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Biomedical subjects

A Yoshida

Publications and source records attributed to A Yoshida.

At least 757 records · Page 42Linked to original sources
PubMed1990

Effect of food-restriction stress on immune response in mice.

Daily 23-h food deprivation for 1-5 days induced gastric ulcers and atrophic changes of the spleen and thymus, accompanied by a rise in plasma cortisol and catecholamine levels in mice. It also modulated several immune cell functions in the spleen including a drop in the B cell population but no change in the mitogen response of the B cells, an increase in T cell population but no change in the L3T4/Lyt2 ratio and an early increase in natural killer activity and O2- production by macrophages. These effects are thought to correlate to the increase in stress-associated humoral factors and this may partly result from stress induced by food restriction.

Animals↗
PubMed1990

The human class I alcohol dehydrogenase gene cluster: three genes are tandemly organized in an 80-kb-long segment of the genome.

The class I alcohol dehydrogenases (ADH; EC 1.1.1.1) play a key role in hepatic alcohol catabolism. Three human class I ADH genes, ADH1, ADH2, and ADH3, which encode the alpha, beta, and gamma subunits respectively, have been isolated and mapped on chromosome 4q21-q23. Genomic cloning using a cosmid vector allowed us to obtain an 88-kb-long genomic segment, which was found to include an entire 80 kb of the class I ADH gene cluster. All three genes lie in the same transcriptional orientation and the order of genes is 5'-ADH3-ADH2-ADH1-3'. It may be of some significance that the order of transcriptional activation in the hepatic development, alpha----beta----gamma, is opposite to the order of gene arrangement. Several members of the AluI family and the KpnI (L1) family of interspersed repetitive sequences were mapped in this region. The divergence of insertional sites suggested that gene multiplication of the class I ADH genes had taken place in the earlier stages of human (or primate) evolution.

Alcohol Dehydrogenase↗
PubMed1990

Involvement of protein kinase C in the regulation of cortisol production by guinea pig adrenocortical cells.

Cytosol of the guinea pig adrenals was found to contain a protein kinase which was dependent on the presence of both calcium and phospholipids (phosphatidylserine and diolein), i.e., calcium/phospholipid-dependent protein kinase (protein kinase C). The peak of protein kinase C was separated from type II cAMP-dependent protein kinase by DE-52 chromatography. 12-0-Tetradecanoylphorbol-13-acetate (TPA) caused dose-dependent increments of cortisol formation without affecting cAMP formation by guinea pig adrenocortical cells as well as angiotensin II did. TPA-activated cortisol production was blocked by the addition of aminoglutethimide and cycloheximide, suggesting that the site of action of TPA might be located at a point before the production of pregnenolone in the mitochondria. Since TPA showed an increase in the cortisol production, protein kinase C may be involved in modulating steroidogenesis in the guinea pig adrenals in addition to the classical cAMP-dependent protein kinase pathway.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Effects of dietary polychlorinated biphenyls on cholesterol catabolism in rats.

Dietary polychlorinated biphenyls (PCBs) caused hypercholesterolaemia in rats. The concentration and output of biliary cholesterol was significantly lower than that of the control group. Biliary output of total bile acids was significantly decreased in rats given the PCB-supplemented diet. Faecal excretion of total steroids (sum of neutral steroids and acidic steroids) was not significantly changed in rats given the PCB-supplemented diet. The present results indicate that dietary PCBs cause hypercholesterolaemia without modifying the faecal total steroids excretion. These results suggest that PCBs produce hypercholesterolaemia accompanied by changes in biliary or faecal excretion of bile acids and neutral steroids in addition to an increase in hepatic cholesterol synthesis.

Animals↗
PubMed1990

Gastric lesions in rats fed salted food materials commonly eaten by Japanese.

