[Lumbosacral radiation myeloneuropathy. Report of a case and effects of prednisolone treatment].
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Adult↗
Biomedical subjects
M Iwata
Publications and source records attributed to M Iwata.
[Vibration hazards in quarry workers].
Vibration hazards were surveyed in a population of quarry workers using chipping hammers and to a lesser extent, rock drills. Sixty-nine male quarry workers, aged 49.1 +/- 8.7 and exposed to vibration for 16.4 +/- 5.1 years, were surveyed in 1981-82. They were exposed to vibration for about 2-4 hours per days, mainly under a piece-work pay system. They had a high prevalence of Raynaud's phenomenon (36.2%) and numbness in upper extremities (53.6%). It is considered that the high prevalence was mainly due to large vibration levels in chipping hammers and rock drills and long daily exposure time. The attacks of Raynaud's phenomenon were found predominantly in the left hand, which held chisels, whereas the restriction of motion in the elbow was predominantly in the right arm which pushed chipping hammers. The same 49 male quarry workers in this population were also surveyed in 1976-77 and the prevalence of their complaints between 1976-77 and 1981-82 was compared. The prevalence of Raynaud's phenomenon was the same, but the frequency of the attacks increased between the two periods. The prevalence of other complaints such as numbness, pain and chills in the upper extremities also increased. Between 1976-77 and 1981-82, the prevalence of Raynaud's phenomenon, numbness, and pain in the upper extremities increased in the population of quarriers exposed to vibration for above 2.6 hours per day and 200 days per year, or 600 hours per year. On the other hand, the prevalence of these complaints mostly decreased in the population of quarriers with less exposure.
Adult↗
[Symposium: cooperation between the professional medical facility and regional health care agencies in the care of patients with refractory diseases].
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Chronic Disease↗
Characterization of sea-urchin fibronectin.
Sea-urchin fibronectin from the ovary of the sea urchin Pseudocentrotus depressus bound to gelatin, fibrin and fibrinogen. After mild digestion of the protein labelled with 125I, a 195 000 Da domain was observed. Sea-urchin fibronectin was aggregated by spermine (1 mM) at neutral pH. When the concentration of spermine was decreased or increased, the aggregation was diminished. The addition of 1 M-NaCl or 4 M-urea inhibited the spermine-induced aggregation. Sea-urchin fibronectin mediated the spreading of baby-hamster kidney cells on the plastic surface.
Animals↗
Relaxation of isolated rabbit veins mediated by latent histamine H2-receptors.
Isolated rabbit veins preconstricted by either norepinephrine, methoxamine or potassium were relaxed by histamine in the presence of mepyramine, a histamine H1-antagonist. The relaxation was not antagonized by atropine, propranolol and indomethacin but by an H2-antagonist cimetidine. It is likely that histamine relaxes the rabbit veins through H2-receptors.
Animals↗
Kinetic aspects and mechanism of liposome disintegration in polyoxyethylene lauryl ether and sodium cholate solutions.
The disintegration behaviour of liposomes in polyoxyethylene lauryl ether (PLE) and sodium cholate solutions was studied by the turbidity disappearance method. In maximally solubilized systems of liposomes, the molar ratios (phosphatidylcholine/surfactant) were 0.43 and 1.8 for PLE and sodium cholate, respectively. The disintegration process of either unilamellar or multilamellar liposomes followed first-order kinetics. Based on a physical model in which liposomes heterogeneous in size were assumed to disintegrate from the outermost shell one by one, a mathematical expression of the turbidity disappearance rate was introduced and applied to explain the data thus obtained. Model calculations suggested that the number of disintegrated shells would not be so large, even if up to 50% reduction of the initial turbidity was observed. From the dependence of the pseudo-first-order rate constant (kobs) on the surfactant concentration for unilamellar liposomes, it was assumed in general that kobs consists of the contributions of the monomer and micellar fractions: for PLE, both fractions shared in the disintegration, but only the micellar fraction with sodium cholate. Furthermore, in the latter case, kobs depended on the initial liposome concentration. These results are likely to be consistent with the proposed modes of surfactant action classified as type A and type B (Helenius, A. and Simons, K. (1975) Biochim. Biophys. Acta 415, 29-79).
