Experimental study of the reactions p-barp--> pi - pi + and K-K+ between 360 and 760 MeV/c.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Y Fujii.
Explore the source record for details and available documents.
The uptake of Na(+)-dependent D-glucose by renal brush-border membrane vesicles (BBMV) isolated from streptozotocin-induced diabetic rats was decreased as compared with controls. Since a Vmax of 4.8 nmol/mg protein per 30 s in diabetic BBMV was significantly decreased as compared with that of controls (Vmax = 7.0 nmol/mg protein per 30 s) without changing an apparent affinity for D-glucose, the decrease in the Na(+)-dependent D-glucose uptake in diabetic rats is likely to be due to the reduction in the number of the transporter. These results are also confirmed by the binding study of [3H]phlorizin to diabetic BBMV. When the blood glucose level is lowered in diabetic rats by both the treatment with insulin and starvation, the decreased Na(+)-dependent D-glucose uptake is returned to control level. These results suggest that Na(+)-dependent D-glucose reabsorption through the apical membrane in proximal tubular kidney cells is dynamically regulated by the change in blood glucose level.
In the normal thymus the number of lymphocytes and the proportion of CD4+CD8+ double-positive cells decrease as a function of age. Six thymomas in elderly patients without myasthenia gravis had a large number of double-positive T cells, as seen in the normal thymic cortex. This suggests that the epithelial cells of thymoma have the function of cortical epithelium and can induce precursor T cells to differentiate to the double-positive stage but not further. In seven thymomas with associated myasthenia gravis, however, there was a conspicuous population of mature single-positive T lymphocytes. These mature T cells may include autoreactive T cells.
Prostaglandin (PG)E2 9-ketoreductase, which catalyzes the conversion of PGE2 to PGF2 alpha, was purified from human brain to apparent homogeneity. The molecular weight, isoelectric point, optimum pH, Km value for PGE2, and turnover number were 34,000, 8.2, 6.5-7.5, 1.0 mM, and 7.6 min-1, respectively. Among PGs tested, the enzyme also catalyzed the reduction of other PGs such as PGA2, PGE1, and 13,14-dihydro-15-keto PGF2 alpha, but not that of PGD2, 11 beta-PGE2, PGH2, PGJ2, or delta 12-PGJ2. The reaction product formed from PGE2 was identified as PGF2 alpha by TLC combined with HPLC. This enzyme, as is the case for carbonyl reductase, was NADPH-dependent, preferred carbonyl compounds such as 9,10-phenanthrenequinone and menadione as substrates, and was sensitive to indomethacin, ethacrynic acid, and Cibacron blue 3G-A. The reduction of PGE2 was competitively inhibited by 9,10-phenanthrenequinone, which is a good substrate of this enzyme, indicating that the enzyme catalyzed the reduction of both substrates at the same active site. These results suggest that PGE2 9-ketoreductase, which belongs to the family of carbonyl reductases, contributes to the enzymatic formation of PGF2 alpha in human brain.
Primary cultured mouse hepatocytes were treated with clofibric acid to induce peroxisome proliferation. They were briefly fixed with paraformaldehyde and centrifuged to prepare pellets. The hepatocytes were split open to remove cytoplasmic soluble proteins and fixed with glutaraldehyde. They were routinely incubated for catalase enzyme cytochemistry and fixed in osmium tetroxide. The specimens were quickly frozen, deeply etched and rotary shadowed by platinum and carbon. Peroxisomes were identified as osmium reaction products on replica membranes. In treated hepatocytes, the number of peroxisomes was considerably increased and smooth membranous structures resembling sER (referred to as 'peroxisome-forming sheets') showed hypertrophy. The rER associated with intermediate filaments was significantly decreased and 'peroxisome-forming sheets' appeared, being accompanied with budding and fragmentation of peroxisomes.
In order to enhance general reactivity of immune system in the tumor-bearing host, we employed extract of Cordyceps sinensis (CSE) as a biological response modifier. Cordyceps sinensis is an interesting material produced by a kind of mushroom parasitic to larval moths and was used to hasten recovery from exhaustion in ancient China. In this experiment, C57BL/6 mice implanted subcutaneously with syngeneic EL-4 lymphoma cells were employed as the host. Oral administration of the extract leads to a reduction of tumor size and prolongation of the host survival time. As judged by plaque-forming cells against T-dependent (sheep erythrocytes) and T-independent (bacterial lipopolysaccharide) antigens, CSE showed to augment the antibody responses. As for the activities of peritoneal macrophages, chemotaxis was dramatically depressed within a few days after EL-4 transplantation up to the end of life, but treatment with CSE at -14, -7, -4, +4, +7 and +10 days after the tumor transplantation augmented the activity about four times stronger than that of control. Phagocytic activity of macrophages was also decreased in tumor-bearing mice treated with cyclophosphamide (100 mg/kg) 3 and 5 days after tumor transplantation. But administration of CSE restored the activity to more than the normal level. The overall efficacy of CSE was tested with protective activity against systemic infection by Salmonella enteritides. The tumor-bearing mice receiving this medicine lived significantly longer than any other groups without CSE.
