Development of an abdominal wall sphincter for the continent ileostomy.
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Biomedical subjects
Publications and source records attributed to B J Murphy.
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The content of free amino acids in whole blood was measured in near-term gravid female Weddell seals (Leptonychotes weddelli) and compared with fetal amino acid profiles during rest and during experimental diving. With the exception of taurine and glutathione, Ninhydrin-reactive components of acid extracts of blood occurred in higher concentrations on the fetal side of the placenta than on the maternal side. Compared with humans the Weddell seal displayed higher ratios of fetal arterial to maternal arterial levels for aspartate, glycine, alanine, valine, tyrosine, phenylalanine, and total branched-chain amino acids. In the resting state the total free amino acid concentration in maternal blood was only about 70% as large as the total amino acid concentration in fetal blood, compared with a value of over 80% for humans. Only modest changes in the concentrations of specific amino acids occurred during simulated awake diving, but the overall maternal pools of glycine, glutamate, and glutamine were augmented, creating favorable conditions for uptake by the fetus.
Motor neuroblasts comprising the brachial segments of the lateral motor column in the dystrophic chicken were counted at 6, 7, 9, 12, and 18 days of incubation and at 5 days' post-hatching. Comparisons with similar counts from normal chick embryos disclosed that there was a significantly greater depletion of motor neurons in normal embryos between days 9 and 12. These findings suggest that nerve-muscle interaction may be altered early in the development of the motor unit in the dystrophic chick embryo.
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In New Hampshire chickens, the primary clinical symptom of dystrophy is limitation of wing motility. Examination of the brachial-level motor unit in chick embryos homozygous for dystrophy reveals abnormalities in both muscular and neural components. Wing motility in these embryos is abnormal as early as six days, and there is a corresponding lack of differentiation of the pectoralis major muscle. The findings suggest that delayed development of brachial-level neuronal pathways is responsible for the decreased wing motility and early degeneration of the pectoral muscle.
Early aspects of in vivo sarcomere organization were studied using normal and dystrophic New Hampshire chick embryos. Brachial somites 17-22 were removed from stages 16 through 28 embryos, processed for electron microscopy, and analyzed. Comparisons of normal and dystrophic material disclosed that thick filaments appeared later in dystrophic myotomal cells. This was correlated with a similar delay in the appearance of long polyribosomes. By stage 28, normal myotomal cells contained well-defined sarcomeres, whereas dystrophic sarcomeres were frequently unorganized, with myofilaments in poor longitudinal alignment. Periodic tubules were poorly developed or lacking.
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The perceived spatial frequency of low-frequency sinusoidal gratings is elevated when the gratings are temporally modulated sufficiently rapidly. Although this phenomenon is usually called "spatial-frequency doubling", the magnitude of this spatial-frequency elevation depends on the spatial and temporal parameters of the grating and may be less than or greater than doubling. Adaptation to such a pattern produces contrast-threshold elevation whose spatial-frequency tuning is centered upon the grating's real rather than perceived spatial frequency. These results suggest that the spatial-frequency elevation occurs later in the visual system than adaptation or that these two processes are independent of one another, at least under the conditions of these experiments.
Fetal responses to normobaric diving simulated by submersion of the maternal head for 20 min were studied in four conscious Weddell seals near term. Microspheres injected into the maternal aorta were distributed to the placenta and kidneys in the ratio of 0.4 in the control period and 19.3 during diving, suggesting minimal placental vasoconstriction. Fetal heart rate fell during diving from a mean control value of 90 to 34 beats/min after 4 min. The onset of fetal bradycardia was not consistently associated with changes in blood gas tensions. Diving was associated with a fall in fetal arterial O2 tension from 24 to 9 Torr, arterial CO2 tension rose from 47 to 85 Torr, and arterial pH fell from 7.35 to 7.24. Fetal-maternal gradients for CO2 and H+ transport remained constant, whereas the gradient for O2 transport fell from 47 Torr before diving to 14 Torr at the end of diving. Blood lactate concentrations increased three- to fourfold during diving and reached peak values 10-15 min after diving ended. The similarity of the fetal and maternal heart rate responses to diving is consistent with the presence of physiological oxygen-conserving reflexes akin to the adult's.
New Hampshire chickens, homozygous for inherited muscular dystrophy, display clinical manifestations at an early age. A fine structural examination of embryos from this strain shows marked degenerative changes four days prior to hatching. The Z bands appear to dissolve progressively to the point where finally the myofibrils become uniformly dense with no detectable banding patterns.
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Dilations of the sarcotubular system and misaligned myofilaments have been reported as early indicators of muscular dystrophy in skeletal muscle. Since the developing tubular component is believed instrumental in initial myofilament alignment during myogenesis, tubular development is evaluated using normal and dystrophic chick embryo skeletal muscle and cultures of normal and dystrophic embryonic pectoral muscle incubated in the presence of horse spleen ferritin. Comparisons of the findings show that periodic tubules are absent from dystrophic somitic muscle and that invaginating tubules from the sarcolemma are found in fewer, randomly located areas of dystrophic pectoral muscle cells. The results indicate that the tubular component is not involved in the bizarre vesiculations seen in mature dystrophic muscle, however, the malalignment of dystrophic myofilaments is probably the result of the poorer development of the T system in this muscle.
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1. Ornithine-2-oxo acid aminotransferase activity was inhibited by amino-oxyacetate (10(-5) M). This permitted the measurement of ornithine decarboxylase in the presence of mitochondria by using the 14CO2-trapping technique. 2. Subcellular fractionation of rat liver by differential centrifugation, followed by the assay of ornithine decarboxylase in the presence of amino oxyacetate and of marker enzymes for each fraction, demonstrated that ornithine decarboxylase was located in the cytosol. 3. The greatly increased ornithine decarboxylase activity observed after growth-hormone administration was also found to be localized in the cytosol. 4. The Km of ornithine decarboxylase from rat liver for ornithine was 28 muM. Administration of growth hormone 4 h before death did not affect the apparent affinity of ornithine decarboxylase for ornithine.