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Biomedical subjects

M Yoshihara

Publications and source records attributed to M Yoshihara.

At least 73 records · Page 4Linked to original sources
PubMed1999

Mea2/Golga3 gene is disrupted in a line of transgenic mice with a reciprocal translocation between Chromosomes 5 and 19 and is responsible for a defective spermatogenesis in homozygotes.

A line of transgenic mouse T604 transmitted a transgene to progeny together with a set of chromosomes with a reciprocal translocation. The transgene was integrated at a single site in the translocated chromosomes, as revealed by fluorescence in situ hybridization. The transgenic hemizygous males, also heterozygous for the translocation of chromosomes, showed apparently normal spermatogenesis, while the males homozygous for the transgene as well as for the translocated chromosomes showed a defect in spermatogenesis. Considering that the genetic rearrangement by either insertion of the transgene or the chromosome translocation in the T604 mouse line might have caused a recessive mutation in a gene indispensable for spermatogenesis, we have mapped the transgene integration site and the translocation breakpoints in mouse chromosomes. Linkage analysis with SSLP markers showed that the loci for the transgene and the translocation breakpoints were closely located to D5Mit24 on Chromosome (Chr) 5, and to a region between D19Mit19 and D19Jpk2 on Chr 19. Mea2 gene, mapped only 2 cM from D5Mit24 and known to show male-specific enhanced expression in the testis, was analyzed as a candidate for the gene disrupted in T604 transgenic mice. Southern blot analysis revealed that Mea2 gene was indeed disrupted in T604 mice, and Northern blot analysis of the testis RNA showed that the expression of Mea2 was annihilated in the testis of T604 transgenic homozygotes.

Animals↗
PubMed1999

Eradication of Helicobacter pylori increases gastric acidity in patients with atrophic gastritis of the corpus-evaluation of 24-h pH monitoring.

BACKGROUND: Recent studies have shown that the eradication of Helicobacter pylori results in a gastric acid secretion which decreases to normal levels in patients with duodenal ulcer disease. The aim of this study was to evaluate the effect of eradication of H. pylori in a 24-h study of gastric acidity in patients with atrophic gastritis of the corpus. METHODS: Intragastric acidity was measured by continuous 24-h pH monitoring, and the histology of the gastric antrum and corpus were evaluated in 14 H. pylori-positive patients with histologically proven atrophic gastritis of the corpus (10 men, 4 women; mean age, 57 years) before and 1 year after anti-H. pylori therapy. RESULTS: H. pylori was absent in 13 of 14 patients 1 year after treatment. Both gastritis and atrophy scores were significantly lower after eradication therapy (P < 0.01). The 24-h median pH and the percentage of 24-h pH readings above 4.0 units were significantly decreased after eradication therapy (from 5.12 +/- 0.36 to 2.69 +/- 0.21, and from 65.5 +/- 6.6% to 28.2 +/- 6.1%, P < 0.01, respectively.) CONCLUSION: Eradication of H. pylori increases 24-h gastric acidity in patients with atrophic gastritis of the corpus. Improvement of the histology of the gastric antrum and corpus may lead to the normalization of gastric acidity.

Aged↗
PubMed1999

The role of endoscopic findings for the diagnosis of Helicobacter pylori infection: evaluation in a country with high prevalence of atrophic gastritis.

BACKGROUND: This study examines endoscopic findings in the diagnosis of Helicobacter pylori (H. pylori) in the Japanese population. MATERIALS AND METHODS: The endoscopic findings (including gastric fold findings and degree of atrophy by the Kimura-Takemoto classification system), histologic severity of inflammation, and glandular atrophy were assessed according to the Sydney system in 642 patients (419 men; 223 women; mean age 43.5 years, range 13-86). H. pylori infection was evaluated by Giemsa staining and serum IgG antibodies. RESULTS: 391 of 642 patients (60.9%) were diagnosed as having endoscopic gastritis. Of the 391 patients with endoscopic gastritis, 318 (82.6%) had histologic gastritis and 310 (79.3%) had H. pylori infection. Of the 251 patients with endoscopically normal stomachs, 43 (17.1%) had histologic gastritis and 32 (12.7%) had H. pylori infection. Atrophic gastritis was the most prevalent finding (56.3%) among those with endoscopic gastritis. The prevalence of H. pylori infection in patients with atrophic gastritis (92.7%) and rugal hyperplastic gastritis (92.3%) was significantly higher than in those with other types of gastritis or with a normal stomach (12. 7%). A markedly high prevalence of H. pylori infection was found in subjects with tortuosity, hyperrugosity, and/or hyporugosity of the gastric folds. CONCLUSIONS: The accurate endoscopic assessment of gastritis according to the Sydney system along with gastric fold findings and the endoscopically identified extent of gastric atrophy are valuable indicators for determining H. pylori infection and histologic gastritis in the Japanese population.

