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Biomedical subjects

S Okada

Publications and source records attributed to S Okada.

At least 1,153 records · Page 64Linked to original sources

[A case of vesical malacoplakia diagnosed by randomized biopsy of the urinary bladder].

Vesical malacoplakia is a relatively rare disease and commonly diagnosed by characteristic cystoscopical findings and histological determination using biopsy specimen. We report here a case of a 53-year-old housewife, with atypical cystoscopical findings, which looked like carcinoma in situ, and in which randomized biopsy helped to make the final diagnosis. This case was successfully controlled by anti-bacterial agents.

Biopsy↗

Glycosaminoglycan-free small proteoglycan core protein is secreted by fibroblasts from a patient with a syndrome resembling progeroid.

A male patient, 4 years 9 mo old and having progeroidal appearance, exhibited delayed mental development and multiple abnormalities of connective tissues including growth failure, osteopenia of all and dysplasia of some bones, defective deciduous teeth, loose but elastic skin, delayed wound healing with formation of thin atrophic scars, scanty scalp hair, hypotonic muscles, and hypermobile joints. Skin fibroblasts of the patient converted only about half of the core protein of the small proteodermatan sulfate to a mature glycosaminoglycan chain-bearing proteoglycan. The remaining core protein, which contained complex-type asparagine-bound oligosaccharides, was secreted with almost normal kinetics. Xylosyltransferase activity and the synthesis of other proteoglycan types were normal. Normal induction of glycosaminoglycan synthesis occurred in the presence of 1 mM, but there was very little induction in the presence of 0.01 mM p-nitrophenyl-beta-xyloside. An antibody against an N-terminal pentadecapeptide of the core protein recognized the glycosaminoglycan-free core protein from the patient less well than the chain-bearing protein treated with chondroitin ABC lyase. Though these results do not define the basic defect unambiguously, they provide the first report of a disorder being due to an abnormality in small proteoglycan biosynthesis.

Abnormalities, Multiple↗

Calmodulin activates adenylate cyclase from rat anterior pituitary.

Bovine brain calmodulin activated adenylate cyclase in calmodulin-deficient rat anterior pituitary membranes. This activation appeared to be specific by the following criteria: 1) calmodulin activation was Ca2+ dependent and responded biphasically to calcium, displaying activation at low and inhibition at higher concentrations; 2) calmidazolium, a potent calmodulin antagonist, inhibited calmodulin activation of adenylate cyclase; 3) activation of the enzyme occurred in a dose-dependent manner, at calmodulin concentrations normally found in most cells (1- to 20-microM range). However, this response was not saturated using calmodulin concentrations as high as 50 microM. The data suggest that endogenous calmodulin can be dissociated from normal anterior pituitary adenylate cyclase, that the enzyme can be subsequently stimulated by addition of micromolar concentrations of calmodulin, and that this enzyme appears to be at least 50-fold less sensitive to calmodulin than is the brain adenylate cyclase.

Adenylyl Cyclases↗

Methylation of the c-myc gene changes during aging process of mice.

The degree of methylation at c-myc proto-oncogene was found to change during aging process of mice by the use of methylation-sensitive restriction enzymes. The spleen DNA showed hypomethylation as mice aged, while hypermethylation was observed in the liver DNA. The brain DNA on the contrary revealed no appreciable difference between young and old mice. When the DNAs were examined at actin and dihydrofolate reductase (DHFR), no significant change was observed. It suggests that an age-related change of oncogene structure may be one of the factors which are related to an age-associated increase of cancer incidence rate.

Actins↗

Treatment of NZB/NZW mice with total lymphoid irradiation: long-lasting suppression of disease without generalized immune suppression.

