Tatsuya Oguni
Osaka Medical College
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Featured researches published by Tatsuya Oguni.
Pediatrics International | 1999
Keisuke Okasora; Ryuzo Takaya; Masakuni Tokuda; Yasuhiro Fukunaga; Tatsuya Oguni; Haruki Tanaka; Kazutaka Konishi; Hiroshi Tamai
Abstract Background: There are a variety of methods for assessing body composition. Bioelectrical impedance analysis (BIA) is an easy and non‐invasive technique, but has limitations in underweight and overweight subjects. Few reports have investigated the validity of BIA in children. In this report, the characteristics of BIA, especially in overweight and underweight children, are assessed and the results are compared with those of dual energy X‐ray absorptiometry (DXA), as a reliable method for assessing body composition.
Diabetes Research and Clinical Practice | 1995
Masanori Iwanishi; Toshiyuki Obata; Schu Yamada; Hiroshi Maegawa; Rie Tachikawa-Ide; Satoshi Ugi; Masaaki Hasegawa; Hideto Kojima; Tatsuya Oguni; Ryuhei Toudo; Yukio Shigeta; Atsunori Kashiwagi
We identified three families having a mutation in the mitochondrial tRNA(LEU(UUR)) gene at bp 3243 in 300 patients with non-insulin dependent diabetes mellitus (NIDDM), who had first degree relatives of patients with NIDDM. We found six individuals with diabetes, one with impaired glucose tolerance (IGT), and five with normal glucose tolerance (NGT) among three families. Insulin secretory response to oral glucose load was impaired in six diabetics, but was normal in IGT and NGT, and the proportion of mutant DNA in the blood did not always associate with the severity of glucose intolerance. Furthermore, both gender and obesity may influence the clinical expression of diabetes in three pairs with an age-matched brother-sister relationship with similar high mutation rate in blood samples. Thus, although patients with mitochondrial gene mutation had a high frequency of diabetes, the proportion of mutant DNA evaluated by blood samples may not necessarily indicate glucose intolerance in the members with the mutation. Unidentified factors including gender, aging, and obesity may alter the clinical manifestation of diabetes.
Biochemical and Biophysical Research Communications | 1987
Masakuni Tokuda; Atsunori Kashiwagi; Eiji Wakamiya; Tatsuya Oguni; Makoto Mino; Hiroyuki Kagamiyama
Glucose tolerance factor partially purified from yeast extract powder stimulated [U-14C]-D-glucose uptake to a level 5.6 times greater than the basal level in the absence of insulin in isolated adipocytes prepared from rats fed with normal laboratory chow. The factor also stimulated 3-O-methylglucose transport 2.2-fold from the basal level in the absence of insulin, but not in the presence of 8 nM insulin. Kinetic analysis revealed that glucose tolerance factor increased 3-O-methylglucose transport by decreasing the Ks value for 3-O-methylglucose with little change in the Vmax.
American Journal of Hematology | 2000
Toshihito Nagata; Hideo Mugishima; Atsushi Yoden; Kenji Yoshikawa; Tatsuya Oguni; Kuniaki Yamashiro; Shiyunji Yamamori; Kensuke Harada
Acute myelomonocytic leukemia (AMMoL) accompanied by monoclonal gammopathy is a rare condition, and its pathogenesis and the cytogenetic mechanism of such leukemogenesis have not been determined in detail. A case of AMMoL with eosinophilia accompanied by immunoglobulin G κ monoclonal gammopathy is described. Immunophenotypic studies of the peripheral blood and bone marrow mononuclear cells revealed no evidence of abnormally proliferating cells of B‐lineage. DNA analyses of bone marrow mononuclear cells containing leukemic cells revealed rearrangement of the κ‐light chain (Igκ) gene and c‐myc and c‐jun proto‐oncogenes. The intensities of the rearranged bands for these genes on Southern blot analysis suggested the existence of a major population of leukemic cells with rearranged Igκ gene and minor population(s) of leukemic cells with rearranged c‐myc and/or c‐jun proto‐oncogene(s) in the patients bone marrow and indicated the occurrence of genetic evolutionary changes in leukemic cells in this patient before starting chemotherapy. These results suggest that these leukemic cells are the most likely candidate for immunoglobulin G κ monoclonal protein production, and structural abnormalities of c‐myc and c‐jun proto‐oncogenes may have contributed to the evolution of leukemic cells in this patient. Am. J. Hematol. 65:66–71, 2000.
