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Biomedical subjects

Y Taguchi

Publications and source records attributed to Y Taguchi.

At least 109 records · Page 6Linked to original sources

Helicobacter pylori inhibits the secretory activity of gastric parietal cells in patients with chronic gastritis. An ultrastructural study.

BACKGROUND: Previous in vitro studies suggested that Helicobacter pylori may inhibit the acid secretion of gastric parietal cells. The aim of this study was to investigate ultrastructurally the influence of H. pylori infection on the gastric parietal cell function in vivo. METHODS: This study comprised 28 patients with chronic gastritis. Biopsy specimens were taken from the gastric body in all cases and examined by electron microscopy. Gastric parietal cells were counted in each ultrathin section and classified into secretory and non-secretory types. The pH of the gastric juice was also measured in all patients. RESULTS: The number of parietal cells in the secretory phase was significantly lower in H. pylori-infected (n = 16) patients than in those (n = 12) without H. pylori infection. The intragastric pH was significantly higher in patients with H. pylori-associated gastritis than in those without H. pylori infection. Parietal cells in secretory phase tended to decrease in proportion to the activity of the gastric mucosal inflammation. CONCLUSIONS: The results of this investigation suggests that H. pylori-associated gastritis is related to a decreased secretory activity of the gastric parietal cells.

Biopsy↗

Gastric juice levels of lactoferrin and Helicobacter pylori infection.

BACKGROUND: Recently, in vitro studies suggested that lactoferrin (Lf) might play an important role in the physiopathology of Helicobacter pylori-associated gastritis. However, whether Lf is present in the gastric juice and its relationship with H. pylori infection have not as yet been reported. In the present investigation the presence of Lf in gastric juice and its correlation with H. pylori infection were assessed. METHODS: This study comprised 30 H. pylori-positive and 14-negative patients with chronic gastritis. Gastric juice levels of Lf were measured with enzyme-linked immunoassays. Gastric juice concentration of Lf was also investigated in accordance with the histologic findings of biopsy specimens in the gastric body and antrum. RESULTS: Lf concentration in gastric juice was significantly higher in H. pylori-positive than in -negative patients (P = 0.033). The pH values are known to influence the levels of Lf. However, intragastric Lf levels were also significantly increased in H. pylori-positive patients as compared with H. pylori-negative patients after correcting the Lf levels for pH values (P = 0.029) or after adjusting the pH values of the gastric juice with NaHCO3 solution in both groups of patients (P = 0.0007). In addition, the gastric juice levels of Lf correlated significantly with the gastric mucosal concentrations of Lf in the gastric body (P < 0.005, r = 0.568) and the antrum (P < 0.05, r = 0.401). CONCLUSIONS: This study showed for the first time that Lf is present in gastric juice and that it correlates with H. pylori infection. Lf may constitute a good marker for H. pylori-associated gastritis. Although correlation does not prove causation, this study suggests that Lf might play an important role in the physiopathology of H. pylori-associated gastritis.

Biomarkers↗

Relation of lactoferrin levels in gastric mucosa with Helicobacter pylori infection and with the degree of gastric inflammation.

