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Articles by H Aoki
Total Records ( 2 ) for H Aoki
  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.

  J. K Akada , H Aoki , Y Torigoe , T Kitagawa , H Kurazono , H Hoshida , J Nishikawa , S Terai , M Matsuzaki , T Hirayama , T Nakazawa , R Akada and K. Nakamura
  Junko K. Akada, Hiroki Aoki, Yuji Torigoe, Takao Kitagawa, Hisao Kurazono, Hisashi Hoshida, Jun Nishikawa, Shuji Terai, Masunori Matsuzaki, Toshiya Hirayama, Teruko Nakazawa, Rinji Akada, and Kazuyuki Nakamura

Helicobacter pylori, a common pathogen that causes chronic gastritis and cancer, has evolved to establish persistent infections in the human stomach. Epidemiological evidence suggests that H. pylori with both highly active vacuolating cytotoxin A (VacA) and cytotoxin-associated gene A (CagA), the major virulence factors, has an advantage in adapting to the host environment. However, the mechanistic relationship between VacA and CagA remains obscure. Here, we report that CagA interferes with eukaryotic endocytosis, as revealed by genome-wide screening in yeast. Moreover, CagA suppresses pinocytic endocytosis and the cytotoxicity of VacA in gastric epithelial cells without affecting clathrin-dependent endocytosis. Our data suggest that H. pylori secretes VacA to attack distant host cells while injecting CagA into the gastric epithelial cells to which the bacteria are directly attached, thereby protecting these attached host cells from the cytotoxicity of VacA and creating a local ecological niche. This mechanism might allow H. pylori to balance damage to one population of host cells with the preservation of another, allowing for persistent infection.

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