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Search Results: 1 - 10 of 30 matches for " Kyota Ashikawa "
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Genome-Wide Association Study of Breast Cancer in the Japanese Population
Siew-Kee Low, Atsushi Takahashi, Kyota Ashikawa, Johji Inazawa, Yoshio Miki, Michiaki Kubo, Yusuke Nakamura, Toyomasa Katagiri
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0076463
Abstract: Breast cancer is the most common malignancy among women in worldwide including Japan. Several studies have identified common genetic variants to be associated with the risk of breast cancer. Due to the complex linkage disequilibrium structure and various environmental exposures in different populations, it is essential to identify variants associated with breast cancer in each population, which subsequently facilitate the better understanding of mammary carcinogenesis. In this study, we conducted a genome-wide association study (GWAS) as well as whole-genome imputation with 2,642 cases and 2,099 unaffected female controls. We further examined 13 suggestive loci (P<1.0×10?5) using an independent sample set of 2,885 cases and 3,395 controls and successfully validated two previously-reported loci, rs2981578 (combined P-value of 1.31×10?12, OR = 1.23; 95% CI = 1.16–.30) on chromosome 10q26 (FGFR2), rs3803662 (combined P-value of 2.79×10?11, OR = 1.21; 95% CI = 1.15–.28) and rs12922061 (combined P-value of 3.97×10?10, OR = 1.23; 95% CI = 1.15–.31) on chromosome 16q12 (TOX3-LOC643714). Weighted genetic risk score on the basis of three significantly associated variants and two previously reported breast cancer associated loci in East Asian population revealed that individuals who carry the most risk alleles in category 5 have 2.2 times higher risk of developing breast cancer in the Japanese population than those who carry the least risk alleles in reference category 1. Although we could not identify additional loci associated with breast cancer, our study utilized one of the largest sample sizes reported to date, and provided genetic status that represent the Japanese population. Further local and international collaborative study is essential to identify additional genetic variants that could lead to a better, accurate prediction for breast cancer.
What is measured when fluctuation of macrovariables is measured in quantum systems
Kyota Fujikura,Akira Shimizu
Physics , 2015,
Abstract: For equilibrium states of macroscopic quantum systems,we study what are measured when fluctuations of macrovariables are measured. To mimic classical ideal measurements, we consider `quasi-classical measurements' which are minimally-disturbing, homogeneous, and unbiased quantum measurements with moderate magnitudes of errors. For all such measurements, we find that the symmetrized time correlation is obtained among many quantum correlations that reduce, in the classical limit, to the same classical time correlation. As an important consequence of this universal result, we show that the fluctuation-dissipation theorem (FDT) is partially violated as a relation between observed quantities in macroscopic quantum systems. The post-measurement state is squeezed by backactions of the measurements, but is macroscopically identical to the pre-measurement equilibrium state. This state evolves with time, in which macrovariables fluctuate and relax, unlike other microstates (such as the Gibbs state) that represent the same equilibrium state.
Carrier doping to pseudo-low-dimensional compound La2RuO5
Masatomo Uehara,Kenich Ashikawa,Yoshimasa Aka,Yoshihide Kimishima
Physics , 2008,
Abstract: Hole carrier doping has been tried to pseudo-low-dimensional material La2RuO5 by substituting La3+ with Cd2+. Single phased samples of La2-xCdxRuO5 with x up to 0.5 have been successfully obtained and also high pressure O2 annealing has been performed to the x=0.5 sample. Although the formal ionic state of Ru is expected to increase from 4+ (at x=0) to 4.5+ (at x=0.5), the magnetic and electrical properties show no significant changes in as-sintered samples. In contrast, high pressure O2 annealed x=0.5 samples show a little reduction of electrical resistivity and the decrease of thermoelectric power at 260 K. From these results, it can be speculated that the doped carriers are mostly compensated by oxygen deficiency in as-sintered samples.