To investigate the mechanism of the inhibitory effects of interferon-gamma (IFN-gamma) on bone resorption, the effects of murine IFN-gamma on 45Ca release from prelabeled fetal mouse forearm bones were investigated. Murine IFN-gamma usually did not affect basal 45Ca release but almost completely and equipotently inhibited bone resorption induced by PTH(1-34), PTH-rP(1-34), 1,25(OH)2D3, and interleukin 1 (IL-1). The half-maximal concentration for inhibition of bone resorption induced by IL-1 alpha was 25.8 +/- 14.6 U/ml (mean +/- SD for 13 experiments), which is not different from those for PTH, PTH-rP, and 1,25(OH)2D3. There was no correlation between prostaglandin E2 concentration in the conditioned medium and 45Ca release from the IFN-gamma-treated forearm bones. The inhibitory effect of IFN-gamma on bone resorption induced by PTH-rP (1-34) or IL-1 alpha continued during 6 days of culture, whereas that of calcitonin disappeared after 2 days of culture. These findings suggest that IFN-gamma non-preferentially inhibits bone resorption induced by various bone-resorbing factors in fetal mouse forearm bones via a PGE2-independent mechanism. As no escape phenomenon developed in IFN-gamma-treated bones, the cytokine may be potentially useful for treatment of certain patients with malignancy-associated hypercalcemia.
A 36-year-old housewife complained of a tight feeling in the pharynx with increasing dysphagia, dyspnea, and mild fever. Chest roentgenogram was interpreted as a cystic mass in the middle mediastinum. Computed tomography showed a cystic mass compressing the carina and the esophagus. Ten days after onset, symptoms were suddenly relieved followed by a tarry stool. The chest mass shadow decreased. Esophagofiberscopy showed two fistulas communicating with a cyst that had two chambers. Thoracotomy performed 40 days after onset showed a true duplication of the esophagus with rupture into the esophagus. This is a rare case in which it was possible to observe the sequence of events of a ruptured intramural duplication cyst by means of chest roentgenography, computed tomography, esophagofiberscopy, and cystogram.
Clostridium perfringens alpha toxin caused contraction of the isolated rat ileum in a dose-dependent manner. The contraction caused by the toxin was inhibited by verapamil, nifedipine, cinnarizine, but not by tetrodotoxin or incubation in a low Na+ medium. The toxin stimulated Ca2+ uptake in the ileum in a dose-dependent manner. Nifedipine completely inhibited the Ca2+ uptake into the ileum induced by the toxin. Furthermore, TMB-8, trifluoperazine, W-7 and H-7 significantly blocked the toxin-induced contraction. On the other hand, the toxin activated de novo production of phosphatidic acid and phosphatidylinositol in the tissue. These data suggest that the toxin-induced contraction is due to an increased Ca2+ permeability across the tissue, and activation of phospholipid metabolism.
ML-1 human myeloblastic leukemia cells are induced to differentiate to monocytes by conditioned medium (CM) derived from tetradecanoylphorbol acetate (TPA)-treated ML-1 cells. Antibodies to tumor necrosis factor (TNF) inhibited the differentiation-stimulating activity of CM, indicating that this activity is due to the presence of TNF in CM. TNF added to non-conditioned medium was as effective as CM in stimulating ML-1 cell differentiation. In the presence of a low (0.12 ng/ml) concentration of TPA, TNF-induced maturation was synergistically increased and Type I macrophages were formed. With higher (1-10 ng/ml) TPA concentrations, Type II macrophages were also obtained. As the TNF/TPA concentration increased, ML-1 cell differentiation was increasingly inhibited. Mature cells derived from ML-1 cells were found to secrete TNF at concentrations ranging from less than 2 U/ml to greater than 180 U/ml, the amount depending upon the number of cells and the stage of cell maturation. These results indicate that TNF participates in the regulation of precursor cell maturation. Low concentrations of TNF produced by small numbers of mature cells stimulate differentiation, whereas high concentrations of TNF generated by elevated numbers of macrophages inhibit the maturation process, possibly in combination with other cytokines. Because TNF serves as a competence factor for ML-1 cells, (Guan X.-P., Takuma T., Hromchak R. & Bloch A. (1990) Competence and progression in cell differentiation. Proc. Am. Assoc. Cancer Res. 31, 28.), the TNF-induced stimulation of differentiation depends additionally on the action of serum-contained differentiation-specific progression factors.
