The acetaldehyde associated with alcoholic beverages is an evident carcinogen for the esophagus. Genetic polymorphisms of the alcohol dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (ALDH2) genes are associated with the risk of esophageal cancer. However, the exact mechanism via which these genetic polymorphisms affect esophageal carcinogenesis has not been elucidated. ADH1B*2 is involved in overproduction of acetaldehyde due to increased ethanol metabolism into acetaldehyde, and ALDH2*2 is involved in accumulation of acetaldehyde due to the deficiency of acetaldehyde metabolism. Acetaldehyde can interact with DNA and form DNA adducts, resulting in DNA damage. N 2 -ethylidene-2′-deoxyguanosine (N 2 -ethylidene-dG) is the most abundant DNA adduct derived from acetaldehyde. Therefore, we quantified N 2 -ethylidene-dG levels in blood samples from 66 Japanese alcoholic patients using liquid chromatography/electrospray tandem mass spectrometry, and investigated the relationship between N 2 -ethylidene-dG levels and ADH1B and ALDH2 genotypes. The median N 2

The entire gene for gramicidin S synthetase 1 (GS 1) was cloned into the plasmid vector pUC18, and the nucleotide sequences of the GS 1 gene and its flanking region were determined. The full-length clone was 4,539 base pairs long and had an open reading frame of 3,294 nucleotides coding for 1,098 amino acids. The calculated molecular weight of 123,474 agreed with the apparent molecular weight of 120,000 found in SDS-PAGE of GS 1 from B. brevis. The nucleotide sequence of GS 1 gene was highly homologous to that of tyrocidine synthetase 1. The overall similarity between the deduced amino acid sequences of the two genes was 57.5%. The gene product of clone GS309 was easily purified to an essentially homogeneous state by ammonium sulfate fractionation followed by DEAE-Sepharose CL-6B, Ultrogel AcA-34, and second DEAE-Sepharose CL-6B column chromatography. The purified protein catalyzed the D-phenylalanine-dependent ATP-32PPi exchange reaction which is specific for GS 1 activity, and the specific activity of the purified product was nearly the same as the purified GS 1 from B. brevis. The product also showed a weak phenylalanine racemase activity.

No abstract

A considerable amount of health record (HR) data has been stored due to recent advances in the digitalization of medical systems. However, it is not always easy to analyze HR data, particularly when the number of persons with a target disease is too small in comparison with the population. This situation is called the imbalanced data problem. Over-sampling and under-sampling are two approaches for redressing an imbalance between minority and majority examples, which can be combined into ensemble algorithms. However, these approaches do not function when the absolute number of minority examples is small, which is called the extremely imbalanced and small minority (EISM) data problem. The present work proposes a new algorithm called boosting combined with heuristic under-sampling and distribution-based sampling (HUSDOS-Boost) to solve the EISM data problem. To make an artificially balanced dataset from the original imbalanced datasets, HUSDOS-Boost uses both under-sampling and over-sampling to eliminate redundant majority examples based on prior boosting results and to generate artificial minority examples by following the minority class distribution. The performance and characteristics of HUSDOS-Boost were evaluated through application to eight imbalanced datasets. In addition, the algorithm was applied to original clinical HR data to detect patients with stomach cancer. These results showed that HUSDOS-Boost outperformed current imbalanced data handling methods, particularly when the data are EISM. Thus, the proposed HUSDOS-Boost is a useful methodology of HR data analysis.

Male Wistar rats, aged 6 weeks, were maintained at 25 degreesC for 9 to 11 weeks (W group), at 10 degreesC for 9 to 11 weeks (C group), and at 25 degreesC for 2 weeks after exposure to 10 degreesC for 9 weeks (D group). Thermogenesis at 10 degreesC was significantly greater than at 25 degreesC. Thermogenesis per body mass in the C group was greater than in the W and D groups. The RQ value at 10 degreesC was greater than at 25 degreesC in the W group, whereas the opposite was observed in the C and D groups. It is suggested that a large part of enhanced thermogenesis, caused by cold acclimation for 9 weeks, is lost because of a decreased secretion of calorigenic hormones, in spite of a slight decrease in BAT mass, during deacclimation for 2 weeks.