Obesity was widely identified as a modifiable risk factor for NODAT. Body mass index (BMI) is the most frequently used diagnostic indication of obesity, and higher pretransplant BMI has been reported to be an independent risk factor of

NODAT. However, the influence of posttransplant increase in BMI on the development of NODAT during outpatient follow-up has not been established. This is a single-centered retrospective study in Japan. We identified 158 consecutive patients who received living donor kidney transplantation in Sendai Shakaihoken Hospital from September 2000 to December 2009. Of these, 101 patients were included in this study. NODAT was defined based on the American Diabetes Association definitions. Fifteen patients developed NODAT selleck inhibitor with a median follow-up period of 27 (3-109) months. Of these 15 patients with NODAT, 13 patients were diagnosed after the first year of transplantation, with a median follow-up of 29 months, and 2 patients were diagnosed at 3 months after transplantation. Recipient age (HR: 1.06 [1.01-1.13]) and increase in BMI (HR: 1.12 [1.01-1.26]) proved to be independent risk factors of

NODAT in multivariate logistic analysis after adjustments for pretransplant 2-hour OGTT level, pretransplant BMI, and use of tacrolimus. This is the first study showing the association between an increase in BMI and the development CRM1 inhibitor of NODAT. The increase in BMI might be a risk factor for NODAT. These findings underline the importance of routine BMI measurements in medical practice.”
“We compared 3 polymerase chain reaction (PCR) methods (mutant-enriched PCR, peptide nucleic acid-locked nucleic acid [PNA-LNA] PCR, and PCR clamp) to detect EGFR mutations in 50 patients with advanced non-small-cell lung cancer (NSCLC). Seventeen were harboring EGFR mutations, 5 of whom showed discrepancies between the results of different PCR methods. All 5 responded to gefitinib, which we consider

to suggest that the discrepancies were false negatives.\n\nBackground: Epidermal growth factor receptor (EGFR) mutations are predictive FK228 order of response to EGFR tyrosine kinase inhibitors (TKIs) in NSCLC. Several methods have been used to detect EGFR mutations; however, it is not clear which is the most suitable for use in the clinic. In this study, we directly compare the clinical sensitivity and specificity of 3 PCR methods. Patients and Methods: We compared the 3 PCR methods (mutant-enriched PCR, PNA-LNA PCR, and PCR clamp) in patients with advanced NSCLC. A patient who showed sensitive mutations by at least 1 PCR method was treated with gefitinib. A patient who showed no sensitive mutations was treated with chemotherapy with cytotoxic agents. Results: Fifty patients with advanced NSCLC previously untreated with EGFR-TKIs were enrolled in this trial. Seventeen patients were harboring EGFR mutations, 5 of whom showed discrepancies between the results of different PCR methods. All 5 patients responded to gefitinib.