Cholic Acid↗
A study on biological monitoring of n-hexane exposure.
n-Hexane is one of the solvents widely used in industry and well known to be neurotoxic. Recently it was clearly revealed that n-hexane is metabolized in vivo and its metabolites are excreted in the urine. However, the relationship between the exposed dose of n-hexane and the metabolites in the urine has not yet been substantially determined. Therefore, in this investigation we intended to clarify the above relationship in order to establish its usefulness for biological monitoring of n-hexane exposure. The exposed dose was measured by means of a personal monitoring badge worn by workers in seven factories manufacturing vinyl sandals. The time-weighted average (TWA) concentration of n-hexane was 0.2-47.4 ppm. The n-hexane metabolites in the urine of 22 workers were measured with modified Perbellini's method [12] in the early morning (6:00-7:00 hrs) and at 17:00 hrs. 2,5-Dimethylfuran, 2,5-hexanedione and gamma-valerolactone were identified by gas chromatography and mass spectrometory. At 17:00 hrs the means +/- SD of the metabolites were 0.21 +/- 0.11 mg/l for 2,5-dimethylfuran, 1.13 +/- 0.71 mg/l for 2,5-hexanedione, and 2.04 +/- 2.31 mg/l for gamma-valerolactone. The metabolites were also found in the urine in the early morning. 2-Hexanol was not detected in the urine of any worker examined. A strong correlation between TWA concentration of n-hexane and 2,5-hexanedione in the urine was found at 17:00 hrs (r = 0.895, P less than 0.001). The results suggest that the urinary metabolites of n-hexane, especially 2,5-hexanedione, could be useful indicators for biological monitoring of n-hexane exposure. Furthermore the present study offers the advantage of a better estimate of n-hexane TWA.
Adolescent↗
Changes of n-hexane metabolites in urine of rats exposed to various concentrations of n-hexane and to its mixture with toluene or MEK.
It is well known that n-hexane produces peripheral neuropathy, and 2,5-hexanedione, one of the metabolites of n-hexane, is thought to be the main causative agent. Recently, the metabolites of n-hexane in urine have been measured by gas chromatography, and 2,5-hexanedione was proved to be useful for the biological monitoring of n-hexane exposure. In the present experiment, we intended to clarify the change of n-hexane metabolites in the urine of rats exposed to various concentrations of n-hexane and to its mixture with toluene of MEK. In the first experiment, five separate groups of five rats each were exposed to 100, 500, 1000, or 3000 ppm of n-hexane, or fresh air respectively in an exposure chamber for 8 h a day. Urinary samples were gathered during exposure, 16, 24, and 40 h after exposure. Half of each sample was analyzed by gas chromatography after hydrolysis with acid and enzymes, and the other half was analyzed without hydrolysis. 2,5-Dimethylfuran, MBK, 2-hexanol, 2,5-hexanedione, and gamma-valerolactone could be identified as n-hexane metabolites in the urine. The main metabolites were 2-hexanol and 2,5-hexanedione. 2-Hexanol was mostly excreted during exposure, while most of the 2,5-hexanedione was excreted after the end of exposure. The amount of metabolites in the urine correlatively increased with the concentration of n-hexane from 100 to 1000 ppm, but the amount of metabolites scarcely increased when the concentration of n-hexane increased from 1000 to 3000 ppm.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
An experimental study of the combined effects of n-hexane and methyl ethyl ketone.
This study was intended to determine whether or not methyl ethyl ketone (MEK) enhances the neurotoxicity of n-hexane at low concentration and after long term exposure. Separate groups of eight rats were exposed to 100 ppm n-hexane, 200 ppm MEK, 100 ppm n-hexane plus 200 ppm MEK, or fresh air in an exposure chamber for 12 hours a day for 24 weeks. The body weight, motor nerve conduction velocity (MCV), distal motor latency (DL), and mixed nerve conduction velocities (MNCVs) were measured before exposure and after four, eight, 12, 16, 20, and 24 weeks' exposure. One rat of each group was histopathologically examined after 24 weeks' exposure. Exposure of 100 ppm n-hexane did not significantly decrease the functions of the peripheral nerve throughout the experiment. Exposure to 200 ppm MEK significantly increased MCV and MNCVs and decreased DL after four weeks' exposure, but at this later stage no significant changes were found throughout the experiment by comparison with the controls. Mixed exposure to 100 ppm n-hexane plus 200 ppm MEK significantly decreased by comparison with the controls. On histopathological examination of the tail nerve, however, no changes were found in any of the exposed groups or the controls. These results suggest that MEK might enhance the neurotoxicity of n-hexane at a low concentration, and mixed exposures to n-hexane and MEK should be avoided.
Animals↗
Detection and characterization of polymers in cephalothin by passive cutaneous anaphylaxis in mice.