We used total lymphoid irradiation (TLI; total dose = 3400 rad) to treat the lupus-like renal disease of 6-mo-old female NZB/NZW mice. Similar to our past studies, this treatment resulted in a marked prolongation of survival, decrease in proteinuria, and decrease in serum anti-DNA antibodies compared with untreated littermate controls. Although there was no evidence of disease recurrence in TLI-treated mice until after 12 mo of age, the in vitro proliferative response to phytohemagglutinin by NZB/NZW spleen cells recovered within 6 wk such that responses were greater than control NZB/NZW animals. A similar recovery and overshoot after TLI were evident in the primary antibody response to the T cell-dependent antigen sheep red blood cells (SRBC). Both the total and IgG anti-SRBC antibody responses after TLI were greater than those of untreated NZB/NZW controls, and were comparable with those of untreated non-autoimmune mice. Despite this increased response to mitogens and antigens after TLI, we noted a decrease in spontaneous splenic IgG-secreting cells and a decrease in IgG but not IgM antinuclear antibody production. Nonspecific suppressor cells of the mixed leukocyte response were detectable in the spleens of NZB/NZW mice early after TLI. However, the disappearance of suppressor cells was not associated with recrudescence of disease activity. Furthermore, transfer of large numbers of spleen cells from TLI-treated NZB/NZW mice did not result in disease suppression in untreated age-matched recipients. In summary, treatment of NZB/NZW mice with TLI results in a prolonged remission in autoimmune disease, which is achieved in the absence of generalized immunosuppression.

Animals↗

Difference in mode of inhibition between alpha-D-xylosyl beta-D-fructoside and alpha-isomaltosyl beta-D-fructoside in synthesis of glucan by Streptococcus mutans D-glucosyltransferase.

Both alpha-isomaltosyl beta-D-fructoside and alpha-D-xylosyl beta-D-fructoside show strong inhibition of the synthesis of water-insoluble and water-soluble D-glucans from sucrose by a partially purified preparation of a D-glucosyltransferase (GTase) from Streptococcus mutans 6715; however, the inhibitory modes differ substantially. In the presence of alpha-isomaltosyl beta-D-fructoside, the production of reducing sugars and the consumption of sucrose are remarkably enhanced, compared with a control of sucrose alone. Under these conditions, a large proportion of low-molecular-weight glycan (lmwg) and a series of nonreducing oligosaccharides (both containing D-fructosyl groups or residues) are produced. In contrast, in the presence of alpha-D-xylosyl beta-D-fructoside, the production of reducing sugars and the sucrose consumption are strikingly suppressed, and no lmwg or oligosaccharides are produced. Thus, it may be concluded that alpha-isomaltosyl beta-D-fructoside acts as an alternative acceptor for the D-glucosyl and/or D-glucanosyl transfer reactions of the enzyme, and serves to lessen the formation of insoluble and soluble D-glucan, although it stimulates the transferring activity of the enzyme. On the other hand, alpha-D-xylosyl beta-D-fructoside competitively inhibits the sucrose-splitting activity of the enzyme as an analog to sucrose, and thereby diminishes the synthesis of D-glucan.

Disaccharides↗

Quantitative fluorographic detection of 3H and 14C on two-dimensional thin-layer chromatographic sheets by an ultra-high-sensitivity TV camera system.

A method for quantitative detection of 3H and 14C on thin layers is described. After impregnation of the TLC sheet with 50% 2,5-diphenyloxazole-tetrahydrofuran, quantitative imaging of the distribution of weak beta-ray-emitting isotopes on the chromatogram was carried out at room temperature by using a TV camera system, which consisted of a two-stage microchannel plate image intensifier, a low-lag vidicon, and an image processor. The method is applicable for 14C- and 3H-labeled samples on TLC sheets (10 X 10 cm) emitting more than 0.17 and 7.5 Bq/mm2, respectively. The method is rapid and has a dynamic range far greater than that of film.

Autoradiography↗

Lysis of the glomerular basement membrane in children with IgA nephropathy and Henoch-Shönlein nephritis.

