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Background/aim: This multi-institutional study aimed to investigate the efficacy and feasibility of proton beam therapy (PBT) for renal cell carcinoma (RCC) in Japan., Patients and Methods: The survival, local control, and toxicities in 22 RCC patients treated between 2001 and 2016 at 6 Japanese PBT institutes were analyzed., Results: The 22 patients comprised 20 men and had a median age of 67 (range=42-88) years. The total irradiation dose was 60-79.6 Gy (relative biological effectiveness). Over a median follow-up of 37 months, the 3-year overall and disease-specific survival rates were 95% and 100%, respectively, and no recurrence occurred. No patient experienced grade 3 or higher adverse events. The serum blood urea nitrogen (p=0.25) and creatinine levels (p=0.95) were not significantly affected, although the mean estimated glomerular filtration rate was reduced by 7.1±11.2 ml/min/1.73 m 2 Conclusion: Despite the small number of patients, high-dose PBT can control RCC while maintaining their renal function with high probability, and could be and alternative curative therapy especially for inoperable patients., (Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Purpose: To investigate the efficacy and safety of proton beam therapy (PBT) for the treatment of stage I non-small cell lung cancer (NSCLC)., Methods and Materials: Six hundred sixty-nine patients with 682 tumors histologically or clinically diagnosed stage I NSCLC according to the seventh edition of Union for International Cancer Control who received passive-scattering PBT from April 2004 and December 2013 in Japan were retrospectively reviewed to analyze survival, local control, and toxicities., Results: Of 669 patients, 486 (72.6%) were men, with a median age of 76 years (range, 42-94 years). NSCLC was histologically confirmed in 440 patients (65.7%). Clinical T stages included T1a (n = 265; 38.9%), T1b (n = 216; 31.7%), and T2a (n = 201; 29.4%). The total irradiation doses of PBT ranged from 74.4 to 131.3 biological effective dose GyE (median, 109.6 biological effective dose GyE). The median follow-up period was 38.2 months (range, 0.6-154.5 months) for all patients. The 3-year overall survival and progression-free survival rates for all patients were 79.5% and 64.1%, respectively. For patients with stage IA tumors, the 3-year overall survival and progression-free survival rates were 82.8% and 70.6%, respectively, and the corresponding rates for patients with stage IB tumors were 70.8% and 47.3%, respectively. The 3-year local progression-free rates for all, stage IA, and stage IB patients were 89.8%, 93.5%, and 79.4%, respectively. The incidence of grade 2, 3, 4, and 5 pneumonitis was 9.8%, 1.0%, 0%, and 0.7%, respectively. The incidence of grade ≥3 dermatitis was 0.4%. No grade 4 or severe adverse events, other than pneumonitis, were observed., Conclusions: PBT appears to yield acceptable survival rates, with a low rate of toxicities., (Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.)

Objective Cardiac rehabilitation (CR) improves the mortality in patients with cardiovascular disease (CVD). Even in elderly patients with CVD, CR may improve the activities of daily living (ADL). Methods Eighty-eight outpatients over 65 years of age at the beginning of a CR program (baseline) at Fukuoka University Hospital who had CVD and could be followed-up for up to 5 years were enrolled. CVD included ischemic heart disease, postoperative valvular heart disease, dissecting aneurysm of the aorta and peripheral artery disease. The patients were divided into 2 groups according to the average estimated glomerular filtration rate (eGFR) at baseline (55.4±14.8 mL/min/1.73 m 2 ): high (≥55.4, n=44) and low (<55.4, n=44)-eGFR groups. The anaerobic threshold (AT) during exercise and left ventricular ejection fraction (LVEF) were measured by cardiopulmonary exercise (CPX) and ultrasound cardiography, respectively. The serum brain natriuretic protein (BNP) was also measured every year. Results The average age at baseline in all patients was 73±6 years. In all patients, the level of eGFR did not significantly change for 5 years (55±15 mL/min/1.73 m 2 at baseline vs. 48±14 at the end of the study). The AT (3.7±1.0 METs at baseline vs. 3.3±0.5), LVEF (57±13% vs. 64±10%) and BNP (260±452 pg/mL vs. 308±345) were also maintained for 5 years. In both the low- and high-eGFR groups, the eGFR, AT during exercise, LVEF and BNP at the end of the study were not significantly changed compared to the baseline values, although some changes were observed during the follow-up period. Conclusion Long-term CR in CVD outpatients over 65 years of age helped maintain the AT, LVEF, BNP and eGFR for 5 years. CR afforded cardio-renal protection in elderly patients with CVD.