A high intake of salted food is thought to be related to the high incidence of stomach cancer in Japan. In the present study, female F344 rats were divided into four groups. They were fed a nutritionally deficient purified diet (Group 1) and standard purified diet (Group 3) for 113 weeks and the same diets supplemented with salted cuttlefish guts, broiled, salted, dried sardines, pickled radish, and soy sauce (Groups 2 and 4). The incidence of papillomas and ulcers of the forestomach was highest in Group 4, which was given the standard diet supplemented with the salty food materials (p less than 0.05). These results suggest the importance of salted food as a suspicious causal factor in human stomach cancer in Japan.

Animals↗
PubMed1990

Effects of excess dietary tyrosine on cholesterol, bile acid metabolism and mixed-function oxidase system in rats.

Excess dietary tyrosine (12%) caused hypercholesterolemia in male Wistar rats and significantly increased cytochrome P-450 and b5 contents. Bile flow and biliary output of total bile acids were significantly increased in rats fed this diet. Biliary output of cholesterol was not significantly altered, whereas that of taurocholic acid was significantly increased. Excess dietary tyrosine significantly decreased the fecal excretion of neutral steroids, whereas total steroid excretion was not significantly changed. The present results indicate that excess dietary tyrosine causes hypercholesterolemia without modifying the fecal total steroid excretion, thus supporting our previous hypothesis that stimulated synthesis of cholesterol is a main reason why excess dietary tyrosine leads to hypercholesterolemia.

Administration, Oral↗
PubMed1990

Molecular characterization of 1,4-dihydropyridine-sensitive calcium channels of chick heart and skeletal muscle.

A monoclonal antibody designated as MAC-L1 immunoprecipitated [3H]PN200-110-labeled calcium channels of chick cardiac and skeletal muscle. On specific immunoprecipitation of 125I-labeled proteins, two large polypeptides (Mr 197,000 and 139,000 for heart, and 172,000 and 135,000 for skeletal muscle, under reducing conditions) were identified as the major components of these channels. Both polypeptides were found to exist together as a complex in 1% digitonin, but to become separated from each other in 1% Triton X-100. The 197 and 172 kDa peptides of cardiac and skeletal muscles, respectively, were photolabeled with [3H]azidopine. Under nonreducing conditions, the 139 kDa polypeptide of heart and the 135 kDa polypeptide of skeletal muscle took on larger molecular weights of 192,000 and 190,000, respectively. The 139 kDa but not the 197 kDa component of the heart was capable of binding to wheat germ agglutinin-Sepharose. Among the polypeptides specifically precipitated by MAC-L1, a 165 kDa peptide of skeletal muscle was phosphorylated by cAMP-dependent protein kinase. In contrast, a minor 99 kDa polypeptide, but not the major 197 kDa polypeptide, of the heart was phosphorylated by this kinase. These results suggest that the dihydropyridine-sensitive cardiac calcium channel has alpha 1 and alpha 2 subunits that are homologous but not identical to those of the skeletal muscle calcium channel.

Animals↗
PubMed1990

Heterogeneity of antigen molecules recognized by anti-tax1 monoclonal antibody Lt-4 in cell lines bearing human T cell leukemia virus type I and related retroviruses.

Using a monoclonal antibody, Lt-4, directed against human T cell leukemia virus type I (HTLV-I) trans-activator (tax1) antigen, we examined the expression of tax1 and related antigens in a variety of T cell lines bearing HTLV-I and related retroviruses, simian T cell leukemia virus type I (STLV-I) and HTLV-II, by immunofluorescence and immunoblot assays. Lt-4 reacted with all HTLV-I-bearing cell lines tested and five out of eight simian cell lines bearing STLV-I, but not with an HTLV-II-bearing cell line. Lt-4 detected 40 kd tax1 antigen molecules in most HTLV-I-bearing cell lines except one cell line that expressed 39 kd tax1 antigen. In the STLV-I-bearing T cell lines, tax1-related antigen molecules detected by Lt-4 were heterogeneous, having molecular weights in the range of 36-41 kd.

Animals↗
PubMed1990

Development of postpartum spontaneously resolving transient Graves' hyperthyroidism followed immediately by transient hypothyroidism.

