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RISS 인기검색어
- 검색키워드
- 저자 : Susumu Sakata (검색결과 5 건)
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Sakata, Susumu,Liang, Lifan,Sakata, Naoya,Sakata, Yuri,Chemaly, Elie R,Lebeche, Djamel,Takewa, Yoshiaki,Chen, Jiqiu,Park, Woo Jin,Kawase, Yoshiaki,Hajjar, Roger J Blackwell Publishing Asia 2007 Clinical and experimental pharmacology & physiolog Vol.34 No.12
<P>SUMMARY</P><OL TYPE='1'><li level='1'>The aim of the present study was to examine the acute and chronic effects of adenoviral gene transfer on cardiac function in terms of left ventricular (LV) mechanoenergetic function. Recombinant adenoviral vector carrying &bgr;-galactosidase and green fluorescent protein genes (Ad.&bgr;gal-GFP) was used. Cardiac function was examined in cross-circulated rat heart preparations, where end-systolic/diastolic pressure–volume relationships (ESPVR/EDPVR), systolic pressure–volume area (PVA), LV relaxation rate, equivalent maximal elastance at mid-range LV volume (eE<SUB>max</SUB> at mLVV), coronary blood flow, coronary vascular resistance and myocardial oxygen consumption (VO<SUB>2</SUB>) were also measured.</LI><li level='1'>To examine the <I>ex vivo</I> acute effects of the adenoviral vector, data were obtained before and 30–90 min after intracoronary infusion of Ad.&bgr;gal-GFP in the excised, cross-circulated hearts that underwent serotonin pretreatment. To examine the <I>in vivo </I>chronic effects of adenoviral gene transfer, normal rat hearts received Ad.&bgr;gal-GFP or saline by a catheter-based technique and data were obtained 3 days after the injection of Ad.&bgr;gal-GFP or saline.</LI><li level='1'>The ESPVR, EDPVR, LV relaxation rate, eE<SUB>max</SUB> at mLVV, coronary blood flow and coronary vascular resistance remained unchanged in Ad.&bgr;gal-GFP-transfected hearts in both <I>ex vivo</I> acute and <I>in vivo </I>chronic experiments. Moreover, the <I>ex vivo</I> and <I>in vivo </I>transfection caused no change in the slope and VO<SUB>2</SUB> intercept of the VO<SUB>2</SUB>–PVA relationship, VO<SUB>2</SUB> for basal metabolism and for Ca<SUP>2+</SUP> handling in excitation–contraction coupling and O<SUB>2</SUB> costs of LV contractility.</LI><li level='1'>These results indicate that adenoviral gene transfer has neither acute nor chronic toxic effects on LV mechanical and energetic function. A special combination of <I>in vivo </I>adenoviral gene transfer and a cross-circulation experimental system may provide a useful novel strategy to explore the functional and mechanoenergetic role of specifically targeted genes in the diseased heart.</LI></OL>
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Possible effects of whole body vibration on bone properties in growing rats
Akira Minematsu,Yasue Nishii,Hidetaka Imagita,Susumu Sakata 대한골다공증학회 2019 Osteoporosis and Sarcopenia Vol.5 No.3
Objectives: To examine the effects of whole body vibration (WBV) on bone properties in growing rats, and to explore the optimal conditions for enhancing bone properties. Methods: Thirty-six 4-week-old male rats were divided into 1 control and 5 experimental groups. Each experimental group underwent WBV at 15, 30, 45, 60, and 90 Hz (0.5 g, 15 min/d, 5 d/wk) for 8 weeks.We measured bone size, muscle weight and bone mechanical strength of the right tibia. Trabecular bone mass and trabecular bone microstructure (TBMS) of the left tibia were analyzed by micro-computed tomography. Serum levels of bone formation/resorption markers were also measured. Results: WBV at 45 Hz and 60 Hz tended to enhance trabecular bone mass and TBMS parameters. However, there was no difference in maximum load of tibias among all groups. Serum levels of bone resorption marker were significantly higher in the 45-Hz WBV group than in the control group. Conclusions: WBV at 45e60 Hz may offer a potent modality for increasing bone mass during the period of rapid growth. Further studies are needed to explore the optimal WBV conditions for increasing peak bone mass and TBMS parameters. WBV modality may be a potent strategy for primary prevention against osteoporosis.