This is the first multi-institutional retrospective survey of the long-term outcomes of proton therapy (PT) for prostate cancer in Japan. This retrospective analysis comprised prostate cancer patients treated with PT at seven centers between January 2008 and December 2011 and was approved by each Institutional Review Board. The NCCN classification was used. Biochemical relapse was based on the Phoenix definition (nadir + 2.0 ng/mL). Toxicities were evaluated with the Common Terminology Criteria for Adverse Events version 4.0. There were 215, 520, and 556 patients in the low-risk, intermediate-risk, and high-risk groups, respectively. The median follow-up period of surviving patients was 69 months (range: 7-107). Among all patients, 98.8% were treated using a conventional fractionation schedule and 1.2% with a hypofractionation schedule; 58.5% and 21.5% received neoadjuvant and adjuvant androgen deprivation therapy, respectively. The 5-year biochemical relapse-free survival (bRFS) and overall survival rates in the low-risk, intermediate-risk, and high-risk groups were 97.0%, 91.1%, and 83.1%, and 98.4%, 96.8%, and 95.2%, respectively. In the multivariate analysis, the NCCN classification was a significant prognostic factor for bRFS, but not overall survival. The incidence rates of grade 2 or more severe late gastrointestinal and genitourinary toxicities were 4.1% and 4.0%, retrospectively. This retrospective analysis of a multi-institutional survey suggested that PT is effective and well-tolerated for prostate cancer. Based on this result, a multi-institutional prospective clinical trial (UMIN000025453) on PT for prostate cancer has just been initiated in order to define its role in Japan., (© 2018 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.)

The purpose of this study was to investigate the factor structure of the Body Image Concern Inventory (BICI) using a Japanese population as a web-based survey. Two thousand and sixty individuals (1030 women, 1030 men) ranging from 20 to 69 years of age (M=40, SD=16) took part in the present research. A confirmatory factor analysis showed that the second-order factor model of the BICI, which had three first-order factors and one second-order factor of dysmorphic appearance concern was an adequate fit to the data. Additionally, the Cronbach's alpha values of the overall and three subscales of the BICI were adequate. Furthermore, measurement invariance tests revealed that the second-order factor model of the BICI had acceptable measurement invariance at the scale and factor-loading levels between genders. These findings suggested that the BICI was reliable, and able to compare its mean scores between women and men in Japan., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Objectives: The use of staplers for thoracic surgery has been widely accepted and regarded as a safe procedure. However, adverse events (AEs) of stapling are occasionally experienced. The aim of this retrospective study was to analyse the AEs of stapling in pulmonary vascular surgery., Methods: A retrospective multi-institutional review was conducted by the 29 institutions of the Central Japan Lung Cancer Surgery Study Group. All staplings of the pulmonary artery (PA) and vein in thoracic surgery were reviewed during the research period., Results: Stapling of the PA and vein was performed 3393 times. The total number of AEs related to stapling was nine (0.27%). Eight events occurred intraoperatively and one occurred immediately after the operation. Intraoperative AE occurred more frequently than postoperative AE. AE in the PA occurred more frequently than in the pulmonary vein. The intraoperative AEs were oozing (n=3), stapling failure (n=2), laceration of the peripheral vasculature at compression (n=2) and technical injury of the vasculature at insertion (n=1). The causes of AEs were reported to be tissue fragility (n=3), stapler rocking during stapling (n=2), stapler-tissue thickness mismatch (n=2) and technical failure (n=1). The only postoperative AE was staple line rupture of the PV stump. No relationship was seen between the incidence of AE and cartridge colours, compression types of staplers or numbers of staple lines., Conclusions: Generally, stapling of the pulmonary vasculatures in recent thoracic surgery has been safe. Furthermore, the knowledge of the possible risks of pulmonary vascular stapling may help to decrease the AEs of stapling.