Immunization of BALB/c mice by repeated injections of cephalothin (CET) - Ascaris suum extract conjugate resulted in formation of IgE antibodies, which were able to sensitize syngeneic animals for passive cutaneous anaphylaxis (PCA). By means of high-pressure liquid chromatography, a fraction with extremely high PCA-eliciting activity, but without appreciable antimicrobial activity, was isolated from the CET preparation. Physicochemical analyses of the fraction identified the major component of polymer impurities as being a proteinaceous complex with a molecular weight of 6,580. Very little cross-reactivity of CET and potassium benzyl penicillin (PcG) was noted when these antibiotics were used as the challenge antigens for PCA induced by corresponding murine antisera. The results of the inhibition studies indicated, however, that at least two antigens were involved in the PCA induced by anti-CET antibodies, one strictly specific for CET and another shared by PcG. Evidence was also presented that the nucleus structure and acyl side-chain structure of CET play the major role in the PCA elicited by the challenge with CET and its polymer, respectively.
Animals↗
[Carcinogenicity study of cholestyramine in rats].
Carcinogenicity study on cholestyramine, an anti-hypercholesterolemic agent, was carried out using Fischer rats by feeding with a normal pellet diet (control) and with three sorts of the pellet diets in which cholestyramine was admixed in the common diet at the rates of 1.25, 2.5 and 5%, respectively. The animals were fed with these diets for 26 months and a normal diet for subsequent 2 months. Some of the male rats fed with the 5% admixed diet revealed a slight growth retardation and occasionally hemorrhagic tendency, without resulting in severe macroscopic and microscopic lesions of the internal organs and in shortening of the mean survival time as compared with that of the control group. The rates of tumor-bearing animals were high in all experimental groups including the control, but the rates were not considered to be drug-related. Incidences of individual tumors were not significantly different each other between cholestyramine-fed groups and control group. Thus, it was not recognized that cholestyramine induced any drug-related specific tumors and an accelerated growth of any tumors.
Animals↗
[Chronic toxicity study of ranitidine hydrochloride orally administered in rats].
Chronic toxicity of ranitidine hydrochloride, a new histamine H2-receptor antagonist, was studied using Sprague Dawley rats. Ranitidine was administered orally at dose levels of 30, 100, 300 and 1000 mg/kg/day for 26 or 53 weeks. In the 1000 mg/kg/day group, ten of 31 females died showing acute toxic signs. In the survived animals of this dose group, changes were observed, such as salivation, depression of body weight gain, increase in water consumption, increase in urinary Na and K excretion, increase in serum albumin content, increase in weights of the liver, kidneys and heart. Main histopathological findings were as follows: centrolobular or midzonal fat deposition in liver, increase in s-ER in hepatocytes, increase in foamy cells in lung and some slight degenerative changes occasionally seen in renal tubules. In the 300 mg/kg/day group, the changes similar to those in the 1000 mg/kg/day group were observed, however, the degree of these changes was more moderate. All of the above-mentioned findings were demonstrated to be reversible in recovery period for 8 weeks. In the 100 and 30 mg/kg/day groups, no remarkable changes were observed in both sexes. It was concluded that the maximum nontoxic dose of ranitidine hydrochloride was 100 mg/kg/day in male and female rats.
Administration, Oral↗
A nationwide survey on organic solvent components in various solvent products: Part 1. Homogeneous products such as thinners, degreasers and reagents.
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Chromatography, Gas↗
Studies on a new nucleoside antibiotic, dapiramicin. I. Producing organism, assay method and fermentation.
A new antibiotic, dapiramicin, has been isolated from the fermentation broth of Micromonospora sp. SF-1917. Since the dapiramicin exhibited essentially no in vitro activity by usual bioassays, two assay methods for dapiramicin were developed, HPLC and a new bioassay by growth inhibition of fungal mycelia on a slide glass. Fermentation of dapiramicin is also described.
Antifungal Agents↗
Role of lipomodulin, a phospholipase inhibitory protein, in immunoregulation by thymocytes.
The treatment of murine thymocytes with anti-lipomodulin antibody during Con A stimulation causes selective loss of suppressor activity, but not of helper activity on PFC assay, when co-cultured with T cell-depleted spleen cells. Interaction of the antibody with responder cells in thymocyte culture were necessary in the early stage rather than in the later stage of lymphocyte activation by Con A, which suggests that anti-lipomodulin antibody acts in the stage of suppressor T cells generation. When thymocytes were cultured with purified lipomodulin for 48 hr, suppressor activity was induced. Lipomodulin as detected by radioimmunoassay was found to be released from T cells with the phenotype of I-J+, Lyt-1-, Lyt-2+. The immunoprecipitates from the media of Con A-stimulated thymocyte with anti-I-Kk antibody and anti-lipomodulin antibody were analyzed on SDS-gel electrophoresis. I-J products had m.w. 36,000 and 24,000, whereas lipomodulin had m.w. 36,000, 24,000, and 15,000. Because anti-I-Jk antibody could precipitate 125I-labeled lipomodulin purified from rabbit neutrophils, these results suggest that lipomodulin is a product of I-J genes that induces suppressor T cells.
