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Biomedical subjects

M Katsumata

Publications and source records attributed to M Katsumata.

At least 73 records · Page 4Linked to original sources
PubMed1990

Influence of a high ambient temperature and administration of clenbuterol on body composition in rats.

This study was conducted to determine the effects of the oral administration of the beta agonist clenbuterol on body composition in growing rats reared under a high ambient temperature. Forty-three male Wistar-strain rats of 5 weeks of age were divided into 6 groups: 2 levels of ambient temperature (26 and 33 degrees C) and 3 dose levels of clenbuterol (0, 50, and 100 micrograms/kg diet) under each ambient temperature. All rats were raised for 7 weeks. From the 3rd week, rats in the clenbuterol-treated groups were fed a diet containing clenbuterol. Both the lipid and cholesterol content in the rat liver, and the epididymal adipose tissue weight were significantly higher in the hot environment than in the temperature environment. Body fat component was significantly higher in rats in the 33 degrees C groups in comparison with that in rats in the 26 degrees C groups. On the other hand, body protein component was significantly lower in the 33 degrees C groups than in the 26 degrees C groups. Although the administration of clenbuterol significantly decreased fat and increased protein in the 26 degrees C groups, no particular influence of clenbuterol administration on body composition was observed in the 33 degrees C groups.

Administration, Oral↗
PubMed1990

Rhabdomyomatous mesenchymal hamartoma of skin.

A 4-year-old boy was seen at the Kanto Teishin Hospital because of a lesion present at birth. Examination revealed a round, soft, soybean-sized, pedunculated nodule on the midline anterior neck region. Histologically, the most conspicuous aberration was the presence of bundles of striated skeletal muscle fibers throughout the dermis. This nodule was diagnosed as rhabdomyomatous mesenchymal hamartoma of skin, a name first given by Mills. We believe this is the first report of this condition in Japan.

Child, Preschool↗
PubMed1990

Methemoglobinemia with oxidized hemoglobins and modified hemoglobins found in bloods of workers handling aromatic compounds and in those of a man who drank cresol solution.

We found that half-oxidized hemoglobins such as (alpha 2+ beta 3+)2 and (alpha 3+ beta 2+)2, and methemoglobin were significantly increased in the erythrocytes of workers handling chemical compounds in a chemical plant of Japan. In addition, we found two unusual anodic hemoglobins (hemoglobin X and hemoglobin Y) to be present to a large extent in the erythrocytes of the workers investigated (21 persons), using isoelectric focusing electrophoresis on polyacrylamide gel plates. For example, the hemoglobin analysis of a worker showed: hemoglobin X, 6.2%; hemoglobin Y, 26.8%; hemoglobin A + hemoglobin F, 54.5%, half-oxidized hemoglobins, 9.8%; methemoglobin, 1.5%; hemoglobin A2, 2%. Since contents of hemoglobin A decreased by more than 40% of normal levels, and those of oxidized and modified hemoglobins increased up to 40% of total hemoglobins in the erythrocytes of several workers in the plant, we may consider these cases as ones having toxic methemoglobinemia with oxidized and modified hemoglobins. The changes of intracellular hemoglobins in these cases may be due to oxidation and modification of the proteins by chemical compounds absorbed from skin and lungs. Therefore, these hemoglobins may be a good indicator to monitor the health of workers in chemical plants. We also studied the formation mechanism of modified hemoglobins such as hemoglobin X and hemoglobin Y, investigating the reactions of hemoglobin with various aromatic compounds in vitro. On the other hand, we had the opportunity to analyze the changes in oxidized hemoglobins and modified hemoglobins in the blood of a man who drank cresol solution to commit suicide and was sent to a hospital.(ABSTRACT TRUNCATED AT 250 WORDS)

Cresols↗
PubMed1989

Clear cell hidradenoma with whorl formation of squamoid cells: immunohistochemical and electron microscopic studies.

Many groups of squamoid cells arranged in whorls were found in a case of clear cell hidradenoma. These cells showed positive staining for carcinoembryonic antigen, but S-100 protein was not detected. Electron microscopic examination showed considerable amounts of tonofilaments, but neither keratohyalin granules nor multivesicular dense bodies were present in these cells. These features suggest that the constituting cells of whorls differentiated toward the eccrine ductal cells, in particular the intraepidermal ductal cells.