Background: Brugada syndrome (BrS) is characterized by specific alterations on ECG in the right precordial leads and associated with ventricular arrhythmia that may manifest as syncope or sudden cardiac death. The major causes of BrS are mutations in SCN5A for a large subunit of the sodium channel, Nav1.5, but a mutation in SCN3B for a small subunit of sodium channel, Navβ3, has been recently reported in an American patient., Methods and Results: A total of 181 unrelated BrS patients, 178 Japanese and 3 Koreans, who had no mutations in SCN5A, were examined for mutations in SCN3B by direct sequencing of all exons and adjacent introns. A mutation, Val110Ile, was identified in 3 of 178 (1.7%) Japanese patients, but was not found in 480 Japanese controls. The SCN3B mutation impaired the cytoplasmic trafficking of Nav1.5, the cell surface expression of which was decreased in transfected cells. Whole-cell patch clamp recordings of the transfected cells revealed that the sodium currents were significantly reduced by the SCN3B mutation., Conclusions: The Val110Ile mutation of SCN3B is a relatively common cause of SCN5A-negative BrS in Japan, which has a reduced sodium current because of the loss of cell surface expression of Nav1.5.

Background: Dilated cardiomyopathy (DCM) is characterized by a dilated left ventricular cavity with systolic dysfunction manifested by heart failure. It has been revealed that mutations in genes for cytoskeleton or sarcomere proteins cause DCM. However, the disease-causing mutations can be found only in far less than half of patients with a family history, indicating that there should be other disease genes for DCM. Formin homology 2 domain containing 3 (FHOD3) is a sarcomeric protein expressed in the heart that plays an essential role in sarcomere organization during myofibrillogenesis. The purpose of this study was to explore a possible novel disease gene for DCM., Methods and Results: We analyzed 48 Japanese familial DCM patients for mutations in FHOD3, and a missense variant, Tyr1249Asn, which was predicted to modify the 3D structure and damage protein function, was found in a case with adult-onset DCM. Functional studies revealed that the DCM-associated mutation significantly reduced the ability to induce actin dynamics-dependent activation of serum response factor, although no remarkable change in the cellular localization was induced in neonatal rat cardiomyocytes transfected with a mutant construct of FHOD3., Conclusions: The DCM-associated FHOD3 variant may cause DCM by interfering with actin filament assembly.

Objective: The primary objectives of the current study were to 1) confirm the three-factor model of the Pain Catastrophizing Scale (PCS) items in a Japanese sample and 2) identify the catastrophizing subdomain(s) most closely associated with measures of pain and functioning in a sample of individuals with chronic pain., Design: This was based on a cross-sectional observational study., Setting: This study was conducted in a university-based clinic., Patients: One hundred and sixty outpatients with chronic pain participated in this study., Outcome Measures: Patients completed the PCS, the Brief Pain Inventory, and the Hospital Anxiety and Depression Scale; 30 patients completed the PCS again between 1 and 4 weeks later., Results: Confirmatory factor analysis supported a three-factor structure of the Japanese version of the PCS, and univariate and multivariate associations with validity criterion supported the validity of the measure. Catastrophic helplessness was shown to make a unique contribution to the prediction of pain intensity, pain interference and depression, and catastrophic magnification made a unique contribution to the prediction of anxiety., Conclusions: The findings support the cross-cultural generalizability of the three-factor structure of the PCS and indicate that the PCS-assessed catastrophizing subdomains provide greater explanatory power than the PCS total score for understanding pain-related functioning., (Wiley Periodicals, Inc.)

