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H Murase

Publications and source records attributed to H Murase.

At least 19 recordsLinked to original sources
PubMed1999

Helicobacter pylori water extract induces interleukin-8 production by gastric epithelial cells.

In Helicobacter pylori-associated gastric mucosal injury, interleukin (IL) -8, a potent leukocyte chemoattractant, is produced by epithelial cells infected by H. pylori and directs neutrophils to the gastric mucosa. According to previous studies, the IL-8 production requires direct contact between the bacteria and epithelial cells. The aims of the present study were to determine whether an H. pylori water extract (HPE) induces IL-8 production by gastric epithelial cells and to characterize IL-8-inducing substances in HPE. Extracts were prepared from a standard strain and from strains obtained from patients with gastric ulcers. After addition of HPE to MKN 45 cells, a gastric cancer cell line, IL-8 in supernatants and IL-8 mRNA were measured by immunoassay and reverse transcription-polymerase chain reaction, respectively. For characterization, active fractions obtained by gel filtration of standard-strain HPE were treated by heating or trypsinization. To study the signal pathway leading to IL-8 production, inhibitors for protein kinase A (PKA), protein kinase C (PKC), or protein tyrosine kinase (PTK) were incubated with MKN45 cells before HPE stimulation. HPE from the standard strain and one of these clinical strains induced IL-8 production. Lipopolysaccharide or cagA in the strains showed no correlation with IL-8 concentration. Standard-strain HPE induced IL-8 mRNA expression in MKN 45 cells. Gel filtration localized activity to a low-molecular-weight fraction of about 7 kDa, which was resistant to heat and trypsin digestion. PKC inhibitors significantly blocked HPE-induced IL-8 production by MKN 45 cells; however, the PKA inhibitor or PTK inhibitors showed a partial inhibitory effect. HPE contains a nonprotein substance of low molecular weight that is responsible for IL-8 induction in gastric epithelial cells. This induction is mainly dependent on the activation of PKC but partially also dependent on PKA or PTK.

Cells, Cultured↗
PubMed1998

Antioxidant activity of a novel vitamin E derivative, 2-(alpha-D glucopyranosyl)methyl-2,5,7,8-tetramethylchroman-6-ol.

A novel vitamin E derivative, 2-(alpha-D-glucopyranosyl)methyl-2,5,7,8-tetramethylchroman-6-ol (TMG), has excellent water-solubility (> 1 x 10[3] mg/ml). The antioxidant activity of TMG was investigated. Kinetic studies of the inhibition of radical-chain reaction of methyl linoleate in solution demonstrated that the peroxyl radical-scavenging activity was not changed by the replacement of phytiyl side chain of vitamin E to glucosyl group. TMG acted as an effective inhibitor on lipid peroxidation of egg yolk phosphatidylcholine (PC)-liposomal suspension induced by a water-soluble and a lipid-soluble radical generator, 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) and 2,2'-azobis(2,4-dimethylvaleronitrile) (AMVN). Its effectiveness was higher than that of ascorbic acid (AsA) when liposomal suspension was exposed to a lipid-soluble radical generator, AMVN. TMG also showed an excellent antioxidant activity on cupric ion-induced lipid peroxidation of PC-liposomal suspension, and suppressed the oxidation of rat brain homogenate which contained trace level of iron ion. On the other hand, AsA acted as a prooxidant on both the cupric ion-induced liposomal peroxidation and the oxidation of rat brain homogenate. When human plasma was exposed to either AAPH or AMVN, the accumulation of cholesteryl ester hydroperoxides was retarded by the addition of TMG.

Adult↗
PubMed1998

In vivo and in vitro effects of AVP and V1a receptor antagonist on Cushing's syndrome due to ACTH-independent bilateral macronodular adrenocortical hyperplasia.