Adenoma, Sweat Gland↗
PubMed1989

Follicular cyst derived from hair matrix and outer root sheath.

A new follicular cyst was reported. The lower part of the cyst wall was composed of both basophilic and shadow cells as seen in pilomatricoma, whereas the upper part of the wall consisted of clear cells. Our case apparently derives from hair matrix and outer root sheath.

Child↗
PubMed1988

John Lattimer lecture. Lipokinins: novel phospholipase A2 activators mediate testosterone effects on embryonic genitalia.

Testosterone-treated calf thymocytes produce increased amounts of proteins, termed lipokinins, that stimulate phospholipase A2 from snake venom and mammalian tissue. The induction of these proteins by testosterone is blocked by cycloheximide and, thus, requires new protein synthesis. These proteins activate phospholipase A2 stoichiometrically. They are inactivated by boiling, trypsin or alkaline phosphatase but not by deoxyribonuclease or ribonuclease. Lipokinins significantly repair the failure of masculinization in the Tfm mouse with an X-linked deficiency of androgen-receptor. Thus, the post-receptor effects of testosterone on embryonic genitalia may be mediated through stimulation of phospholipase A2 by lipokinins. Moreover, lipokinins may be involved as stimulators of the arachidonic acid cascade, as lipocortins are inhibitors.

Animals↗
PubMed1988

Organization of chromosomes in the mouse nucleus: analysis by in situ hybridization.

We used in situ hybridization with various biotinylated DNA probes to characterize the distribution of mouse chromosomes in the nucleus. This entailed an examination of plasmid-marked chromosomes from two strains of transgenic mice and also an examination of the distribution of centromeres and total mouse genomic DNA. Our results show that, regardless of the hybridization probes used or the tissue types examined, with sections of mouse tissues embedded in paraffin all chromosomal DNA appeared to be localized to the nuclear periphery. This was observed in tissues fixed with either crosslinking or non-crosslinking fixatives, and submitted to a variety of prehybridization treatments. Further experiments with non-embedded nuclei fractionated from mouse liver revealed a similar distribution of DNA at the telomeric end of chromosome 3, but for centromeric DNA and total mouse genomic DNA, hybridization signals were observed both in the interior and at the periphery of the nucleus. These observations preclude the exclusive localization of chromosomes to the nuclear periphery. However, they indicate that a subset of centromeres are likely to be associated with the nuclear membrane, and that there is such an association at the telomeric end of chromosome 3. Overall, these results are compatible with previous observations of other investigators showing regions of contact between chromosomes and the nuclear membrane.

Animals↗
PubMed1987

Elevated glucocorticoid receptor levels in lymphocytes of children with the fetal hydantoin syndrome (FHS).

Our recent studies of the teratogenic mechanisms of phenytoin (DPH) and glucocorticoids in mice have indicated that DPH utilizes the anti-inflammatory pathway of glucocorticoids in producing congenital defects, such as cleft palate. This pathway is influenced by H-2 and H-3 histocompatibility-linked genes in the mouse, such that congenic strains have H-2 or H-3 alleles that confer susceptibility to DPH-induced congenital defects, and susceptible H-2 congenic strains have high glucocorticoid receptor levels. However, other H-2 or H-3 alleles confer resistance to these defects in their otherwise genetically identical congenic partner strains, and "resistant" H-2 alleles are associated with low levels of these receptors. To determine whether this animal work is applicable to the human, we have sought to investigate whether the level of glucocorticoid receptors in circulating lymphocytes of children with the fetal hydantoin syndrome (FHS) is as it is in the animals. We found that children with FHS had glucocorticoid receptor levels significantly elevated above those of unaffected children with similar DPH exposure in control families. The receptor level of affected children was also significantly elevated above that of fathers of children with the FHS and of fathers and mothers of control children. These findings are consistent with those documented in the animal models and suggest that an elevated level of glucocorticoid receptors in lymphocytes may be a marker for susceptibility to the FHS syndrome.

Abnormalities, Drug-Induced↗
PubMed1986

A rapid assay for activity of phospholipase A2 using radioactive substrate.

