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Search Results: 1 - 10 of 2383 matches for " Midori Kato "
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Model of the Effects of Improving TB Diagnosis on Infection Dynamics in Differing Demographic and HIV-Prevalence Scenarios  [PDF]
Allison S. Rhines, Midori Kato-Maeda, Marcus W. Feldman
Journal of Tuberculosis Research (JTR) , 2015, DOI: 10.4236/jtr.2015.31001
Abstract: This paper seeks to examine the sensitivity of tuberculosis transmission (TB) dynamics to the rate at which infectious individuals with active TB begin a TB treatment course, and therefore cease to be infectious to others. We model this by varying both the rate at which individuals are diagnosed and begin treatment, and the demographic conditions in which the epidemic occurs. An agestructured deterministic ordinary differential equation model is used to study the sensitivity of TB transmission dynamics to the implementation of a more effective diagnostic such as Xpert MTB/ RIF in a high HIV prevalence setting. Sensitivity analysis of the effectiveness of the diagnostic (λ) shows the interim disease dynamics in three demographic scenarios defined by differences in HIV prevalence and age structure at a constant transmission rate. In the near future, we expect the diagnostic to have the most effect in areas of high HIV prevalence. In the long term, we expect the diagnostic to have the most significant impact at high transmission rates regardless of HIV prevalence and age structure.
Synthesis and Spectroscopic Properties of Ferrocenyl Derivative Containing Donor and Acceptor Groups  [PDF]
Makoto Minato, Chiharu Sorai, Takashi Ito, Masashi Kiguchi, Midori Kato
International Journal of Organic Chemistry (IJOC) , 2017, DOI: 10.4236/ijoc.2017.73022
Abstract: Much interest has been devoted to organometallic NLO materials. We have become interested in exploring the utility of ferrocenyl group as the conjugating bridge. Thus, we synthesized 1-{{[1,3-(5-methylbenzo)dithiol]-2-yli- dene}methyl}-1’-[2-(p-nitrophenyl)-(E)-ethenyl]ferrocene (1). This new ferrocenyl compound has a donor and an acceptor group in 1,1’-positions. Investigations of the solvatochromic property of the compound revealed that it has polarized structure in a polar solvent, such as DMF. SHG efficiency of the compound was estimated by an SHEW (second-harmonic generation with the evanescent wave) method.
On characters and formal degrees of discrete series of affine Hecke algebras of classical types
Dan Ciubotaru,Midori Kato,Syu Kato
Mathematics , 2010,
Abstract: We address two fundamental questions in the representation theory of affine Hecke algebras of classical types. One is an inductive algorithm to compute characters of tempered modules, and the other is the determination of the constants in the formal degrees of discrete series (in the form conjectured by Reeder \cite{Re}). The former is completely different than the Lusztig-Shoji algorithm \cite{Sh, L}, and it is more effective in a number of cases. The main idea in our proof is to introduce a new family of representations which behave like tempered modules, but for which it is easier to analyze the effect of parameter specializations. Our proof also requires a comparison of the $C^{\ast}$-theoretic results of Opdam, Delorme, Slooten, Solleveld \cite{O, DO, Sl2, OSa, OS}, and the geometric construction from \cite{K1,K2,CK}.
Link between Aluminum and the Pathogenesis of Alzheimer's Disease: The Integration of the Aluminum and Amyloid Cascade Hypotheses
Masahiro Kawahara,Midori Kato-Negishi
International Journal of Alzheimer's Disease , 2011, DOI: 10.4061/2011/276393
Abstract: Whilst being environmentally abundant, aluminum is not essential for life. On the contrary, aluminum is a widely recognized neurotoxin that inhibits more than 200 biologically important functions and causes various adverse effects in plants, animals, and humans. The relationship between aluminum exposure and neurodegenerative diseases, including dialysis encephalopathy, amyotrophic lateral sclerosis and Parkinsonism dementia in the Kii Peninsula and Guam, and Alzheimer's disease (AD) has been suggested. In particular, the link between aluminum and Alzheimer's disease has been the subject of scientific debate for several decades. However, the complex characteristics of aluminum bioavailability make it difficult to evaluate its toxicity and therefore, the relationship remains to be established. Mounting evidence has suggested that significance of oligomerization of -amyloid protein and neurotoxicity in the molecular mechanism of AD pathogenesis. Aluminum may play crucial roles as a cross-linker in -amyloid oligomerization. Here, we review the detailed characteristics of aluminum neurotoxicity based on our own studies and the recent literatures. Our aim is to revisit the link between aluminum and AD and to integrate aluminum and amyloid cascade hypotheses in the context of -amyloid oligomerization and the interactions with other metals.