Therapeutic Effects of Hydrogen in Animal Models of Parkinson's Disease
Kyota Fujita,Yusaku Nakabeppu,Mami Noda
Parkinson's Disease , 2011, DOI: 10.4061/2011/307875
Abstract: Since the first description of Parkinson's disease (PD) nearly two centuries ago, a number of studies have revealed the clinical symptoms, pathology, and therapeutic approaches to overcome this intractable neurodegenerative disease. 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) are neurotoxins which produce Parkinsonian pathology. From the animal studies using these neurotoxins, it has become well established that oxidative stress is a primary cause of, and essential for, cellular apoptosis in dopaminergic neurons. Here, we describe the mechanism whereby oxidative stress evokes irreversible cell death, and propose a novel therapeutic strategy for PD using molecular hydrogen. Hydrogen has an ability to reduce oxidative damage and ameliorate the loss of nigrostriatal dopaminergic neuronal pathway in two experimental animal models. Thus, it is strongly suggested that hydrogen might provide a great advantage to prevent or minimize the onset and progression of PD. 1. Introduction The central pathological feature of PD was loss of neurons in substantia nigra pars compacta (SNpc). DA depletion by the loss of dopaminergic neurons in SNpc is a primary symptom of PD [1]. PD is one of the most common neurodegenerative and progressive diseases, along with Alzheimer’s disease (AD) [2, 3]. In these last two decades, many lines of evidence have emerged to suggest that oxidative stress is closely related to the onset and the progression of PD and AD. Using neurotoxins in experimental animal models, an enormous number of studies have been undertaken to develop neuroprotective drugs against PD. MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) was found to be a by-product of the chemical synthesis of a meperidine analog with potent heroin-like effects [4, 5]. MPTP has the ability to induce PD-like pathology and has been used in various species including nonhuman primates, and rodents. Among the neurotoxic mechanism of MPTP, mitochondrial impairment is highly associated with oxidative damage and related neurodegeneration; the detailed mechanism and the linkage between oxidative damage and neurodegeneration are discussed in this review. Although MPTP-induced PD model animals are regarded as the best reproducible model, another neurotoxin, 6-hydroxydopamine (6-OHDA; 2,4,5-trihydroxyphenylethylamine), is also used for toxin-induced animal model of PD [6]. Many trials have focused on the reduction of oxidative stress as a therapeutic strategy because oxidative stress is regarded as one of the major risk factors in the onset of PD as
Ventricular Fibrillation Caused by Traumatic Coronary Artery Dissection  [PDF]
Jun-ya Ishikawa, Naoto Morimura, Eri Nagai, Kyota Nakamura, Makoto Shimizu, Keiji Uchida
Case Reports in Clinical Medicine (CRCM) , 2015, DOI: 10.4236/crcm.2015.44026
Abstract:
Coronary artery dissection due to blunt chest trauma (traumatic coronary artery dissection [TCAD]) may heal spontaneously, and some surgeons believe that conservative or elective treat-ments are sufficient, provided that there are no progressing ischemic symptoms. However, we report a patient who experienced sudden ventricular fibrillation (VF) during initial medical care for trauma injuries. The 32-year-old woman was riding in a passenger car when an accident occurred, and was subsequently transported to our emergency department. Twelve-lead electrocardiography revealed ST segment elevation in leads II, III, and aVF, although her vital signs remained stable. Therefore, we prioritized assessing the trauma at other sites, and VF suddenly occurred. Coronary angiography was performed with repeated defibrillation and chest compressions, which resulted in recovery of spontaneous circulation. Occlusion was observed in the right coronary artery, which we treated with balloon angioplasty. However, intravascular ultrasonography (IVUS) subsequently revealed coronary artery dissection, a stent was placed, and the patient successfully recovered. Therefore, IVUS may be useful for diagnosing TCAD, and swift intervention is needed if TCAD is detected.
Therapeutic Approach to Neurodegenerative Diseases by Medical Gases: Focusing on Redox Signaling and Related Antioxidant Enzymes
Kyota Fujita,Megumi Yamafuji,Yusaku Nakabeppu,Mami Noda
Oxidative Medicine and Cellular Longevity , 2012, DOI: 10.1155/2012/324256
Abstract: Oxidative stress in the central nervous system is strongly associated with neuronal cell death in the pathogenesis of several neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. In order to overcome the oxidative damage, there are some protective signaling pathways related to transcriptional upregulation of antioxidant enzymes, such as heme oxygenase-1 (HO-1) and superoxide dismutase (SOD)-1/-2. Their expression is regulated by several transcription factors and/or cofactors like nuclear factor-erythroid 2 (NF-E2) related factor 2 (Nrf2) and peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α). These antioxidant enzymes are associated with, and in some cases, prevent neuronal death in animal models of neurodegenerative diseases. They are activated by endogenous mediators and phytochemicals, and also by several gases such as carbon monoxide (CO), hydrogen sulphide (H2S), and hydrogen (H2). These might thereby protect the brain from severe oxidative damage and resultant neurodegenerative diseases. In this paper, we discuss how the expression levels of these antioxidant enzymes are regulated. We also introduce recent advances in the therapeutic uses of medical gases against neurodegenerative diseases.
Near Infrared Spectroscopy Study of the Frontopolar Hemodynamic Response and Depressive Mood in Children with Major Depressive Disorder: A Pilot Study
Masahide Usami, Yoshitaka Iwadare, Masaki Kodaira, Kyota Watanabe, Kazuhiko Saito
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0086290
Abstract: AIM The aim of this study was to evaluate the frontopolar hemodynamic response and depressive mood in children with mild or moderate major depressive disorder during six weeks treatment without medication. METHODS The subjects were 10 patients with mild or moderate depression. They were depressive drug-naive children and adolescents. The scores of Depression Self Rating Scale (DSRS), the results of the Verbal Fluency Test (VFT), and the concentrations of oxy-hemoglobin (Oxy-Hb) of frontal pole brain assessed by two-channel near infrared spectroscopy (NIRS) after six weeks of treatment was compared with those of initial treatment. RESULTS The score of DSRS was significantly reduced after six weeks of initial treatment (p<0.001, t-test). The word number of VFT was not significantly changed after six weeks of treatment. The oxy-Hb concentration significantly increased after six weeks of treatment (p<0.001, t-test). CONCLUSIONS This study demonstrated that the concentration of oxy-Hb of frontopolar cortex in children with mild and moderate depression improved along with their depressive mood. These results suggested that concentration of oxy-Hb using NIRS may be used as the state maker for change in depressive mood of children having depression, similar to that in adults.