A rapid method for the assay of phospholipase A2 has been developed using a radioactive substrate, L-alpha-dipalmitoyl-(2-[9,10(N)-3H]palmitoyl)-phosphatidylcholine. The substrate diluted with cold carrier (1 mM) is dissolved in 80% ethanol containing 25 mM sodium deoxycholate. The enzymatic reaction is performed in 1.0 ml 0.1 M glycine-NaOH buffer, pH 9.0, containing 2 mumol CaCl2, 10 micrograms bovine serum albumin, 2.5 mumol sodium deoxycholate, 0.01 unit (or less) phospholipase A2, and 40-100 nmol substrate. The enzymatic reaction is terminated by adding 0.2 ml 5% Triton X-100 solution containing 40 mumol EDTA. The product of the enzymatic reaction, radioactive palmitic acid, is extracted by 10 ml hexane containing 0.1% acetic acid in the presence of anhydrous sodium sulfate (0.5 g/ml). Activity of phospholipase A2 is directly determined from the radioactivity in the hexane extract. The present method achieves a quick separation of the radioactive product, [3H]palmitic acid, from the radioactive substrate, L-alpha-dipalmitoyl-(2-[3H]palmitoyl)-phosphatidylcholine, without the need of separation by TLC.

1-Propanol↗
PubMed1986

Murine glucocorticoid receptors: new evidence for a discrete receptor influenced by H-2.

The glucocorticoid receptor contents in the lungs of females of two congenic strains of mice, B10.A (H-2a) and B10 (H-2b), differing only in the H-2 histocompatibility region of chromosome 17, have been measured by the dextran-charcoal method and by our previously described methods of molecular sieving and ion exchange chromatography [M. Katsumata, C. Gupta, and A. S. Goldman (1985) Arch. Biochem. Biophys. 243, 385-395]. As reported, two receptors, II and IB, are demonstrable by each column chromatographic method, and 5,5-diphenylhydantoin binds to receptor IB but not to receptor II. Receptor IB cannot be detected unless molybdate is added in cytosols prepared with hypotonic buffer [10 mM 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid and 10 mM dithiothreitol, pH 7.35) according to S. L. Liu, J. F. Grippo, R. P. Erickson, and W. B. Pratt (1984) J. Steroid Biochem. 21, 633-637], a method which has been reported to give maximal receptor levels. Using hypotonic buffer containing 10 mM molybdate we observed a small but significantly higher content of receptor IB in B10.A mice than that in B10 mice, but no significant difference in receptor II or total receptor content. On the other hand, cytosols prepared with isotonic buffer (50 mM Tris-HCl, 120 mM NaCl, 1 mM EDTA, 10 mM dithiothreitol, and 10 mM molybdate, a modification of the buffer used in our previous report) contained significantly higher levels of receptor IB and of total binding in pulmonary cytosols of B10.A as compared to those of B10. There was no difference in receptor II content. Molybdate stabilizes receptor IB in both buffers. These results explain the apparent contradiction between our results and those of Liu et al. by showing that the hypotonic buffer used by them allows for determination of maximal levels of receptor II, but permits selective destruction of receptor IB. However, the use of isotonic buffer gives maximal values of both receptors II and IB. With isotonic buffer, it is demonstrated that only the level of receptor IB is influenced by H-2-linked genes.

Animals↗
PubMed1985

Involvement of central catecholamines in mediation of pressor responses of the rat to carotid occlusion.

Carotid occlusion evoked a pressor response in rats after transection of the spinal cord. Intraventricular pretreatment with 6-hydroxydopamine inhibited the pressor response. The pressor response to occlusion was also diminished by the intraventricular but not by the intravenous injection of guanethidine. Intravenous atropine or mecamylamine, or intraventricular captopril did not affect the pressor response. Thus, it appears that central catecholaminergic mechanisms are involved in the mediation of the pressor response to carotid occlusion.

Animals↗
PubMed1985

Glucocorticoid receptor IB: mediator of anti-inflammatory and teratogenic functions of both glucocorticoids and phenytoin.

