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Biomedical subjects

M Asaka

Publications and source records attributed to M Asaka.

At least 217 records · Page 12Linked to original sources
PubMed1995

Relationship between Helicobacter pylori infection, atrophic gastritis and gastric carcinoma in a Japanese population.

AIM: To evaluate the possible relationship between Helicobacter pylori infection and gastric carcinoma, and its precursor lesion, intestinal metaplasia, in a Japanese population. SUBJECTS AND METHODS: H. pylori infection was identified by the presence of anti-H. pylori immunoglobulin (Ig)G. The frequency of H. pylori infection was compared in 109 patients with gastric carcinoma, the same number of patients with atrophic gastritis and asymptomatic controls matched for age, sex and place of birth. To study the relation between H. pylori and intestinal metaplasia, sera and gastric antral and corpus mucosal biopsies were obtained from 58 asymptomatic controls, 92 patients with chronic gastritis and 80 patients with peptic ulcer. RESULTS: The presence of IgG antibody to H. pylori was significantly more frequent in those with gastric carcinoma than in asymptomatic controls (87.2 versus 74.3%; odds ratio 2.4; 95% confidence interval 1.2-4.8). The positive rates of H. pylori IgG antibody were 80.7% in patients with atrophic gastritis. Mean serum gastrin and pepsinogen II levels in H. pylori-positive patients were higher than those in H. pylori-negative patients. Serum gastrin and pepsinogen I levels were significantly higher in controls than gastric carcinoma patients (P < 0.01 and P < 0.05, respectively). Serum pepsinogen I:II ratios were significantly lower in controls than in gastric carcinoma patients (P < 0.01). Intestinal metaplasia was strongly associated with H. pylori infection, and was only found in patients with IgG antibodies to H. pylori. CONCLUSIONS: These results suggest that H. pylori infection is associated with the development of gastric cancer by providing a suitable environment for carcinogenesis of the gastric mucosa, such as gastric atrophy and intestinal metaplasia.

Enzyme-Linked Immunosorbent Assay↗
PubMed1995

Role of Helicobacter pylori in chronic gastritis: a prospective study.

We conducted a prospective study to evaluate the relationship between Helicobacter pylori infection and chronic gastritis in a Japanese population. H. pylori was found in 67% of patients positive for mononuclear cell (MN cell) infiltration and in 75.8% of patients positive for polymorphonuclear cell (PMN cell) infiltration, whereas H. pylori was found in 14.2% of patients without MN cell infiltration and in 33.2% of patients without PMN cell infiltration. The frequency of MN and PMN cell infiltration in H. pylori-positive patients was significantly higher than that in H. pylori-negative patients. The frequency of H. pylori infection did not differ in those with atrophic gastritis from those without, whereas the frequency of intestinal metaplasia became significantly higher in those with moderate and severe atrophy. There was no significant difference between serum pepsinogen I (PG I) levels in H. pylori-positive and -negative patients. However serum PG II levels were significantly increased in H. pylori-positive patients aged 40-69 years. The serum PG I-II ratio was significantly lower in H. pylori-positive patients aged 40-59 years. These results suggest that H. pylori infection in the gastric mucosa plays an important role in the pathogenesis of chronic and atrophic gastritis and in the development of intestinal metaplasia.

Adult↗
PubMed1994

Possible role of Helicobacter pylori infection in early gastric cancer development.

BACKGROUND: Gastric cancer is the most frequently diagnosed malignancy in Japan. The possible relationship between Helicobacter pylori infection and gastric cancer in Japan was evaluated. METHODS: H. pylori infection was identified by the presence of anti-H. pylori IgG. The frequency of H. pylori infection was compared in 213 patients with gastric cancer and the same number of asymptomatic control subjects matched for age and sex. RESULTS: The presence of IgG antibody to H. pylori was significantly more prevalent (P < 0.001) in those with gastric cancer compared with asymptomatic control subjects (88.2% versus 74.6%). H. pylori positive rates were significantly greater in patients with the intestinal type (90.4%, P < 0.001) and diffuse type (86.4%, P < 0.05) of gastric cancer than in control subjects. Ninety-three percent of the patients with early gastric cancer tested positive for H. pylori (P < 0.001 compared with control subjects), whereas no significant difference was observed between those with advanced gastric cancer and control subjects. The intestinal type of early gastric cancer showed only the significantly increased frequency of high titer (optical density > 1.50) of H. pylori IgG antibody (P < 0.001) compared with control subjects without cancer. CONCLUSIONS: These results suggest that H. pylori infection may be associated with the development of early gastric cancer in Japan.

