A new technology and field test of advance cue usage in volleyball.
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Biomedical subjects
Publications and source records attributed to P Edwards.
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Hospitals run on paper, or sometimes so it seems. The patient accounts department at Cabell Huntington Hospital was having an increasingly difficult time handling the hospital's growing patient accounts load, which was creating a forest of paperwork to be processed, filed, retrieved, updated, and refiled.
Connective tissue allografts are treated commonly with deep freezing to facilitate their storage in tissue banks and to reduce their immunogenicity. The influence of freezing on the healing of these grafts is unknown. The effect of an aggressive freezing protocol on ligament graft healing in a nonimmunogenic autograft model was investigated. The femoral-medial collateral ligament-tibial complex of the rabbit knee was transplanted orthotopically into the site from which it had just been harvested. The fresh group had their grafts rinsed in normal saline, and the frozen-thawed group had their grafts repetitively frozen-thawed in liquid nitrogen immediately before reimplantation. The healing of the ligament complexes were evaluated mechanically at intervals as long as 1 year after transplantation. Repeated freezing had little effect on the initial mechanical behavior of the graft complexes but was found to be detrimental to subsequent graft incorporation. The frozen-thawed grafts were weaker than the fresh grafts overall, and this effect persisted over time. The failure load and stress of the frozen-thawed grafts reached only 87% and 75% of that of the fresh grafts after 48 weeks. Because the initial mechanical effects of freezing were minimal, subsequent effects on graft healing must be attributed to factors other than gross structural injury. Despite showing almost no signs of damage to bone-ligament-bone grafts initially, freezing procedures may have important subsequent biologic consequences that may influence the clinical success of stored connective tissue grafts used in ligament reconstruction.
Many elderly people have difficulty in taking their drugs correctly after discharge home from hospital. Individualised teaching can improve their compliance and quality of life.
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This study was carried out to test the hypothesis that a relationship exists between ligament tension and ligament cell geometry. Rabbit knee joints were positioned at 70 degrees of joint flexion and the medial collateral ligament (MCL) was mechanically isolated and the femur-MCL-tibia complex was stretched or compressed by displacing the crosshead of a materials testing machine: -2.0 mm (relative compression), 0.0 mm (a reproducible no-load starting point), +/-0.7 mm or + 1.4 mm (relative tension). Each MCL complex was then fixed immediately in 10% neutral buffered formalin. Contralateral knees were dissected similarly with MCLs exposed and fixed in situ at 70 degrees of flexion. Subsequent to histological processing, measurements were made of the profiles of fibrocyte nuclei (since previous work has shown that nuclear shape closely approximates fibrocyte shape) that were located in the central portion of each MCL midsubstance using a video-based computerized morphometry system. Results showed that the dimensions of nuclei in the midsubstance of experimental MCLs were significantly longer and thinner at crosshead displacements that corresponded to increased ligament tension. At +1.4 mm of displacement fibrocyte nuclei were approximately 4 microm longer and 1 microm thinner than those fixed at 0.0 mm, an observation supported by a statistically significant increase in the mean maximum-to-minimum-diameter ratio and a significant decrease in mean cell roundness. These results strongly suggest that mechanical load can directly affect ligament fibrocyte geometry in situ. If a similar phenomenon also occurs in vivo, the metabolism of ligament fibrocytes may be influenced considerably by their loading history.
Auditing the outcome from vascular surgery with regard to graft occlusion is made difficult by variations in the type of surgery performed and the case mix. These difficulties are compounded when attempting to compare units. In the present study we have attempted to develop a scoring system to predict the risk of graft occlusion, and thus compensate for these variables. Prospectively collected data from 214 consecutive patients undergoing vascular reconstructive surgery (233 arterial grafts) were analysed. Graft occlusion occurred in 82 patients (35.2%). Using a multivariate linear regression analysis of these data a five-factor, five-grade scoring system has been devised (GORA: Graft Occlusive Risk Assessment). Logistic regression analysis of the observed risk of occlusion with this derived score produced the following relationship between the odds ratio of occlusive risk and GORA score: (logeR/1 - R = (0.229 x score) - 4.165). The score was then validated in a different group of 186 patients (196 arterial grafts). In both groups the score was found to predict accurately the risk of graft occlusion (P < 0.001). There was no significant difference in the receiver operating characteristic curves between the estimation and validation groups.