Responses of canine lymphoid tissues to mitogens were studied in five normal dogs and in two dogs with acquired myasthenia gravis (MG). In the normal dogs, lymph-node-derived lymphocytes gave the most consistent proliferative responses to concanavalin A (Con A), phytohemagglutinin (PHA), and pokeweed mitogen (PWM), as determined by thymidine incorporation; and in most cases PHA, lipopolysaccharide (LPS), and PWM stimulated total IgG production, as determined by ELISA. Splenic lymphocytes had the greatest capacity for increased total IgG production. In the myasthenic dogs total IgG production by unstimulated lymph-node-derived lymphocytes was 88 micrograms/ml and 153 micrograms/ml, much higher than that of unstimulated normal dog lymphocytes (mean less than 1.0 microgram/ml). All mitogens resulted in suppression rather than stimulation of IgG production by lymphocytes from dogs with MG. Production of antibodies to acetylcholine receptors (AChRs) was detected in the supernatants of lymphocyte cultures from one of the dogs with MG at a rate of 78 fmol/5 x 10(5) cells per week and was not detected in culture supernatants of control dogs. This study demonstrates that lymph nodes may be an important site of antibody production in myasthenic dogs and provides the necessary groundwork for future studies of the cellular immunology of canine MG.
The balloon catheter technique is being utilized in various intravascular procedures and transluminal angioplasty, but the type of morphological changes which take place in intracranial vessels after balloon inflation and dilatation are still unknown. This study reports on morphological changes in normal canine basilar arteries after transluminal angioplasty (TA) with 1.5 Atmospheres of inflation pressure and 30% dilatation. Histological changes 1 h after TA consisted of denudation of endothelial cells, deposition of fibrin which covered the denuded endothelium, stretching and focal dehiscence of internal elastic lamina and altered myocytes in media. These morphological changes were more prominent when the balloon was inflated longer. Seven days after TA, however, the endothelium had been regenerated almost completely, while slight chronic changes still remained in the internal elastic lamina and media. Angiographical and morphometrical analyses did not disclose any significant differences. This report proposes that under some conditions intra-arterial inflation and dilatation of the intracranial arteries causes reversible changes, which are noted mainly in the endothelium. In addition, a new in vivo experimental model which could be of use for physiological or pathophysiological investigations of intracranial arteries is introduced.
A micro high-performance liquid chromatographic (micro-HPLC) procedure for the assay of digitoxin tablets and deslanoside injections has been developed. Micro-HPLC is performed on an ODS micro column, with acetonitrile-methanol-water (10:20:17) for digitoxin tablets and acetonitrile-water (21:70) for deslanoside injections. The effluent is monitored by UV absorption at 220 nm. Quantitation of cardiac glycosides in tablets and injections is carried out by the internal standard method. The composite assay results for digitoxin tablets and deslanoside injections provide average values of 101.2 and 99.9% with standard deviations of 1.2 and 0.93%, respectively. This micro-HPLC method is sensitive, quantitative, and reproducible. It is suitable for use in examining the content uniformity of pharmaceutical preparations.
To identify cortical and subcortical structures in the brain which are associated with septic encephalopathy, local cerebral glucose utilization (LCGU) in the 31 discrete regions were evaluated with a quantitative (14C)-2.deoxyglucose autoradiographic method in the septic rat model. Sepsis was produced by cecal ligation and punctures. Forty rats were subjected to behavioral study and divided into two groups (control, n = 15; sepsis, n = 25). Septic rats died within 36 h, and the rats developed behavioral depression, and showed EEG slowing and an increase in pain threshold. The latter was evaluated by a tail flick method within 8 h after the surgical procedures, while control rats did not show significant change in either behaviors or pain threshold. In another study, LCGU was measured when behavioral depression, increase in pain threshold, and EEG slowing developed in the sepsis group (n = 7). In this group, the mean LCGU in auditory and parietal cortices, lateral geniculate, superior colliculus, hippocampus, and locus ceruleus was 95, 74, 67, 69, 72, and 53 mumol.100 g-1.min-1, being lower by 23%, 22%, 18%, 19%, 14%, and 27% than that in the sham-operated control group (n = 7), respectively. However, the mean LCGU in septal and raphe nuclei was 52 and 84 mumol.100 g-1.min-1, being significantly higher by 27% and 33% than that in the control group, respectively. These results suggest that septic encephalopathy is associated with metabolic changes in the discrete brain regions, which are related to the serotonergic or noradrenergic system.