Adult↗
PubMed1994

Alteration of aldolase isozymes in serum and tissues of patients with cancer and other diseases.

We studied the alteration of aldolase isozymes in the serum and tissues of patients with cancer and other diseases using radioimmunoassays specific for aldolase A, B, and C subunits. Aldolase B was predominantly found in adult liver, where aldolase A and C were distinctly low. Aldolase A and B showed almost the same concentration in fetal liver, while in neonatal liver aldolase B protein concentrations were much higher than aldolase A. In contrast, aldolase A was the predominant isozyme found in hepatoma and gastric cancer tissues, whereas aldolase B was distinctly low in hepatoma tissues, and extremely low in gastric cancer tissues. These results suggest that the aldolase A is a more fetal type of liver isozyme than the aldolase B and C, and aldolase B is a more differentiated type of liver isozyme than aldolase A and C. Serum FDP aldolase activities were elevated in half of patients with liver diseases, all patients with muscle diseases and a few patients with cancer. Serum aldolase A levels were elevated in patients with muscle diseases and cancer, but not elevated in patients with liver diseases. In contrast, serum aldolase B levels were elevated in patients with liver disease, but not elevated in patients with muscle diseases and other diseases without liver injury. Serum aldolase B levels showed a trend to decrease in cancer patients with normal GPT levels. Serum aldolase A/B ratios were significantly increased in cancer patients with normal GPT levels, whereas they showed the decreased levels in patients with liver diseases.(ABSTRACT TRUNCATED AT 250 WORDS)

Fructose-Bisphosphate Aldolase↗
PubMed1994

Point mutation of K-ras gene codon 12 in biliary tract tumors.

BACKGROUND/AIMS: Point mutations of the K-ras gene have been reported in a wide variety of human tumors. However, there might be conflicting data about its presence or incidence in biliary tract tumors. The aim of this study is to elucidate the presence and types of point mutation in biliary tract tumors, including gallbladder carcinoma and adenoma, extrahepatic bile duct carcinoma, and ampullary carcinoma. METHODS: Mutation bands detected in modified two-step polymerase chain reaction were eluted from agarose gel and analyzed by dideoxy sequencing method. RESULTS: Of 20 biliary tract tumors showing a mutation band, G to A single base substitutions were confirmed in 15 cases as the most frequent changes, which were divided into changes for aspartic acid (GAT) and (14) serine (AGT) (1). Changes for valine (GTT) were found in two cases. In extrahepatic bile duct carcinoma, duplicate mutations (GA/TT) were found in two cases and triplicate mutation (A/GA/TT) in one case. The adenoma portion of one "cancer in adenoma" case of gallbladder showed the single base transition (GAT) in the second position, same as in the carcinoma portion. CONCLUSIONS: Most of the biliary tract tumors comprised point mutation in K-ras gene codon 12, and G to A transition was the most frequent.

Adenoma↗
PubMed1994

Helicobacter pylori infection in gastric carcinoma.

PURPOSE: This study was undertaken to compare the pathoclinical findings in gastric adenocarcinoma with serum IgG antibody to Helicobacter pylori. MATERIALS AND METHODS: We examined 185 patients with histologically established gastric cancer. The presence of immunoglobulin (Ig)G antibody in the high molecular cell-associated antigen of H. pylori was determined by enzyme-linked immunosorbent assay. Pepsinogens I and II were measured by radioimmunoassay. The distribution of H. pylori on the gastric mucosa was assessed by the Campylobacter-like organism test and phenol red dye spraying. RESULTS: H. pylori IgG antibody was detected in 93.1% of patients with gastric cancer (mean age 61.7 years), 94.3% of patients with early gastric cancer and 91.2% with advanced gastric cancer. No statistical difference in serology was observed between type of gastric cancer, depth of cancer invasion, tumor size or histology. Only in patients with diffuse-type cancer of the cardia was there a lower percentage of positive results (80.0%). The ratio of pepsinogen I to pepsinogen II was higher in the patients who exhibited no H. pylori antibodies. CONCLUSIONS: H. pylori antibodies were common in patients with gastric cancer, and were not correlated with histological type nor stage of cancer. In the Niigata district, a higher percentage of patients with gastric carcinoma displayed H. pylori antibodies compared with other districts in Japan.

Adenocarcinoma↗
PubMed1994

The role of Helicobacter pylori infection in the pathogenesis of gastritis.

