Wakayama Wellness Foundation

Wakayama-shi, Japan

Wakayama Wellness Foundation

Wakayama-shi, Japan
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Morita Y.,Osaka University | Morita Y.,Seichokai Hannan City Hospital | Morita N.,Social Insurance Kinan Hospital | Morita N.,Wakayama Wellness Foundation | And 7 more authors.
Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology | Year: 2014

Objective This study aimed to determine the relationship of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor-c (VEGF-C) expression with lymphangiogenesis, lymph node metastasis (LNM), and other clinicopathologic features in human oral tongue cancers. Study Design Forty tongue cancer specimens were immunohistochemically examined for COX-2 and VEGF-C expression and for lymphatic vessel density (LVD). We analyzed the relationships between COX-2 and VEGF-C expression and the relationships of such expression with clinicopathologic findings and survival of patients. Results Eighteen tumors out of 40 (45%) showed COX-2 expression, and 18 tumors (45%) expressed VEGF-C. Twelve tumors (30%) coexpressed COX-2/VEGF-C. A significant correlation was found between COX-2 and VEGF-C expression (P <.01). Of note, COX-2/VEGF-C coexpression significantly correlated with lymphangiogenesis, LNM, TNM stage (P <.01), and LVD (P <.05). In Cox regression for survival, COX-2/VEGF-C coexpression was identified as an independent prognostic factor (P <.05). Conclusions Our results suggest that examination of immunohistochemical expression of COX-2 and VEGF-C predicts LNM and survival in human oral tongue cancers. © 2014 Elsevier Inc. All rights reserved.

Yoshida T.,Wakayama Medical University | Kato J.,Wakayama Medical University | Inoue I.,Wakayama Medical University | Yoshimura N.,University of Tokyo | And 16 more authors.
International Journal of Cancer | Year: 2014

Our study investigated the relationship between gastric cancer development and activity of Helicobacter pylori-associated chronic gastritis or the resulting chronic atrophic gastritis (CAG). A cohort of 4,655 healthy asymptomatic subjects, in whom serum pepsinogen (PG) and H. pylori antibody titer had been measured to assess the activity and stage of H. pylori-associated chronic gastritis, was followed for up to 16 years, and cancer development was investigated. In subjects with a serologically diagnosed healthy stomach (H. pylori-negative/CAG-negative), cancer incidence rate was low, at 16/100,000 person-years. With the establishment of H. pylori infection and progression of chronic gastritis, significant stepwise cancer risk elevations were seen from CAG-free subjects (H. pylori-positive/CAG-negative) [hazard ratio (HR) = 8.9, 95% confidence interval (CI) = 2.7-54.7] to subjects with CAG (H. pylori-positive/CAG-positive) (HR = 17.7, 95% CI = 5.4-108.6) and finally to subjects with metaplastic gastritis (H. pylori-negative/CAG-positive) (HR = 69.7, 95% CI = 13.6-502.9). In H. pylori-infected CAG-free subjects, significantly elevated cancer risk was observed in the subgroup with active inflammation-based high PG II level or potent immune response-based high H. pylori antibody titer; the former was associated with a particularly high risk of diffuse-type cancer, and both subgroups showed high cancer incidence rates of around 250/100,000 person-years, comparable to that in subjects with CAG. No such risk elevation was observed in H. pylori-infected subjects with CAG. These results clearly indicate that gastric cancer develops mainly from the gastritis-atrophy-metaplasia-cancer sequence and partly from active inflammation-based direct carcinogenesis, and that serum levels of PG and H. pylori antibody titer provide indices of cancer development in H. pylori-infected subjects. What's new? Infection with the bacteria H. pylori is the most common risk factor for developing gastric cancer. The infection causes chronic inflammation leading to a sequence of gastritis, atrophy, metaplasia, dysplasia, cancer. This study follows up a cohort of 6,000 men after 16 years and showed that cancer risk increased with the progression of inflammation and atrophy, which can be measured by serum tests. These tests, the authors suggest, would be useful in assessing risk among people infected with H. pylori. © 2013 UICC.

