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Biomedical subjects

Y Ikari

Publications and source records attributed to Y Ikari.

64 records · Page 4Linked to original sources
PubMed1987

Dystrophic symptoms prevented by phenobarbital in avian muscular dystrophy.

New Hampshire normal (line 412) and dystrophic (line 413) chickens were treated with central stimulants and central depressants, respectively, once a day from the 2nd to the 10th day after hatching, and effects of the treatment were examined on a number of muscle fibers, areas of muscle fibers, and the coefficient of variation of a muscle on the 13th day. Central depressants, especially phenobarbital, effectively prevented development of the dystrophic symptoms, whereas central stimulants made normal chickens "dystrophic". The righting ability of the dystrophic chickens was normal after treatment with 10 mg/kg of phenobarbital during the early postnatal period from the 2nd to the 28th day after hatching.

Age Factors↗
PubMed1984

Development and growth of extensor carpi radialis longus muscle in normal and dystrophic chickens.

The development and growth of the skeletal muscles in normal and dystrophic chickens were studied to obtain a clue to the mechanism of dystrophic pathogenesis. A relatively small and isolated muscle--the extensor carpi radialis longus (ECRL) muscle--was utilized to analyze quantitatively the histologic and physiologic parameters. Both normal and dystrophic chickens attained qualitatively the same parameters, but there were some quantitative differences. The first disorder to appear in the dystrophic muscle was a substantial retardation of muscle cell proliferation in the early postnatal development, and the fiber loss was fully compensated by hypertrophy of the remaining cells. The succeeding abnormalities in the dystrophic muscle, e.g., reduction of efficiency in the tension output per unit area, were interpreted as compensating reactions. Therefore, it is likely that the dystrophic lesions in avian muscular dystrophy are caused by retardation of muscle cell proliferation in the early postnatal period. Possible mechanisms for the retardation are discussed in terms of the nerve--muscle trophic interactions which could be greatly intensified in the early postnatal period.

Animals↗
PubMed1984

Transplantation of extensor carpi radialis longus muscle in normal and dystrophic chicks.

The etiology of avian muscular dystrophy was examined by a cross-transplantation technique. Care was taken for the transplants to regenerate and develop under neural influence, by using the small extensor carpi radialis longus (ECRL) muscle. The ECRL muscles were exchanged between normal and dystrophic chicks 2 to 3 days ex ovo, and the muscle weight, number of muscle fibers, muscle fiber size, and contractile properties of the transplanted muscles were observed 60 to 65 days after operation when the tissue reconstitution was virtually complete. The results obtained for the physiologic, anatomic, and histologic parameters strongly suggested that there exists some failure in the host environment of the dystrophic chicken. The analyses of the histologic parameters suggested that a genetic disorder may also reside in the muscle tissue itself. The myotonic nature of the muscle membrane, however, probably does not contribute significantly to the abnormal behavior of dystrophic chickens. The importance of some neurogenic abnormalities in avian muscular dystrophy is discussed in relation to the results reported by other investigators.

Action Potentials↗
PubMed1980

Ionic mechanism of the resting membrane depolarization of frog sartorius muscle induced by dimorpholamine.

Ionic mechanism of the resting membrane depolarization of frog sartorius muscle induced by dimorpholamine was studied in a variety of ionic conditions. The resting membrane was depolarized in a dose-dependent manner reaching a maximum with a dose of 6 X 10(-5) M. The amount of the depolarization (1.4 mV) was suppressed with doses over 10(-4) M. This dose-dependent response was accompanied by change in the membrane conductance. The chloride conductance was increased by 16% and the potassium conductance by 7%, however the sodium conductance did not significantly change with a dose of 2 X 10(-5) M. The slight depolarization induced by the drug was well explained by the changes in the ionic conductance. The effects of these actions on the membrane action potentials were simulated, suggesting that this drug possesses the nature of a stimulant on excitable membranes yet does not produce any appreciable depolarization blockade.

Animals↗
PubMedDate not supplied

Elastic recoil following percutaneous transluminal coronary angioplasty and Palmaz-Schatz stent implantation.

The post-procedural elastic recoil in 133 lesions treated with the Palmaz-Schatz stent was compared to 133 matched lesions treated with balloon angioplasty to determine the role of prevention of elastic recoil in the creation of a larger initial luminal diameter. Elastic recoil was defined as the difference between the maximal diameter of the inflated balloon and the minimal luminal diameter of the dilated segment immediately after the procedure and was evaluated by quantitative coronary angiography. Overdilatation was defined as a dilatation induced by a balloon with a maximal diameter larger than the pre-procedure reference diameter. The percent diameter stenosis was reduced from 73% to 31% in the balloon angioplasty group and from 72% to -4% in the stent group (31% vs. -4%, p < 0.01). Elastic recoil was significantly larger in the balloon angioplasty group than in the stent group (0.94 +/- 0.29 mm vs. 0.09 +/- 0.09 mm, p < 0.01). Overdilatation and lesion morphology had no significant effects on elastic recoil in the stent group. In the balloon angioplasty group, overdilatation, noncalcified lesions and eccentric lesions were associated with increased elastic recoil. These results indicated that the larger post-procedural luminal diameter associated with the Palmaz-Schatz stent was primarily the result of prevention of elastic recoil, which was not influenced by the degree of overdilatation or lesion morphology.

Angioplasty, Balloon, Coronary↗
PubMedDate not supplied

Enhancement of ascorbate cytotoxicity by chelation with ferrous ions through prolonged duration of the action.

Fe(II)-L-ascorbic acid complex (FeAsc) exhibited a greater cytotoxicity [50% inhibitory dose (IC50), 24-32 microM] to human carcinoma A 549 or rat SV40-transformed W3Y cells than ascorbic acid (Asc) (IC50, 460-660 microM); a simple mixture of Fe(II) and Asc, or Fe(II) alone was also less cytotoxic. Malignant cells from a variety of tissues of different species were also susceptible to FeAsc. FeAsc exhibited a longer half-life (66-82 hours) during cell contact than that of Asc (2.5-3.1 hours). Thus chelated Fe(II) but not unbound Fe (II) was responsible for the enhanced cytotoxicity of FeAsc, which was attributed primarily to its prolonged duration of action.

Animals↗
PubMedDate not supplied

[Outcome of coronary angioplasty and coronary artery bypass grafting in patients over 75 years old].

Mortality, morbidity, and 3-year survival rates were evaluated in patients aged over 75 years undergoing initial revascularization by percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass grafting (CABG). The groups of 74 patients undergoing PTCA and 27 undergoing CABG had similar clinical characteristics including age, sex, emergency operation, prior myocardial infarction, and ejection fraction. The PTCA group contained significantly more patients with single vessel disease (44% vs 8%, p < 0.01) while the CABG group had more three-vessel or left main trunk disease (30% vs 70%, p < 0.01). The patients in the PTCA group demonstrated more prior cerebral vascular events, renal insufficiency, and abdominal aortic aneurysms. Angiographic revascularization was achieved in 112 of 130 lesions (86%) and in 63 of the 74 (84%) patients in the PTCA group. Hospital mortality for the PTCA group was 5.4% (two cardiac deaths and two non-cardiac deaths), but 0% for the CABG group. Myocardial infarction occurred in 1.3% and 3.7%, respectively (p = NS). Three-year survival, excluding hospital deaths, was 90% for patients with PTCA and 96% for those with CABG (p = NS). All these deaths were of non-cardiac origin. Both PTCA and CABG are safe and effective for selected patients over the age of 75 years.

Aged↗