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Biomedical subjects

M Asaka

Publications and source records attributed to M Asaka.

At least 163 records · Page 9Linked to original sources
PubMed1998

Detection of coccoid Helicobacter pylori: light microscopical immunogold silver enhancing stain.

BACKGROUND: Helicobacter pylori (H. pylori) can be morphologically divided into spiral and coccoid forms. Although many different staining procedures for light microscopy have been developed to detect H. pylori, there are no reports that the coccoid forms can be specially identified by a staining method. The ability to identify the coccoid form of H. pylori by light microscopy would be important for studies evaluating its possible role in gastric disease. We examined whether both the coccoid and the spiral forms could be stained using anti-H. pylori antibody. METHODS: Specimens from the stomachs of dyspeptic patients with proven H. pylori infection and H. pylori from culture (1st and 4th day) were stained with the light microscopic immunogold silver enhancing stain using the rabbit IgG specific for H. pylori. Cultured H. pylori was also stained with electron microscopic immunogold staining method using the same antibody. The number of coccoid forms was counted by scanning electron microscopy. RESULTS: Biopsies and H. pylori from 6 patients were studied. H. pylori from both biopsy material and culture appeared as black organisms by light microscopic immunogold silver enhancing stain. The coccoid forms constituted 0.4% and 98.3% on days 1 and 4 of culture, respectively (by scanning electron microscopy). The antigen recognized by the anti-H. pylori antibody was located on the surface of the flagella, the cell wall, or in the cytoplasm by immunoelectron microscopy. CONCLUSION: This study shows that both spiral and coccoid forms of H. pylori can be detected by light microscopic immunogold silver enhancing stain using anti-H. pylori antibody. This simple stain is to be proven useful for studies aimed at understanding whether the coccoid form plays a role in disease.

Animals↗
PubMed1998

Modification of Helicobacter pylori adhesion to human gastric epithelial cells by antiadhesion agents.

Helicobacter pylori is a major etiological agent in gastroduodenal disorders. H. pylori adhesion to human gastric mucosa is the initial step of H. pylori colonization. Inhibition of H. pylori adhesion is thus a therapeutic target in preventing H. pylori infection. We have previously established a method using the enzyme-linked immunosorbent assay to analyze quantitatively H. pylori adhesion to gastric epithelial cells. This method is suitable for screening antiadhesion agents. Some mucoprotective agents are proved to have antiadhesion effects in vitro, and they may modify H. pylori adhesion. This evidence gives us a useful clue to analyze the molecular mechanism of H. pylori adhesion to mucosa. Furthermore, in clinical trials, these mucoprotective agents enhanced the eradication rate when administered with antibiotics. In conclusion, the antiadhesion agents may have potential as therapeutic regimens against H. pylori infection.

Bacterial Adhesion↗
PubMed1998

Effects of rebamipide in combination with lansoprazole and amoxicillin on Helicobacter pylori-infected gastric ulcer patients.

The aim of this study was to compare the additive effect of rebamipide with that of teprenone in combination with dual therapy on H. pylori eradication. A total of 102 H. pylori-positive gastric ulcer patients were assigned at random to two groups; in addition to dual therapy (amoxicillin 500 mg thrice daily and lansoprazole 30 mg every morning for two weeks), one group received rebamipide 100 mg thrice daily for eight weeks, while the other group received teprenone 50 mg thrice daily for eight weeks. H. pylori diagnosis after treatment was made by [13C]UBT. The ulcer healing rate was 85.7% in the rebamipide group and 79.5% in the teprenone group (P = NS). The eradication rate was 68.4% (95% CI = 54-83%) in the rebamipide group and 47.7% (95% CI = 32-61%) in the teprenone group (P = 0.043) by per-protocol analysis. These findings suggest that the efficacy of dual therapy may be increased by the administration of rebamipide.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1998

Clinical studies of 13C-urea breath test in Japan.