Adolescent↗
PubMed1999

Effect of smoking and histological gastritis severity on the rate of H. pylori eradication with omeprazole, amoxicillin, and clarithromycin.

BACKGROUND: The combination of omeprazole, amoxicillin, and clarithromycin is a common regimen against Helicobacter pylori. Several recent studies have shown that smoking, high intragastric acidity, and the degree of histological gastritis are associated with H. pylori eradication failure. MATERIALS AND METHODS: One hundred and thirty-seven H. pylori-positive patients were treated with a 1-week regimen composed of omeprazole, 20 mg once daily; amoxicillin, 500 mg; and clarithromycin, 200 mg thrice daily. Success of the treatment was evaluated by histology and the 13C-urea breath test at least 4 weeks after completion of therapy. Data about age, gender, alcohol intake, smoking habits, and previous proton pump inhibitor intake were collected in patient interviews. We evaluated fasting gastric pH and the degree of histological gastritis before eradication of H. pylori. RESULTS: The overall eradication of H. pylori at 4 weeks was successful in 98 of 137 patients (72%). On the multivariate analysis, a low grade of inflammation in the antrum (p </=.01; 95% confidence interval [CI], 2.34-16.75), low grade of activity in the fundus (p </=.05; 95% CI, 1.31-9.65), and smoking (p </=.05; 95% CI, 1.27-6.82) were the significant independent factors predicting treatment failure. CONCLUSIONS: These findings indicate that H. pylori eradication therapy with omeprazole, amoxicillin, and clarithromycin is less effective in patients who smoke and more effective in patients with high scores of antral inflammation and fundal activity at baseline biopsy.

Adult↗
PubMed1999

MUC1 expression in intramucosal colorectal neoplasms. Possible involvement in histogenesis and progression.

PURPOSE: The mucin core peptide MUC1 often is detectable in colorectal carcinoma (CRC) tissue and cell lines. However, whether MUC1 in CRC correlates with tumor histogenesis and progression is unclear. We studied the relationship between MUC1 expression in intramucosal CRC and clinicopathologic features, expression of Ki-67, and p53 protein, and apoptosis. METHODS: The intramucosal CRC we studied included 140 endoscopically or surgically resected lesions, including 106 low-grade carcinomas and 34 high-grade carcinomas. De novo carcinoma, defined as carcinoma with no adenomatous component, represented 9 of 140 tumors. Three macroscopic types were identified: 57 lesions were polypoid, 55 were superficial and flat, and 28 were granular-type laterally spreading tumors (G-LST). MUC1, Ki-67, and p53 expression were examined immunohistochemically. Apoptotic cells were identified by in situ DNA nick end labeling. RESULTS: MUC1 expression in high-grade carcinomas was significantly more frequent (p < 0.01) than in low-grade carcinomas; expression in adenomas was almost nil. MUC1 expression in polypoid carcinomas was significantly more frequent (p < 0.05) than in superficial carcinomas or G-LST. MUC1 expression in carcinomas with p53 expression was significantly more frequent (p < 0.01) than in carcinomas not expressing p53. No significant correlation was found between expression of MUC1 and Ki-67 labeling index. MUC1 was expressed more frequently in carcinomas with relatively high apoptotic index (p < 0.01). MUC1 expression did not differ between de novo carcinomas and those developing from adenomas. CONCLUSIONS: The results suggest that MUC1 is likely to be expressed in the course of colorectal carcinoma development when p53 protein is overexpressed and apoptosis is prominent.

