Publications by authors named "Reiji Hattori"

A photoplethysmography (PPG) sensor is a cost-effective and efficacious way of measuring health conditions such as heart rate, oxygen saturation, and respiration rate. In this work, we present a hybrid PPG sensor system working in a reflective mode with an optoelectronic module, i.e.

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The promising possibility of an organic photodetector (OPD) is emerging in the field of sensing applications for its tunable absorption range, flexibility, and large-scale fabrication abilities. In this work, we fabricated a bulk heterojunction OPD with a device structure of glass/ITO/PEDOT:PSS/P3HT:PCBM/Al using the spin-coating process and characterized the dark and photocurrent densities at different applied bias conditions for red, green, and blue incident LEDs. The OPD photocurrent density exhibited a magnitude up to 2.

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The temperature dependence thermal conductivity of the indium-gallium-zinc oxide (IGZO) thin films was investigated with the differential three-omega method for the clear demonstration of nanocrystallinity. The thin films were deposited on an alumina (α-AlO) substrate by direct current (DC) magnetron sputtering at different oxygen partial pressures ([PO] = 0%, 10%, and 65%). Their thermal conductivities at room temperature were measured to be 1.

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This paper compares the structural design of two organic biosensors that minimize power consumption in wireless photoplethysmogram (PPG) waveform monitoring. Both devices were fabricated on the same substrate with a red organic light-emitting diode (OLED) and an organic photodiode (OPD). Both were designed with a circular OLED at the center of the device surrounded by OPD.

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This paper demonstrated a new design structure for minimizing the power consumption of a pulse meter. Monolithic devices composed of a red (625 nm) organic light-emitting diode (OLED) and an organic photodiode (OPD) were fabricated on the same substrate. Two organic devices were designed differently.

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Active infective endocarditis may progress to annular abscess formation. We describe a patch annuloplasty technique to treat the fragile aortic root tissue in these patients.

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The occurrence of infective aortic pseudoaneurysms tends to be intractable and difficult to treat. We experienced a very rare case of a recurrent infective pseudoaneurysm in the ascending aorta that occurred after cardiac surgery in an atomic bomb survivor with myelodysplastic syndrome. The pseudoaneurysm was successfully repaired using a femoral artery autograft with an omentopexy and the patient recovered well without any recurrence.

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Background: We hypothesized that enhanced mesenchymal cell (MC) engraftment with insulin-like growth factor-1 (IGF-1) improves left ventricular (LV) function and survival.

Methods And Results: IGF-1 (10 microg/ml) increased adhesion and inhibited apoptosis under hypoxia in vitro through activation of phosphatidylinositol 3-kinase (PI3K) in bone marrow-derived MCs obtained from transgenic rats expressing green fluorescence protein. Myocardial infarction (MI) in rats was produced by ligature of the left coronary artery.

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We investigated the mechanism of exercise-induced late cardioprotection against ischemia-reperfusion (I/R) injury. C57BL/6 mice received treadmill exercise (60 min/day) for 7 days at a work rate of 60-70% maximal oxygen uptake. Exercise transiently increased oxidative stress and activated endothelial isoform of nitric oxide synthase (eNOS) during exercise and increased expression of inducible isoform of NOS (iNOS) in the heart after 7 days of exercise.

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Background: The hypothesis that mechanical stress during reperfusion produces myocyte oncosis and inhibits apoptosis was tested in the present study.

Methods And Results: Isolated and perfused rat hearts were subjected to 30 min ischemia followed by 150 min reperfusion. In the control-reperfusion heart, the form of myocyte death was a mixture of apoptosis only, oncosis only, and both apoptosis and oncosis.

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We investigated the role of oxidative/nitrosative stress in the tolerance to ischemia/reperfusion (I/R) injury in BIO14.6 cardiomyopathy hamster hearts at 6 weeks of age. These hearts showed no significant morphologic change and left ventricular (LV) dysfunction.

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Objective: Dystrophin is a sarcolemmal membrane protein that prevents the myocyte from oncosis induced by physical stress. Because ischemic preconditioning (IPC) protects mitochondria and prevents oncosis during reperfusion, we hypothesized that dystrophin is an end-target of IPC distal to mitochondrial protection.

Methods And Results: Isolated rat hearts were subjected to 30 min ischemia followed by reperfusion.

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Activation of p38 mitogen-activated protein (MAP) kinase (MAPK) has been implicated in the mechanism of cardiomyocyte (CMC) protection and injury. The p38 MAPK controversy may be related to differential effects of this kinase on apoptosis and necrosis. We have hypothesized that p38 MAPK-mediated F-actin reorganization promotes apoptotic cell death, whereas it protects from osmotic stress-induced necrotic cell death.

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Although protein kinase C (PKC) and phosphatidylinositol 3 (PI3)-kinase are implicated in cardioprotective signal transduction mediated by ischemic preconditioning, their role in pharmacological preconditioning (PPC) has not been determined. Cultured neonatal rat cardiomyocytes (CMCs) were subjected to simulated ischemia for 2 h followed by 15 min of reoxygenation. PPC of CMCs consisted of administration of 50 microM adenosine, 50 microM diazoxide, and 50 microM S-nitroso-N-acetylpenicillamine (SNAP), each alone or in combination, for 15 min followed by 30 min of washout before simulated ischemia.

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Conventional therapies for severe ischemic heart disease are limited in applicability. While several angiogenesis researches have shown novel efficacy, safety and feasibility for clinical use, recently we have started the clinical trial of a sole cell therapy using autologous bone marrow mononuclear cells transplantation targeted into ischemic hibernating myocardium. Here, we review the background of bone marrow cell research and introduce therapeutic angiogenesis for severe ischemic heart disease by autologous bone marrow cells transplantation.

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Resveratrol (trans-3,4',5-trihydroxystilbene), a recently described grape-derived polyphenolic antioxidant, has been found to protect the heart from ischemic-reperfusion injury. The present study sought to determine the mechanism of cardioprotection by investigating the ability of resveratrol to precondition the heart. Isolated perfused rat hearts were randomly divided into six groups: group I was perfused for 15 min with Kreb-Henseleit buffer (KHB) only; group II was perfused with 10 microM resveratrol; group III was perfused with 10 microM resveratrol plus 100 microM N(G)-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide (NO) synthase (NOS) inhibitor; group IV was perfused with 10 microM resveratrol plus 100 microM aminoguanidine (AG), an inducible NOS (iNOS) blocker; and groups V and VI consisted of hearts perfused with L-NAME and AG, respectively.

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