Trisomy 21, Down syndrome individuals demonstrate Alzheimer's disease-associated neuropathology at post mortem. The amyloid precursor protein, one of the pathological proteins is encoded for on chromosome 21. Mouse chromosome 16 is syntenic to human chromosome 21 for the region spanning the amyloid gene. We have previously reported the appearance of Alzheimer's disease-associated neuropathological proteins in cortical grafts derived from Trisomy 16 mice at 4-6 months survival. This paper reports the ultrastructural observations of large and multiple deposits of intracellular lipofuscin within these trisomic grafts at 12 months survival along with increased numbers of free ribosomes, extended Golgi apparatus and endoplasmic reticulum, membrane degeneration and abnormal axonal profiles. Similar but less severe neuro-degeneration is occasionally observed within 18-month-old normal, mouse hippocampal tissue and rarely observed in age-matched control grafts.
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This is a case of late-onset (6 weeks) radial nerve paralysis following open reduction and internal fixation of a comminuted distal humerus fracture. A transected radial nerve within the callus was found at reoperation. The mechanism of transection was thought to be repetitive motion of the nerve across an edge of new bone. The nerve was repaired and tendon transfers done subsequently with less than full functional recovery at 16 months. No such case has been previously reported.
Optically pure L-(+)-C alpha-methyl-arginine and D-(-)-C alpha-methyl-arginine were synthesized. Experimental results indicated that DL-C alpha-methyl-arginine methyl ester could be resolved by trypsin, but workup posed a technical difficulty. Chemical resolution at the stage of DL-C alpha-methyl-ornithine, followed by selective guanidination using N,N'-di-Cbz-S-methylisothiourea and hydrogenolysis provided a effective and practical method for the synthesis of optically pure C alpha-methyl-arginine.
The in-vivo pharmacological properties have been examined of FCC5 (2-N-carboxamidino-1,2,-3, 4, 10, 14b-hexahydrodibenzo (c.f.) pyrazino (1, 2-alpha)azepine hydrochloride), a guanidino analogue of mianserin. FCC5 (30-100 micrograms kg-1, i.v.) caused long-lasting (> 1 h) attenuation of histamine- and 5-hydroxytryptamine (5-HT)-induced bronchoconstriction in the anaesthetized guinea-pig. FCC5 (< or = 1 mg kg-1, i.v.) had no effect on submaximal bronchoconstrictor responses caused by i.v. acetylcholine or the thromboxane A2-mimetic U46619 ((15S)-hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5Z,13E-dienoic acid). The pressor effects of 5-HT in anaesthetized and pithed rats were inhibited by FCC5 (0.3-1.0 mg kg-1, i.v.). Higher doses of FCC5 (3 mg kg-1, i.v.) reduced bradycardia and depressor responses to 5-HT in anaesthetized rats. In anaesthetized cats and rats and also pithed rats, FCC5 (0.1-1.0 mg kg-1, i.v.) caused sympathomimetic effects as demonstrated by pressor responses and tachycardia. FCC5 (0.1-0.3 mg kg-1, i.v.) inhibited pressor responses to tyramine whereas those to noradrenaline and sympathetic nerve stimulation were potentiated. Oedema in the rat paw caused by intraplantar 5-HT was inhibited by FCC5 (ID50 0.76 mg kg-1, i.p.; and 2.7 mg kg-1, p.o.). In decerebrate rats which had been spinalized at T6-8, fenfluramine-induced facilitation of the flexor reflex of the anterior tibialis muscle was inhibited by mianserin (ID50 0.36 mg kg-1, i.p.) but not by FCC5 (< or = 3 mg kg-1, i.p.).(ABSTRACT TRUNCATED AT 250 WORDS)
The strain of athymic nude male mice (ANM) developed at the University of Southern California (USC) exhibits spontaneous hyperglycemia and relative hypoinsulinemia in vivo. To investigate factors that influence insulin secretion in this animal model of non-insulin-dependent diabetes mellitus, we utilized the isolated perfused mouse pancreas of the ANM-USC and control BALB/c mice. We compared in vitro glucose-induced insulin secretion in ANM-USC and control mice, inhibition of secretion by somatostatin, and variability of insulin secretion over the two-year period it took to complete these experiments. Glucose-induced insulin secretion from the isolated pancreas was biphasic in both ANM-USC and controls. Insulin secretion was quantitatively equal to or greater than control mice, depending on the phase of secretion analyzed and the source of the control mice. In contrast to pancreases of control mice, insulin secretion from ANM-USC pancreases was relatively resistant to inhibition of insulin secretion by somatostatin. Variability in insulin secretion over the two years in which these experiments were performed was greater from pancreases of control than that observed from pancreases of the ANM-USC. The hyperglycemic ANM-USC mouse does not demonstrate diminished insulin secretion in vitro yet is relatively hypoinsulinemic in vivo. Thus circulating factors other than somatostatin might contribute to the insulinopenic stage in this animal model.
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