The uPA/PAI-1 complex typically constituted about 5% of the uPA antigen (total uPA). The concentration of complex was found to correlate more strongly to the concentration of PAI-1 (r = 0.72; p < 0.0001) than to the concentration of uPA (r = 0.55: p < 0.0001). Interestingly, in this material the uPA/PAI-1 complex (using an optimised cutoff level of 0.22 ng microg(-1) DNA) had a stronger prognostic value than optimised cut-off valuesfor uPA or PAI-1. The data suggest that activation of prourokinase within the tumour, which is a prerequisite for the formation of the uPA/PAI-1 complex, is of better prognostic value than the production of prourokinase or PAI-1 in the breast cancer tumour.
In pig coronary artery rings contracted by the thromboxane analogue U 46619 (9,11-dideoxy-11 alpha, 9 alpha-epoxy-methano-prostaglandin F 2 alpha), spiperone induced a relaxation which, at 30 mumol/l, corresponded to a complete reversal of the U 46619-induced contraction. The concentration-response curve for spiperone was bell-shaped. The second phase, i.e. the reduction of the relaxant effect (at concentrations above 30 mumol/l) was due to a contractile effect which was the only response in (1) endothelium-denuded arteries, (2) arteries treated with gossypol or methylene blue, or (3) arteries not precontracted with U 46619. Suramin and reactive blue 2 antagonized the relaxing effect, whereas metitepine, spiroxatrine, propranolol, idazoxan, flupenthixol, atropine and 8-phenyltheophylline did not. The endothelium-independent contraction was not reduced by metitepine. In strips of arteries with intact endothelium, incubated with [3H]adenosine and subsequently superfused with physiological salt solution containing dipyridamole, spiperone evoked an increase in tritium overflow above basal efflux. The present results are compatible with the hypothesis that spiperone releases ATP from the pig coronary artery. ATP, in turn, seems to activate endothelial P2 purinoceptors, leading to the release of endothelium-derived relaxing factor (NO) with a subsequent vascular relaxation.
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