OBJECTIVES: Lactoferrin (Lf) is an iron-binding glycoprotein present in milk, lacrimae, saliva, and gastroduodenal secretions. In vitro studies disclosed contradicting results regarding the relation of Lf with Helicobacter pylori (HP) infection. This study aimed to investigate the relationship between the gastric mucosal concentration of Lf and HP infection of the stomach. The relationship of the gastric mucosal level of Lf with the gastric mucosal concentration of interleukin-8 (IL-8) and with the intragastric ammonia levels was also assessed. In addition, the gastric mucosal Lf levels before and after irradication of HP infection were also evaluated. METHODS: This study was composed of 27 HP-positive and 12 HP-negative patients with chronic gastritis. Gastric mucosal biopsy specimens were obtained from all subjects by endoscopy, and the degree of histological inflammatory changes were assessed according to the Sydney system. The gastric mucosal levels of Lf and IL-8 were measured by immunoassays. Assessment of the effect of therapy on the gastric mucosal level of Lf was performed in 10 patients with HP-associated duodenal ulcer. RESULTS: Lf, IL-8, and ammonia levels were significantly higher in patients with HP-positive gastritis compared with those with HP-negative gastritis in both the antrum and the gastric body. Histologically, the degree of inflammatory changes correlated significantly with the Lf levels in the gastric mucosa. Furthermore, the degree of HP colonization was more significant in biopsy samples from the antrum than in those from the corpus of the stomach. The gastric mucosal levels of Lf and IL-8 correlated significantly in the antrum and the gastric body. The ammonia intragastric level significantly correlated with the mucosal Lf level in the antrum and in the gastric body. Therapy significantly decreased the Lf levels in the gastric mucosa of the antrum (p < 0.005) and the gastric body (p < 0.005). CONCLUSION: The results of the present investigation showed, for the first time in vivo, that Lf concentration is increased in the biopsy specimens of patients with HP-related gastritis, and that the levels of Lf correlate significantly with the degree of inflammation of the gastric mucosa. The gastric mucosal level of Lf may constitute an excellent marker of HP infection.

2-Pyridinylmethylsulfinylbenzimidazoles↗

[Abducens palsy].

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Abducens Nerve↗

[Prediction of outcome after acute exacerbation of idiopathic interstitial pneumonia].

Some patients with chronic idiopathic interstitial pneumonia (IIP) experience acute exacerbations (AE). Because the precise mechanisms of AE in patients with IIP remain unclear, the treatment for AE is not established and the efficacy of steroids is controversial. Consequently, it is difficult to predict outcomes in patients with AE of IIP. We therefore studied the relationship between clinical findings, efficacy of treatment, and clinical outcome in patients with AE of IIP. Thirty-two patients were enrolled, and were divided into two groups: 10 who were alive more than one year after the onset of the AE survivors, 8 men and 2 women, and 22 who died within one year of the AE (non-survivors, 17 men and 5 women). Survivors were significantly younger than non-survivors (59.7 +/- 9.9 vs 67.5 +/- 8.2 years, respectively, p < 0.05). The values of PaCO2 measured before the AE were higher in survivors than in non-survivors (43.0 +/- 3.7 vs 38.4 +/- 4.0 torr, respectively, p < 0.05). At the onset of the AE the levels of C-reactive protein in serum were higher in survivors than in non-survivors (13.9 +/- 7.9 vs 7.3 +/- 5.8 mg/dl, respectively, p < 0.05). Chest X-ray films showed progression of ground-glass shadows in both groups when the AE occurred; the radiographic findings did not differ markedly between groups. Of the 22 non-survivors, 7 had received medication before the AE; none of the survivors had received medication before the AE. At the time of the AE all patients were treated with steroid pulse therapy, and the dose of methylprednisolone used, did not differ significantly between groups. These data suggest that three factors are closely related to responsiveness to steroid therapy and to clinical outcomes after AE in patients with IIP: 1) age at the onset on IIP, 2) respiratory status before the AE, and 3) disease activity as reflected by inflammatory reactions.

Age Factors↗

[Skew deviation].

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Brain Diseases↗

[Venous angioma].

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Brain Neoplasms↗

[Creutzfeldt-Jakob disease with a widespread presence of kuru-type plaques after cadaveric dural graft replacement. An autopsy case].