We conducted a prospective study to evaluate the relationship between H. pylori infection and gastritis in a Japanese population. The study population consisted of 92 patients with endoscopically proven gastritis. Biopsy specimens were taken from the gastric mucosa from the corpus and antrum according to the Sydney system for the new classification of gastritis. H. pylori was histologically found in 84.3% of patients for mononuclear (MN) cell infiltration and in 88.1% of those positive for polymorphonuclear (PMN) cells. H. pylori was not found in any of nine patients without MN cell infiltration (P < 0.001), while 68.8% of patients without PMN cell infiltration were positive for H. pylori (P < 0.03). The frequency of MN cell infiltration in H. pylori-positive patients was significantly higher than that in H. pylori-negative patients (100% vs 65.4%; P < 0.001). The frequency of PMN cell infiltration in H. pylori-positive patients was also significantly higher than that in H. pylori-negative patients (54.5% vs 23.1%; P < 0.01). The incidence of MN cell infiltration in the antrum was significantly higher than that in the gastric corpus in H. pylori-positive gastritis patients (93.2% vs 65.1%; P < 0.001). The incidence of PMN cell infiltration was also higher in the antrum than in the corpus in H. pylori-positive gastritis patients, although the difference was not significant (42.0% vs 31.7%).(ABSTRACT TRUNCATED AT 250 WORDS)

Gastric Mucosa↗
PubMed1994

Causal role of Helicobacter pylori in peptic ulcer relapse.

Helicobacter pylori has been shown to infect the gastric mucous layer of almost all patients with duodenal ulcer disease, as well as that of most patients with gastric ulcer disease. Recent studies have suggested that the eradication of H. pylori affects the natural history of duodenal ulcer disease such that the rate of relapse decreases markedly. We evaluated the relationship between H. pylori infection and peptic ulcer relapse in a Japanese population following a prospective study. Seven of 18 (38.9%) gastric ulcer patients positive for H. pylori relapsed by the end of 1 year, whereas only 1 of 9 (11.1%) gastric ulcer patients without H. pylori developed ulcer relapse (P < 0.05). Relapse rates of duodenal ulcer patients negative for H. pylori were significantly lower than those positive for H. pylori within 1 year (0% vs 66.7%; P < 0.01). The effects of anti-H. pylori drugs on the eradication of H. pylori were examined in 50 patients with peptic ulcers. Eradication rates with a proton pump inhibitor (PPI) alone (omeprazole 20 mg) showed the lowest values (4 of 13; 30.8%). The rates were: 44.4% for amoxicillin alone (4 of 9); 70% for triple therapy consisting of amoxicillin, metronidazole, and bismuth subnitrate (14 of 20); and 87.5% for concomitant therapy of the PPI plus amoxicillin (7 of 8). Reinfection rates of H. pylori within 1 year after eradication of this organism were distinctly higher in the PPI alone group (80%) than in other groups (18.2%-32.4%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

The role of Helicobacter pylori in peptic ulcer disease.

The linking of relapse of duodenal as well as gastric ulcers with Helicobacter pylori (H. pylori) has been a considerable advance in managing patients with peptic ulcer disease. However, pathogenetic role of H. pylori in peptic ulcer still remains unclear. The aim of this study was to assess the relationship between H. pylori infection and inflammatory cell infiltration in gastric mucosa in peptic ulcer disease. Sixty-four patients with endoscopically proven gastric ulcer and 26 patients with duodenal ulcer were evaluated by prospective study. Biopsy specimens were taken from the ulcer margin, corpus and antrum. Eradication of H. pylori was attempted by concomitant administration of amoxycillin 500 mg, metronidazole 250 mg and bismuth subnitrate 1 g twice daily for 2 weeks. H. pylori positive rates in clinical stages of gastric and duodenal ulcer showed almost the same values of more than 90%. The prevalence of H. pylori at the antrum and corpus was almost the same as that between gastric and duodenal ulcer patients, whereas a dramatic difference in the positive rates at the ulcer margin was observed between gastric and duodenal ulcer patients (83.9% and 35.0%, respectively). The prevalence of polymorphonuclear (PMN) cell infiltration at the ulcer margin was still high even at the scarring stage of gastric and duodenal ulcer with positive H. pylori, whereas a dramatic decrease of PMN cell infiltration was observed at the ulcer margin after successful eradication of H. pylori. These results suggest that H. pylori may play an important role in the pathogenesis of gastric and duodenal ulcer by inducing inflammatory cells such as PMN cells in gastric mocosa.

