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Biomedical subjects

K Endoh

Publications and source records attributed to K Endoh.

At least 55 records · Page 3Linked to original sources
PubMed1995

[Acute myeloid leukemia (M1) following chemotherapy for Ki-1 lymphoma complicated with rheumatoid arthritis].

A 58-year-old woman complicated with rheumatoid arthritis (RA) was admitted to our hospital with right axillar lymphadenopathy and splenomegaly in November 1992. She was diagnosed as an anaplastic large-cell lymphoma (Ki-1 +) (stage IIIB) on the histological findings of the right axillar lymph nodes. She was treated with 11 courses of CHOP regimen between February 1992 and May 1993, and with mitoxantrone, etoposide (VP-16) and predonisolone in April 1992 and May 1993. The right axillar lymph nodes and spleen were irradiated at a dose of 36Gy in October 1992 and May 1993 respectively. In May 1993, peripheral blood showed WBC 89,000/microliter with 96% myeloblasts, Hb 8.3 g/dl, and Plt 124,000/microliter. Bone marrow aspirate revealed hypercellularity with 90% myeloblasts, which were positive for CD13 and HLA-DR. She was diagnosed as AML (M1). The karyotype showed normal. Southern blot analysis did not reveal the rearrangement of the MLL gene. She received the BHAC-DMP regimen and obtained complete remission. However, she relapsed during consolidation therapy, and died of cerebral bleeding. An autopsy revealed absence of a residual tumor. The mean interval from exposure to alkylating agent to the onset of secondary leukemia has been reported to be about 5 years, in contrast to a shortened interval of about 2 years for VP-16-induced leukemia. In our patient, it took only 1 year to have AML following chemotherapy for Ki-1 lymphoma. This suggests that her AML might be induced not only by treatments for RA and Ki-1 lymphoma, but also by immunological background such as RA.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1994

Intragastric nicotine protects against 40% ethanol-induced gastric injury despite pretreatment with NG-nitro-L-arginine methyl ester or adrenal medullectomy in rats.

We tested the hypotheses that the protective effect of intragastric nicotine against ethanol-induced gastric mucosal injury is dependent on endogenous nitric oxide or peripheral sympathoadrenal mechanisms. Rats were pretreated with NG-nitro-L-arginine methyl ester (3 mg/kg subcutaneous, 1 h prior to study) to block endogenous nitric oxide synthesis or with adrenal medullectomy (three weeks prior to study) to ablate the effect of the adrenal medulla. At 1-h intervals, vehicle or nicotine (4 mg/kg) and 40% ethanol were then given intragastrically. The total lengths of the linear gastric corpus mucosal lesions were measured unbiasedly. The protective effect of intragastric nicotine was not modified by either pretreatment. We conclude that the mechanism mediating intragastric nicotine protection against 40% ethanol-induced gastric mucosal injury is independent of endogenous nitric oxide or the adrenal medulla.

Administration, Oral↗
PubMed1994

Effects of smoking and nicotine on the gastric mucosa: a review of clinical and experimental evidence.

Epidemiological and experimental evidence have shown that nicotine has harmful effects on the gastric mucosa. The mechanisms by which cigarette smoking or nicotine adversely affect the gastric mucosa have not been fully elucidated. In this report, clinical and experimental data are reviewed. The effects of nicotine from smoking on gastric aggressive or defensive factors are discussed. Nicotine potentiates gastric aggressive factors and attenuates defensive factors; it also increases acid and pepsin secretions, gastric motility, duodenogastric reflux of bile salts, the risk of Helicobacter pylori infection, levels of free radicals, and platelet-activating factor, endothelin generation, and vasopressin secretion. Additionally, nicotine impairs the therapeutic effect of H2-receptor antagonists and decreases prostaglandin synthesis, gastric mucosal blood flow, mucus secretion, and epidermal growth factor secretion. Although many of the studies provide conflicting results, the bulk of the evidence supports the hypothesis that nicotine is harmful to the gastric mucosa.

Epidermal Growth Factor↗
PubMed1994

Schwannoma of the duodenum causing melena.