A case of Creutzfeldt-Jakob disease (CJD) is reported in a 48-year-old woman who had received a cadaveric dural graft after a clipping procedure of a cerebral artery aneurysm in September 1985. In November 1994, she noticed unsteady gait and blurred vision at first. She successively developed ataxic gait, dementia and myoclonus, and became mute. Serial CT scans revealed no abnormal findings, and serial EEGs showed diffuse slow activity without periodic discharge. The patient died in March 1996, 17 months after the initial symptoms. A brain autopsy demonstrated extensive spongiform degeneration in the cerebral neocortex, thalamus, striatum, and cerebellum especially in the granular layer, with associated astrocytosis and marked neuronal loss. Immunohistochemically, PrP plaques, so called kuru-type plaques, were extensively distributed throughout the cerebrum and cerebellum. Moreover, some of these plaques resembled "florid" plaques, which were surrounded by a zone of spongiform change. The PrP gene analysis of her blood and brain tissue revealed no mutations with homozygosity, Met/Met, at codon 129. The unusual features of this case, that is the absence of PSD on EEG and the widespread presence of kuru-type plaques including "florid" plaques, may be similar to the features of "new variant" CJD.

Cadaver↗

Aureobasidin A, an antifungal cyclic depsipeptide antibiotic, is a substrate for both human MDR1 and MDR2/P-glycoproteins.

The human MDR1 gene encodes the multidrug transporter P-glycoprotein (Pgp). Although the MDR2/Pgp shares about 80% identity at the amino acid level with the MDR1/Pgp, the MDR2/Pgp cannot act as a multidrug transporter. We examined the drug sensitivity of Saccharomyces cerevisiae expressing either the human MDR1/Pgp or MDR2/ Pgp. The human MDR1/Pgp conferred about 4-fold resistance to aureobasidin A, a cyclic depsipeptide antifungal antibiotic, on the drug-sensitive yeast strains. Interestingly the human MDR2/Pgp also conferred about 2.5-fold resistance to aureobasidin A. The resistance to aureobasidin A conferred by the MDR2/Pgp as well as by the MDR1/Pgp was overcome by vinblastine, verapamil, and cyclosporin A, depending on their concentrations, but not by colchicine. Aureobasidin A probably interacts directly with Pgps, because it overcame multidrug resistance of human cells and inhibited azidopine photoaffinity labeling of MDR1/Pgp in human cell membranes. These results suggest the possibility that the human MDR1 and MDR2/Pgps have conserved domain(s) for drug recognition.

ATP Binding Cassette Transporter, Subfamily B↗

Advance directives and withdrawal of dialysis in the United States, Germany, and Japan.

OBJECTIVE: To determine the role of advance directives in decisions to withdraw chronic dialysis in the United States, Germany, and Japan. DESIGN: Survey by questionnaire. PARTICIPANTS: Seventy-two American, 87 German, and 73 Japanese nephrologists. MAIN OUTCOME MEASURES: Each nephrologist's total number of (1) dialysis patients, (2) cases of withdrawal of dialysis, (3) patients with advance directives, and (4) uses of such directives. Nephrologists also stated whether they would continue or stop dialysis in 8 hypothetical cases. RESULTS: American, German, and Japanese nephrologists reported withdrawing dialysis for 5.1%, 1.6%, and 0.7% of their patients in the last year, respectively. Thirty percent of American patients had advance directives, and such directives were used in decision making for 3.2% of all patients. Only 0.3% of German and Japanese patients had advance directives, and such directives were used in decision making for 0.09% of patients. When asked about a hypothetical mentally incompetent patient whose family requests withdrawal of dialysis, American nephrologists were much more likely to stop dialysis in the absence of an advance directive than German or Japanese nephrologists. However, almost all nephrologists from the 3 countries would stop dialysis when a family request to withdraw was supported by a patient advance directive. CONCLUSIONS: There is a high prevalence of advance directives among American dialysis patients, and such directives frequently play a role in decision making. German and Japanese nephrologists appear willing to follow advance directives, but the low prevalence of such directives limits the frequency of their use.

Advance Directive Adherence↗

A dnaA box can functionally substitute for the priming signals in the oriV of the broad host-range plasmid RSF1010.

