In the past Hiromi Sato has collaborated on articles with Teruo Mozume and Yoshie Maitani. One of their most recent publications is Effect of source-supply interruptions on the interface abruptness in gas source molecular beam epitaxy grown InGaAs/InP heterostructures. Which was published in journal Journal of Crystal Growth.

More information about Hiromi Sato research including statistics on their citations can be found on their Copernicus Academic profile page.

Hiromi Sato's Articles: (12)

Effect of source-supply interruptions on the interface abruptness in gas source molecular beam epitaxy grown InGaAs/InP heterostructures

AbstractThe effect of source-supply interruptions on the InGaAsInP heterointerface abruptness in gas-source molecular-beam epitaxy grown lattice-matched InGaAs/InP has been investigated. It is confirmed by observing high-resolution transmission electron microscope (HRTEM) images and photoluminescence (PL) peak energy shifts that the thickness of the InGaAs well becomes narrower as the source-supply interruption (SSI) becomes longer. When the SSI is not optimized, an interface layer forms, consisting of one to several strained monolayers as confirmed by PL and HRTEM. When the SSI is optimized, Auger electron microscopy, PL, and HRTEM reveal abrupt heterointerface formation.

Research paperEffect of ethanol on the true diffusion coefficient of diclofenac and its sodium salt in silicone membrane

AbstractThe effect of ethanol on the diffusion coefficient of free diclofenac (DH) as a hydrophobic drug in a silicone membrane was studied and the value was compared with that of sodium diclofenac (DNa) as a hydrophilic material. The silicone membrane permeation of DH was described as a lipid pathway up to 60% w/w ethanol. The change in the partition coefficient of DH between the silicone membrane and ethanol-aqueous solution as a function of ethanol concentration seems to correspond with that of the partition coefficient of many drugs between octanol and water or a buffer. The apparent diffusion coefficient of DH and DNa in ethanol-aqueous solution was dependent on the ethanol concentration, i.e., it was related to the partition coefficient. The true diffusion coefficient of a lipid layer can be calculated by subtracting the partition coefficient from the apparent diffusion coefficient by changing the ethanol concentration.

DNA-adduct formation in lungs, nasal mucosa, and livers of rats exposed to urban roadside air in Kawasaki City, Japan

AbstractThe potency of ambient air for DNA-adduct formation was estimated using Wistar rats. The animals were maintained in a small-animal facility located beside a main highway intersection in Kawasaki City, Japan, for up to 60 weeks and were exposed to roadside air contaminated mainly with automobile emission (exposure group, EG) or to clean air (control group, CG). Compared to CG, the relative adduct levels (RAL) were increased significantly in EG lungs (17.1-fold (P<0.05)), nasal mucosa, and livers after exposure for 4 weeks. However, there were no significant differences in RAL between EG and CG after exposure for 12 weeks, but they were elevated again in EG after exposure for 48 or 60 weeks. These results suggest that roadside air in this region can cause the generation of DNA adducts. This activity of ambient roadside air can be estimated using experimental animals, indicating that biological monitoring of DNA-adduct formation may be a powerful tool to assess the effect of ambient air on human health.

Endocrine pharmacologyActivation of AMPK–Sirt1 pathway by telmisartan in white adipose tissue: A possible link to anti-metabolic effects

AbstractTelmisartan exerts anti-metabolic effects beyond its angiotensin receptor blockade activities, but the mechanisms have hitherto remained elusive. We sought to elucidate the peroxisome proliferator-activated receptor-γ (PPAR-γ)-dependent and PPAR-γ-independent mechanisms underlying the anti-metabolic effects of telmisartan in white adipose tissue. Nine-week-old male C57BL/6 mice were fed with a 60% high-fat diet for 6 weeks, with 1 mg/kg telmisartan or vehicle administrated orally during the last 3 weeks. 3T3-L1 adipocytes were cultured with telmisartan either with 2-chloro-5-nitro-N-phenylbenzamide (GW9662), a selective irreversible antagonist of PPAR-γ, or compound C, an ATP-competitive inhibitor of AMPK. Western blotting and semiquantitative RT-PCR analysis were used to assess adiponectin, Sirt1, and AMPK levels. Lipid accumulation was assessed by Oil red O staining. The activation of transcription factor PPAR-γ2 was evaluated by using a luciferase reporter assay for mPPAR-γ2 expression plasmid vector. Treatment with telmisartan increased serum adiponectin levels in high-fat diet-fed mice concomitantly with an upregulation of adiponectin mRNA in visceral adipose tissue. In vitro telmisartan treatment dose-dependently increased adiponectin mRNA in 3T3-L1 cells; the increase was inhibited by compound C, but not by GW9662. Telmisartan increased expression of Sirt1 mRNA and Sirt1 protein as well as the phosphorylation of AMPK in 3T3-L1 cells. Telmisartan can increase adiponectin production in white adipose tissue partly via a PPAR-γ2-independent mechanism. Precise understanding of this molecular mechanism will require further investigation.

