Biomedical subjects

K Asagoe

Publications and source records attributed to K Asagoe.

26 records · Page 2Linked to original sources

PubMed1995

Therapeutic effects of lansoprazole on peptic ulcers in elderly patients.

We studied the effects of lansoprazole on ulcer healing and Helicobacter pylori infection in elderly patients with peptic ulcers. In a group of 24 patients with gastric ulcers, the H. pylori infection rate was 100%. In the course of gastric ulcer healing with famotidine or lansoprazole alone, the H. pylori infection showed no signs of decline. The ulcer healing rates after 8 weeks were similar between the H2-receptor antagonist famotidine (73%), and the proton pump inhibitor lansoprazole (82%). When eradication of H. pylori infection was attempted by concomitant administration of lansoprazole and amoxicillin 500 mg b.i.d. for 2 weeks, the eradication rate was 33% in the group given lansoprazole 30 mg q.d. plus ampicillin 500 mg b.i.d., whereas it was 77% in the group given lansoprazole 30 mg b.i.d. plus ampicillin 500 mg b.i.d. Lansoprazole is considered to be a useful agent for the treatment of patients with peptic ulcers and H. pylori infection and its effectiveness in H. pylori eradication is improved by b.i.d. administration along with ampicillin.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1995

[Complete remission in acute myeloblastic leukemia (M0) after treatment with rhG-CSF].

A 57-year-old man was admitted because of fever and night sweat. The bone marrow was hypercellular with 86.4% blast cells. The diagnosis of AML (M0) was made, because the blast cells were negative for peroxidase stain and had CD13 and no lymphoid antigens in marker analysis. The patient was treated with BH-AC.TMP, BH-AC.MVP and low dose Ara-C without any hematological improvement, and even additional treatment with medium dose Ara-C resulted in 66.4% blast cells in the bone marrow. Subsequent administration of rhG-CSF (150 micrograms/day) by continuous intravenous infusion resulted in the decrease of the blast cells in the bone marrow to a level that was evaluated as complete remission. He remains in complete hematological remission at present. As shown in this case, rhG-CSF might be an effective agent for the treatment of AML, even if the mechanism of its effectiveness is unclear at present. Further clinical studies should will supply useful information to analyze the pathophysiology of AML.

Granulocyte Colony-Stimulating Factor↗

PubMed1994

Effect of gastric mucosal blood flow on the pathogenesis of ammonia in Helicobacter pylori-induced gastric mucosal injury.

PURPOSE: We investigated the effects of the gastric mucosal blood flow on the pathophysiology of ammonia-induced gastric mucosal damage. DESIGN: The study was designed to show whether the damaging effect of ammonia, a product of Helicobacter pylori urease, on the gastric mucosa is increased by the decrease in gastric mucosal blood flow in rats subjected to ischemia. RESULTS: Although ammonium chloride at concentrations of 15-60 mmol/l produced no significant macroscopical lesion in normotensive rats, it caused severe macroscopic hemorrhagic gastric lesions in the stomachs of rats subjected to ischemia. Exposure of the stomach to the combination of ischemia and ammonium chloride (60-600 mmol/l, pH adjusted to 7-9 with sodium hydroxide) produced macroscopic hemorrhagic lesions. However, exposure of the mucosa to the combination of ischemia and sodium hydroxide (60-600 mmol/l, pH was reduced to 7-9 with hydrochloric acid) produced no significant lesions. CONCLUSIONS: These results indicate that the mucosal lesions observed in patients infected with H. pylori are not caused by the alkalinity of H. pylori-produced ammonia and suggest that concomitant infection with H. pylori in the ischemic stomach may lead to the development of ulceration in these patients.

Ammonium Hydroxide↗

PubMed1994

[Analysis of platelet-derived factors that modulate functions of polymorphonuclear leukocytes].