Apoptosis↗
PubMed1999

Enhanced expression of inducible nitric oxide synthase and nitrotyrosine in gastric mucosa of gastric cancer patients.

Recent studies (K. Komoto et al., Am. J. Gastroenterol., 93: 1271-1276, 1998) have shown that Helicobacter pylori infection is associated with gastric cancer. However, the mechanism of H. pylori in carcinogenesis has not been clarified. H. pylori infection leads to a sustained production of reactive nitrogen species that may contribute to cause DNA damage. In this study, we examined the expression of inducible nitric oxide synthase (iNOS) and nitrotyrosine in gastric mucosa. The expression of iNOS and nitrotyrosine was examined by immunohistochemistry in 93 patients who initially underwent gastric biopsies between 1975 and 1992. Thirty-four individuals were later found to have gastric cancer at least 2 years after the initial biopsies (group A). The other 59 subjects have shown no evidence of gastric cancer during long-term follow-up. Fifty-one of these patients were positive for H. pylori (group B), and eight were negative for H. pylori (group C). The expression of iNOS and nitrotyrosine in the gastric mucosa was significantly higher in H. pylori-positive groups A and B than in H. pylori-negative group C. Among the H. pylori-positive patients, the expression of iNOS and nitrotyrosine was significantly higher in group A than in group B. These results suggest that high production of iNOS and nitrotyrosine in the gastric mucosa infected with H. pylori may contribute to the carcinogenesis of gastric cancer.

Adult↗
PubMed1998

Differential diagnosis of NPH and brain atrophy assessed by measurement of intracranial and ventricular CSF volume with 3D FASE MRI.

Differential diagnosis of NPH and brain atrophy is sometimes difficult. Recently, a new method using MRI was introduced as a noninvasive, direct technique for the measurement of intracranial CSF volume. Using this new technique, we measured the intracranial and ventricle CSF volume in patients with enlarged ventricles in order to differentiate between NPH and brain atrophy. Ten healthy volunteers (control group) and 21 patients with enlarged ventricles were enrolled in this study. Eleven out of 21 patients were clinically diagnosed as having NPH (shunted group) and the remaining 10 patients were considered to have cerebral atrophy (non-shunted group). Intracranial and ventricular CSF volume in each case were measured by 3D FASE (Fast Asymmetric Spine-Echo) MR imaging sequence with region growing method. Ventricular/intracranial CSF volume ratio was also calculated. Ten out of 11 patients showed improvement in clinical symptoms and/or dementia scale after shunting. Our results clearly indicate that the ventricular volume in the shunted group was enlarged and that the ventricular/intracranial CSF ratio was significantly high. Thus we concluded that enlarged ventricle with high ventricular/intracranial CSF volume ratio strongly suggests NPH.

Adult↗
PubMed1998

Growth patterns in various macroscopic types of noninvasive intramucosal colorectal carcinoma with special reference to apoptosis and cell proliferation.

PURPOSE: Apoptotic cell death and cell proliferation play important roles in the histogenesis and development of colorectal carcinoma. The aim of this study was to examine the relationship between apoptosis and cell proliferation in various macroscopic types of intramucosal colorectal carcinoma in relation to the expression of p53 and bcl-2. METHODS: One hundred forty cases with endoscopically or surgically resected intramucosal colorectal carcinoma were studied. There were 57 cases of polypoid-type carcinomas, 55 cases of superficial-type carcinomas, and 28 cases of granular-type, laterally spreading tumors. Polypoid-type carcinomas were pedunculated, subpedunculated, or sessile polyps. Superficial-type carcinomas were flat lesions with a smooth, even surface. Granular-type, laterally spreading tumors were superficially spreading lesions with aggregates of nodules and a granular surface. Apoptotic cells were identified by the in situ DNA nick end labeling method. Ki-67, p53, and bcl-2 expression were examined immunohistochemically. RESULTS: The superficial-type carcinoma apoptotic index (30.9 percent) was significantly lower than that of polypoid-type carcinoma (54.4 percent) and granular-type, laterally spreading tumor (60.7 percent). The superficial-type carcinoma proliferative index (67.3 percent) was significantly higher than that of polypoid-type carcinoma (42.1 percent) and granular-type, laterally spreading tumor (28.6 percent). In superficial-type carcinomas the proliferative index in p53-positive carcinomas was significantly higher, and the apoptotic index was higher in carcinomas with a lower proliferative index. There was no significant difference in apoptotic index, proliferative index, or p53 protein overexpression between de novo carcinomas and those that had arisen in precursor adenomas. CONCLUSIONS: The pattern of cell death and proliferation may vary with different macroscopic types of intramucosal colorectal carcinoma. Superficial-type colorectal carcinomas especially demonstrate diminished apoptosis and increased cell proliferation. This may be useful in understanding their biologic behavior.