A 25-year-old woman with a history of Graves' disease, in remission for 8.5 years following 6 months of methimazole therapy, first came to our attention 5 months after her first delivery with clinical and biochemical hypothyroidism, markedly elevated titre of anti-thyroid microsomal antibody (MCHA; 1:102400) and mildly elevated activity of thyrotropin-binding inhibitory immunoglobulins (TBII; 29.5%). After short-term (3 months) treatment with L-thyroxine therapy, the development of hyperthyroidism in the first trimester of the second pregnancy, which remitted through the second and third trimesters, was observed. TBII showed a peak value (93.1%) 1 month after the onset of hyperthyroidism, and a normal value (12.4%) 6 d after delivery. One month after the second delivery, the patient developed hyperthyroidism, with an elevation of 99mTc thyroid uptake (5.58%; normal range 0.5-2.5%), which was immediately followed by transient clinical and biochemical hypothyroidism. Concomitant increases in MCHA titre and TBII activity were observed after delivery, and both reached peak levels (1:409600 and 81.0%, respectively) one and a half months after the onset of hypothyroidism. Thyroid-stimulating antibody (TSAb), measured using FRTL-5 thyroid cells, was detected at a weakly positive level (161%) on initial examination, and the serial change in TSAb was almost identical to that in TBII. Patients with Graves' disease may develop Graves' type hyperthyroidism, followed immediately by transient hypothyroidism due to coexisting destructive autoimmune thyroiditis during the early postpartum period, despite increasing TSAb activity.

Adult↗
PubMed1990

Arthritis in a human T lymphotropic virus type I (HTLV-I) carrier.

The case is described of a 57 year old woman with polyarthritis fulfilling the 1987 revised criteria of the American Rheumatism Association for rheumatoid arthritis, accompanied by clinical carrier state infection of HTLV-I. Anti-HTLV-I IgM antibodies were detected by western blot analysis in her synovial fluid and serum. Atypical lymphocytes with nuclear convolutions were found in synovial fluid and synovial tissue obtained from the affected knee joint, suggesting in situ activation of HTLV-I infected lymphocytes in the affected synovial compartment. The HTLV-I antigens were detected (1.2%) in short term cultured synovial fluid lymphocytes, by indirect immunofluorescence. These findings supported the possibility that HTLV-I has a role in triggering or modifying inflammation in the synovial compartment.

Arthritis, Rheumatoid↗
PubMed1990

Steroid-responsive sensorineural hearing loss associated with aortitis syndrome.

Five cases of sensorineural hearing loss associated with aortitis syndrome are presented, and their clinical features are discussed in detail. All patients were middle-aged females. Pure-tone audiometry revealed a high-tone gradual-loss type of configuration, and the recruitment phenomenon was proved to be positive in most cases. The degree of hearing loss correlated well with the erythrocyte sedimentation rate. However, the most remarkable clinical feature was that the hearing loss showed steroid responsiveness in all cases. Based on these clinical features, it was suggested that the steroid-responsive sensorineural hearing loss associated with this syndrome might not be an incidental accompanying symptom but rather one of the local manifestations of the disease arising from similar mechanisms as the systemic inflammatory process. Associated conductive disturbance is also discussed.

Adult↗
PubMed1990

The mechanism involved in the conversion of thyrotropin receptor-bound blocking-type immunoglobulin G (IgG) to the stimulating-type by anti-human IgG antibodies.