Objectives: The present study aimed to develop a Japanese version of the Short-Form McGill Pain Questionnaire (SF-MPQ-J) that focuses on cross-culturally equivalence to the original English version and to test its reliability and validity., Design: Cross-sectional design., Method: In study 1, SF-MPQ was translated and adapted into Japanese. It included construction of response scales equivalent to the original using a variation of the Thurstone method of equal-appearing intervals. A total of 147 undergraduate students and 44 pain patients participated in the development of the Japanese response scales. To measure the equivalence of pain descriptors, 62 pain patients in four diagnostic groups were asked to choose pain descriptors that described their pain. In study 2, chronic pain patients (N=126) completed the SF-MPQ-J, the Long-Form McGill Pain Questionnaire Japanese version (LF-MPQ-J), and the 11-point numerical rating scale of pain intensity. Correlation analysis examined the construct validity of the SF-MPQ-J., Results: The results from study 1 were used to develop SF-MPQ-J, which is linguistically equivalent to the original questionnaire. Response scales from SF-MPQ-J represented the original scale values. All pain descriptors, except one, were used by >33% in at least one of the four diagnostic groups. Study 2 exhibited adequate internal consistency and test-retest reliability, with the construct validity of SF-MPQ-J comparable to the original., Conclusion: These findings suggested that SF-MPQ-J is reliable, valid, and cross-culturally equivalent to the original questionnaire. Researchers might consider using this scale in multicenter, multi-ethnical trials or cross-cultural studies that include Japanese-speaking patients., (Wiley Periodicals, Inc.)

Background: Hypertrophic cardiomyopathy (HCM), which is inherited as an autosomal dominant trait, is the most prevalent hereditary cardiac disease. Although there are several reports on the systematic screening of mutations in the disease-causing genes in European and American populations, only limited information is available for Asian populations, including Japanese., Methods and Results: Genetic screening of disease-associated mutations in 8 genes for sarcomeric proteins, MYH7, MYBPC3, MYL2, MYL3, TNNT2, TNNI3, TPM1, and ACTC, was performed by direct sequencing in 112 unrelated Japanese proband patients with familial HCM; 37 different mutations, including 13 novel ones in 5 genes, MYH7, MYBPC3, TNNT2, TNNI3, and TPM1, were identified in 49 (43.8%) patients. Among them, 3 carried compound heterozygous mutations in MYBPC3 or TNNT2. The frequency of patients carrying the MYBPC3, MYH7, and TNNT2 mutations were 19.6%, 10.7%, and 8.9%, respectively, and the most frequently affected genes in the northeastern and southwestern parts of Japan were MYBPC3 and MYH7, respectively. Several mutations were found in multiple unrelated proband patients, for which the geographic distribution suggested founder effects of the mutations., Conclusions: This study demonstrated the frequency and distribution of mutations in a large cohort of familial HCM in Japan.

Background: Hypertrophic cardiomyopathy (HCM) is a primary myocardial disorder with an autosomal-dominant pattern of inheritance mainly caused by single heterozygous mutations in sarcomere genes. Although multiple gene mutations have recently been reported in Western countries, clinical implications of multiple mutations in Japanese subjects are not clear., Methods and Results: A comprehensive genetic analysis of 5 sarcomere genes (cardiac β-myosin heavy chain gene [MYH7], cardiac myosin-binding protein C gene [MYBPC3], cardiac troponin T gene [TNNT2], α-tropomyosin gene [TPM1] and cardiac troponin I gene [TNNI3]) was performed in 93 unrelated patients and 14 mutations were identified in 28 patients. Twenty-six patients had single heterozygosity (20 in MYBPC3, 4 in MYH7, 1 in TNNT2, 1 in TNNI3), whereas 2 proband patients with familial HCM had double heterozygosity: 1 with P106fs in MYBPC3 and R869C in MYH7 and 1 with R945fs in MYBPC3 and E1049D in MYH7. From the results of the family survey and the previous literature on HCM mutations, P106fs, R945fs and R869C seemed to be pathological mutations and E1049D might be a rare polymorphism. The proband patient with P106fs and R869C double mutation was diagnosed as having HCM at an earlier age (28 years of age) than her relatives with single mutation, and had greater wall thickness with left ventricular outflow obstruction., Conclusions: One double mutation was identified in a Japanese cohort of HCM patients. Further studies are needed to clarify the clinical significance of multiple mutations including phenotypic severity.