Neurosteroids block the increase in intracellular calcium level induced by Alzheimer’s β-amyloid protein in long-term cultured rat hippocampal neurons
Midori Kato-Negishi,Masahiro Kawahara
Neuropsychiatric Disease and Treatment , 2008,
Abstract: Midori Kato-Negishi1, Masahiro Kawahara21Department of Developmental Morphology, Tokyo Metropolitan Institute for Neuroscience, 2-6 Musashidai, Fuchu-shi, Tokyo 183- 8526, Japan; 2Department of Analytical Chemistry, School of Pharmaceutical Sciences, Kyushu University of Health and Welfare, 1714-1 Yoshino-cho, Nobeoka-shi, Miyazaki 882-8508, JapanAbstract: The neurotoxicity of β-amyloid protein (AβP) is implicated in the etiology of Alzheimer’s disease. We previously have demonstrated that AβP forms Ca2+-permeable pores on neuronal membranes, causes a marked increase in intracellular calcium level, and leads to neuronal death. Here, we investigated in detail the features of AβP-induced changes in intracellular Ca2+ level in primary cultured rat hippocampal neurons using a multisite Ca2+- imaging system with fura-2 as a fluorescent probe. Only a small fraction of short-term cultured hippocampal neurons (ca 1 week in vitro) exhibited changes in intracellular Ca2+ level after AβP exposure. However, AβP caused an acute increase in intracellular Ca2+ level in long-term cultured neurons (ca 1 month in vitro). The responses to AβP were highly heterogeneous, and immunohistochemical analysis using an antibody to AβP revealed that AβP is deposited on some but not all neurons. Considering that the disruption of Ca2+ homeostasis is the primary event in AβP neurotoxicity, substances that protect neurons from an AβP-induced intracellular Ca2+ level increase may be candidates as therapeutic drugs for Alzheimer’s disease. In line with the search for such protective substances, we found that the preadministration of neurosteroids including dehydroepiandrosterone, dehydroepiandrosterone sulfate, and pregnenolone significantly inhibits the increase in intracellular calcium level induced by AβP. Our results suggest the possible significance of neurosteroids, whose levels are reduced in the elderly, in preventing AβP neurotoxicity.Keywords: neurotoxicity, pore, calcium homeostasis, channel, aging
Membrane Incorporation, Channel Formation, and Disruption of Calcium Homeostasis by Alzheimer's β-Amyloid Protein
Masahiro Kawahara,Isao Ohtsuka,Shoko Yokoyama,Midori Kato-Negishi,Yutaka Sadakane
International Journal of Alzheimer's Disease , 2011, DOI: 10.4061/2011/304583
Abstract: Oligomerization, conformational changes, and the consequent neurodegeneration of Alzheimer's β-amyloid protein (AβP) play crucial roles in the pathogenesis of Alzheimer's disease (AD). Mounting evidence suggests that oligomeric AβPs cause the disruption of calcium homeostasis, eventually leading to neuronal death. We have demonstrated that oligomeric AβPs directly incorporate into neuronal membranes, form cation-sensitive ion channels (“amyloid channels”), and cause the disruption of calcium homeostasis via the amyloid channels. Other disease-related amyloidogenic proteins, such as prion protein in prion diseases or α-synuclein in dementia with Lewy bodies, exhibit similarities in the incorporation into membranes and the formation of calcium-permeable channels. Here, based on our experimental results and those of numerous other studies, we review the current understanding of the direct binding of AβP into membrane surfaces and the formation of calcium-permeable channels. The implication of composition of membrane lipids and the possible development of new drugs by influencing membrane properties and attenuating amyloid channels for the treatment and prevention of AD is also discussed. 1. Introduction Alzheimer’s disease (AD) is a severe type of senile dementia, affecting a large portion of elderly people worldwide. It is characterized by profound memory loss and inability to form new memories. The pathological hallmarks of AD are the presence of numerous extracellular deposits, termed senile plaques, and intraneuronal neurofibrillary tangles (NFTs). The degeneration of synapses and neurons in the hippocampus or cerebral cortex is also observed [1]. The major components of NFTs are phosphorylated tau proteins, and that of senile plaques are β-amyloid proteins (AβPs). Although the precise cause of AD remains elusive, it is widely accepted that oligomerization of AβP and the consequent neurodegeneration might be the cause of neuronal death in AD patients [2, 3]. There is considerable interest regarding the mechanism by which AβPs cause neurodegeneration. AβPs have been reported to cause various adverse effects on neuronal survivals, such as the production of reactive oxygen species, the induction of cytokines, the induction of endoplasmic reticulum (ER) stresses, and the abnormal increase in intracellular calcium levels ([Ca2+]i) [4]. These adverse effects are complex and may be interwoven. Of these effects, the disruption of calcium homeostasis could be the earliest and primary event, since Ca2+ ions are essential for various neuronal functions. The
