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Articles by A Tanaka
Total Records ( 5 ) for A Tanaka
  M Ai , A Tanaka , K Shimokado , R Ohtani , A Inazu , J Kobayashi , H Mabuchi , T Nakano and K. Nakajima

We found a unique cholesteryl ester transfer protein (CETP) deficient case with markedly elevated serum triglyceride (TG) as well as high-density lipoprotein cholesterol (HDL-C) levels. Most of the CETP deficiency cases were reported to have normal or reduced serum TG with elevated HDL-C.


The case subject was a 40-year-old male with a compound heterozygous CETP deficiency. Two heterozygous CETP deficient cases and 10 normal volunteers were also recruited as controls. They underwent an oral fat tolerance test (OFTT) and their blood was taken at fasting and during the OFTT to be used for laboratory tests.


The case subject had apolipoprotein E (apo-E) phenotype 4/2 with fatty liver but without any cardiovascular disease. His serum TG, HDL-C, apo-AI and apo-B48 levels were significantly higher, but the low-density lipoprotein cholesterol level was lower than controls. Although post-heparin plasma lipoprotein lipase and hepatic lipase (both mass and activity) were nearly normal, the serum level of angiopoietin-like-protein-3 was extremely elevated. While his serum remnant-like particles-TG (RLP-TG) and total TG levels significantly increased after a fat load, the RLP-cholesterol (RLP-C) level did not increase during OFTT.


The case subject was different from the common CETP deficient cases reported previously. Also, the results indicated that the metabolic pathways of RLP-C and RLP-TG formation in the postprandial state are controlled independently in CETP deficient cases. CETP deficiency itself may not be atherogenic, while one with elevated RLPs may be atherogenic. These cases may have raised the controversy of whether CETP deficiency is atherogenic or not.

  J Grewal , R Suri , S Mankad , A Tanaka , D. W Mahoney , H. V Schaff , F. A Miller and M. Enriquez Sarano

Background— Mitral annulus is a complex structure of poorly understood physiology. Full-volume real-time 3-dimensional transesophageal echocardiography offers a unique opportunity to completely image and quantify mitral annulus size and motion.

Methods and Results— Real-time 3-dimensional transesophageal echocardiography of the mitral valve was acquired in 32 patients with myxomatous valve disease (MVD) and moderate to severe regurgitation, 15 normal control subjects, and 10 patients with ischemic mitral regurgitation of identical body surface area. Mitral annular dimensions (circumference, area, anteroposterior and intercommissural diameters, height, and ratio of height to intercommissural diameter ratio, which appraises annular saddle-shape depth) were measured throughout the cardiac cycle with dedicated quantification software. Compared with direct surgical measurement, 3-dimensional anterior annular dimension provided reliable measurements (mean difference, 0.1±0.1 mm; P=0.73; 95% confidence interval, ±4.4 mm). Annular dimensions were larger in MVD patients compared with control subjects in diastole (all P<0.05). Normal annulus displayed early-systolic anteroposterior (P<0.001) and area (P=0.04) contraction, increased height (P<0.001), and deeper saddle shape (ratio of height to intercommissural diameter, 15±1% to 21±1%; P<0.001), whereas intercommissural diameter was unchanged (P=0.30). In contrast, MVD showed early-systolic intercommissural dilatation (P=0.02) and no area contraction (P=0.99), height increase (P=0.11), or saddle-shape deepening (P=0.35). Late-systolic MVD annular saddle shape deepened but annular area excessively enlarged (P<0.04) as a result of persistent intercommissural widening (P<0.02). MVD annulus also contrasts with ischemic mitral regurgitation annulus, which, despite similar anteroposterior enlargement, is narrower and essentially adynamic. After MVD repair, the annulus remained dynamic without systolic saddle-shape accentuation (P=0.30).

Conclusions— Real-time 3-dimensional transesophageal echocardiography provides insights into normal, dynamic mitral annulus function with early-systolic area contraction and saddle-shape deepening contributing to mitral competency. MVD annulus is also dynamic but considerably different with loss of early-systolic area contraction and saddle-shape deepening despite similar magnitude of ventricular contraction, suggestive of ventricular-annular decoupling. Subsequent area enlargement may contribute to mitral incompetence. After mitral repair, MVD annulus remains dynamic without systolic saddle-shape accentuation. Thus, real-time 3-dimensional transesophageal echocardiography provides new insights that allow the refining of mitral pathophysiology concepts and repair strategies.