Background: Although plasma pigment epithelium-derived factor (PEDF) levels have been shown to be significantly correlated with the levels of creatinine (Cr) in type 2 diabetes, little is known about the association between PEDF levels and renal dysfunction in patients with coronary artery disease (CAD)., Methods: We enrolled 134 consecutive patients with diagnosed CAD and measured plasma levels of PEDF, serum Cr, uric acid (UA) and high-sensitive C-reactive protein (hsCRP)., Results: Plasma PEDF levels were positively correlated with serum Cr (p 〈 0.0001) and UA (p 〈 0.0001) and negatively correlated with the estimated glomerular filtration rate (eGFR) (p 〈 0.0001), whereas there was no association between plasma PEDF and age or hsCRP. When the subjects were divided into five groups (0-4) according to the number of metabolic factors (obesity, diabetes, hypertension and dyslipidemia), PEDF levels in patients with four factors were significantly higher than those in patients without factors. Next, we divided the patients into quartiles according to their plasma PEDF levels (〈 9.9 μg/mL, 9.9-12.8, 12.9- -15.7, 〉 15.7). The eGFR in the first group was significantly higher than those in the third and fourth groups. Multivariate logistic analysis indicated that eGFR (p 〈 0.0001) and age (p = 0.030) were significant independent variables that correlated with the quartile classification according to PEDF levels., Conclusions: This study revealed that PEDF may play a role in renal dysfunction in CAD patients.

Coronary artery disease (CAD) is based on the atherosclerosis of coronary artery and may manifest with myocardial infarction or angina pectoris. Although it is widely accepted that genetic factors are linked to CAD and several disease-related genes have been reported, only a few could be replicated suggesting that there might be some other CAD-related genes. To identify novel susceptibility loci for CAD, we used microsatellite markers in the screening and found six different candidate CAD loci. Subsequent single nucleotide polymorphism (SNP) association studies revealed an association between CAD and megakaryoblastic leukemia factor-1 gene (MKL1). The association with a promoter SNP of MKL1, -184C > T, was found in a Japanese population and the association was replicated in another Japanese population and a Korean population. Functional analysis of the MKL1 promoter SNP suggested that the higher MKL1 expression was associated with CAD. These findings suggest that MKL1 is involved in the pathogenesis of CAD.

Background: Mutations in FKTN encoding for fukutin cause Fukuyama-type congenital muscular dystrophy characterized by severe muscle wasting and hypotonia with mental retardation. Fukuyama-type congenital muscular dystrophy is a recessive genetic trait. FKTN mutations in patients with dilated cardiomyopathy (DCM) have been investigated by our research group. The patients showed hyper-CKemia with mild or no muscle weakness and without mental retardation, suggesting that the clinical spectrum of FKTN mutations are wider than previously thought. The current study was designed to further explore the association of FKTN mutations with DCM or hypertrophic cardiomyopathy (HCM)., Methods and Results: A total of 172 patients with DCM, 144 patients with familial HCM and 384 control individuals were analyzed for FKTN mutations. There was a DCM patient who was a compound heterozygote of a 3-kb insertion mutation and a missense mutation Cys101Phe. The patient showed hyper-CKemia with mild muscle involvement and no brain involvement. In contrast, 2 other DCM patients and 3 controls were heterozygous for the insertion mutation and normal allele, showing that the heterozygous insertion mutation itself was not associated with DCM. No mutation was found in the HCM patients., Conclusions: These observations indicated that the compound heterozygous FKTN mutation was a rare cause of DCM. Hyper-CKemia might be indicative of FKTN mutation in DCM.