Animals↗
Modulation of the biologic activities of IgE-binding factors. III. Switching of a T cell hybrid clone from the formation of IgE-suppressive factor to the formation of IgE-potentiating factor.
Incubation of rat-mouse T cell hybridoma cells, 23B6, with rat immunoglobulin E (IgE) results in the formation of the 15,000-dalton IgE-suppressive factor and the 30,000-dalton IgE-binding factor, which has neither potentiating activity nor suppressive activity on the IgE response. Another T cell hybridoma, 23A4 cells, produces the 30,000-dalton "inactive" IgE-binding factor upon incubation with IgE. Both the 15,000-dalton IgE-suppressive factor and the 30,000-dalton IgE-binding factor lacked affinity for lentil lectin but bound to peanut agglutinin. When the 23B6 cells were incubated with IgE in the presence of lysolecithin, the majority of the 15,000-dalton IgE-binding factor formed by the cells gained affinity for lentil lectin, and this factor selectively potentiated the IgE response. The glycosylation-enhancing factor, which was formed by stimulation of normal spleen cells with lymphocytosis-promoting factor (LPF or pertussigen), also switched 23B6 cells from the formation of IgE-suppressive factor to the formation of IgE-potentiating factor. It was also found that the 30,000-dalton "inactive" IgE-binding factor, formed by both 23B6 and 23A4 cells, gained the ability to potentiate the IgE response, when the cells were cultured with IgE in the presence of glycosylation-enhancing factor. The results indicate that IgE-potentiating factor and IgE-suppressive factor share common precursors, and that biologic activities of IgE-binding factors are decided by their carbohydrate moieties. Incubation of the two hybridoma cells with lysolecithin or glycosylation-enhancing factor results in an increase in the proportion of FC epsilon R+ cells, suggesting that the assembly of N-linked oligosaccharide to precursor molecules is intrinsic for the expression of FC epsilon R.
Animals↗
[People active in the ALSSOA. Amyotrophic Lateral Sclerosis Society of America].
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Amyotrophic Lateral Sclerosis↗
Modulation of the biologic activities of IgE-binding factor. IV. Identification of glycosylation-enhancing factor as a kallikrein-like enzyme.
Stimulation of normal rat splenic T cells with pertussigen (lymphocytosis-promoting factor, LPF, from Bordetella pertussis) resulted in the release of a soluble factor that enhanced the glycosylation of IgE-binding factors during their biosynthesis. The soluble factor was detected by the ability of a culture filtrate of LPF-stimulated spleen cells to switch a T cell hybridoma, 23A4, from the formation of unglycosylated IgE-binding factor to the formation of glycosylated IgE-binding factor. The glycosylation-enhancing factor (GEF) had affinity for D-galactose, and the binding of the factor to hybridoma cells via a cell surface galactose was essential for modulation of IgE-binding factors. The GEF was inactivated by irreversible inhibitors of serine proteases such as phenylmethylsulfonyl fluoride, diisopropylfluorophosphate, and p-nitrophenyl ethylpentylphosphonate but was not affected by nonphosphorylating analogues of the organophosphorus compounds. Benzamidine, a competitive and reversible inhibitor of trypsin, also inhibited the glycosylation of IgE-binding factors by GEF. The factor could be purified by absorption to p-aminobenzamidine agarose followed by elution with benzamidine. The capacity of GEF to enhance the glycosylation of IgE-binding factors was inhibited by synthetic substrates of trypsin but not by substrates of chymotrypsin, indicating that GEF is a trypsin-like enzyme. Indeed, trypsin, plasmin, and kallikrein enhanced the glycosylation of IgE-binding factors during their biosynthesis. An inhibitor of trypsin-like enzyme(s), N-alpha-p-tosyl-L-lysine chloromethylketone (TLCK), inhibited trypsin and plasmin but not kallikrein, and TLCK failed to inhibit the GEF-mediated enhancement of glycosylation. It was also found that bradykinin, the biologically active product of cleavage of kininogen by kallikrein, enhanced the glycosylation of IgE-binding factors. The results indicate that GEF is a kallikrein-like enzyme.
Animals↗