A rare case of duodenal schwannoma is reported. A 69-year-old man was admitted for evaluation of melena. Endoscopy and hypotonic duodenography showed a submucosal tumor in the third part of the duodenum. Biopsy findings were suggestive of leiomyosarcoma, therefore pancreatoduodenectomy was performed. Hematoxylin-eosin staining of the resected specimen showed interlacing bundles of spindle-shaped cells with palisading nuclei. Immunohistochemical staining showed positivity for S-100 protein and neuron-specific enolase, but desmin was negative, thus a diagnosis of schwannoma was made. Schwannoma is often difficult to distinguish from leiomyogenic tumors by standard staining, but immunohistochemical staining proved useful in this case.

Aged↗
PubMed1994

Size-regulation and biochemical activities of the multicellular spheroid composed of rat liver cells.

It was reported that cell-sheets composed of rat liver cells could be obtained by using a collagen-conjugated thermo-responsive polymer, poly-N-isopropyl acrylamide, as a cell substratum and they were then able to transform into multicellular spheroids in the hydrophobic dish. In this study, we succeeded in easily obtaining the cell-sheets with the intended size by using the etched substratum. Biochemical analyses of spheroids derived from cell-sheets with areas of 0.2, 0.5 and 2.5 cm2 were carried out. Each cell-sheet rapidly aggregated at the same rate and finally turned into a multicellular spheroid within 5 days after the detachment. However, both decreases of DNA and LDH contents in cell-sheets with an area of 2.5 cm2 within 24 hr after the detachment were more obvious than in the others, respectively. It is tempting to speculate from these data that the vital spheroids with the desired size can be easily obtained by using our new method.

Acrylamides↗
PubMed1993

Mechanism of intragastric tetramethylammonium protection against 40% ethanol injury in rat stomach.

The effect of tetramethylammonium (TMA), a ganglionic stimulant, on gastric mucosal injury induced by 40% ethanol was examined. In studies I-III, rats were treated with intragastric vehicle or TMA (1 or 10 mg/kg). In study I, 1 hr after the treatment, 40% ethanol was given intragastrically. The length of the linear corpus mucosal lesions was measured unbiasedly with a caliper after another hour. In study II, mean blood pressure was assessed before and after the treatment. In study III, 1 hr after the treatment, gastric mucus and juice volumes, and titratable acid were measured. In study IV, 40% ethanol (10 ml/kg) was administered intragastrically immediately after 0.2 or 1.4 ml of intragastric vehicle treatment. One hour later, gastric lesions score was assessed as in study I. Results show that (1) intragastric TMA dose-dependently protected against 40% ethanol-induced gastric injury; (2) neither dose of intragastric TMA increased mean blood pressure; (3) there was a dose-related increase in gastric mucus secretion for TMA 1 and 10 mg/kg, and a significant increase in gastric juice volume only for TMA 10 mg/kg; and (4) the rats treated with 1.4 ml of vehicle plus 40% ethanol had significantly less injury than those treated with 0.2 ml of vehicle plus 40% ethanol. We conclude that the protective effect of intragastric TMA can be explained by its dose-related effect in enhancing gastric mucus secretion for TMA 1 and 10 mg/kg and the significantly greater increase in gastric juice volume for TMA 10 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1993

Involvement of alpha 2-adrenoceptors in mechanism of intragastric nicotine protection against ethanol injury in rat stomach.

To elucidate the role of alpha- and beta-adrenoceptors in the mechanism of intragastric nicotine protection against ethanol-induced gastric mucosal injury, the following studies were performed. At 0.5-hr prior to the injury study, rats were pretreated with: subcutaneous control, prazosin (0.5 mg/kg) or yohimbine (5 mg/kg) to block alpha 1- or alpha 2-adrenoceptors; or intraperitoneal control, metoprolol (2 mg/kg) or butoxamine (4 mg/kg) to block beta 1- or beta 2-adrenoceptors, respectively. At 1-hr intervals, rats received intragastric vehicle or nicotine (4 mg/kg) and 40% ethanol (10 ml/kg). Total lengths of the linear gastric corpus mucosal lesions were measured by an unbiased observer using a caliper. In a separate study, 0.5-hr after subcutaneous control or yohimbine (5 mg/kg), rats were treated with intragastric vehicle or nicotine (4 mg/kg). One hour later, gastric mucus volume, gastric juice volume and pH, and titratable acid in the gastric juice were measured. In the rat stomach, the intragastric nicotine protection against 40% ethanol-induced mucosal injury was not blocked by selective alpha 1-(prazosin), beta 1-(metoprolol), or beta 2-(butoxamine) adrenoceptor antagonists. The protection was significantly reduced although not completely abolished by selective alpha 2-(yohimbine) adrenoceptor antagonist. Yohimbine also significantly reduced basal and nicotine-stimulated increase in gastric mucus volume. These data suggest that alpha 2-adrenoceptors are involved in the protective effect of intragastric nicotine against 40% ethanol-induced gastric mucosal injury possibly by a mucus-dependent mechanism.