An electron-microscopic study of the glomerular basement membrane was made on 242 renal biopsies from 222 children with a variety of renal diseases. Lysis of the basement membrane was observed in 16 of the 25 children with Henoch-Schönlein nephritis, 36 of the 72 with IgA nephropathy and one with acute poststreptococcal glomerulonephritis. Lysis was frequently associated with subepithelial dense deposits and polymorphonuclear leukocytes, and these are thought to play a role in the lytic process. There was a significant correlation between the presence of lysis of the basement membrane, the degree of proteinuria and the severity of glomerular changes by light microscopy. These findings suggest that the degree of lysis is an indication of the severity of the disease and lysis is associated with progressive disease and a worse prognosis in Henoch-Schönlein nephritis and IgA nephropathy.

Adolescent↗

Pathological study on a severe sialidosis (alpha-neuraminidase deficiency).

A 56-day-old infant with alpha-neuraminidase deficiency, whose clinical features included severe edema of extremities and ascites which resembled those in severe infantile sialidosis, was autopsied. Perforation, whose pathogenesis was unclear, was found on the descending portion of the duodenum. Light and electron microscope studies showed that neurons in the cerebral and cerebellar corticies, and the thoracic spinal cord contained membrane-bound vacuoles but no membranous cytoplasmic bodies. Zebra bodies were found only in the neurons of the spinal cord. The neurons in the paraganglion and in the Auerbach's myenteric plexus were also distended with numerous membrane-bound vacuoles. Hepatocytes, endothelial cells and Kupffer cells in the liver and glomerular and tubular epithelial cells in the kidney were swollen with a number of vacuoles, although the patient showed none of the clinical features of renal involvement. These pathological changes were similar to those in nephrosialidosis reported by Le Sec et al. [Arch Fr Pediatr 35:819-829 (1978)].

Cerebral Cortex↗

Presence of glycoproteins containing the polylactosamine structure in brain and liver of GM1 gangliosidosis patients. Comparative study between clinical types I and II, using endo-beta-galactosidase enzyme.

The material derived from defective degradation of glycoproteins, which accumulates in brain and liver of a patient with GM1 gangliosidosis type I, was investigated, and the structure of the main storage compounds determined. For comparison, brain and liver of a patient with GM1 gangliosidosis type II were also analyzed. Analysis of the glycopeptides obtained after pronase digestion of the defatted residue indicates the storage of glycoprotein-like material in type I, but not in type II. Treatment with endo-beta-galactosidase showed that the stored material contained N-acetyllactosamine repeating units. Two major oligosaccharides, OS I and OS II, were isolated after the enzyme treatment, whose structures are: GlcNAc beta 1----3 Gal (OS I) and Gal beta l----4GlcNAc beta 1----3 Gal (OS II). Treatment with exo-beta-galactosidase transformed the trisaccharide OS II into the disaccharide OS I, indicating that the deficiency of beta-galactosidase in GM1 gangliosidosis type I, but not in type II, also affects glycoprotein catabolism, leading to the accumulation of glycopeptides containing terminal beta-galactosyl residues and N-acetyllactosamine repeating units. These results indicate the severe impairment in the catabolism of glycoconjugates with beta-linked galactose in type I, although this impairment is not as pronounced in type II.

Brain Chemistry↗

Enhancement of in vitro ribonucleic acid synthesis on chromium(III)-bound chromatin.

Z chromatin-chromium (Cr) complex, prepared from mouse liver chromatin and CrCl3, showed a significantly enhanced template activity for in vitro RNA synthesis. Digestion experiments with this complex using micrococcal nuclease and DNase I suggested that Cr(III) preferentially binds to linker regions rather than core regions of chromatin. Further, it was found that Cr(III) binds to DNA and nonhistone proteins (NHP), but hardly to histones. Moreover, the template activity of an NHP-Cr complex, when added to a DNA-histones complex, was inhibited remarkably. The template activity of the chromatin-Cr complex was not significantly altered by proteinase K digestion. Furthermore, experiments using rifampicin and [gamma-32P]guanosine 5'-triphosphate (GTP) demonstrated an increase in the number of initiation sites in the chromatin-Cr complex. These results suggest that, in this in vitro system, Cr(III) preferentially binds to DNA in chromatin and causes an increase in the number of initiation sites, thus enhancing RNA synthesis.