We examined the possibility that AVP and V1a receptors were involved in regulating cortisol production in a 49 year old man with ACTH-independent bilateral macronodular adrenocortical hyperplasia (AIMAH), and investigated the effects of a V1a receptor antagonist. An i.v. injection of a small dose (0.1 or 0.3 U) of AVP, insulin-induced hypoglycaemia, upright posture tests, and oral administration of a V1a receptor antagonist (OPC-21268; 300 mg), and its repeated administration at a dose of 600 mg/day for 8 days were performed. An in vitro study of dispersed cells obtained from resected AIMAH tissue was also conducted. Plasma ACTH, AVP and cortisol levels and 24-h urinary free cortisol excretion were measured in the in vivo studies and cortisol concentrations in incubation media in the in vitro study. Injection of small doses of AVP stimulated cortisol secretion without any elevation of plasma ACTH. Insulin-induced hypoglycaemia caused a rise in plasma AVP followed by an increase in plasma cortisol. Although plasma cortisol levels were not affected by single or repeated administrations of OPC-21268, 24-h urinary free cortisol excretion was significantly decreased by the repeated treatment. In the in vitro study, more cortisol was stimulated by AVP from adrenal cells of the AIMAH tissue than from those of a normal adrenal gland, and this secretion was completely suppressed by OPC-21268. These results suggested that hypersensitivity to AVP may have contributed to overproduction of cortisol in this case of ACTH-independent bilateral macronodular adrenocortical hyperplasia, and may have contributed to its pathogenesis.

Adrenal Cortex↗
PubMed1997

Synthesis of a novel vitamin E derivative, 2-(alpha-D-glucopyranosyl) methyl-2,5,7,8-tetramethylchroman-6-ol, by alpha-glucosidase-catalyzed transglycosylation.

A novel derivative of vitamin E, vitamin E glucoside, was synthesized from 2-hydroxymethyl-2,5,7,8-tetramethylchroman-6-ol and maltose in a solution containing DMSO by transglycosylation with alpha-glucosidase from Saccharomyces species. The glycosylated product was identified as 2-(alpha-D-glucopyranosyl)methyl-2,5,7,8-tetramethylchroman-6-ol (TMG) by mass spectrometry and nuclear magnetic resonance spectroscopy. The optimal pH of transglycosylation was 5.5, and the yield of TMG increased as the concentration of maltose increased. TMG has high solubility in water (> 1 x 10(3) mg/mL). The 1,1-diphenyl-2-picrylhydrazyl radical scavenging activity of TMG was found to be nearly the same as those of alpha-tocopherol, Trolox (2-carboxy-2,5,7,8-tetramethylchroman-6-ol), and ascorbic acid.

Antioxidants↗
PubMed1997

Effect of glucocorticoid receptor antagonist RU 38486 on acute glucocorticoid-induced insulin resistance in rat adipocytes.

We examined the mechanism of acute glucocorticoid-induced insulin resistance in rat adipocytes using the glucocorticoid receptor antagonist RU 38486. Pretreatment with dexamethasone (DEX) and prednisolone for 60 minutes resulted in 50% inhibition of insulin-induced [3H]2-deoxyglucose (DOG) uptake at 10(-8) and 10(-7) mol/L, respectively, in rat adipocytes and 20% and 25% inhibition of insulin-induced [3H]2-DOG uptake, respectively, in soleus muscles. Our previous experiments indicated that DEX and prednisolone alone stimulate protein kinase C (PKC) in rat adipocytes. Accordingly, we examined [3H]DEX binding to PKC from MonoQ column-purified rat brain cytosol. Specific [3H]DEX binding to MonoQ column-purified PKC was observed (kd, 56.8 nmol/L; Bmax, 725 fmol/mg protein). Thus, insulin-induced PKC translocation from the cytosol to the membrane was suppressed by pretreatment with 10(-7) mol/L DEX and 10(-6) mol/L prednisolone for 80 minutes. During treatment with RU 38486 for 60 minutes, there was no change in the glucocorticoid-induced inhibitory effect on insulin-induced [3H]2-DOG uptake and PKC translocation from the cytosol to the membrane. Moreover, pretreatment with RU 38486 for 120 minutes slightly prevented the DEX-mediated inhibition of insulin-induced glucose uptake. These results suggest that acute glucocorticoid-induced insulin resistance may be mainly mediated through the other non-glucocorticoid receptor pathway.