Amoxicillin↗
PubMed1993

The mechanisms of aspirin-induced gastric mucosal injury.

We examined changes in intracellular pH with the fluorescent probe BCECF after treatment with aspirin (ASA) in gastric mucosal cells isolated from guinea pigs at various extracellular, pH levels. The cytotoxic activities of ASA and the intracellular trapping of ASA at various extracellular pH levels were also examined by colorimetric MTT assay and counting the influx of [14C](carboxyl-14C)-ASA. Under acid extracellular pH, ASA reduced intracellular pH in gastric mucosal cells and exhibited cytotoxicity. Intracellular trapping of ASA was also observed only under acidic extracellular conditions. The present study suggests that ASA causes gastric mucosal cell injury in vitro by reducing intracellular pH, resulting from intracellular trapping of ASA under acidic extracellular conditions.

Animals↗
PubMed1993

Effect of a novel immunosuppressant, FK506, on spontaneous lupus nephritis in MRL/MpJ-lpr/lpr mice.

We evaluated the effect of the novel immunosuppressive agent, FK506, which is known to inhibit T cell immunity, on the development of lupus nephritis in MRL/MpJ-lpr/lpr (MRL/l) mice. FK506 was administered subcutaneously (1 mg/kg body weight) from 12 to 20 weeks of age in 13 MRL/l mice with spontaneous lupus nephritis. Nine animals receiving no treatment were used as the control. FK506 significantly reduced the development of proteinuria, lowered the level of BUN, and suppressed the elevation of serum anti-dsDNA antibodies. Histopathological study showed that FK506 significantly inhibited the progression of glomerular hypercellularity and crescent formation. Glomerular deposition of C3 was significantly reduced in the FK506-treated mice compared to the nontreated controls. These findings suggest that FK506 may protect against progression of lupus nephritis in MRL/l mice, an animal model of systemic lupus erythematosus.

Animals↗
PubMed1993

The protective effect of 4-hydroxy-2-methyl-N-[2-(tetrazol-5-yl)- phenyl]-2H-1, 2-benzothiazine-3-carboxamide-1, 1-dioxide monosodium salt (HX-1920) on cisplatin-induced toxicity in rats.

The protective effect of 4-hydroxy-2-methyl-N-[2-(tetrazol-5-yl)-phenyl]-2H-1, 2-benzothiazine-3-carboxamide-1, 1-dioxide monosodium salt (HX-1920) on the nephrotoxicity of cisplatin was studied in rats. Effects of HX-1920 on antitumor activity and emesis induced by cisplatin were also examined using mice and ferrets, respectively. All 10 rats injected with both HX-1920 and LD50 of cisplatin survived for 14 days. After 24 hr, co-administration of HX-1920 significantly increased the urinary excretion of cisplatin in rats. HX-1920 also significantly inhibited the cisplatin-induced elevation of urinary N-acetyl-beta-D-glucosaminidase, blood urea nitrogen and plasma creatinine concentrations in rats. HX-1920 had no effect on the number of white blood cell. HX-1920 tended to reduce the emesis induced by cisplatin in ferrets. Furthermore, there was no difference in the survival curve between the cisplatin group and the HX-1920 plus cisplatin group in mice inoculated with P 388 leukemia cells. Thus, HX-1920 did not modify the antitumor activity of cisplatin. These results suggest that HX-1920 has a protective effect on the nephrotoxicity of cisplatin without inhibiting its antitumor activity.

Acetylglucosaminidase↗
PubMed1993

Glomerulosclerosis in the rat induced by repeated immune-mediated mesangial cell injury.

Glomerulosclerosis is a common feature of progressive glomerular injury. We investigated whether experimental glomerulosclerosis could be induced by repeated immunologic injury to mesangial cells. Chronic mesangial proliferative glomerulonephritis (GN) was induced by repeated injections of polyclonal antibody directed against the Thy 1 antigen present on the mesangial cell membrane. An intravenous injection of anti-Thy 1 serum (ATS) was given weekly to 18 male Wistar rats, which were sacrificed at weeks 2, 4 and 6 after induction of GN. Blood urea nitrogen and serum creatinine were significantly elevated in rats with anti-Thy 1 nephritis at weeks 4 and 6 compared to normal rats. Progressive expansion of the mesangial matrix with diffuse sclerosis was observed at weeks 4 and 6 by silver methenamine staining. Ultrastructurally there was a prominent rough endoplasmic reticulum in the mesangial cells and collagenous fibrils in an expanded mesangial matrix. Immunohistochemical staining revealed a marked increase in type IV collagen and laminin in the mesangium at weeks 4 and 6. Thus, repeated immunologic injury restricted to the mesangium may result in the accumulation of extracellular matrix and the development of glomerulosclerosis. These studies emphasize the importance of the mesangial cell in progressive glomerular injury.