  A Tanaka , T Imanishi , H Kitabata , T Kubo , S Takarada , T Tanimoto , A Kuroi , H Tsujioka , H Ikejima , K Komukai , H Kataiwa , K Okouchi , M Kashiwaghi , K Ishibashi , H Matsumoto , K Takemoto , N Nakamura , K Hirata , M Mizukoshi and T. Akasaka

Although some recent guidelines recommend an early invasive strategy for non-ST-segment elevation acute coronary syndrome (NSTEACS), several studies have failed to identify any benefit for very early intervention for NSTEACS. The no-reflow phenomenon may inhibit the expected benefit from very early recanalization for NSTEACS subjects. The aim of this study was to investigate whether optical coherence tomography (OCT) could predict no-reflow in patients with NSTEACS.

Methods and results

This study comprised 83 consecutive patients with NSTEACS who underwent OCT and successful emergent primary stenting. On the basis of post-stent TIMI flow, patients were divided into two groups: no-reflow group (n = 14) and reflow group (n = 69). Thin-cap fibroatheroma (TCFA) was defined as a plaque presenting lipid content for >90°, and with thinnest part of the fibrous cap measuring <70 µm. Thin-cap fibroatheroma were more frequently observed in the no-reflow group than in the reflow group (50% vs. 16%, P = 0.005). The frequency of the no-reflow phenomenon increases according to the size of the lipid arc in the culprit plaque. Final TIMI blush grade also deteriorated according to the increase in the lipid arc. A multivariable logistic regression model revealed that lipid arc alone was an independent predictor of no-reflow (odds ratio 1.018; CI 1.004–1.033; P = 0.01).


Optical coherence tomography can predict no-reflow after percutaneous coronary intervention (PCI) in NSTEACS. The lipid contents of a culprit plaque may play a key role in damage to the microcirculation after PCI for NSTEACS. From our results, it is found that OCT is useful tool for stratifying risk for PCI for NSTEACS.

  K Kobayashi , A Tanaka , H Takahashi , J Igarashi , Y Ishitsuka , N Yokota and T. Shimizu

A phosphodiesterase (PDE) from Escherichia coli (Ec DOS) is a novel haem-based oxygen sensor enzyme. Binding of O2 to the reduced haem in the sensor domain enhances PDE activity exerted by the catalytic domain. Kinetic analysis of oxygen-dependent catalytic enhancement showed a sigmoidal curve with a Hill coefficient value of 2.8. To establish the molecular mechanism underlying allosteric regulation, we analysed binding of the O2 ligand following reduction of haem in the isolated dimeric sensor domain using pulse radiolysis. Spectral changes accompanying O2 binding were composed of two phases as a result of reduction of two haem complexes when high-dose electron beams were applied. In contrast, upon reduction of the dimer with a low-dose beam, the kinetics of O2 ligation displayed single-phase behaviour as a result of the reduction of one haem complex within dimer. Based on these results, we propose that the faster phase corresponds to binding of the first O2 molecule to one subunit of the dimer, followed by binding of the second O2 molecule to the other subunit. Notably, for the haem axial ligand mutant proteins, M95A and M95L, O2 binding displayed single-phase kinetics and was independent of electron beam dose.

  A Tanaka , H. M Shen , S Ratnam , P Kodgire and U. Storb

The process of somatic hypermutation (SHM) of immunoglobulin (Ig) genes requires activation-induced cytidine deaminase (AID). Although mistargeting of AID is detrimental to genome integrity, the mechanism and the cis-elements responsible for targeting of AID are largely unknown. We show that three CAGGTG cis-elements in the context of Ig enhancers are sufficient to target SHM to a nearby transcribed gene. The CAGGTG motif binds E47 in nuclear extracts of the mutating cells. Replacing CAGGTG with AAGGTG in the construct without any other E47 binding site eliminates SHM. The CA versus AA effect requires AID. CAGGTG does not enhance transcription, chromatin acetylation, or overall target gene activity. The other cis-elements of Ig enhancers alone cannot attract the SHM machinery. Collectively with other recent findings, we postulate that AID targets all genes expressed in mutating B cells that are associated with CAGGTG motifs in the appropriate context. Ig genes are the most highly mutated genes, presumably because of multiple CAGGTG motifs within the Ig genes, high transcription activity, and the presence of other cooperating elements in Ig enhancers.

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