Adipocytes↗
PubMed1996

Antinociceptive activity of deltorphin analogs in the formalin test.

Two deltorphin (DLT: Tyr-D-Met-Phe-His-Leu-Met-Asp-NH2) analogs, [N alpha-n-butyl-Gly6]DLT ([nBuG6]DLT) and [N alpha-iso-butyl-Gly6]DLT ([isoBuG6]DLT), were examined for their antinociceptive activities by a formalin test in mice after subcutaneous (s.c.) injection. [nBuG6]DLT exhibited potent dose-dependent antinociceptive activities at doses of more than 0.02 mumol/kg at the first and second phases, while morphine similarly inhibited of the pain responses at doses more than 0.01 mumol/kg in the formalin test. [isoBuG6]DLT showed potent antinociceptive activity at the second phase, but did not inhibit the pain response at the first phase. This phenomenon may be caused by a mu-antagonist/delta-agonist property of this compound. The antinociceptive effects of these analogs were antagonized by delta-antagonist naltrindole, but not by the mu-antagonist naloxone. These findings suggest that the antinociceptive effects were mediated via delta-receptors. These compounds may be useful as delta-agonists for clarifying the mechanism of analgesia mediated by delta-opioid receptors.

Analgesics, Opioid↗
PubMed1995

Manganese ions penetrate via L-type Ca2+ channels and induce contraction in high-K+ medium in ileal longitudinal muscle of guinea-pig.

1. Mn2+ (5 mM) completely inhibited the K+ (10-60 mM)-induced ileal tonic tension to the baseline, however, the tension and Mn2+ uptake increased progressively, depending on the K+ concentration of above 35 mM. 2. The L-type Ca2+ channel blocker, D-600 and nifedipine inhibited the tension development and Mn2+ uptake after addition of Mn2+ in the high-K+ (60 mM) medium, however, T-type Ca2+ channel blocker, Ni2+ and amiloride had no effect on it. 3. D-600 and nifedipine inhibited the tension development and Mn2+ uptake in the presence of 5 mM Mn2+ in the Ca(2+)-free, high-K+ (60 mM) medium. 4. The results suggest that Mn2+ penetrates via L-type Ca2+ channels in the ileal cell membrane in a state of prolonged depolarization and activates the contractile elements.

Amiloride↗
PubMed1995

Heterotransplantation of human parathyroid glands into nude mice.

Heterotransplantation of human parathyroid tissues into nude mice was performed to investigate the characteristics of grafted tissues. Grafts prepared from hyperplasia, adenoma and normal glands which were resected at operation were implanted in the gluteus muscle of the recipient mice (female, KSNnu/nu strain). Graft function was evaluated by measuring human intact PTH concentrations in sera of the mice. Serum PTH concentrations 12 weeks after transplantation were correlated with the tissue volume in the mice which received one, two, four or eight pieces of 1 mm3 hyperplastic tissues. Changes in graft function were examined in the mice which received four grafts prepared from hyperplasia, adenoma or normal glands. Transplantation of parathyroid tissues resulted in an increase in PTH concentrations for 4 weeks, reaching a plateau thereafter. The level remained unchanged for 8 weeks. Serum PTH levels in the mice with grafts prepared from hyperplasia or adenoma were significantly higher than in those with grafts from normal glands, though without a significant difference between the mice with grafts from adenoma and from hyperplasia. Serum calcium levels were similar in all three groups. We also observed the response of grafted parathyroid tissue to a low calcium level in sera: there was higher PTH secretion four weeks after the administration of the low calcium diet. The success of heterotransplantation was histologically proven by the presence of grafts which were not atrophic in the muscle 12 weeks after transplantation. Nucleoli were found more frequently, and nuclear pleomorphism was observed in the cells of heterografts.

Adenoma↗
PubMed1995

[A case of Sjögren's syndrome with rheumatoid arthritis manifesting transverse myelitis with antineuronal antibody].