Pathophysiology | 1996
Jin Yamaguchi; Tatsuya Oguni; Kazutaka Konishi; Makoto Mino
Abstract The aim of this study was to assess the influence of intra-abdominal fat accumulation in obese children upon lipids, glucose metabolism, and blood pressure. Intra-abdominal fat accumulation was quantified by the intra-abdominal visceral fat to extra-abdominal fat ratio (VS ratio) using CT scanning. The subjects were simple obese boys (35) and girls (24) aged 10.6 ± 2.1 years. The following parameters were calculated: VS ratio from CT analysis at umbilical level, percentage of ideal body weight (%IBW), body mass index (BMI), and waist-to-hip ratio (WHR) from anthropometric measurements. Replies to questionnaires concerning duration of obesity and history of family obesity were obtained. Blood pressure and biochemical parameters including transaminases, serum lipids, blood glucose and insulin were measured. Visceral fat obesity was present in 15.7% of all the subjects. Visceral fat syndrome was seen in some cases. The VS ratio displayed a weak positive correlation with GOT ( r = 0.352, P = 0.0078) and GPT ( r = 0.351, P = 0.0075), but no correlation with serum lipids, blood glucose, insulin, or blood pressure. Stepwise and multiple regression analysis revealed that GOT and GPT depended upon the VS ratio, age, and duration of obesity. It was concluded that intra-abdominal fat accumulation in childhood can cause fatty liver when combined with aging and persistent obesity, and that obese children with fatty liver are likely to develop visceral fat syndrome in the future.
Pediatrics International | 2014
Tohru Fujiwara; Tatsuya Oguni; Gen Unishi; Takuya Tanabe; Kazuhiko Ohbayashi; Kazunari Kaneko
Children with early adiposity rebound (AR), measured using individual body mass index (BMI) growth curves, have an increased risk of metabolic disease as adults. The children with early AR, however, are not fully characterized. The aim of this study was to investigate the prevalence and characteristics of the infants who develop early AR.
Pediatrics International | 2018
Akihisa Okumura; Shinobu Ida; Setsuko Ito; Tatsuya Oguni; Mitsuyoshi Suzuki; Masaaki Mori; Toshiaki Shimizu
The aim of this study was to investigate consumer perception of ionic beverage consumption by young children as a potential link to their excessive use.
Pathophysiology | 1996
Kazuo Watanabe; Naohisa Kawamura; Masakuni Tokuda; Tatsuya Oguni; Kazutaka Konishi; Makoto Mino
Abstract The serum level of soluble interleukin-2 receptor (sIL-2R) has been proposed as a clinical marker for various autoimmune diseases. Serum in patients with insulin-dependent diabetes mellitus (IDDM), as an organ-specific autoimmune disease, was investigated by sIL-2R assay. Although serum sIL-2R levels were very much higher in patients with acute lymphocytic leukemia and chronically or subchronically inflammatory diseases including Schoenlein-Henoch disease, juvenile rheumatoid arthritis (JRA), systemic lupus erythematosus (SLE), ulcerative colitis (UC) and mucocutaneous lymph node syndrome (MCLS), the level in IDDM children who were newly diagnosed (within 6 months after onset) was also moderately higher (628 ± 64 U/ml; P 1c level, or patient. ThesThese findings suggest that slowly progressing T-cell activation and an imbalanced cellular immune response exist in newly diagnosed IDDM children.
Clinical Pediatric Endocrinology | 2001
Keisuke Okasora; Masakuni Tokuda; Kazutaka Konishi; Tatsuya Oguni; Ryuzo Takaya; Takashi Uemura; Naoki Namba; Noriko Nariyama; Yasuhiro Kawasaki; Yasuhiro Fukunaga; Hiroshi Tamai
Japanese Journal of Clinical Oncology | 1992
Toshihito Nagata; Naohisa Kawamura; Tadashi Motoyama; Munenori Miyake; Atushi Yoden; Kenji Yoshikawa; Tatsuya Oguni; Kuniaki Yamasiro; Makoto Mino