Adrenergic alpha-Antagonists↗
PubMed1993

Mechanism of gastric hyperemia induced by intragastric hypertonic saline in rats.

BACKGROUND: Intragastric hypertonic (2 mol/L) saline produces injury in the gastric mucosa and a significant increase in gastric blood flow (hyperemia) in anesthetized rats. We studied the mechanism of this hyperemia. METHODS: Rats were treated with intravenous boluses of NG-nitro-L-arginine methyl ester (3 mg/kg) to block synthesis of endogenous nitric oxide, pyrilamine (1 mg/kg) to inhibit H1 receptors, or indomethacin (5 mg/kg) to block synthesis of endogenous prostaglandins during blood flow studies or with subcutaneous capsaicin (125 mg/kg) 10-14 days before blood flow studies to ablate capsaicin-sensitive afferent nerves. Gastric mucosal blood flow was measured by hydrogen gas clearance before and during intragastric administration of 2 mol/L saline. RESULTS: The gastric hyperemia induced by intragastric 2 mol/L saline was completely blocked only by indomethacin. The associated gastric mucosal damage was increased significantly. CONCLUSIONS: In the rat stomach, the gastric hyperemia induced by intragastric 2 mol/L saline is mediated by endogenous prostaglandins and plays a protective role. Endogenous nitric oxide, H1 receptors, and capsaicin-sensitive afferent nerves are not involved in this protective hyperemia.

Analysis of Variance↗
PubMed1993

[Influence of urine pH and cations on antimicrobial activities of penems].

We compared the antimicrobial activities of penems in human urine with those in Mueller-Hinton broth in order to clarify the usefulness of penems for urinary tract infections. Furthermore, we also investigated the influence of urine components, such as pH, magnesium concentration and calcium concentration, on the antimicrobial activities of penems. Three penems, i.e., imipenem, panipenem and meropenem were employed. And two bacterial strains, i.e., Escherichia coli NIHJ JC-2 and Pseudomonas aeruginosa 18s, were tested. There was no significant difference in MBCs between human urine and Mueller-Hinton broth against E. coli. However, MBCs of penems in human urine was lower than those in Mueller-Hinton broth against P. aeruginosa. On the other hand, MBCs of penems against these two strains were low when urine pH was high or urine calcium concentration was low. No influence of urine magnesium concentration on MBCs of penems was seen. From these results, it was suggested that we should measure the antimicrobial activities of penems not only in Mueller-Hinton broth, but also in human urine, when we administer penems to patients with urinary tract infections. And we should foresee the clinical effects of penems against urinary tract infections paying attention to urine pH of the patients.

Cations, Divalent↗
PubMed1993

Mutagenicity of activated carbon adsorbate of drinking water in the Ames assay.

Mutagenicity of activated carbon adsorbate from drinking water collected in Niigata City was assayed by the Ames assay. Adsorbate was extracted from activated carbon with benzene, and then with ethanol. Although the benzene extract was not mutagenic, the ethanol one showed the mutagenic activity for Salmonella typhimurium strains TA98 and TA100 with and without S9 mix. The ethanol extract was much more mutagenic on TA100 than TA98 both with and without S9 mix. The mutagenic activity per liter of water was found to be the strongest in winter and the weakest in summer.

Animals↗
PubMed1993

[MRI study of the brain in aged volunteers: T2 high signal intensity lesions and high cortical function].