Fiber types in human extraocular muscle (h-EOM) were examined immunohistochemically with antibodies against slow tonic (anti-ALD) and slow twitch (anti-SOL) myosins. Four types of muscle fiber in h-EOM were distinguishable according to their reactivities with these antibodies. Groups 1 and 2 fibers reacted with both antibodies, group 1 fibers showing stronger reactivity than group 2 fibers with anti-ALD. Group 3 fibers reacted only with anti-SOL. Group 4 fibers did not react with either antibody. The latter were the most common, and were the main fibers in both the peripheral (outer orbital) and central zones of h-EOM. The next most common were group 1 fibers, which were located mainly in the peripheral layer. Group 2 fibers were less common, but were the second most common type in the central layer. Group 3 fibers were only minor constituents. Multiple innervations were observed in some fibers of groups 1 and 2, and group 1 fibers were suggested to be slow tonic myofibers in h-EOM. These specific immunohistochemical and physiological features of h-EOM seem to be the basis of the low morbidity seen in the usual types of muscular dystrophy.
Sustained exposure to aldosterone (Aldo) increases the abundance and activity of the Na-K pump in cortical collecting tubules (CCT). However, the onset and mechanism of the early interaction of Aldo with the CCT pump, especially in adrenal-intact animals, are unclear. We evaluated the short-term effects of the hormone on Na-K-adenosinetriphosphatase (ATPase) activity and on ouabain-sensitive 86Rb uptake, a measure of the transporting rate of the pump, in microdissected CCT from adrenal-intact rats. Incubation with Aldo (10(-8) M, 2 h) had no effect on Na-K-ATPase activity (Vmax), whereas it produced at least a twofold increase in 86Rb uptake. This effect was generated by physiological concentrations of the hormone (threshold 10(-10) M; apparent K1/2 approximately 10(-9) M), after a short lag of less than or equal to 30 min. Incubation with Aldo in the presence of amiloride or nystatin or in a Na-free medium (choline chloride) did not prevent the enhanced 86Rb uptake seen after Aldo alone; possible interpretations of these observations are discussed. We conclude that Aldo produces a rapid stimulation of pump function in CCT that precedes its induction of new pump synthesis; the physiological significance of this effect is suggested by its occurrence in tubules from adrenal-intact animals within the time frame and concentration range of the hormone's effects on electrolyte transport.
Etiology and pathogenesis of focal and segmental glomerulosclerosis (FSGS) in patients with toxemia of pregnancy remain controversial. We examined 15 preeclamptic patients presenting with nephrotic syndrome. None of the patients had urinary abnormalities and hypertension before pregnancy. Clinically, proteinuria first developed during pregnancy and disappeared completely in all but one patient lost to follow-up after 1-30 months from delivery. Renal dysfunction, hypertension and edema rapidly resolved in the postpartum period. None of the patients had a progressive clinical course. Renal biopsy specimens obtained postpartum revealed typical features of preeclamptic nephropathy. In addition, findings compatible with FSGS were observed in 13 patients including 4 in which such lesions were unearthed by additional serial sectioning. These results indicate that FSGS may not only be induced by preeclampsia but also be one of the representative glomerular changes in preeclamptic patients with nephrotic syndrome. A favorable clinical course ensues in a manner similar to that of patients with the garden - variety of preeclampsia.
The 4-methoxy-5-methylpyrano[4,3-b]indole-1,3(4H,5H)-dione (9), prepared from methyl 3-methoxycarbonyl-1-methylindol-2-yl acetate (6), underwent a strong base-induced cycloaddition reaction with 2-chloro-6,6-ethylenedioxy-5,6,7,8-tetrahydro-1,4-naphthoquinone (11) to give the tetrahydronaphtho[2,3-b]carbazole-7,12-dione (10), regioselectively. The cycloadduct (10) was successfully converted to a D-ring indole analogue of daunomycin (1a).