Coronary artery disease (CAD) has become a major health problem in many countries. Recent genome-wide association studies have identified the association between rs1333049 on chromosome 9p21 and susceptibility to CAD in Caucasoid populations. In this study, we evaluated the associations of rs1333049 with CAD in Japanese (604 patients and 1,151 controls) and Koreans (679 patients and 706 controls). We found a significant association in both Japanese [odds ratio (OR)=1.30, 95% confidence interval (CI); 1.13-1.49, p=0.00027, allele count model] and Koreans (OR=1.19, 95% CI; 1.02-1.38, p=0.025, allele count model). These observations demonstrated that chromosome 9p21 was the susceptibility locus for CAD also in East Asians.

We examined whether the use of non-steroidal anti-inflammatory drugs (NSAIDs) can affect the anemia and iron status of hemodialysis patients. We recruited patients from six dialysis centers who had undergone maintenance hemodialysis for at least four months. We examined the use of NSAIDs during the past three months based on their medical records and assigned the patients to three groups (group A, non-NSAID group; group B, aspirin group; and group C, non-aspirin NSAID group). Of the 446 patients, 95 (21.3%) were treated with aspirin and 103 (23.1%) were treated with non-aspirin NSAIDs. The serum iron level and transferrin saturation (TSAT) were significantly lower in group C patients than those in group A. However, the ratio of the patients who were administrated iron preparations during the past three months was significantly higher than that in the other two groups. The incidences of positive fecal occult blood tests did not differ substantially between the three groups. The ratios of the patients who were administrated recombinant human erythropoietin were the same between three groups. Using a multiple regression analysis, the administration of non-aspirin NSAIDs was identified as an independent factor for the decreased serum iron and the decreased TSAT levels. A multiple logistic regression analysis revealed that the patients using non-aspirin NSAIDs had an increased the requirement for iron preparation therapy (OR 2.03, 95% CI, 1.28-3.22). The use of non-aspirin NSAIDs may therefore increase the risk of the iron deficiency in patients undergoing hemodialysis.

Background: Idiopathic cardiomyopathy was by definition a disease of unknown etiology and there are two major clinical forms, hypertrophic cardiomyopathy and dilated cardiomyopathy. Recent molecular genetic analyses have now revealed that mutations in genes for sarcomere cause hypertrophic cardiomyopathy leading to a hypothesis of hypertrophic cardiomyopathy as sarcomeropathy. On the other hand, mutations in genes for Z-disc component cause dilated cardiomyopathy speculating that dilated cardiomyopathy is cytoskeletopathy at least in part., Methods: A large panel of Asian patients and families with hypertrophic cardiomyopathy or dilated cardiomyopathy was analyzed for gene abnormalities in all exons and adjacent introns of the known disease-related genes and in a part of several candidates of novel disease-related genes., Results: Mutations in the genes for sarcomere were found in 47% of familial cases and 14% of sporadic cases of hypertrophic cardiomyopathy and there were locus and allelic differences in clinical phenotypes of hypertrophic cardiomyopathy patients. In contrast, only a few patients with dilated cardiomyopathy were identified for mutations in the known disease-causing genes. Mutations in the gene for titin, a giant molecule linking Z-disc with sarcomere components, were found in hypertrophic cardiomyopathy patients., Conclusions: The molecular etiologies of cardiomyopathy can be identified in about half of hypertrophic cardiomyopathy and a small part of dilated cardiomyopathy, suggesting that there are several novel disease-causing genes. Identification of titin mutation in hypertrophic cardiomyopathy indicate that hypertrophic cardiomyopathy is in part considered as the cytoskeletopathy.