In order to characterize age-related and chronological changes of the brain, longitudinal studies of aged volunteers were conducted using computed tomography since 1982. The present paper discusses correlations between brain function and findings of MR images which were obtained a using 1.5 T superconductive MR instrument since 1989. A total of 118 volunteers aged 60 to 88 years old with a mean age of 75.0 +/- 6.7 participated in the study, which consisted of MRI, EEG recording, the Benton Visual Retention Test and a medical interview. Subjects with a past history or clinical evidence of CVD, head trauma or dementia were excluded from the study. Incidence of T2 high signal intensity lesions increased with age. Some showing T1 low signal intensity in the same lesion were considered to be lacunar infarction, over all incidence of which was 24.6%. Numbers of correct responses on the BVRT showed a negative correlation with numbers of T2 high signal intensity lesions. Although the aged volunteers in the present study could achieve all activity of daily living without any trouble, high cortical function evaluated by visuoperceptual performance of BVRT was somewhat disturbed in participants with multiple T2 high signal intensity lesions. Brain atrophy seems to be more advanced in groups with T2 hyper intensity lesions than in the group without them. These findings may support the notion that T2 high signal intensity lesions are not merely an index of ageing but pathologic lesions accompanied with senescence, although further studies including clinicopathological correlation are necessary to establish this concept.

Aged↗
PubMed1993

An experimental model of acute liver injury using multicellular spheroids composed of rat parenchymal and non-parenchymal liver cells.

Massive hepatic cell necrosis can be induced by Corynebacterium parvum and lipopolysaccharide (LPS) in rats. In this model, serum LDH, GOT and GPT activities are significantly increased in vivo within several hours after LPS injection. An in vitro experimental acute liver injury animal model was produced by using multicellular spheroids composed of rat parenchymal and non-parenchymal liver cells. These multicellular spheroids were prepared by detaching the confluent monolayer on the collagen-conjugated thermo-responsive polymer coated culture dish at a temperature below the lower critical solution temperature and culturing it on the non-adhesive substratum. LPS caused clear elevations of GOT, GPT and LDH activities from these spheroids into the medium. However, the increase of LDH activity was only observed in the monolayer culture system. These results suggest that the multicellular spheroids of liver cells are useful models as an alternative to animal tests for hepatotoxicity.

Alanine Transaminase↗
PubMed1992

Intragastric nicotine protects against 40% ethanol-induced gastric mucosal injury despite pretreatment with propranolol or N-ethylmaleimide in rats.

We tested the hypotheses that the protective effect of intragastric nicotine against ethanol-induced gastric mucosal injury is dependent on propranolol- or N-ethylmaleimide-sensitive mechanisms. Propranolol was administered in doses (2 and 20 mg/kg) that provided dose-related blockade of beta-adrenoceptors (significant decreases in heart rate). N-Ethylmaleimide was administered in doses that previously had been shown to increase gastric vascular permeability (10 mg/kg) or inhibit gastric mucosal sulfhydryl compounds (50 mg/kg). At 0.5 hr after these or control subcutaneous pretreatments, the rats received intragastric nicotine (4 mg/kg) or vehicle. One hour later 40% ethanol was given intragastrically. The gastric corpus mucosal lesions were recorded by polaroid photographs after another hour, and their areas measured unbiasedly by computerized image analysis. The results showed that N-ethylmaleimide, but not propranolol, aggravated ethanol-induced gastric mucosal injury. The protective effect of intragastric nicotine was not modified by either pretreatment. We conclude that the mechanism mediating intragastric nicotine protection against 40% ethanol-induced gastric mucosal injury is independent of propranolol- or N-ethylmaleimide-sensitive mechanisms.

Animals↗
PubMed1992

Intragastric nicotine protection against 40% ethanol injury in rat stomach. Role of ganglionic stimulation or blockade.