Molecular and cellular pharmacologyElacridar enhances the cytotoxic effects of sunitinib and prevents multidrug resistance in renal carcinoma cells

AbstractIntrinsic drug resistance occurs in many renal carcinomas and is associated with increased expression of multidrug resistant proteins, which inhibits intracellular drug accumulation. Multidrug resistant protein 1, also known as P-glycoprotein, is a membrane drug efflux pump belonging to the ATP-binding cassette (ABC) transporter superfamily. ABC Sub-family B Member 2 (ABCG2) is widely distributed and is involved in the multidrug resistant phenotype. Sunitinib is a tyrosine kinase inhibitor used to treat kidney cancer that disrupts signaling pathways responsible for abnormal cancer cell proliferation and tumor angiogenesis. Multiple drug resistance is important in tyrosine kinase inhibitor-induced resistance. We hypothesized that inhibition of multidrug resistant transporters by elacridar (dual inhibitor of P-glycoprotein and ABCG 2) might overcome sunitinib resistance in experimental renal cell carcinoma.Human renal carcinoma cell lines 786-O, ACHN, and Caki-1 were treated with sunitinib or elacridar alone, or in combination. We showed that elacridar significantly enhanced sunitinib cytotoxicity in 786-O cells. P-glycoprotein activity, confirmed by P-glycoprotein function assay, was found to be inhibited by elacridar. ABCG2 expression was low in all renal carcinoma cell lines, and was suppressed only by combination treatment in 786-O cells. ABCG2 function was inhibited by sunitinib alone or combination with elacridar but not elacridar alone. These findings suggest that sunitinib resistance involves multidrug resistance transporters, and in combination with elacridar, can be reversed in renal carcinoma cells by P-glycoprotein inhibition.

A Src family inhibitor (PP1) potentiates tumor-suppressive effect of connexin 32 gene in renal cancer cells

AbstractConnexin (Cx) genes exert negative growth effects on tumor cells with certain cell specificity. We have recently reported that Cx32 acts as a tumor suppressor gene in renal cancer cells due to the inhibition of Src-dependent signaling. In line with the previous study, here we examined if a Src family inhibitor (PP1) could potentiate tumor-suppressive effect of Cx32 in Caki-2 cell from human renal cell carcinoma. In order to clarify the potentialization of PP1, using Cx32-transfected Caki-2 cells and mock-transfected Caki-2 cells, we estimated difference in cytotoxic effect of PP1 on the two cell clones in vitro as well as in vivo. PP1 showed more cytotoxic effect on Caki-2 cells having Cx32 positive expression than that of Cx32 negative expression at lower doses. This potentialization was also observed in xenograft model of nude mice. The potentialization of the effect mainly depended on the induction of apoptosis but not the control of cell growth. In conjugation with this event, the reduction of anti-apoptotic molecules (Bcl-2 and Bcl-xL) was caused by the combination of Cx32 expression and PP1 treatment in Caki-2 cells. These results suggest that PP1 potentiates tumor-suppressive effect of connexin 32 gene in renal cancer cells through the reduction of anti-apoptotic molecules.

Detection of single optical photons with STJ detectors in RIKEN

AbstractWe fabricated high quality Nb/Al/AlOx/Al/Nb superconducting tunnel junction (STJ) detectors in RIKEN, and succeeded detecting single optical photons. The normal resistance of the STJ device was 2×10−6Ωcm2 and the ratio of normal resistance and dynamic resistance (Rn/Rd) at 0.2mV was 10−5 operated at 0.35K. The intrinsic energy resolution for 2.64eV(470nm) photon was 1.0eV. Good linearity was observed.

Development of a low energy particle detector using a superconducting transition edge sensor

AbstractIt is possible for a superconductive transition edge sensor (TES) to detect directly the low energy proton generated in the neutron beta decay. The precision measurement of the proton spectrum is important to test the prediction of the Standard Model of electroweak interaction. Therefore, we are developing a TES microcalorimeter with a large effective area for a proton detector. Our first TES device consists of four-pixels using a Ti/Au bilayer. All pixels are parallel biased and X-rays from a 55Fe source are detected successfully.