The initiation of replication from oriV RSF1010, the replication origin of the broad host-range plasmid RSF1010, depends on RepA (helicase), RepB' (primase), and RepC (initiator protein), encoded by RSF1010 itself, while this initiation event in E. coli is independent of dnaA, dnaB, dnaC, and dnaG [Scherzinger et al. (1984) Proc. Natl. Acad. Sci. USA 81, 654-658; Scholz et al. (1985) in: Plasmids in Bacteria, pp. 243-259, Plenum, New York; Haring and Scherzinger (1989) in: Promiscuous Plasmids of Gram-negative Bacteria, pp. 95-124, Academic Press, London; Scherzinger et al. (1991) Nucl. Acids Res. 19, 1203-1211]. We showed in this work that a newly constructed origin consisting of an oriV RSF1010 and a DnaA protein binding site, the dnaA box, inserted near oriV RSF1010 (oriV RSF1010-dnaA box) could function without RepB' primase, but required RepA and RepC. This oriV RsF1010-dnaA box could not replicate in a dnaA46 strain in which only RepA and RepC were supplied, even at a permissive temperature. These results indicate that an inserted dnaA box can functionally substitute for the RSF1010-specific ssi signals, the RepB' dependent priming signals in oriV RSF1010, and can direct a priming pathway different from the RSF1010-specific one, but related to DnaA protein.

Bacterial Proteins↗

Helicobacter pylori infection in patients with gastric carcinoma in biopsy and surgical resection specimens.

BACKGROUND: The discrepancy between the high seropositivity for Helicobacter pylori (H. pylori) and the low diagnostic yield of H. pylori organism in gastric biopsies of patients with gastric carcinoma has yet to be clarified. The present study attempted to clarify this controversial point by performing a comparative evaluation between the detection rate of H. pylori in biopsy and in surgical specimens. METHODS: The presence of H. pylori in biopsy samples from 50 patients with gastric carcinoma and 50 age-matched controls was evaluated histologically. Six histologic sections were obtained from gastric noncancerous areas and the presence of H. pylori was evaluated in those H. pylori negative patients who underwent gastrectomy. RESULTS: H. pylori was positive in 35 of 50 controls (70%). In biopsy samples, H. pylori was detected in 29 of 37 patients (78.4%) with early gastric carcinoma, 7 of 13 (53.8%) with advanced carcinoma, 16 of 23 (69.6%) with intestinal type of gastric carcinoma, and 20 of 27 (74.1%) with diffuse type of carcinoma. Studies carried out in gastrectomy specimens increased the diagnostic yield of H. pylori to 33 (89.2%), 12 (92.3%), 19 (82.6%), and 26 (96.3%) in patients with early, advanced intestinal, and diffuse types of gastric carcinoma, respectively. Overall, H. pylori was positive in 36 biopsy specimens (72%) and 45 gastrectomy specimens (90%). Namely, the detection of H. pylori infection was significantly higher in patients with gastric carcinoma using gastrectomy specimens than in patients with gastric carcinoma using biopsy specimens only (P < 0.05). CONCLUSIONS: These results indicate that the actual prevalence of H. pylori in patients with gastric carcinoma is considerably higher than that previously reported.

Biopsy↗

Multiple myeloma-associated systemic vasculopathy due to crystalglobulin or polyarteritis nodosa.

Systemic vasculopathy is a rare complication of multiple myeloma (MM). We describe a patient diagnosed with MM who developed clinical features of systemic vasculopathy including gangrene, livedo reticularis, hypertension, renal failure, and perforation of the small intestine. Histopathologic examination of the small intestine revealed necrotizing vasculitis in the small arteries, along with crystalline deposits in the small vessels. To our knowledge, previously reported cases of systemic vasculopathy associated with MM include at least 9 cases due to crystalglobulin deposition in vessels and 2 due to polyarteritis nodosa. Deposits of crystalglobulin may have induced systemic necrotizing vasculitis in our patient.

Adult↗