Peak Serum AST Is a Better Predictor of Acute Liver Graft Injury after Liver Transplantation When Adjusted for Donor/Recipient BSA Size Mismatch (ASTi)
Kyota Fukazawa,Seigo Nishida,Ernesto A. Pretto Jr.
Journal of Transplantation , 2014, DOI: 10.1155/2014/351984
Abstract: Background. Despite the marked advances in the perioperative management of the liver transplant recipient, an assessment of clinically significant graft injury following preservation and reperfusion remains difficult. In this study, we hypothesized that size-adjusted AST could better approximate real AST values and consequently provide a better reflection of the extent of graft damage, with better sensitivity and specificity than current criteria. Methods. We reviewed data on 930 orthotopic liver transplant recipients. Size-adjusted AST (ASTi) was calculated by dividing peak AST by our previously reported index for donor-recipient size mismatch, the BSAi. The predictive value of ASTi of primary nonfunction (PNF) and graft survival was assessed by receiver operating characteristic curve, logistic regression, Kaplan-Meier survival, and Cox proportional hazard model. Results. Size-adjusted peak AST (ASTi) was significantly associated with subsequent occurrence of PNF and graft failure. In our study cohort, the prediction of PNF by the combination of ASTi and PT-INR had a higher sensitivity and specificity compared to current UNOS criteria. Conclusions. We conclude that size-adjusted AST (ASTi) is a simple, reproducible, and sensitive marker of clinically significant graft damage. 1. Introduction Despite the marked advances in the perioperative management of the liver transplant recipient, an assessment of clinically significant graft injury following preservation and reperfusion remains difficult [1]. The lack of a sensitive clinical marker of acute liver injury has a profound impact on clinical practice and the success of translational research in liver transplantation. Such a clinical marker could aid the management of graft dysfunction in early identification of recipients who will require retransplantation. Currently, posttransplant peak aspartate aminotransferase (AST) is a widely accepted clinical marker for graft damage in liver transplant practice [2–6]. In fact, the United Network for Organ Sharing (UNOS) suggests relisting criteria for the recipients with primary graft dysfunction (PNF) on the basis of the post-transplant peak AST [7]. AST is an enzyme that is involved in amino acid metabolism, primarily existing in hepatocytes. During transplantation graft hepatocytes are inevitably injured, and intracellular enzymes are subsequently released into the systemic circulation of the recipient. We theorized that the recipient AST serum concentration is a function of the total amount of AST released by the graft liver diluted by the total circulating
Collective Excitations of Bose-Einstein Condensates in a Double-Well Potential
Ippei Danshita,Kyota Egawa,Nobuhiko Yokoshi,Susumu Kurihara
Physics , 2005, DOI: 10.1143/JPSJ.74.3179
Abstract: We investigate collective excitations of Bose-Einstein condensates at absolute zero in a double-well trap. We solve the Bogoliubov equations with a double-well trap, and show that the crossover from the dipole mode to the Josephson plasma mode occurs in the lowest energy excitation. It is found that the anomalous tunneling property of low energy excitations is crucial to the crossover.
K-134, a Phosphodiesterase 3 Inhibitor, Prevents Brain Damage by Inhibiting Thrombus Formation in a Rat Cerebral Infarction Model
Hideo Yoshida, Yuka Ashikawa, Shinsuke Itoh, Takashi Nakagawa, Akimune Asanuma, Sohei Tanabe, Yoshihiro Inoue, Hiroyoshi Hidaka
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0046432
Abstract: Background K-134 is a more potent antiplatelet drug with a selective inhibitory effect on phosphodiesterase 3 (PDE3) compared with its analogue, cilostazol. Objectives This study was performed to compare the ameliorating effects of K-134 and cilostazol on brain damage in an experimental photothrombotic cerebral infarction model. Methods and Results We investigated the effects of oral preadministration of PDE3 inhibitors in a rat stroke model established by photothrombotic middle cerebral artery (MCA) occlusion. K-134 significantly prolonged MCA occlusion time at doses >10 mg/kg, and reduced cerebral infarct size at 30 mg/kg in the stroke model (n = 12, 87.5±5.6 vs. 126.8±7.5 mm3, P<0.01), indicating its potent antithrombotic effect. On the other hand, the effects of cilostazol on MCA occlusion time and cerebral infarct size are relatively weak even at the high dosage of 300 mg/kg. Furthermore, K-134 blocked rat platelet aggregation more potently than cilostazol in vitro. Also in an arteriovenous shunt thrombosis model, K-134 showed an antithrombotic effect greater than cilostazol. Conclusions These findings suggest that K-134, which has strong antithrombotic activity, is a promising drug for prevention of cerebral infarction associated with platelet hyperaggregability.
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