We report a sixty-year-old woman with transverse myelitis who had suffered from rheumatoid arthritis since age of 52. She was admitted to our department because of muscle weakness and painful tonic spasm in the bilateral lower extremities, sensory disturbance below the mamillary level and bladder disturbance. She had sicca symptoms. As a result of sialography, Sjögren's syndrome was diagnosed. Antineuronal antibody was found in the sera of the patient. She had no symptom of systemic vasculitis. Lupus anticoagulant and anticaldiolipin antibody were negative. The pathogenesis of transverse myelitis in rheumatic disease is still uncertain. Vasculitis and the immunological reaction of antineuronal antibody have been suggested as possible causes. This report suggests the influence of direct immunological reaction on the central nervous system.

Arthritis, Rheumatoid↗
PubMed1995

[Corticosterone].

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Corticosterone↗
PubMed1994

Temperature high sensitivity of manganese uptake in ileal longitudinal smooth muscle of guinea-pig.

1. Mn2+ (5 mM) inhibited completely the K+ (60 mM)-induced ileal tonic tension to the base line, however, the tension increased progressively to the above level of the original K+ tonic response after 3 hr of the Mn2+ application at 37 degrees C. 2. At 30, 32 or 34 degrees C, the tensions which developed after 3 hr of the addition of 5 mM Mn2+ in the high-K+ medium was 0, 21, 48% of their original K+ tonic levels, respectively. 3. The tension development and manganese uptake in the presence of Mn2+ in the high-K+ medium was highly dependent on the temperature in very narrow range of 32-37 degrees C in the suspending medium.

Animals↗
PubMed1994

Manganese ions induce tonic contraction after relaxation in a high-K+ medium in ileal longitudinal smooth muscle of guinea-pig.

In ileal longitudinal muscle 5 mM Mn2+ inhibited completely the K+ (60 mM)-induced tonic tension to the base line; however, the tension progressively increased to above the level of original tonic response evoked by K+ after 3 h in the presence of Mn2+. Tetrodotoxin 5 x 10(-5) M) had no influence on the tension development in the presence of Mn2+ in the high-K+ medium. Mn2+ also increased the tension in a high-K+, Ca(2+)-free medium. The Ca2+ antagonist, gallopamil (10(-6) M) inhibited the development of tension in the presence of Mn2+ in the high-K+ medium. The 45Ca uptake determined by the lanthanum method remained unchanged from control levels after 3 h of the 5 mM Mn2+ application in the high-K+ medium in spite of the development of the tension. The manganese uptake in the high-K+ medium, increased in accordance with the increase of duration of 5 mM Mn2+ application. Gallopamil inhibited manganese uptake in the high-K+ medium. These results suggest that Mn2+ firstly reduces K(+)-induced tension by inhibition of Ca2+ influx, subsequently, Mn2+ ions accumulate in the intracellular compartments through voltage-operated Ca2+ channels and may activate contractile proteins in the ileal muscle.

Animals↗
PubMed1994

Emphysematous pyelonephritis successfully treated with nephrectomy and granulocyte colony-stimulating factor.

A 58-year-old woman developed diabetic ketoacidosis and emphysematous pyelonephritis caused by Escherichia coli. She was successfully treated with nephrectomy, antibiotics, and recombinant human granulocyte colony-stimulating factor (rhG-CSF). RhG-CSF therapy may be an effective adjunct for diabetic patients with severe infection, even when neutropenia is not present.

Anti-Bacterial Agents↗
PubMed1993

Aldosterone binding to mineralocorticoid receptors of mononuclear leukocytes in diabetic subjects.

