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Articles by N Takeda
Total Records ( 3 ) for N Takeda
  J Wohlschlaeger , B Levkau , G Brockhoff , K. J Schmitz , M von Winterfeld , A Takeda , N Takeda , J Stypmann , C Vahlhaus , C Schmid , N Pomjanski , A Bocking and H. A. Baba

Background— Whether adult cardiomyocytes have the capacity to regenerate in response to injury and, if so, to what extent are still issues of intense debate. In human heart failure, cardiomyocytes harbor a polyploid genome. A unique opportunity to study the mechanism of polyploidization is provided through the setting of hemodynamic support by left ventricular assist devices. Hence, the cardiomyocyte DNA content, nuclear morphology, and number of nuclei per cell were assessed before and after left ventricular assist device support.

Methods and Results— In 23 paired myocardial samples, cardiomyocyte ploidy was investigated by DNA image cytometry, flow cytometry, and in situ hybridization. Nuclear cross-sectional area and perimeters were measured morphometrically, and the binucleated cardiomyocytes were counted. The median of the cardiomyocyte DNA content and the number of polyploid cardiomyocytes both declined significantly from 6.79 c to 4.7 c and 40.2% to 23%, whereas a significant increase in diploid cardiomyocytes from 33.4% to 50.3% and in binucleated cardiomyocytes from 4.5% to 10% after unloading was observed.

Conclusions— The decrease in polyploidy and increase in diploidy after left ventricular assist device suggest a numeric increase in diploid cardiomyocytes (eg, through cell cycle progression with completion of mitosis or by increased stem cells). The cardiac regeneration that follows may serve as a morphological correlate of the recovery observed in some patients after unloading.

  I Matsunari , H Aoki , Y Nomura , N Takeda , W. P Chen , J Taki , K Nakajima , S. G Nekolla , S Kinuya and K. Kajinami

Although both 123I-metaiodobenzylguanidine (123I-MIBG) imaging and 11C-hydroxyephedrine (11C-HED) positron emission tomography (PET) are used for assessing cardiac sympathetic innervation, their relationship remains unknown. The aims were to determine whether 123I-MIBG parameters such as heart-to-mediastinum ratio (H/M) are associated with quantitative measures by 11C-HED PET and to compare image quality, defect size, and location between 123I-MIBG single-photon emission computed tomography (SPECT) and 11C-HED PET.

Methods and Results—

Twenty-one patients (mean left ventricular ejection fraction, 39±15%) underwent 123I-MIBG imaging and 11C-HED PET. Early (15-minute), late (3-hour) H/M, and washout rate (WR) were calculated for 123I-MIBG. Myocardial retention and WR was calculated for 11C-HED. Using a polar map approach, defect was defined as the area with relative activity <60% of the maximum. Both the early (r=0.76) and late (r=0.84) 123I-MIBG H/M were correlated with 11C-HED retention. 123I-MIBG WR was correlated with 11C-HED WR (r=0.57). Defect size could not be measured in 3 patients because of poor quality 123I-MIBG SPECT, whereas 11C-HED defect was measurable in all patients. Although defect size measured by early or late 123I-MIBG SPECT was closely correlated with that by 11C-HED PET (early: r=0.94; late: r=0.88), the late 123I-MIBG overestimated defect size particularly in the inferior and septal regions.


123I-MIBG H/M gives a reliable estimate of cardiac sympathetic innervation as measured by 11C-HED PET. Furthermore, despite the close correlation in defect size, 11C-HED PET appears to be more suitable for assessing regional abnormalities than does 123I-MIBG SPECT.

  N Takeda , E. L O'Dea , A Doedens , J. w Kim , A Weidemann , C Stockmann , M Asagiri , M. C Simon , A Hoffmann and R. S. Johnson

Hypoxic response and inflammation both involve the action of the hypoxia-inducible transcription factors HIF-1 and HIF-2. Previous studies have revealed that both HIF- proteins are in a number of aspects similarly regulated post-translationally. However, the functional interrelationship of these two isoforms remains largely unclear. The polarization of macrophages controls functionally divergent processes; one of these is nitric oxide (NO) production, which in turn is controlled in part by HIF factors. We show here that the HIF- isoforms can be differentially activated: HIF-1 is induced by Th1 cytokines in M1 macrophage polarization, whereas HIF-2 is induced by Th2 cytokines during an M2 response. This differential response was most evident in polarized macrophages through HIF- isoform-specific regulation of the inducible NO synthase gene by HIF-1, and the arginase1 gene by HIF-2. In silico modeling predicted that regulation of overall NO availability is due to differential regulation of HIF-1 versus HIF-2, acting to, respectively, either increase or suppress NO synthesis. An in vivo model of endotoxin challenge confirmed this; thus, these studies reveal that the two homologous transcription factors, HIF-1 and HIF-2, can have physiologically antagonistic functions, but that their antiphase regulation allows them to coordinately regulate NO production in a cytokine-induced and transcription-dependent fashion.

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