[Problems in teaching the nursing process in relation to nursing theories--analysis by systems approach].
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Biomedical subjects
Publications and source records attributed to R Ito.
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The use of hydrogen peroxide as a labile and safe food preservative in fish cake and boiled noodles has recently been restricted by the Japanese government, since hyperplasia has been found in the duodenum of mice after long-term peroral study. The action of compounds with resembling mode of action, potassium bromate as an improving agent in bread, and sodium chlorate as a weed killer are discussed in this paper in view of developmental and environmental pharmacology.
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The amidolytic activity of activated kallikrein in plasma can be measured by use of the chromogenic substrate, S-2302 (H-D-Pro-Phe-Arg-pNA). Plasma prekallikrein was activated to kallikrein by exposure to 50 mg/L dextran sulfate in acetone/water (35/65 by vol) at 0 degrees C for 15 min. The acetone slows anti-kallikrein activity and increases the kallikrein activity by 30%. The 37 degrees C reaction mixture contained 0.54 mmol of S-2302 substrate per liter of Tris buffer (pH 7.5 at 37 degrees C). We monitored the change in absorbance at 405 nm for 60 s. The specificity of the substrate for kallikrein was demonstrated by using plasma deficient in prekallikrein (Fletcher trait) diluted with pooled normal human plasma. We recommend collecting blood specimens with sodium citrate as the anticoagulant and with use of a double-syringe technique and all-plastic containers. Plasma kallikrein activity with Chromozym-PK (Bz-Pro-Phe-Arg-pNA) as substrate (y-axis) compared with S-2302 as substrate (x-axis) gave the relation: y = 0.28x + 0.82 (r = 0.94). Day-to-day analytical variation was 2.4% for a pooled plasma with a mean value of 85.9 mukat/L. The mean (and 2 SD) for 50 healthy adults was 86.4 (32.4) mukat/L.
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The axonal initial segment of the Mauthner cell of tadpoles of Rana catesbeiana and its surrounding neuropil, the axon cap, were examined by electron microscopy. The initial segment is almost completely covered by numerous synaptic terminals with profuse clear spherical synaptic vesicles. These synaptic terminals are of one uniform type and are found to be extensions of preterminal swellings, which are filled with accumulated mitochondria and glycogen granules in addition to the synaptic vesicles. Some swelling were shown to have two or more terminals. The synaptic terminals as well as the preterminal swelling are occasionally linked by small synaptic junctions. The significance of this structural organization in the inhibitory control of the Mauthner cell activation was discussed.
Effects of 5-methyl-7-diethylamino-s-triazolo-1, 5-a) pyrimidine (trapidil, Rocornal), a therapeutic agent for ischemic heart disease, on various types of experimental hyperlipemias were studied. With administration of trapidil, elevation of serum high density lipoprotein cholesterol (HDL-C) levels and reduction in serum total cholesterol (TC), low density lipoprotein and very low density lipoprotein cholesterol (LDL-C) and the ratio of HDL-C to LDL-C (LDL-C/HDL-c) were observed in most disease models. Changes in HDL-C levels and LDL-C/HDL-C in the hyperlipemia induced by lipid-enriched diet in mice and in the hyperlipemia induced by high cholesterol diet in Japanese quails were of statistical significance. Also, amelioration of reduction in HDL-C induced by high fat emulsion plus 6-n-propyl-2-thiouracil in rats was observed to be significant. Moreover, trapidil significantly reduced TC, LDL-C levels and LDL-C/HDL-C in the hyperlipemia in hamsters. To investigate possible mechanisms of therapeutic effects of trapidil, blood enzyme activities in Japanese quails with hyperlipemia were assayed. Trapidil showed increases in plasma lipoprotein lipase and serum lecithin-cholesterol acyltransferase activities. These results suggest that trapidil may be an effective chemotherapeutic agent for treating ischemic heart disease.
The identification of carpronium chloride and a metabolite in human urine has been performed by means of field desorption mass spectrometry using deuterium labelling. Essential points in this study are the simultaneous administration of a deuterium labelled drug ([2H9]carpronium chloride), a purification procedure by ion pair extraction with an iodine reagent, and the use of paper electrophoresis to examine the degree of clean-up. The field desorption mass spectra of the purified extracts obtained from sample urine gave a characteristic pattern resulting from the carpronium cation (m/z 160, m/z 169) and a metabolite of the N-(3-carbohydroxypropyl)trimethyl ammonium cation (m/z 146, m/z 155).
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The excitation/emission spectra maxima obtained from orange fluorescing small cell clusters and greenish yellow fluorescing ganglion cell bodies were at 400--410/490--560 nm and at 400--410/470--500 nm, respectively.
Myotendon junctions in the rectus abdominis muscles of bull frogs were examined by the fixation combination of tannic acid and glutaraldehyde using electron microscopy. The features observed on myotendon junctions were the following: (1) There were many deep invaginations of muscle cell membrane at the end of the muscle fibers. Terminal thin filaments of myofibrils were attached to the electron-dense layer lining under the muscle cell membrane on the lateral walls of invaginations. (2) The basement membrane covering the muscle cell membrane was thicker in the invaginations than on the other sites of muscle fibers. (3) Collagen fibers in the invaginations gradually tapered off toward the bottom of the invaginations. But it was not seen that the collagen fibers were attached to both the basement membrane and cell membrane of muscle cells. (4) On the observations using the tannic acid-glutaraldehyde fixation, it was clearly seen that the microfibrils extend from the outer leaflets of the cell membrane to the collagen fibers in invaginations via the basement membrane. It was concluded that the myofibrils might be fastened to the collagen fibers of the tendon by the intermediates of the microfibrils.
Cellular and biochemical changes which occurred in the tissues of newborn mice infected with Mokola virus, a rabies-related virus (rhabdovirus group), were described. The virus was transmitted along the peripheral nerves and appeared in various tissues of the body, but did not replicate in any except the nervous system, where it manifested its gross effects. While Mokola virus increased the synthesis of glycogen and total protein in infected brain, liver, lung, spleen and heart, it reduced the activity of monoamine oxidase in the brain. Virus multiplication occurred in the normal rough endoplasmic reticulum. During virus reproduction the membranes of the endoplasmic reticulum, Golgi complex and mitochondria were destroyed and replaced by a viral matrix. Virus maturation also occurred within the rough endoplasmic reticulum.
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