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Articles by N Tanaka
Total Records ( 6 ) for N Tanaka
  Y Bando , H Kanehara , D Toya , N Tanaka , S Kasayama and M. Koga

In patients with chronic liver disease (CLD), glycated haemoglobin (HbA1C) levels have been shown to be apparently lower than real values, whereas serum glycated albumin (GA) levels are apparently higher. The present study was aimed to examine whether both glycaemic indices are influenced by hepatic function.


Subjects consisted of 82 patients with CLD. Various indicators for hepatic function as well as HbA1C and GA were also measured. Estimated HbA1C values were calculated from the mean plasma glucose levels. Two hundred and two type 2 diabetic patients without CLD were studied as controls.


Although GA was strongly correlated with HbA1C in patients with CLD as well as diabetic patients, GA levels in patients with CLD were relatively higher than those in diabetic patients. In patients with estimated HbA1C ≤5.8%, GA levels significantly increased but HbA1C levels decreased as a function of decreasing hepaplastin test (HPT). The ratio of GA/HbA1C (G/H ratio) increased as a function of decreasing HPT. In patients with estimated HbA1C >5.8%, in contrast, GA levels were independent of HPT levels. In the patients with CLD, GA and HbA1C were associated with mean plasma glucose levels and some indicators for hepatic function. The multivariate analysis revealed a significant association of G/H ratio with HPT, cholinesterase and direct bilirubin. The G/H ratio was not associated with the mean plasma glucose but with HPT and cholinesterase levels.


The G/H ratio correlates with hepatic function but not with plasma glucose levels. Therefore, CLD should be suspected for diabetic patients with an elevated G/H ratio.

  S Hirano , H Shinotoh , H Shimada , A Aotsuka , N Tanaka , T Ota , K Sato , H Ito , S Kuwabara , K Fukushi , T Irie and T. Suhara

Corticobasal syndrome, progressive supranuclear palsy and frontotemporal dementia are all part of a disease spectrum that includes common cognitive impairment and movement disorders. The aim of this study was to characterize brain cholinergic deficits in these disorders. We measured brain acetylcholinesterase activity by [11C] N-methylpiperidin-4-yl acetate and positron emission tomography in seven patients with corticobasal syndrome (67.6 ± 5.9 years), 12 with progressive supranuclear palsy (68.5 ± 4.1 years), eight with frontotemporal dementia (59.8 ± 6.9 years) and 16 healthy controls (61.2 ± 8.5 years). Two-tissue compartment three-parameter model and non-linear least squares analysis with arterial input function were performed. k3 value, an index of acetylcholinesterase activity, was calculated voxel-by-voxel in the brain of each subject. The k3 images in each disease group were compared with the control group by using Statistical Parametric Mapping 2. Volume of interest analysis was performed on spatially normalized k3 images. The corticobasal syndrome group showed decreased acetylcholinesterase activity (k3 values) in the paracentral region, frontal, parietal and occipital cortices (P < 0.05, cluster corrected). The group with progressive supranuclear palsy had reduced acetylcholinesterase activity in the paracentral region and thalamus (P < 0.05, cluster corrected). The frontotemporal dementia group showed no significant differences in acetylcholinesterase activity. Volume of interest analysis showed mean cortical acetylcholinesterase activity to be reduced by 17.5% in corticobasal syndrome (P < 0.001), 9.4% in progressive supranuclear palsy (P < 0.05) and 4.4% in frontotemporal dementia (non-significant), when compared with the control group. Thalamic acetylcholinesterase activity was reduced by 6.4% in corticobasal syndrome (non-significant), 24.0% in progressive supranuclear palsy (P < 0.03) and increased by 3.3% in frontotemporal dementia (non-significant). Both corticobasal syndrome and progressive supranuclear palsy showed brain cholinergic deficits, but their distribution differed somewhat. Significant brain cholinergic deficits were not seen in frontotemporal dementia, which may explain the unresponsiveness of this condition to cholinergic modulation therapy.

  S Rathore , O Katoh , H Matsuo , M Terashima , N Tanaka , Y Kinoshita , M Kimura , E Tsuchikane , K Nasu , M Ehara , K Asakura , Y Asakura and T. Suzuki

Background— Retrograde approach through collaterals has been introduced for percutaneous recanalization of chronic total occlusion (CTO) of the coronary arteries. We investigated the safety and efficacy of retrograde approaches used for percutaneous recanalization of CTO in a consecutive series of patients.

Methods and Results— We studied 157 consecutive patients who underwent retrograde CTO recanalization between 2003 and 2008 at a single center. A total of 118 (75.2%) of these patients have had previously failed antegrade attempts. Septal, epicardial, and saphenous vein graft collaterals were used in 67.5%, 24.8%, and 7.6% of cases, respectively. Collateral channel was crossed by guide wire successfully in 115 (73.2%) cases, and the procedure was successful by retrograde approach in 103 (65.6%) cases. Collateral channels (CCs) were graded as follows: CC0, no continuous connection; CC1, continuous thread-like connection; and CC2, continuous, small sidebranch-like connection. CC1, collateral tortuosity <90°, and angle with recipient vessel <90° (P<0.0001) were significant predictors of success. Epicardial channel use (P=0.01), CC0, corkscrew channel (P<0.0001), angle with recipient vessel >90° (P=0.0007), and nonvisibility of connection with recipient vessel were found to be significant predictors of procedural failure. The CC dissection was observed in 6 patients, with 1 needing coil embolization and others who were managed conservatively. The major adverse cardiac events were low, with 1 coronary artery bypass graft, 1 Q-wave myocardial infarction, 5 non–Q-wave myocardial infarctions, and no deaths in this group of patients.