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Femoral bone structure in Otsuka Long-Evans Tokushima Fatty rats
Akira Minematsu,Tomoko Hanaoka,Yoshihiro Takada,Shunji Okuda,Hidetaka Imagita,Susumu Sakata 대한골다공증학회 2016 Osteoporosis and Sarcopenia Vol.2 No.1
Objectives: Type 2 diabetes mellitus (T2DM) increases fracture risk despite normal to high levels of bone mineral density. Bone quality is known to affect bone fragility in T2DM. The aim of this study was to clarify the trabecular bone microstructure and cortical bone geometry of the femur in T2DM model rats. Methods: Five-week-old Otsuka Long-Evans Tokushima Fatty (OLETF; n ¼ 5) and Long-Evans Tokushima Otsuka (LETO; n ¼ 5) rats were used. At the age of 18 months, femurs were scanned with micro-computed tomography, and trabecular bone microstructure and cortical bone geometry were analyzed. Results: Trabecular bone microstructure and cortical bone geometry deteriorated in the femur in OLETF rats. Compared with in LETO rats, in OLETF rats, bone volume fraction, trabecular number and connectivity density decreased, and trabecular space significantly increased. Moreover, in OLETF rats, cortical bone volume and section area decreased, and medullary volume significantly increased. Conclusions: Long-term T2DM leaded to deterioration in trabecular and cortical bone structure. Therefore, OLETF rats may serve as a useful animal model for investigating the relationship between T2DM and bone quality. © 2016 The Korean Society of Osteoporosis. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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PICOT Inhibits Cardiac Hypertrophy and Enhances Ventricular Function and Cardiomyocyte Contractility
Jeong, Dongtak,Cha, Hyeseon,Kim, Eunyoung,Kang, Misuk,Yang, Dong Kwon,Kim, Ji Myoung,Yoon, Pyoung Oh,Oh, Jae Gyun,Bernecker, Oliver Y.,Sakata, Susumu,Thu, Le Thi,Cui, Lei,Lee, Young-Hoon,Kim, Do Han,W Grune & Stratton 2006 Circulation research Vol.99 No.3
<P>Multiple signaling pathways involving protein kinase C (PKC) have been implicated in the development of cardiac hypertrophy. We observed that a putative PKC inhibitor, PICOT (PKC-Interacting Cousin Of Thioredoxin) was upregulated in response to hypertrophic stimuli both in vitro and in vivo. This suggested that PICOT may act as an endogenous negative feedback regulator of cardiac hypertrophy through its ability to inhibit PKC activity, which is elevated during cardiac hypertrophy. Adenovirus-mediated gene transfer of PICOT completely blocked the hypertrophic response of neonatal rat cardiomyocytes to enthothelin-1 and phenylephrine, as demonstrated by cell size, sarcomere rearrangement, atrial natriuretic factor expression, and rates of protein synthesis. Transgenic mice with cardiac-specific overexpression of PICOT showed that PICOT is a potent inhibitor of cardiac hypertrophy induced by pressure overload. In addition, PICOT overexpression dramatically increased the ventricular function and cardiomyocyte contractility as measured by ejection fraction and end-systolic pressure of transgenic hearts and peak shortening of isolated cardiomyocytes, respectively. Intracellular Ca(2+) handing analysis revealed that increases in myofilament Ca(2+) responsiveness, together with increased rate of sarcoplasmic reticulum Ca(2+) reuptake, are associated with the enhanced contractility in PICOT-overexpressing cardiomyocytes. The inhibition of cardiac remodeling by of PICOT with a concomitant increase in ventricular function and cardiomyocyte contractility suggests that PICOT may provide an efficient modality for treatment of cardiac hypertrophy and heart failure.</P>
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