We present the characteristic features of mineralocorticoid receptor regulation in human mononuclear leukocytes in patients with diabetes mellitus. Eighteen diabetic patients (3M and 15F, aged from 28 to 77 years with a mean of 53 +/- 14 (mean +/- SD) years) and 7 normal subjects (6M and 1F, aged from 29 to 59 years with a mean of 41 +/- 13 years) were studied. The mean plasma aldosterone concentration in the diabetic patients was significantly lower than that in the normal subjects (137 +/- 62 vs 189 +/- 36 pmol/l, p < 0.05). Seven of the 18 diabetic patients were hypoaldosteronemic. These 7 patients, however, showed normokalemia, except one with mild hyperpotassemia. The number of binding sites of [3H]aldosterone to mineralocorticoid receptor in the diabetic patients was significantly higher than that in the normal subjects (853 +/- 281 vs 488 +/- 109 sites/cell, p < 0.05), but there was no significant difference in Kd of [3H]aldosterone binding to mineralocorticoid receptor between the diabetic patients and normal subjects (1.34 +/- 0.37 vs 0.99 +/- 0.61 nmol/l). In the diabetic patients, a significant negative correlation was observed (r = 0.70, p < 0.01) between plasma aldosterone concentration and the binding sites, but not between plasma aldosterone concentration and Kd. In the total subjects, including normal subjects and diabetic patients, a significant negative correlation was also found between plasma aldosterone concentration and binding sites (r = 0.72, p < 0.001). These results suggest that increased binding sites of mineralocorticoid receptor may help to prevent diabetic patients from being hyperkalemic.

Adult↗
PubMed1992

Glycyrrhizin (licorice)-induced hypokalemic myopathy. Report of 2 cases and review of the literature.

Fifty-nine cases of glycyrrhizin (licorice)-induced hypokalemic myopathy (GIHM), 2 females treated in our departments (85 and 73 years old) and 57 cases reported in the literature were studied, and conditions leading to the onset, factors, clinical manifestations, laboratory assessments, muscle biopsy findings, treatment and outcome were discussed. The 59 GIHM cases comprised 32 men, 25 women and 2 patients without record of sex; the average age was 55.2 years. In many cases, conditions leading to the onset of GIHM were habitual licorice ingestion, ingestion of antituberculosis agents containing licorice and long-term ingestion of licorice-containing agents for chronic gastritis, chronic hepatitis or chronic dermatitis. The combined use of hypotensive diuretic agents increased the risk of GIHM in an overwhelming number of cases. The main clinical symptom was flaccid quadriplegia in almost all cases, with muscle pain in 32.2% and peripheral dysesthesia in the extremities, manifested mainly by numbness (27.1%). Laboratory findings included a mean serum K+ value of 1.98 mEq/l (56 GIHM cases), a mean creatine kinase of 5,385.7 IU/l (n = 30), a mean blood aldosterone concentration of 2.92 ng/dl (n = 30; normal: 2.0-13.0 ng/dl) and a mean plasma renin activity of 0.17 ng/ml/h (n = 27; normal: 0.8-4.4 ng/ml/h). Muscle biopsy was performed in 17 of the 59 cases with resultant findings of myopathic changes consisting mainly of phagocytosis, necrotic fibers, vacuolar degeneration, together with sporadic neurogenic changes. Complete cure was attained in 57 of the 59 cases of GIHM by discontinued ingestion of glycyrrhizin (licorice) and potassium supplement.

Aged↗
PubMed1991

19-hydroxyandrostenedione does not modulate [3H]aldosterone binding to human mononuclear leucocytes and rat renal cytosol.