Idiopathic dilated cardiomyopathy (IDC) is characterized by a thin-walled heart with systolic dysfunction of unknown etiology. Because abnormalities in genes for cytoskeletal proteins related to Z-disc function have recently been reported to cause IDC, genomic organization of the gene for nebulette, a novel actin-binding Z-disc protein, was determined and its sequence variations were searched for in Japanese patients with IDC and healthy controls. The nebulette gene consists of 28 exons, and four sequence variations leading to amino acid replacement (Gln187His, Met351Val, Asn654Lys, and Thr728Ala) were identified in the patients. These variations were also found in the healthy controls and hence they were polymorphisms and not disease-specific mutations. Frequencies of Gln187His, Met351Val, and Thr728Ala variants were similar in the patients and controls. However, the frequency of homozygotes for Lys at codon 654, a variant at a relatively conserved residue in an actinbinding motif, was significantly increased in nonfamilial IDC patients (n=106) as compared with healthy control subjects (n=331) (7.54% vs 1.21%, OR=6.25, P=0.002, 95% CI=1.92-20.29), while this association was not found in familial IDC patients (n=24). These observations suggest that the nebulette polymorphism in the actin-binding motif was a novel genetic marker of susceptibility to nonfamilial IDC.

The biofield breast examination (BBE) is a new, noninvasive and cost-effective method for diagnosing breast lesions currently undergoing multicenter evaluation in the USA and Europe. The test analyzes subtle differences in electrical potential caused by dysregulated epithelial proliferation. This report summarizes a prospective evaluation of BBE in a population of 101 patients with suspicious breast lesions scheduled either for open surgical biopsy or fine needle aspiration biopsy. Of the 101 patients included in the study, 49 were found to have a breast malignancy and 52 were found to have a benign breast lesion. BBE correctly identified 44 of 49 biopsy-proven cancers (sensitivity=90%) and correctly indicated no cancer in 31 of 52 biopsy-proven benign cases (specificity=60%). Sensitivity increased to 95% for cancers less than 2.5 cm in size. These results indicate that BBE may be an effective adjunctive test to help to resolve abnormalities discovered by physical examination or other screening methods.

According to a national survey of dialysis patients in Japan conducted by the Japanese Society for Dialysis Therapy, there were 1,033 patients on dialysis in the Shiga area which has a population of about 1.2 million. Of these 1,033 dialysis patients 140 were the result of diabetic nephropathy. From four hospitals affiliated to Shiga University of Medical Science the medical records of 90 diabetic subjects on dialysis therapy were reviewed and various clinical parameters were analysed and compared with those of patients with chronic glomerulonephritis. Since only one patient had Type 1 (insulin-dependent) diabetes, the remaining 89 with Type 2 (non-insulin-dependent) diabetes were used for this study. The significantly different variables between patients with Type 2 diabetes and chronic glomerulonephritis were age (60.4 vs 54.6 years, p < 0.05), BMI (22.4 vs 20.6 kg/m2, p < 0.001), cardiothoracic ratio (56.4 vs 53.3%, p < 0.001), mean blood pressure (110 vs 117 mmHg, p < 0.05), serum creatinine (9.0 vs 11.5 mg/dl, p < 0.001), serum urea-N (98.2 vs 115.5 mg/dl, p < 0.001), serum total protein (6.0 vs 6.5 g/dl, p < 0.001) and serum albumin (3.5 vs. 3.9 g/dl, p < 0.001). Serum levels of cholesterol and triglyceride were not significantly different between two groups, though the prevalence of electrocardiogram abnormalities, oedema, neuropathy, myocardial infarction and cerebrovascular diseases was significantly higher in the Type 2 diabetic group. These results suggested that Type 2 diabetic patients with end-stage renal disease were older, more malnourished, fluid overloaded and multi-morbid as a result of vasculopathy and neuropathy.(ABSTRACT TRUNCATED AT 250 WORDS)