Watanabe M.,Wakayama Medical University | Kato J.,Wakayama Medical University | Inoue I.,Wakayama Medical University | Yoshimura N.,University of Tokyo | And 16 more authors.
International Journal of Cancer | Year: 2012

This study aimed to elucidate groups at high risk of developing cancer among patients with serologically identified Helicobacter pylori infection and nonatrophic stomach. Annual endoscopy was performed for a mean of 5.4 years in 496 asymptomatic middle-aged men who were H. pylori antibody-positive and pepsinogen (PG) test-negative. Subjects were stratified according to the activity of H. pylori-associated gastritis measured by serum levels of PG and H. pylori antibody, and/or by endoscopic findings of rugal hyperplastic gastritis (RHG), and cancer development was investigated. During the study period, seven cases of cancer developed in the cohort (incidence rate, 261/100,000 person-years), with 85.7% developing in the group showing a PGI/II ratio ≤3.0, reflecting active inflammation-based high PGII levels. Cancer incidence was significantly higher in this group (750/100,000 person-years) than in groups with less active gastritis. Furthermore, cancer incidence for this group was significantly higher in the subgroup with high H. pylori antibody titers than in the low-titer subgroup. Meanwhile, endoscopic findings revealed that 11.7% of subjects showed RHG reflecting localized highly active inflammation, and cancer risk was significantly higher in patients with RHG than in patients without. Combining the two serum tests and endoscopic examination for RHG allowed identification of subjects with more active gastritis and higher cancer risk. No cancer development was observed in these high-risk subjects after H. pylori eradication. Subjects with highly active gastritis identified by the two serological tests and endoscopic RHG constitute a group at high risk of cancer development with H. pylori-infected nonatrophic stomach. © Copyright 2012 UICC.

Enomoto S.,Wakayama Medical University | Watanabe M.,Wakayama Medical University | Yoshida T.,Wakayama Medical University | Mukoubayashi C.,Wakayama Medical University | And 14 more authors.
Digestive Endoscopy | Year: 2012

Aim: Although frequent vomiting reflexes during esophagogastroduodenoscopy (EGD) causes suffering in patients, very few studies have investigated the characteristics of subjects who frequently develop vomiting reflexes. This study examined the incidence of the vomiting reflex and related factors, especially upper gastrointestinal symptoms, among individuals undergoing transoral EGD. Methods: Subjects included 488 consecutive adults (mean age, 56.1 ± 8.9 years) who underwent transoral EGD for gastric cancer screening between February 2010 and March 2011. All procedures were performed by an endoscopist with 15 years of experience. Based on a questionnaire survey using the frequency scale for the symptoms of gastroesophageal reflux disease (FSSG), symptoms (dyspepsia and acid reflux symptoms) and the number of vomiting reflexes during EGD were recorded. Results: Of the 488 subjects, 271 (56%) developed vomiting reflexes (mean, 4.2 times). This reflex-positive group was younger (54.3 ± 9.5 years) than the reflex-negative group (58.3 ± 7.7 years, P < 0.001). The number of subjects in the reflex-positive group with a high FSSG dyspepsia score (2.27 ± 2.57 vs 1.23 ± 1.84; P < 0.001), acid reflux symptom score (1.96 ± 2.22 vs 1.34 ± 2.14; P < 0.01) or an esophageal hiatal hernia (14.8% vs 4.6%; P < 0.001) was significantly higher than in the reflex-negative group. Multivariate analysis also showed a significant correlation between these four factors and the occurrence of vomiting reflexes. Using an FSSG dyspepsia score of 1 as the cut-off offered 68% sensitivity and 57% specificity for predicting the occurrence of vomiting reflexes. Conclusion: Based on FSSG questionnaire responses on upper gastrointestinal symptoms, dyspepsia symptoms, in particular, are related to presence of vomiting reflexes during EGD. © 2012 Japan Gastroenterological Endoscopy Society.

Inoue I.,Wakayama Medical University | Mukoubayashi C.,Wakayama Medical University | Yoshimura N.,University of Tokyo | Niwa T.,Wakayama Medical University | And 15 more authors.
International Journal of Cancer | Year: 2011

This study investigated correlations between Helicobacter pylori infection or chronic atrophic gastritis (CAG) and risk of colorectal adenoma in a population-based case-control study. Subjects comprised asymptomatic, middle-aged, male Japanese factory workers who participated in an annual health check-up program, including cancer screening with colonoscopy. We selected 239 colorectal adenoma cases based on histological evaluation and 239 age-matched adenoma-free controls, and evaluated colorectal adenoma risk according to stage of H. pylori-related chronic gastritis as determined by serum tests for H. pylori antibody titer and pepsinogen. Subjects with colorectal adenoma were more likely to be smokers and have hypercholesterolemia. H. pylori infection was a risk factor for adenoma as a whole (crude odds ratio [OR]: 2.26, 95% confidence interval [CI]: 1.44-3.55). Analysis of distal adenoma cases showed that adenoma risk was significantly increased in the presence of H. pylori infection, but there was no further increase in risk with CAG. In contrast, proximal adenoma risk increased stepwise with the presence and progression of H. pylori-related chronic gastritis and showed a maximal and significant increase with CAG (crude OR: 4.51, 95% CI: 1.43-14.2). Subjects with more extensive and severe gastritis showed still higher risk not only for proximal but also for distal adenoma. H. pylori-related chronic gastritis is likely to be involved in the development of colorectal neoplasms, and its progression appears to increase the risk, particularly for proximal adenomas. Knowing the H. pylori-related chronic gastritis stage will probably be useful for evaluation of risk for colorectal neoplasia. Copyright © 2011 UICC.