The urea breath test (UBT) using isotope carbon is a non-invasive method for diagnosing H. pylori infection. In Japan, only 13C-UBT using a stable isotope is available, since the clinical use of radioactive isotope 14C-compounds is prohibited. Since there is no worldwide standard protocol for the 13C-UBT, it is therefore important to standardize this test to obtain a cheap, easy, reproducible method. Factors affecting the outcome of 13C-UBT values include sampling times and frequency, the amount of 13C-urea, the cut-off value, the avoidance of oral urease activity, and changes in gastric emptying times and 13C-urea distribution. Mouth rinsing reduces false-positive results due to oral urease activity, particularly within 20 min after ingestion of 13C-urea. A Japanese multicenter trial has shown that the diagnostic utility of 13C-UBT is superb, with the cut-off value 2.5/1000 in 20-min samples after ingestion of 100 mg 13C-urea. The 13C-UBT is a very useful method for diagnosing H. pylori infection.

Breath Tests↗
PubMed1998

Ten minute 13C-urea breath test for the diagnosis of Helicobacter pylori infection.

We investigated the utility of a 10-min 13C-urea breath test (13C-UBT) using 100mg of 13C-urea; this is a simple and rapid method for the detection of Helicobacter pylori infection. One hundred and fifty-one patients in whom the identification of H. pylori was established by rapid urease test, culture, and histology of six biopsy specimens underwent 254 13C-UBT examinations before and/or after eradication treatment. In the 133 patients who did not receive eradication treatment, the calculated sensitivity of the 10-min 13C-UBT was 99.4% and specificity 100% when the cut-off point was set at 3.5/1000, using a mass spectrometer. In the 121 patients who received eradication treatment, this cut-off point gave a sensitivity of 86.7%, a specificity of 99.1%, and a positive predictive value of 92.9%, with a negative predictive value of 98.1%. There were no significant differences between the diagnosis of H. pylori infection at 1 month and more than 3 months after the endpoint of eradication treatment. The 10-min 13C-UBT is suitable for the diagnosis of H. pylori infection before and after eradication treatment.

Breath Tests↗
PubMed1997

What role does Helicobacter pylori play in gastric cancer?

Several lines of evidence support an association between Helicobacter pylori infection and gastric cancer. The natural history of H. pylori-associated gastritis is inexorable progression ultimately leading to gastric atrophy. In general, this process requires between 20 and 40 years to complete. Atrophic gastritis is widely considered to be a precursor lesion of the intestinal type of gastric cancer. Moreover, areas with a high prevalence of H. pylori infection also have a high prevalence of gastric cancer. Strong evidence from three prospective studies shows the risk of gastric cancer to be increased fourfold in H. pylori-positive persons. Several retrospective studies have also confirmed that H. pylori infection is associated with development of gastric cancer, especially in the younger generation, early gastric cancer, and noncardiac gastric cancer. H. pylori alone is not likely responsible for gastric cancer. Rather, it may provide a suitable environment, including chronic gastritis and intestinal metaplasia, for neoplastic change. Recognition of an association between H. pylori infection and gastric cancer has led to a major shift in emphasis on the cause of the disease. Research into H. pylori has focused attention on the importance of chronic inflammation and impaired host defense mechanisms as factors in the development of gastric cancer. H. pylori infection leads to changes in many factors that are important to the pathogenesis of gastric cancer, including vitamin C content of gastric juice, reactive oxygen metabolites, and epithelial cell proliferation. Eradication of the organism may reverse these changes. Therefore, eradication of H. pylori in infected persons might be a route to preventing gastric cancer, although many questions still remain as to the effectiveness of this strategy.

Chronic Disease↗
PubMed1997

The important balance between cytokines derived from type 1 and type 2 helper T cells in the control of graft-versus-host disease.

We have investigated cytokine mRNA expression in the peripheral blood mononuclear cells of 20 patients who received allogeneic hematopoietic stem cell transplants to assess the cytokine network after transplantation. IL-4 mRNA expression decreased in five of five (100%) patients with > or = grade III (severe) acute GVHD and increased in 10 of 22 (45%) patients without severe GVHD. In contrast, IL-12 mRNA expression increased in two of two (100%) patients with severe GVHD, but increased in only six of 18 (33%) patients without severe GVHD. Furthermore, IL-10 and/or IL-13 mRNA expression increased in 19 of 22 (86%) patients without severe GVHD, but increased in only one of three (33%) patients with severe GVHD. In patients with allogeneic PBSCT who had severe acute GVHD, the cytokine mRNA expression in patients with allogeneic PBSCT, who had no severe GVHD, showed a similar pattern to that in patients with allogeneic BMT. IL-4 mRNA expression increased in three of five (60%) patients and IL-10 and/or IL-13 mRNA expression increased in five of five (100%) patients. In contrast, IL-12 mRNA expression increased in only one of three (33%) patients. Serum IL-4 concentration in allogeneic PBSCT patients in the early engraftment phase was relatively high, while serum IL-12 concentration was low. These findings suggest that severe GVHD may be related to the cytokine imbalance between type 1 helper T (Th1) cells and type 2 helper T (Th2) cells.