To verify the aldosterone amplifying action of 19-hydroxyandrostenedione (19-OH-AD), we investigated [3H]aldosterone and [3H]19-OH-AD binding to type I (mineralocorticoid) receptor in the renal cytosol of adrenalectomized and ovariectomized rat, and human mononuclear leucocytes (MNL). In the [3H]aldosterone binding study, the cytosol was incubated with [3H]aldosterone and 200-fold RU28362 (11 beta,17 beta-dihydroxy-6-methyl,17 alpha-(1-propynyl)-androsta-1,4,6- trien-3-one), a pure glucocorticoid, with or without 19-OH-AD. Scatchard plots of [3H]aldosterone binding to cytosol with 0.2 or 20 nM 19-OH-AD or without 19-OH-AD were linear. Dissociation constants (Kd) and maximum bindings (Bmax) without 19-OH-AD, and with 0.2 and 20 nM 19-OH-AD were: 0.71 +/- 0.03 nM and 23.0 +/- 3.4 fmol/mg protein (mean +/- SD, n = 3), 0.72 +/- 0.05 nM and 23.1 +/- 2.3 fmol/mg protein (n = 3), and 0.77 +/- 0.04 nM and 22.9 +/- 4.8 fmol/mg protein (n = 3), respectively. 19-OH-AD did not significantly change the Kd and Bmax of [3H]aldosterone binding. A high concentration of 19-OH-AD slightly displaced 0.2 or 5 nM [3H]aldosterone bound to cytosol. In human MNL, Scatchard plots of [3H]aldosterone binding with both 0.2 and 20 nM 19-OH-AD and without 19-OH-AD were linear. Kd and Bmax were, respectively, 1.00 nM and 780 sites/cell in the absence of 19-OH-AD, and 1.07 nM and 774 sites/cell in the presence of 0.2 nM 19-OH-AD. Without 19-OH-AD they were, respectively, 0.95 nM and 551 sites/cell, and 1.10 nM and 560 sites/cell with 20 nM 19-OH-AD. A high concentration of 19-OH-AD slightly displaced 0.2 or 5 nM of [3H]aldosterone bound to MNL. In both tissues, there was no obvious specific binding of [3H]19-OH-AD within the range of 1-60 nM. The above results suggest that the amplifying effect of 19-OH-AD on aldosterone mineralocorticoid action may not occur at the binding site of aldosterone to type I receptor, and that 19-OH-AD itself may not have any direct or indirect mineralocorticoid actions on the steroid receptor-mediated process in the rat kidney and human MNL.

Adrenalectomy↗
PubMed1990

[A case of glucocorticoid-responsive hyperaldosteronism: follow-up study for 21 years--comparison with cases of 17 alpha-hydroxylase deficiency in Japan].

A study of the pathophysiology in our previously reported case of glucocorticoid-responsive hyperaldosteronism (Case E.H., 17 yrs old, female; JCEM, 28: 1807, 1968), who had undergone a long-term successful treatment for 21 yrs of daily 0.5 mg dexamethasone (Dex), suggested again that the patient had 17 alpha-hydroxylase deficiency (17-OH-D) in the adrenal with minimum enzyme deficiency in the ovary. When Case E.H. was injected with zinc-ACTH for 3 days with daily 0.5 mg Dex administration, plasma levels of 17-deoxy-steroids were moderately or dramatically increased, but those of 17 alpha-hydroxy-steroids (17-OH-steroids) responded poorly or not at all. Plasma level of estradiol and urine estrogens were found to be normal in repeated measurements. Plasma basal levels of LH and FSH were normal, and their responses to LH-RH were high normal or slightly exaggerated. Her menstruation was almost regular, and the basal body temperature was at least biphasic with daily 0.5 mg Dex treatment. However, she did not become pregnant during the 17 yrs of her married life. Then, we surveyed 31 Japanese cases of 17-OH-D with suppressed plasma renin activity (PRA) to ascertain whether similar patients to our case, 17-OH-D with suppressed PRA and with hyperaldosteronism, has been reported or not. In this survey work, 9 such cases were found to have high plasma aldosterone (Ald) concentration (PAC) (group I). The other 21 cases had normal or low normal PAC, and the one remaining case had low urine Ald (group II). 17-Deoxy-steroids such as corticosterone, 11-deoxycorticosterone and progesterone, which were elevated in this disorder, were added to control plasma, and PAC was measured with Dainabot's "ALDOSTERONE.RIAKIT" used for the measurement of PAC in all group I patients. With the total of large amounts of 600 ng of these 17-deoxy-steroids (200 ng for each), however, the incremental PAC value was much less than the lowest PAC value in patients of group I. PAC of one group I patient was measured directly by "ALDOSTERONE.RIAKIT" and also by RIA after extraction and purification procedure using LH-20 column chromatography. The PAC values obtained by both methods were high and the same (285 pg/ml). In 5 out of 22 group II patients, PAC was also measured with the same RIA kit "ALDOSTERONE.RIAKIT" mentioned above, and yet it was low or low normal.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