Conclusions— The retrograde approach in CTO percutaneous coronary intervention is effective in recanalizing CTO. The success rate by retrograde approach was 65.6%, and final success was 85% in this group with acceptable overall adverse events. We have identified predictors of failure related to collateral morphology.

  T Nagasaka , N Tanaka , H. M Cullings , D. S Sun , H Sasamoto , T Uchida , M Koi , N Nishida , Y Naomoto , C. R Boland , N Matsubara and A. Goel

The development of noninvasive screening tests is important to reduce mortality from gastrointestinal neoplasia. We sought to develop such a test by analysis of DNA methylation from exfoliated cancer cells in feces.


We first analyzed methylation of the RASSF2 and SFRP2 gene promoters from 788 primary gastric and colorectal tissue specimens to determine whether methylation patterns could act as stage-dependent biomarkers of gastrointestinal tumorigenesis. Next, we developed a novel strategy that uses single-step modification of DNA with sodium bisulfite and fluorescence polymerase chain reaction methodology to measure aberrant methylation in fecal DNA. Methylation of the RASSF2 and SFRP2 promoters was analyzed in 296 fecal samples obtained from a variety of patients, including 21 with gastric tumors, 152 with colorectal tumors, and 10 with non-neoplastic or inflammatory lesions in the gastrointestinal lumen.


Analysis of DNA from tissues showed presence of extensive methylation in both gene promoters exclusively in advanced gastric and colorectal tumors. The assay successfully identified one or more methylated markers in fecal DNA from 57.1% of patients with gastric cancer, 75.0% of patients with colorectal cancer, and 44.4% of patients with advanced colorectal adenomas, but only 10.6% of subjects without neoplastic or active diseases (difference, gastric cancer vs undiseased = 46.5%, 95% confidence interval (CI) = 24.6% to 68.4%, P < .001; difference, colorectal cancer vs undiseased = 64.4%, 95% CI = 53.5% to 75.2%, P < .001; difference, colorectal adenoma vs undiseased = 33.8%, 95% CI = 14.2% to 53.4%, P < .001).


Methylation of the RASSF2 and SFRP2 promoters in fecal DNA is associated with the presence of gastrointestinal tumors relative to non-neoplastic conditions. Our novel fecal DNA methylation assay provides a possible means to noninvasively screen not only for colorectal tumors but also for gastric tumors.

  R. A Herring , K Saitoh , N Tanaka and T. Tanji

For the first time, the electron intensity on the diffraction plane from amorphous transmission electron microscope (TEM) specimens has been found to have sufficient coherence to produce fringes in interferograms that were created using a wavefront splitting method of diffracted beam interferometry. The fringes were found to exist from low to high electron-scattering angles. Their spatial frequency depended on the angular overlap of the interfering beams, which was controlled by an electron biprism. From these interferograms, phase information of amorphous materials, which is information now lacking and required for determining their atomic structures, was obtained. An immediate application of this interference is a new method to determine the spatial resolution of the TEM that occurs at the shear angle for fringe disappearance.

  K Hanai , T Babazono , I Nyumura , K Toya , N Tanaka , M Tanaka , A Ishii and Y. Iwamoto

Background. Nitric oxide (NO) is thought to play an important role in the pathogenesis of diabetic nephropathy. We conducted a prospective, observational cohort study to explore the relationship between plasma levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, and the development and progression of nephropathy in patients with type 2 diabetes.

Methods. This was a hospital-based observational cohort study in Japanese type 2 diabetic patients with normoalbuminuria [urinary albumin-to-creatinine ratio (ACR) <30 mg/g creatinine] or microalbuminuria (30 ≤ ACR <300 mg/g creatinine). The primary endpoint was the development or progression of diabetic nephropathy, based on transition from any given stage to a more advanced stage of albuminuria.

Results. We studied 225 diabetic patients, 81 women and 144 men, with a mean (±SD) age of 64 ± 10 years. The majority (183) of patients were normoalbuminuric, with the remainder microalbuminuric (42). During the median follow-up period of 5.2 years, 27 normoalbuminuric and 10 microalbuminuric patients reached the primary endpoint. When patients were separated according to the median ADMA level (0.46 µmol/l), patients with higher ADMA levels had a greater incidence of reaching the endpoint (P = 0.014 by the log-rank test). In the multivariate Cox proportional hazard model, the hazard ratio for reaching the endpoint for patients with higher versus lower ADMA levels was 2.72 (95% confidence interval 1.25–5.95; P = 0.012).

Conclusions. Higher plasma levels of ADMA may be a novel and potent predictor of the progression of nephropathy in adult Japanese type 2 diabetic patients.

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