Animals↗

Increment of prostaglandin E2 in association with elevation of urinary sodium excretion following lead administration.

Lead administered to semi-fasted rats caused an elevation of urinary sodium excretion but no increase of urinary potassium excretion as previously observed in fasted rats. Moreover, in this experiment it was found that urinary and serum prostaglandin E2 (PG E2) contents were increased in association with the elevation of urinary sodium excretion by lead and that natriuresis was suppressed by indomethacine treatment. These findings suggest a stimulation of prostaglandin synthetase rather than to a suppression of the renin-angiotensin-aldosterone system as a primary reaction caused by the lead administration.

Administration, Oral↗

Two cases of intratemporal facial nerve neurilemmomas.

The patients with neurilemmomas of the facial nerve within the temporal bone were treated. Although most of cases of the facial nerve neurilemmoma in the temporal bone present with a facial palsy, a few cases have normal facial nerve function and are especially difficult to diagnose preoperatively because of few symptoms. Case 1, a 31-year-old man, developed progressive left facial palsy with protrusion of the posterior wall of the external auditory meatus over a five-month period. Case 2, a 64-year-old man, complained of only fullness and tinnitus of the right ear without any facial nerve symptoms. Polytomography of the temporal bone demonstrated no abnormal findings in both cases. However, computed tomography revealed a soft-tissue density area in the left mastoid cavity with destruction of the posterior wall of the external auditory meatus in case 1. A similar soft-tissue density mass was found in the right tympanic cavity in case 2, suggesting the presence of the tumor in the temporal bone. At operation, the tumors were found to originate from the vertical portion of the facial nerve in both cases. It was assumed that normally existing dehiscences of fallopian canal might account for why some patients have normal facial nerve function.

Adult↗

Action of the protease from Streptomyces cellulosae on L-Leu-Gly.

The protease from Streptomyces cellulosae preferentially catalyzed the formation of (L-Leu-Gly)2 (P1) and (L-Leu-Gly)3 (P2) in highly concentrated solutions of L-Leu-Gly, although it weakly hydrolyzed the substrate at the same time. The formation of P1, P2, L-Leu, and Gly was studied at various pH values, temperatures, and substrate concentrations. The initial velocities (v1, v2, and vH) of formation of P1, P2, and L-Leu (or Gly) and the sum (v1T) of v1 and v2 were determined. The effects of pH and temperature on v1, v2, vH, and v1T were examined at a fixed substrate concentration. The optimum pH and optimum temperature for each of the processes forming P1, P2, L-Leu, and Gly were 8.0 and 65 degrees C, respectively. In the study on the effect of substrate concentration, the plots of the initial velocities versus substrate concentrations were sigmoidal at lower substrate concentrations. The dependence of v1T on the substrate concentration could be explained by a mechanism involving a single active center forming the peptide bonds and two substrate-binding sites located on the left sites (S1 and S2) and the right sites (S1' and S2') of the active center of this enzyme.

Catalysis↗

Effect of clonidine on insulin secretion: a case report.

We have recently seen a case of non-insulin-dependent diabetes mellitus with hypertension in which chronic treatment with oral clonidine gave rise to elevation of blood glucose and decreased insulin secretion. When the response of insulin secretion to glucose administration during clonidine therapy was compared with that after 12 days of wash-out for clonidine in this patient (who was then receiving phentolamine mesylate), there was a marked suppression of insulin secretion to stimulation by intravenous glucose during oral clonidine therapy. This result indicates that the decreased insulin secretion associated with oral clonidine therapy is very unlikely to be due to any direct action of clonidine on beta cells of the pancreatic islets and may be due to suppression of catecholamine release via central alpha-adrenergic receptor stimulation.

Blood Glucose↗