Animals↗
PubMed1993

[13C-urea breath test].

The 13C-urea breath test is now a practical and readily available alternative to endoscopy- and serology-based methods for the detection of H. pylori infection. It can detect very low levels of H. pylori colonization within the stomach by assessing the entire mucosa, and avoids the risks of sampling error. We performed the 13C-urea breath test in asymptomatic volunteers and patients with gastric and duodenal ulcers in order to compare the sensitivity and specificity by measurement of H. pylori antibody by ELISA. The positive rates of H. pylori in the 13C-urea breath test was correspondent with the results from the H. pylori antibody test, although no correlation in the antibody titers and urease activities was observed between the two methods. The 13C-urea breath test was the most useful method in evaluation of eradication of H. pylori after administration of antibiotics, compared to serological and pathological methods. These results suggest that the 13C-urea breath test is highly useful for the diagnosis of H. pylori infection of the gastric mucosa.

Adolescent↗
PubMed1992

Relationship of Helicobacter pylori to serum pepsinogens in an asymptomatic Japanese population.

A seroepidemiologic study of the prevalence of Helicobacter pylori infection in Japan was performed, and the relationship between serum pepsinogen I and II levels (markers of gastritis and gastric atrophy) and H. pylori infection was investigated. Four hundred and eighteen asymptomatic children and adults were studied. The prevalence of anti-H. pylori immunoglobulin G antibody increased with age. For persons born after 1950, the frequency of H. pylori infection increased at approximately 1% per year; for those born before 1950 the prevalence was high (70%-80%) and relatively constant. Serum pepsinogen I and II levels were significantly higher in H. pylori-infected volunteers than in H. pylori-uninfected volunteers [51.6 +/- 3 vs. 42.9 +/- 2 ng/mL (P less than 0.05) for pepsinogen I; 16.0 +/- 1 vs. 7.5 +/- 0.8 ng/mL (P less than 0.001) for pepsinogen II]. The ratio of pepsinogen I to pepsinogen II was significantly lower in H. pylori-infected volunteers (3.5 +/- 0.2) than in uninfected volunteers (6.3 +/- 0.3; P less than 0.001). The apparent decrease in prevalence of H. pylori accompanying the Westernization of Japan may eventually be accompanied by a reduction in the frequency of atrophic gastritis, the precursor lesion of the epidemic form of gastric carcinoma, and ultimately result in a decrease in the incidence of gastric carcinoma in Japan.

Adolescent↗
PubMed1992

Stress-induced gastric mucosal lesion and platelet aggregation in rats.

The effect of cold-restraint stress on platelet function in vitro was studied in the rat model. Platelet function was assessed by platelet aggregation in response to adenosine diphosphate (ADP) and thrombin. ADP-induced platelet aggregation was reduced in platelet-rich plasma after 2 h of cold-restraint stress. Thrombin-induced platelet aggregation was reduced with time during cold-restraint stress with a parallel increase in the lesion index. Although pretreatment of animals with atropine prevented the development of gastric mucosal lesions, platelet dysfunction was not reversed by this treatment. These results suggest that cold-restraint stress may impair platelet function, probably due to platelet activation in vivo, and that the abnormalities in platelet function may be associated with the development of gastric mucosal lesions.

Adenosine Diphosphate↗
PubMed1992

Effects of the platelet-activating factor antagonists CV-6209 and CV-3988 on nephrotoxic serum nephritis in the rat.

Platelet-activating factor (PAF) is known as an important mediator in the pathogenesis of glomerular injury. In the present study, we evaluated the effect of the specific PAF antagonists CV-6209 and CV-3988 on accelerated nephrotoxic serum nephritis (NTN) in the rat. The amount of urinary protein excretion was significantly less in the rats treated with CV-6209 or CV-3988 on the 5th and 7th day of treatment than in the nontreated controls. The results of light- and immunofluorescence-microscopic examination did not demonstrate any favorable effect on glomerular changes by these PAF antagonists. However, CV-6209 protected against the loss of glomerular anionic charges in rats with NTN. Thus, it is suggested that PAF is a potent mediator of protein excretion, and that the loss of glomerular anionic charges is an important mechanism for the mediation of PAF in glomerulonephritis.

Animals↗