Interactions between platelets and polymorphonuclear leukocytes (PMN) modulate their functions and play a role in the development of pathogenesis of some disease. Platelets secret various kinds of factors that affect PMN functions. They seemed to have important role in vivo, but little has been elucidated on exact mechanism of action and physiological meaning of each factor in relation to PMN functions. We studied the effects of platelets and released substances from activated platelets on the functions of PMN. Results were as follows. 1) Platelets enhanced bactericidal activities of PMN against E.coli. 2) Platelets had effects on the generation of superoxide anion (O2-) of PMN. Their effects were quite different according to the assay condition of PMN, that is, platelets inhibited O2- generation when PMN were at rest or stimulated slightly and they enhanced O2-generation of PMN that were stimulated with optimal condition. 3) Thrombin-activated platelets and their supernatant elicited a transient elevation of [Ca2] of PMN. The activity of the supernatant decreased by treating with hexokinase that decomposed ATP. Further treatment with trypsin abolished its activity almost completely. Considering with our additional experiments, factors that induced [Ca2+] elevation of PMN were ATP, beta-thromboglobulin and some trypsin-sensitive factor(s). 4) Supernatant of thrombin-activated platelets decreased random migration and chemokinesis of PMN.

Adenosine Triphosphate↗

PubMed1993

Gastric ammonia has a potent ulcerogenic action on the rat stomach.

BACKGROUND: The pathophysiological mechanism by which Helicobacter pylori induces mucosal injury has not been clarified. The aim of this study was to investigate the role of urea, urease, and ammonia in rat gastric mucosal lesions using an ex vivo chamber model. METHODS: Two groups of rats, normotensive rats and those subjected to ischemia, were studied. The gastric mucosa was examined histologically and macroscopically, and the transmucosal potential difference was measured. RESULTS: Instillation of urea into the stomach generated ammonia in the presence of urease. The amount of ammonia was increased depending on the concentration of urea and was closely associated with the severity of the histological lesions. The exposure of the stomach to 15-60 mmol/L ammonium hydroxide induced both a reduction in transmucosal potential difference and microscopic damage to the gastric mucosa in normotensive rats. Moreover, 15-60 mmol/L ammonium hydroxide produced severe macroscopic gastric lesions in the rats subjected to ischemia. CONCLUSIONS: These results show that ammonia is deleterious to the gastric mucosa and suggest the importance of urea, urease, and ammonia in the pathophysiology of gastric diseases in H. pylori-infected patients.

Action Potentials↗

PubMed1992

Helicobacter pylori has an ulcerogenic action in the ischemic stomach of rats.

Helicobacter pylori (H. pylori) is now accepted as an important cause of chronic active gastritis. There also seems to be an association between the colonization of H. pylori in the gastric mucosa and peptic ulceration. However, it has not demonstrated that the instillation of H. pylori into the stomach produces the ulcerative gastric lesions in animals or humans. We carried out an experiment to study whether or not H. pylori has an ulcerogenic action in the ischemic stomach of rats, using an ex vivo gastric chamber. The rat stomachs were exposed to 1 ml of H. pylori solution (200 IU of urease/ml) and 1 ml of urea (400 mg/dl) for 60 min after the creation of ischemia in the stomach (by withdrawal of 3 ml of blood). The exposure of the stomach to both H. pylori and urea resulted in severe hemorrhagic gastric mucosal lesions with a marked decrease in potential difference (PD) with a concomitant increase in ammonia concentration in rats with ischemia, whereas gastric lesions and a fall in PD were hardly observed in rats without ischemia. These results have demonstrated that H. pylori has an ulcerogenic action on the stomach subjected to mucosal ischemia.

Animals↗

PubMedDate not supplied

CA125-positive papillary tumor of the peritoneum.

A 71-year-old female visited our outpatient unit with chief complaints of anorexia and a sense of abdominal distension. The abnormalities found after admission were conspicious increases in CA125 levels in serum and ascites as well as anemia, accelerated erythrocyte sedimentation and increased serum LDH. The patient underwent an emergency operation for ileus. The histological diagnosis was serous papillomatous cancer. Immunohistologic staining of the cancer tissue demonstrated the production of CA125. In this very rare the remnant of the Müllerian duct in the peritoneum is thought to have been cancerous.

Aged↗

PubMedDate not supplied

Koebner phenomenon on skin graft donor site in cutaneous angiosarcoma.

An 81-year-old woman developed a necrotic plaque and a surrounding purple-red, irregularly shaped macule on her scalp. The diagnosis of angiosarcoma was confirmed histologically. A wide surgical excision was made followed by a split-thickness skin graft from her right buttock. Nine months later, she noticed a dark purple-red lesion on the donor site which grew rapidly into a large mass. Histological examination revealed irregular clefts and vascular channels lined by atypical endothelial cells. Lung metastasis and pneumothorax were also noted. The secondary tumor appeared to represent Koebner phenomenon in a patient with angiosarcoma of the scalp.

Aged↗