Cyclolepis genistoides D. Don (palo azul) promotes differentiation of adipocytes and regulates adipokine expression

AbstractCyclolepis genistoides D. Don is a herbaceous perennial belonging to the family Asteraceae, and its vernacular name is “palo azul” (palo). Palo has been reported to exhibit many physiological effects that contribute to the prevention of metabolic syndromes, although its mechanism is unclear. Among palo's various activities, we investigated the hypothesis that palo promotes adipocytes differentiation and regulates adipokine profiles in 3T3-L1 adipocytes by modulation of peroxisome proliferator–activated receptor (PPAR) γ, a major regulator of adipose differentiation. 3T3-L1 adipocytes were cultured and differentiated in Dulbecco modified Eagle medium with 50 to 200 μg/mL palo for 7 days or were cultured with palo without differentiation protocol for 14 days. Palo down-regulated the expression of 2 types of expressed/secreted adipokines, leptin and resistin, in a concentration-dependent manner. Under a nondifferentiated condition, palo promoted the accumulation of lipid droplets in cells. Real-time polymerase chain reaction and luciferase reporter assay showed that palo up-regulated expression and transcriptional activity of PPARγ. Furthermore, palo increased the expression of insulin-sensitizing adipokine, adiponectin, which is a directly target of PPARγ, both at the messenger RNA level and at the protein level. In summary, palo demonstrated the potential to improve insulin resistance by promoting adipocyte differentiation via PPARγ activation. Results suggest an increase in adiponectin secretion and a decrease in insulin-resistant factors such as leptin and resistin.

Quantitative changes in glycosaminoglycans in the lungs of rats exposed to diesel exhaust

AbstractExposure to diesel exhaust (DE) induces lesions in lung epithelium by generation of reactive oxygen species. Glycosaminoglycans (GAG), components of extracellar matrix, are thought to play important roles in cell proliferation and differentiation in the repair process of injured tissue. We investigated how GAG are related to the recovery of lung tissue from injury. Using high-performance liquid chromatography analysis, we determined the amounts of GAG, such as chondroitin sulfate (CS), dermatan sulfate (DS), and hyaluronan (HA) in the lungs of rats exposed to DE for 4 weeks at concentrations of 0.3 or 3 mg/m3 as suspended particulate matter, or to filtered air. The contents of CS and HA in the surroundings of the bronchi were significantly increased after exposure to DE. In addition, immunohistochemical staining showed that the number of 8-hydroxydeoxyguanosine-positive cells as a marker of cell damage, and proliferating cell nuclear antigen-positive cells also increased in the same areas in which the levels of GAG were elevated in the lungs of rats exposed to 3 mg/m3 DE. These results suggest that CS and HA in the lung contribute to cell proliferation and remodeling in the process of recovery from injury caused by exposure to DE.

Development of measurement system of neutron β decay

AbstractPrecise measurement of neutron β decay allows determining the coupling constant of weak interaction independent of any nuclear structure. We have developed measurement system of neutron β decay at a thermal neutron beamline in JRR-3, JAEA. By using coincidence technique of two kinds of detectors, we have succeeded in detecting the signal of neutron β decay with S/N of 0.63 and count rate of 0.40 cps.

Full paperEffect of enhanced expression of connexin 43 on sunitinib-induced cytotoxicity in mesothelioma cells

AbstractConnexin (Cx) makes up a type of intercellular channel called gap junction (GJ). GJ plays a regulatory role in cellular physiology. The Cx expression level is often decreased in cancer cells compared to that in healthy ones, and the restoration of its expression has been shown to exert antiproliferative effects. This work aims to evaluate the effect of the restoration of connexin 43 (Cx43) (the most ubiquitous Cx subtype) expression on sunitinib (SU)-induced cytotoxicity in malignant mesothelioma (MM) cells. Increased Cx43 expression in an MM cell line (H28) improved the ability of SU to inhibit receptor tyrosine kinase (RTK) signaling. Moreover, higher Cx43 expression promoted SU-induced apoptosis. The cell viability test revealed that Cx43 enhanced the cytotoxic effect of SU in a GJ-independent manner. The effect of Cx43 on a proapoptotic factor, Bax, was then investigated. The interaction between Cx43 and Bax was confirmed by immunoprecipitation. Furthermore, higher Cx43 expression increased the production of a cleaved (active) form of Bax during SU-induced apoptosis with no alteration in total Bax expression. These findings indicate that Cx43 most likely increases sensitivity to SU in H28 through direct interaction with Bax. In conclusion, we found that Cx43 overcame the chemoresistance of MM cells.

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