It has been reported that the addition of antibody (Ab) against human immunoglobulin G (IgG) converts TSH receptor-bound blocking-type IgG to stimulating-type IgG. However, the detail of converting mechanism remains unclear. In this study we examined the mechanism involved in this conversion using FRTL-5 cells. Blocking-type IgG was obtained from a patient with hypothyroidism. FRTL-5 cells were first incubated with IgG solution, then washed with PBS and exposed to antihuman IgG Ab. The effect of antihuman IgG Ab on converting activity was dose dependent. Maximal stimulation of cAMP was achieved with an antiserum dilution of 1:75. It seems likely that antimicrosomal Ab does not interfere with cAMP production, since IgG with a high anti-hemagglutination antibody titer did not show converting activity. Of the several kinds of antibodies tested, Ab against human IgG-Fab fragment was the most effective in converting ability, while the least effective were those against human IgG-Fc fragment. Although the divalent F(ab')2 fragment of antihuman IgG was significantly more effective in its converting ability than the monovalent Fab fragment, the Fab fragment itself also converted blocking IgG to the stimulating type in a dose-dependent manner. Accordingly, receptor cross-linking or aggregation does not play a major role in promoting this converting phenomenon. When cells were first exposed to blocking-type IgG and then to both antihuman IgG Ab and bovine TSH, cAMP production was much greater than the sum of each alone. However, anti-IgG Ab alone did not affect the binding of blocking-type IgG to receptor. These results suggest that the addition of antihuman IgG Ab not only converts blocking-type IgG to the stimulating type but also recovers TSH activity via a postreceptor step. Forskolin, like TSH, showed an additive effect on cAMP stimulatory action with antihuman IgG. In contrast, cholera toxin and antihuman IgG Ab were not additive. The reason for this discrepancy remains unknown. In summary, our observation indicates that 1) the converting phenomenon is induced via IgG-TSH receptor complexes; 2) the mechanism aside from receptor aggregation, i.e. the recognition of a critical domain in TSH receptor molecule, seems necessary for promoting converting phenomenon; and 3) the addition of antihuman IgG Ab affects a postreceptor step via TSH receptor structures that differ from the TSH-binding site.

Adult↗
PubMed1990

Chronic thyroiditis with painful tender thyroid enlargement and transient thyrotoxicosis.

Clinical and laboratory findings and long term outcome (1.5-9 yr) in 7 women and 1 man with chronic thyroiditis (CT) who had painful tender thyroid enlargement were evaluated and compared with those in 11 women with subacute thyroiditis (SAT). Histological features consistent with SAT were not demonstrable, and various forms of CT (fibrous variant, diffuse, or focal lymphocytic thyroiditis) were observed. There were no differences in mean age, duration of symptoms, erythrocyte sedimentation rate, and C-reactive protein values in the 2 diseases. Seven patients had a history of goiter, and none had a history of a preceding upper respiratory tract infection. The mean white blood cell count was significantly lower in CT than in SAT patients. Six CT patients had transient thyrotoxicosis with a marked depression of radioactive iodine uptake. Mean serum T4 and T3 levels and T3 to T4 ratio in these 6 patients did not differ from those in the SAT patients. Five (all with high antimicrosomal antibody titers) of 8 CT patients developed persistent hypothyroidism. In contrast, none of the SAT patients became permanently hypothyroid. TSH binding inhibitory immunoglobulins and thyroid stimulation-blocking antibody at recent examination were negative in these 5 patients. Patients with this disorder present with transient thyrotoxicosis, with a marked depression of the thyroid radioactive iodine uptake, and often develop goitrous or atropic persistent hypothyroidism. This disorder may represent acute exacerbation of an underlying immunological process during the course of CT. To differentiate this syndrome from SAT, thyroid biopsy is necessary.

Adult↗
PubMed1990

Estimation of neuroblast numbers in insect neurogenesis using the lateral inhibition hypothesis of cell differentiation.

Cells in the neurogenic region of an insect ectoderm have two alternative fates, making neurons or epidermis. The fates seem to be determined through a laterally inhibitory interaction among cells. That is, initially homogeneous cells are all competent to differentiate into neuroblasts. Once a cell has differentiated as a neuroblast, it inhibits its immediate neighbors from following this pathway. The differentiation process is simulated by a digital computer in a planar array of polygonal domains similar to a cell pattern. We find that the number of cells differentiating as neuronal precursors in insect neurogenesis is that expected under the hypothesis of lateral inhibition of cell differentiation between immediate neighbors.

Animals↗
PubMed1990

Utility of 2-hydroxypropyl-beta-cyclodextrin in an intramuscular injectable preparation of nimodipine.