Adult↗
PubMed1997

Inhaled vancomycin-induced allergic reaction in decontamination of respiratory tracts for allogeneic bone marrow transplantation.

A 34-year-old male suffered from an allergic reaction after inhalation of decontaminating drugs for BMT. Clinical challenge tests were undertaken to determine the causal drug. It was found that vancomycin hydrochloride (VCM) repeatedly induced dyspnea, fever, hypoxia, eosinophilia, and elevation of CRP. Therefore, clindamycin (CLDM) was used instead of VCM for decontamination of patient respiratory tract. Although complete decontamination of the respiratory tract was not achieved during the leukocytopenic period, BMT was successful, and there were no life-threatening infectious complications. Although inhaled VCM-induced allergic reaction may be a very rare complication in the BMT setting, careful clinical attention should be paid to such patients.

Administration, Inhalation↗
PubMed1997

Studies on gastric mucosal cell injury induced by Helicobacter pylori.

The cause of gastric cell injury induced by Helicobacter pylori was investigated in vitro using gastric mucosal cells derived from male Japanese white rabbits. To evaluate the contribution of the potent urease activity of H. pylori to gastric mucosal cell injury, the supernatant of the H. pylori bacterial pellet, solubilized with N-octyl-glucoside, was added to the gastric mucosal cell suspension. Cell injury was assessed by lactate dehydrogenase (LDH) release into the extracellular fluid. Treatment of cells with H. pylori extracts together with urea resulted in high levels of LDH release, suggesting definite gastric mucosal cell injury, and elevation of ammonia concentration was also observed. In contrast, incubation with H. pylori extracts alone or urea solution alone did not result in increased LDH release or elevated ammonia concentrations. The degree of LDH release from gastric mucosal cells due to H. pylori extracts in the presence of urea was similar to that induced by administration of the same amount of exogenous ammonia. The addition of acetohydroxamic acid, a potent specific urease inhibitor, remarkably inhibited ammonia production, the elevation of pH of extracellular fluid, and LDH release in a dose-dependent manner. These results suggest that ammonia produced by potent urease activity of H. pylori in the presence of urea plays an important role in the pathogenesis of gastric mucosal cell injury.

Ammonia↗
PubMed1997

Increased cytokine production by gastric mucosa in patients with Helicobacter pylori infection.

To determine the mechanisms of gastric mucosal injury associated with Helicobacter pylori infection, we investigated the contents of cytokines and inflammatory cell infiltration in the gastric mucosa. Ninety-six patients with dyspepsia were studied (58 gastric ulcer, 38 nonulcer dyspepsia). Of the 96 patients, 63 were infected with H. pylori as determined by microscopic examination with HE staining, culture of H. pylori, or the rapid urease test. Endoscopic biopsy specimens were obtained from both the antrum and the body to examine interleukin (IL)-8, IL-6, IL-1 beta, and tumor necrosis factor-alpha contents in the gastric mucosa by enzyme-linked immunosorbent assay. Inflammatory cell infiltration was assessed according to the Sydney system. IL-8 content was enhanced in both the antral and body mucosa of the H. pylori-positive patients compared with the H. pylori-negative patients. Furthermore, IL-8 content correlated well with the infiltration of both mononuclear cells and polymorphonuclear cells. These results suggest that IL-8 plays important roles in the pathogenesis of gastric mucosal injury associated with H. pylori infection.

Case-Control Studies↗
PubMed1997

Fifteen-year follow-up of acquired renal cystic disease - a gender difference.