Apoptosis↗
PubMed1998

MUC-1 expression as a predictor of the curative endoscopic treatment of submucosally invasive colorectal carcinoma.

PURPOSE: This study was undertaken to clarify the clinical significance of MUC-1 expression in the endoscopic treatment of colorectal carcinoma with submucosal invasion. METHODS: One hundred eighty-four colorectal carcinomas with submucosal invasion were examined. The depth of submucosal invasion was classified as scanty or massive. The histologic subclassification at the deepest invasive portion was defined as well-differentiated, moderately well-differentiated, moderately to poorly differentiated, poorly differentiated, or mucinous adenocarcinoma. MUC-1 expression was examined immunohistochemically at the deepest invasive portion. In addition, the Ki67 labeling index was also examined immunohistochemically. RESULTS: Lymph node metastases were detected in 28 (15.2 percent) of 184 lesions. Lesions with both scanty submucosal invasion and well-differentiated or moderately well-differentiated adenocarcinomas had no lymph node metastases. MUC-1 expression was detected in 88 (47.8 percent) of 184 lesions and correlated significantly with the presence of lymph node metastases. The Ki67 labeling index also correlated significantly with lymph node metastases. Furthermore, lesions with both MUC-1-negative and low Ki67 labeling index showed no lymph node metastases, even in lesions with massive submucosal invasion. Multivariate analysis indicated that MUC-1 expression was one of the most important risk factors for lymph node metastases and histologic grade among the clinicopathologic factors usually examined. CONCLUSION: MUC-1 expression is one of the accurate predictors of the presence of lymph node metastases among the clinicopathologic factors commonly used. Combined analysis of MUC-1 expression and Ki67 labeling index may be a useful indicator of lymph node metastases and may broaden the indications for the curative endoscopic treatment of carcinoma with massive submucosal invasion.

Adenocarcinoma↗
PubMed1998

Correlation of ratio of serum pepsinogen I and II with prevalence of gastric cancer and adenoma in Japanese subjects.

OBJECTIVE: Gastric cancer (GC) and adenoma (GA) are reported to be related to atrophic gastritis, in which the serum pepsinogen (PG) I level and the PGI/PGII ratio (I/II ratio) are reduced. To verify that the finding of a low PG level increases the risk for GC and GA, we investigated the correlation between low PG levels and the prevalence of GC and GA in individuals. METHODS: The 2,039 subjects (734 Japanese men, mean age 68.5 yr, and 1,305 women, mean age 66.7 yr), selected from among 10,996 local residents who underwent health check-ups based on reductions in their serum PG levels, underwent upper gastrointestinal endoscopy. RESULTS: Gastrointestinal endoscopy detected 21 GCs and 15 GAs. The prevalence of GC was higher than that in the residents without low serum PG. The percentage of early stage of GC (90%) was significantly higher than that of GC detected in unscreened residents (56.9%). The prevalence of GC in men was closely and significantly correlated with the I/II ratio (r = 0.935, p = 0.0063), whereas there was less correlation with age (r = 0.842, p = 0.0734). The prevalence of GA was also closely and significantly correlated with the I/II ratio in men (r = 0.881, p = 0.0203), but not with age (r = 0.163, p = 0.7928). In women the prevalence of GC (r = 0.744, p = 0.090) and GA (r = 0.678, p = 0.1392) did not correlate as strongly with the I/II ratio, although the highest prevalence was seen in the group with the lowest I/II ratio. CONCLUSION: Our study verified that a low I/II ratio signifies a high risk for GC and GA and that measuring serum PG levels can be used as a screening method for GC and GA.