We studied the glucocorticoid receptor complexes of pulmonary and thymic cytosols of female A/J and CD-1 mice and of hepatoma G2 cells by two column-chromatographic systems, using both [3H]dexamethasone (DEX) and [3H]phenytoin (DPH) as ligands. Three DNA-cellulose adsorbable [3H]DEX-receptor complexes were separated in each system. Molecular sieving gave a 7-, a 5.4-, and a 3.5-nm complex (Stokes radii), and DEAE-Sephadex A-50 chromatography gave a complex eluting in the wash, one at 0.14 M KCl, and one at 0.20 M KCl by a KCl gradient. DPH blocked the binding of the 7- and 3.5-nm, wash, and 0.14 M KCl [3H]DEX complexes. Only two DNA-cellulose adsorbable [3H]DPH complexes, each blocked by DEX, were obtained in each system: a 7- and a 3.5-nm, a wash, and a 0.14 M KCl complex. Thus, there is a common receptor for both DPH and DEX. This receptor has two properties which distinguish it from the 5.4-nm DEX-specific receptor: (i) it binds with a variety of steroids other than glucocorticoids and DPH, and (ii) it rebinds new [3H]DEX or [3H]DPH after loss of ligand during chromatographic separation. These results indicate that DPH binds to receptor IB and not to receptor II of Litwack. [G. Litwack, 1976, in Glutathion: Metabolism and Function (Arias, I.M., and Jakoby, W.B., eds.), pp. 285-299, Raven Press, New York]. We have also found that hepatoma G2 cells have only receptor II. DPH affects neither the induction of tyrosine aminotransferase by DEX nor the basal level of this enzyme in these cells. Moreover, neither DEX nor DPH inhibits the release of [3H]arachidonic acid prelabeled in these cells, as they do in thymocytes which have the common receptor. Thus, it appears that glucocorticoid receptor IB binds DEX and DPH as glucocorticoid agonists mediating the anti-inflammatory and teratogenic action of these drugs, while receptor II apparently is responsible for the induction of tyrosine aminotransferase by DEX.

Animals↗
PubMed1985

Production of monozygotic twins following the transfer of bisected embryos in the goats.

Embryos at the morula, blastocyst and hatched blastocyst stage were obtained from superovulated and naturally ovulated Japanese native goats. They were bisected into halves with a glass needle, and transferred immediately or after culture (for morula) to recipients. None of five does which received bisected morula became pregnant. Three of nine goats became pregnant after transfer of bisected hatched blastocysts, six of eleven recipients became pregnant. Four of them produced monozygotic twins and the remaining two produced singles. The present study demonstrated that the hatched blastocyst is suitable for bisection in the goat.

Journal Article↗
PubMed1985

Further studies on vasopressin-induced pressor responses to kainic acid injected into the nucleus tractus solitarii of the rat.

Kainic acid, an analogue of L-glutamate, was microinjected into the nucleus tractus solitarii of cordotomized rats. Kainic acid (30 ng) injected bilaterally into the nucleus elicited hypertension. The pressor response to kainic acid was restricted to sites in the intermediate one-third of the nucleus tractus solitarii. Plasma vasopressin levels were markedly increased during the kainic acid-induced pressor response. Intravenous injection of atropine sulphate or mecamylamine, or intraventricular injection of captopril did not affect the pressor response. It is concluded that in cordotomized rats the pressor response to kainic acid injected into the nucleus tractus solitarii is mainly mediated via increased release of vasopressin. It seems unlikely that the central cholinergic and angiotensin mechanisms are mainly responsible for the response to kainic acid.

Animals↗
PubMed1985

H-2 histocompatibility region influences the inhibition of arachidonic acid cascade by dexamethasone and phenytoin in mouse embryonic palates.

We have reported that susceptibility to glucocorticoid- and phenytoin-induced cleft palate and glucocorticoid receptor levels in mice are influenced by the H-2 histocompatibility complex on chromosome 17. Phenytoin competes with glucocorticoids for the glucocorticoid receptor and inhibits production of prostaglandins and thromboxanes. In this paper, we have investigated whether glucocorticoids and phenytoin inhibit arachidonic acid release and prostaglandin biosynthesis directly in the embryonic palates and whether the H-2 gene complex influences the degree of inhibition. Using congenic strains varying only in the H-2 region, we demonstrate here that both glucocorticoids and phenytoin inhibit the release of 3H-arachidonic acid and prostaglandin biosynthesis from embryonic palatal tissue, prelabeled with 3H-arachidonic acid. The degree of inhibition of arachidonic acid release and of prostaglandin biosynthesis is greater in the strain with H-2a (A/Wy) than in its corresponding congenic partner H-2b (A.BY). Thus, these results provide further evidence for a similar genetic and biochemical pathway for the teratogenic action of both phenytoin and glucocorticoids.

Abnormalities, Drug-Induced↗