In 1979, 96 patients who had undergone hemodialysis for a mean of 3 years and 4 months were entered into this study. This follow-up study revealed that the bilateral kidney volume significantly increased over 10 years in 33 male patients. Kidneys were found to have enlarged 2.7 times over the 10-year follow-up period. However, in 24 females kidney volume did not change over 10 years. This paper reports further results in 39 dialysis patients (21 males and 18 females) who were followed from the 10th to 15th year. In male patients, mean volume was 196 +/- 218 ml (mean +/- SD) at the 10th year and had significantly increased to 225 +/- 213 ml at the 15th year (p < 0.02). In female patients, mean kidney volume was 78 +/- 51 ml at the 10th year and had increased to 117 +/- 91 ml at the 15th year (p < 0.01). The enlargement in kidney volume during the recent 5 years was 1.26 +/- 0.39-fold in males and 1.43 +/- 0.45-fold in females. These rates did not significantly differ between males and females. During this recent 5-year period, there were no surgical cases due to renal cell carcinoma. Therefore, over the entire patient-time dialysis period, there were 6 renal cell carcinomas in 1,470 patient years. In conclusion, 10- to 15-year follow-up studies of kidney size revealed that the enlargement in the kidney due to acquired cysts persisted in male patients, but the rate of increase slowed after 13.0 years of hemodialysis, while the enlargement in the kidney in female patients became significant at 17.7 years of hemodialysis, revealing the slowly progressive nature of acquired cysts in women.

Adult↗
PubMed1997

Invasive pulmonary aspergillosis complicated by subclavian artery occlusion following allogeneic stem cell transplantation.

We describe an unusual case of invasive pulmonary aspergillosis (IPA) complicated by subclavian artery occlusion in a 32-year-old man with severe aplastic anemia, who underwent allogeneic stem cell transplantation. He was severely neutropenic after the conditioning for transplantation, but he had no history of fungal infection. Five days after the transplantation, he developed IPA in the left upper lung, complicated by left subclavian artery occlusion. Extensive chronic graft-versus-host disease, which required the administration of potent immunosuppressants for a long period of time, interfered with the resolution of the IPA.

Adult↗
PubMed1997

Clinical relevance of serum soluble interleukin-2 receptor levels in acute and chronic graft-versus-host disease.

Soluble interleukin-2 receptor (sIL-2R) levels were analyzed in the sera from 27 patients who underwent allogeneic bone marrow transplantation (BMT) in order to to examine whether there was any correlation between sIL-2R levels and graft-versus-host disease (GVHD). The sIL-2R levels markedly increased at the engraftment period, mainly due to cytokine administration shortly after BMT. Although the sIL-2R levels increased at the onset of acute GVHD, the subsequent development of GVHD could not be predicted by the sIL-2R levels documented before acute GVHD. As acute GVHD improved, the sIL-2R levels decreased, thus showing that the sIL-2R levels correlated with the disease status. In patients without acute GVHD, the sIL-2R levels gradually decreased with time and returned to the pretransplant levels after about 12 weeks post BMT. The sIL-2R levels were higher in unrelated allogeneic BMT patients with acute GVHD when compared with related allogeneic BMT patients. There was a significant increase in the sIL-2R levels at the engraftment period and at the onset of acute GVHD. At the onset of chronic GVHD, the sIL-2R levels once again increased and then decreased as chronic GVHD improved. Prolonged increase in sIL-2R levels was followed by subsequent development of chronic GVHD. Patients with a poor prognosis had higher sIL-2R levels than those with a good prognosis. Therefore, it seems that sIL-2R is a useful marker for monitoring the disease status of acute and chronic GVHD.

Adolescent↗
PubMed1997

A translocation t(8;14) and c-myc gene rearrangement associated with the histological transformation of B-cell acute lymphocytic leukemia (FAB-L2) into Burkitt's type (FAB-L3) leukemia.

We report a case of B-cell acute lymphocytic leukemia which showed histological transformation from an FAB-L2 into a Burkitt's type (FAB-L3). Both leukemias had identical immunoglobulin heavy-chain joining gene and kappa light-chain joining gene rearrangements, indicating the clonal identity of the two leukemias. A chromosomal analysis of leukemia cells on the onset indicated normal karyotype, whereas that of the transformed FAB-L3 showed t(8;14)(q24;q32). Furthermore, the proto-oncogene c-myc was in the germline configuration in the initial leukemia but in the rearranged configuration after transformation. Presence of t(8;14)(q24;q32) and the c-myc gene rearrangement after transformation suggested that the chromosomal translocation followed by the activation of the c-myc proto-oncogene might be involved in the Burkitt's type transformation of the FAB-L2 leukemic clone, but not in the leukemogenesis of the initial FAB-L2 leukemia.

Adolescent↗