Adenocarcinoma↗
PubMed1998

Helicobacter pylori infection and gastric neoplasia: correlations with histological gastritis and tumor histology.

OBJECTIVE: Several authors have reported an association between Helicobacter pylori (H. pylori) and gastric carcinoma, but the data are conflicting. Atrophic gastritis and intestinal metaplasia (IM) have also been linked to gastric carcinoma, especially the intestinal tumor type. We investigated the relationship between H. pylori infection, gastric neoplasms, and histological gastritis. METHODS: A total of 105 patients with gastric carcinoma, 36 patients with gastric adenoma, and 105 age- and sex-matched control subjects were examined for H. pylori infection and histological gastritis. H. pylori status was evaluated by Giemsa staining and IgG serology. Mucosal inflammation, atrophy, and IM were evaluated in biopsy specimens from antrum and corpus. RESULTS: H. pylori seroprevalence was higher in patients with gastric carcinoma (98 of 105, 93%) and adenoma (34 of 36, 94%) than in control subjects (82 of 105, 71%, p < 0.05). H. pylori was more prevalent in patients with noncardia (OR, 5.67; 95% CI, 2.25-14.44) than cardia (OR, 5.20; 95% CI, 0.65-41.68) tumors. Histologic types and tumor stage (early; OR, 6.60; 95% CI, 2.23-19.69, advanced; OR, 4.27; 95% CI, 1.21-15.03) showed no difference in H. pylori prevalence. Atrophy and IM scores were higher in patients with the intestinal- but not diffuse-type of carcinoma and adenoma than in H. pylori-positive control subjects. Smoking was associated with gastric carcinoma (OR, 3.05; 95% CI, 1.58-5.93) but not alcohol or coffee use, blood group A, or a family history of gastric cancer. CONCLUSIONS: Our results confirm a strong association between H. pylori and gastric carcinoma and adenoma. The intestinal-type gastric carcinoma is associated with atrophic gastritis and IM.

Adenoma↗
PubMed1998

The association between antral G and D cells and mucosal inflammation, atrophy, and Helicobacter pylori infection in subjects with normal mucosa, chronic gastritis, and duodenal ulcer.

OBJECTIVE: The aim of this study was to clarify the mechanism of inappropriate hypergastrinemia in Helicobacter pylori (H. pylori)-infected subjects. METHODS: We measured fasting serum gastrin (SG) concentrations, and investigated immunohistochemically G and D cell numbers in 47 subjects with normal mucosa, 24 subjects with chronic gastritis, and 24 subjects with duodenal ulcer (DU). The degree of inflammation and atrophy were classified into four categories based on criteria established in the Sydney System: none, mild, moderate, and severe. Avidin-biotin complex methods were used to identify G and D cells, which were counted per unit square (0.25 mm2) in five random fields from each of two well-oriented antral and fundic biopsies. SG concentrations were measured by radioimmunoassay. RESULTS: The G cell number was not significantly different between 24 subjects with H. pylori-associated gastritis and those with DU. However, the number of antral D cells was significantly lower and the G/D cell ratio was significantly higher in subjects with DU than in those with H. pylori-associated gastritis (p < 0.01), although the degree of inflammation and atrophy in the antrum and H. pylori status were similar between the two groups. The mean fasting SG concentration was higher in subjects with DU than in those with H. pylori-associated gastritis, but the difference was not statistically significant. CONCLUSIONS: Our results demonstrate that a marked decrease in antral D cell number with a high G/D cell ratio may contribute to hypergastrinemia and the pathogenesis of DU.

Adult↗
PubMed1998

[Epidemiology of gastrointestinal hemorrhage].

We mentioned about epidemiology of gastrointestinal hemorrhage according to the clinical statistics. Most of recent reports has been investigated by emergency endoscopic examinations. Upper gastrointestinal hemorrhage was the most frequent and its clinical severity was severer than that of lower gastrointestinal hemorrhage. Hemorrhage from small intestine was rare, however they were mostly severe hemorrhage. Peptic ulcer was the most frequent disease as the upper gastrointestinal hemorrhage. Inflammation of colon was the most in the lower gastrointestinal hemorrhage. However, the varied diseases were recognized as origin of small intestinal hemorrhage, non epithelial tumor and inflammation were important.