Possible utility of hydroxyalkylated beta-cyclodextrin (beta-CyD) derivatives as parenteral drug carriers was investigated, using nimodipine, a dihydropyridine derivative with calcium antagonistic action, as a model drug. The aqueous solubility of nimodipine increased linearly with increase in the concentration of hydroxyalkylated beta-CyDs, showing an AL-type phase solubility diagram. The stability constant of nimodipine--hydroxyalkylated beta-CyD complexes was in the order of 2,3-dihydroxypropyl-beta-CyD less than beta-CyD less than 2-hydroxyethyl-beta-CyD less than 3-hydroxypropyl-beta-CyD less than 2-hydroxypropyl-beta-CyD, and the solubilizing ability of the beta-CyDs was also in that order. The results of powder X-ray diffractometry and thermal analysis suggested 1:3 (guest:host) complex formation of nimodipine with 2-hydroxypropyl-beta-CyD in the solid state. The dissolution rate of nimodipine-2-hydroxypropyl-beta-CyD complex was much faster than that of the drug alone. Nimodipine-2-hydroxypropyl-beta-CyD complex gave higher plasma levels of the drug after intramuscular administration to rabbits, i.e., the area under the plasma concentration--time curve and the maximum plasma concentration of the complex were about 2.5 times higher than those of the drug alone. The muscular damage after the injection of nimodipine was reduced by the administration of the complexed form.

2-Hydroxypropyl-beta-cyclodextrin↗
PubMed1990

111In monoclonal antimyosin antibody imaging: imaging of myocardial infarction and myocarditis.

A new scintigraphic method to detect myocardial necrosis has been developed using antimyosin monoclonal antibody Fab labeled with indium-111. Using this method, we studied 35 patients with myocardial infarction, 5 patients with myocarditis and 3 patients with angina pectoris. 111In antimyosin Fab was administered intravenously and antimyosin images were recorded by planar and single photon emission computed tomography (SPECT) 48 hours after injection. Planar images showed discrete localization of 111In antimyosin in 25 of 26 patients within 14 days after the onset of acute myocardial infarction. In 14 of these patients creatine kinase, glutamic oxaloacetic transaminase and lactic dehydrogenase had already normalized. Positive scans were also obtained in 6 of 12 patients between the third week to the ninth year after the onset of the disease. Three patients with acute myocarditis had positive scans 2 and 4 weeks after the onset of the disease. Thus, 111In antimyosin imaging may be a useful noninvasive method for the diagnosis of coronary diseases and myocarditis. Although the mechanism of persistent positive antimyosin images in the chronic stage remains to be clarified, 111In antimyosin scintigraphy holds potential promise as a non-invasive method for the detection of myocardial injury in the subacute to chronic stage as well as in the acute stage.

Adult↗
PubMed1990

[Interaction of CN-100, a novel non-steroidal anti-inflammatory drug, on biopolymers].

Interaction of CN-100, a novel non-steroidal anti-inflammatory drug, with biopolymers were investigated. In collagen induced rat platelet aggregation, the inhibitory effect of CN-100 was almost equipotent as indomethacin (IM) but less potent than that of pranoprofen (PP). The effect of CN-100 on rat platelet aggregation induced by arachidonic acid (AA) was less potent than that of IM and PP. CN-100 inhibited rat platelet functions, serotonin release and malondialdehyde formation, induced by collagen more potently than those induced by AA. In heat-induced rat erythrocyte lysis and Ca2(+)-induced liposome aggregation, the inhibitory effect of CN-100 was less potent than IM but more than those of PP. CN-100 was inhibited with heat denaturation of BSA, and the effect was more potent than IM and PP. The metachromagy based on the binding of an azodye, HABA, to BSA was potentiated weakly by CN-100, but IM had no effect on it. CN-100 and IM increased the fluorescence of the binding of dansyl amide (site I probe) to BSA. These results support that there is considerable interaction between CN-100 and membrane protein, and this effect influences the membrane to increase its stability.

Anti-Inflammatory Agents, Non-Steroidal↗