Intragastric nicotine (4 mg/kg) protects against 40% ethanol-induced gastric mucosal injury and raises mean blood pressure. We postulated that this protective effect was mediated by the ganglionic stimulatory property of nicotine and therefore could be abolished by ganglionic blockers. Rats were pretreated with intraperitoneal hexamethonium (10 mg/kg) or mecamylamine (2 mg/kg) to block peripheral or central autonomic ganglia, respectively. Intragastric vehicle or nicotine (4 mg/kg) was then administered. The total lengths of the linear gastric corpus mucosal lesions induced by intragastric 40% ethanol were measured by an unbiased observer using a caliper. The results showed that both intraperitoneal hexamethonium and mecamylamine pretreatments protected against 40% ethanol-induced gastric mucosal injury. Neither modified the protective effect of intragastric nicotine. The protective effect of hexamethonium and mecamylamine was associated with a significant increase in the volume of gastric mucus and gastric juice. The increase in the volume of gastric content (mucus and juice) was partially responsible for the protective effect of these ganglionic blockers. In a separate experiment, intraperitoneal nicotine (4 mg/kg) also protected against 40% ethanol-induced gastric mucosal injury and raised mean blood pressure. These data indicate that the protection against 40% ethanol-induced gastric mucosal injury is not unique to intragastric nicotine. Such protection can be induced by ganglionic blocking doses of hexamethonium and mecamylamine, or a ganglionic stimulatory dose of intraperitoneally administered nicotine. Whether ganglionic stimulation or blockade plays a role in the mechanism of intragastric nicotine protection, however, remains to be determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Frequency of mutant T lymphocytes defective in the expression of the T-cell antigen receptor gene among radiation-exposed people.

The frequency of mutant T lymphocytes defective in T-cell receptor gene (alpha or beta) expression was measured using the 2-color flow cytometric technique. Results for a total of 203 atomic bomb survivors, 78 of whom were proximally exposed (DS86 doses of greater than or equal to 1.5 Gy) and 125 of whom were distally exposed (DS86 dose of less than 0.005 Gy), showed that the mutant frequency was significantly higher in males than in females. No significant dose effects were observed. In contrast, a significant increase of mutant frequency was observed for 6 patients treated with Thorotrast, a contrast medium containing thorium-232 formerly used for radioligands. In addition, thyroid disease patients treated with 131I showed a dose-related increase of mutant frequency. It was suggested that the present T-cell receptor mutation assay has a unique characteristic as a biological dosimeter for measurement of recent exposures to genotoxic agents.

Adult↗
PubMed1992

Acute toxicity of tri-n-butyltin chloride (TBTC) in the Syrian golden hamster.

The effects of tri-n-butyltin chloride (TBTC) on Syrian golden hamsters were studied. TBTC in single doses of 0, 29.6, 44.4, 66.7, 100 or 150 mg/kg were given to 10 male hamsters in each group and the mortality rates were determined two weeks thereafter. They were 0% (0/10), 0% (0/10), 10% (1/10), 10% (1/10), 30% (3/10) and 70% (7/10) for 0, 29.6, 44.4, 66.7, 100 and 150 mg/kg groups, respectively. In the case of females, seven groups consisting of 10 animals each were given TBTC at doses of 0, 29.6, 44.4, 66.7, 100, 150, or 225 mg/kg. The mortality rates determined two weeks after the TBTC treatment were 0% (0/10), 10% (1/10), 10% (1/10), 0% (0/10), 40% (4/10), 30% (3/10) and 90% (9/10) for 0, 29.6, 44.4, 66.7, 100, and 225 mg/kg groups, respectively. Based on these mortality data, the LD50s via oral administration were determined as 146.9 mg/kg (95% C.I. 111.8-193.3 mg/kg) for the male and 172 mg/kg (95% C.I. 127.2-233.4 mg/kg) for the female. Regarding pathological changes, animals experienced lesions in the bile duct, such as the dilatation of the common bile duct and cholestasis, and/or adhesion of the bile duct to the liver, gallbladder, pancreas and duodenum. In a separate experiment, a single dose of 44.4 mg/kg TBTC was administered orally to 12 male hamsters, then the concentrations of TBTC and its metabolite, di-n-butyltin chloride (DBTC), in the liver were analyzed by means of gas chromatography for 14 days after the treatment. The maximum concentrations of TBTC and DBTC appeared one day after the administration, and decreased rapidly thereafter. The concentration of DBTC was found to be higher than that of TBTC throughout the experimental period.

Alanine Transaminase↗