Age Factors↗
PubMed1998

[Ishikawa's classification of cavernous sinus lesions by clinico-anatomical findings].

Jefferson's classification (1938) has been used to localize lesions of the cavernous sinus. However, we think this classification is sometimes incorrect in identifying localization based on clinico-anatomical evidence. We investigated the efficacy of the newly proposed Ishikawa's classification. Based on the analysis on serial sections of human cavernous sinus, it classifies the locus of the lesion into three groups: anterior, middle, and posterior, corresponding to the location of the intracranial orifice of the optic canal and of the penetration of the maxillary nerve into the cavernous sinus. The subjects were 162 cases with cavernous sinus lesions. They were classified by the two methods. There was a total of 111 cases (69%) of unclassified cases in Jefferson's classification and 45 (28%) in Ishikawa's classification. The anterior type was frequently encountered in cases caused by inflammations and both posterior and whole types were caused by tumors in Ishikawa's classification. It was concluded that Ishikawa's classification is clinically useful to identify and classify the localization of cavernous sinus lesions.

Aneurysm↗
PubMed1997

Transition from growth cone to functional motor nerve terminal in Drosophila embryos.

As a motor axon grows from the CNS to its target muscle, the terminal has the form of a flattened growth cone with a planar central region, lamellipodia, and filopodia. A mature terminal usually has a stereotyped shape that may be elongated with varicosities, as in several invertebrate species, or have short branches with boutons, as in mammals. We examined in Drosophila the developmental changes between growth cone and mature terminal using ultrastructural and immunocytochemical methods. The transition period, which occurs 2-3 hr after the first growth cone reaches its target muscle, is marked by the formation of "prevaricosities," smoothly contoured enlargements of the axons at the point where the nerve trunk first contacts the muscle fiber (MF). There is a 15-30 min ventral-to-dorsal gradient in the formation of prevaricosities on the individual abdominal MFs. Multineuronal innervation of each MF has occurred by this time, and two or more different axons undergo prevaricosity formation while they are intimately intertwined at the nerve entry point (NEP). Presynaptic active zones, both nerve-nerve and nerve-muscle, occur within the prevaricosities along broad contact regions. Synaptotagmin immunoreactive clusters form concurrently. The first varicosities then develop as a result of constrictions of the larger prevaricosities rather than as enlargement of discrete portions of the filopodia or neurites. The prevaricosity stage therefore may include the key steps that lead to the differentiation of functional differences in terminal subtypes as well as those leading to the formation of a stable neuromuscular junction.

Abdominal Muscles↗
PubMed1997

Specific activation of a c-Jun NH2-terminal kinase isoform and induction of neurite outgrowth in PC-12 cells by staurosporine.

Staurosporine, a protein kinase inhibitor, is known to mimic the effect of nerve growth factor (NGF) in promoting neurite outgrowth. To elucidate the mechanism by which staurosporine induces neurite outgrowth in PC-12 cells, we performed an in-gel kinase assay using myelin basic protein as a substrate, and found that staurosporine induced the activation of a kinase with an apparent molecular mass of 57 kDa. The dose of staurosporine required to activate this kinase was consistent with that required to induce neurite outgrowth. Interestingly, the staurosporine-activated kinase was immunoprecipitated by anti-c-Jun NH2-terminal kinase (JNK) isoforms antibody, but not by anti-JNK1-specific antibody or anti-ERK1 antibody, raising the possibility that this kinase is a novel JNK isoform. The substrate specificity of the kinase was distinct from those of osmotic shock-activated JNKs and NGF-activated ERK1. The kinase phosphorylates transcription factors including c-Jun, Elk-1, and ATF2, as well as myelin basic protein, suggesting that it plays a role in gene induction. Furthermore, staurosporine induced immediate-early genes including Nur77 and fos, but not jun. The activation of the staurosporine-activated kinase, as well as the induction of neurite outgrowth, did not require Ras function, while Ras was required for the activation of ERKs and neurite outgrowth induced by NGF. Taken together, these results indicate staurosporine specifically activates a JNK isoform, which may contribute to biological activities including neurite outgrowth.

Activating Transcription Factor 2↗