Maeda S.,Wakayama Medical University | Maeda S.,Wakayama Wellness Foundation | Mure K.,Wakayama Medical University | Mugitani K.,Wakayama Wellness Foundation | And 4 more authors.
Alcoholism: Clinical and Experimental Research | Year: 2014

Background: Adiponectin secreted from adipose tissue is assumed to mediate protective effects on development of metabolic syndrome (MetS) and MetS-related diseases such as cardiovascular diseases and cancer. Relationship between alcohol intake and circulating adiponectin levels is not consistent among the several previous studies. In the present study, we investigated effects of alcohol intake and the alcohol-related polymorphisms on serum adiponectin levels among Japanese male workers. Methods: We conducted a cross-sectional design study with 541 male workers aged 51.5 ± 5.9 (mean ± SD) years in a Japanese plant. Information on alcohol intake and other lifestyles was obtained by a self-administered questionnaire. Serum total adiponectin (T-Ad), high-molecular-weight adiponectin (HMW-Ad), medium-molecular-weight adiponectin (MMW-Ad), and low-molecular-weight adiponectin (LMW-Ad) levels were measured by the enzyme-linked immune assay system kit. Two genotypes in the alcohol dehydrogenase-1B (ADH1B) and aldehyde dehydrogenase-2 (ALDH2) genes were determined using blood sample. In multivariate regression analyses, we adjusted for age, body mass index, smoking, and physical exercise. Results: Among all subjects, high alcohol consumption of 12 units (1 unit contains 22.9 g of ethanol) a week or more was negatively associated with T-Ad levels in the multivariate model, although not significant. When we performed analyses separately for each genotype, high alcohol consumption was negatively associated with T-Ad, HMW-Ad, and LMW-Ad levels only in those with ADH1B *2/*2. Such relationships were not observed in each ALDH2 genotype group. Conclusions: High alcohol consumption was inversely associated with T-Ad, HMW-Ad, and LMW-Ad levels in those with ADH1B *2/*2 genotype, but not in those with the other ADH1B genotypes. To our knowledge, this is the first study that reports combined effects of the alcohol-related polymorphisms and alcohol intake on serum adiponectin levels. Additional studies are required to confirm the present finding. © 2014 by the Research Society on Alcoholism.

Mure K.,Wakayama Medical University | Maeda S.,Wakayama Medical University | Maeda S.,Wakayama Wellness Foundation | Mukoubayashi C.,Wakayama Wellness Foundation | And 5 more authors.
Nutrition | Year: 2013

Objectives: The goal of this cross-sectional study was to assess whether habitual coffee consumption shows beneficial association with metabolic syndrome (MetS) in adults. Methods: The association of coffee consumption and MetS-related biomarkers including visceral fat area (VFA) and subcutaneous fat area (SFA), total serum adiponectin (T-Ad), low-molecular-weight serum adiponectin (LMW-AD), medium-molecular-weight serum adiponectin (MMW-Ad), and high-molecular-weight serum adiponectin (HMW-Ad) levels were analyzed among 364 Japanese men (36-61 y old) using two models of multivariate regression analyses; model 1 (adjusted for age, alcohol drinking, smoking, and walking status) and model 2 (adjusted for body mass index in addition to model 1 analysis). Participants were categorized into two groups according to their MetS risk score (raised blood pressure and hemoglobin A1c levels, and reduced high-density lipoprotein cholesterol levels). Results: Both light (1-3 cups/d) and moderate (≥4 cups/d) coffee consumption showed significant inverse associations with VFA and VFA/SFA ratio (P < 0.0001). Moderate coffee consumption showed a favorable tendency toward these associations with T-Ad (P = 0.06) and HMW-Ad (P=0.07) levels in model 1 analysis. In participants with lower MetS risk score (≤1), moderate coffee consumption showed significant associations with T-Ad and HMW-Ad levels (P < 0.05) in both analyses, whereas no significant associations of coffee consumption with adiponectin levels were seen in the men with higher MetS risk scores (≥2). Conclusions: Habitual moderate coffee consumption shows significant inverse associations with MetS-related biomarkers possibly involving adiponectin, which is inversely related to visceral fat accumulation. © 2013 Elsevier Inc.

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