Likelihood-Based Inference for Discretely Observed Birth-Death-Shift Processes, with Applications to Evolution of Mobile Genetic Elements
Jason Xu,Peter Guttorp,Midori Kato-Maeda,Vladimir N. Minin
Quantitative Biology , 2014,
Abstract: Continuous-time birth-death-shift (BDS) processes are frequently used in stochastic modeling, with many applications in ecology and epidemiology. In particular, such processes can model evolutionary dynamics of transposable elements - important genetic markers in molecular epidemiology. Estimation of the effects of individual covariates on the birth, death, and shift rates of the process can be accomplished by analyzing patient data, but inferring these rates in a discretely and unevenly observed setting presents computational challenges. We propose a mutli-type branching process approximation to BDS processes and develop a corresponding expectation maximization (EM) algorithm, where we use spectral techniques to reduce calculation of expected sufficient statistics to low dimensional integration. These techniques yield an efficient and robust optimization routine for inferring the rates of the BDS process, and apply more broadly to multi-type branching processes where rates can depend on many covariates. After rigorously testing our methodology in simulation studies, we apply our method to study intrapatient time evolution of IS6110 transposable element, a frequently used element during estimation of epidemiological clusters of Mycobacterium tuberculosis infections.
Fitting birth-death processes to panel data with applications to bacterial DNA fingerprinting
Charles R. Doss,Marc A. Suchard,Ian Holmes,Midori Kato-Maeda,Vladimir N. Minin
Quantitative Biology , 2010, DOI: 10.1214/13-AOAS673
Abstract: Continuous-time linear birth-death-immigration (BDI) processes are frequently used in ecology and epidemiology to model stochastic dynamics of the population of interest. In clinical settings, multiple birth-death processes can describe disease trajectories of individual patients, allowing for estimation of the effects of individual covariates on the birth and death rates of the process. Such estimation is usually accomplished by analyzing patient data collected at unevenly spaced time points, referred to as panel data in the biostatistics literature. Fitting linear BDI processes to panel data is a nontrivial optimization problem because birth and death rates can be functions of many parameters related to the covariates of interest. We propose a novel expectation--maximization (EM) algorithm for fitting linear BDI models with covariates to panel data. We derive a closed-form expression for the joint generating function of some of the BDI process statistics and use this generating function to reduce the E-step of the EM algorithm, as well as calculation of the Fisher information, to one-dimensional integration. This analytical technique yields a computationally efficient and robust optimization algorithm that we implemented in an open-source R package. We apply our method to DNA fingerprinting of Mycobacterium tuberculosis, the causative agent of tuberculosis, to study intrapatient time evolution of IS6110 copy number, a genetic marker frequently used during estimation of epidemiological clusters of Mycobacterium tuberculosis infections. Our analysis reveals previously undocumented differences in IS6110 birth-death rates among three major lineages of Mycobacterium tuberculosis, which has important implications for epidemiologists that use IS6110 for DNA fingerprinting of Mycobacterium tuberculosis.
Altered Energy Homeostasis and Resistance to Diet-Induced Obesity in KRAP-Deficient Mice
Takahiro Fujimoto, Kyoko Miyasaka, Midori Koyanagi, Toshiyuki Tsunoda, Iwai Baba, Keiko Doi, Minoru Ohta, Norihiro Kato, Takehiko Sasazuki, Senji Shirasawa
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0004240
Abstract: Obesity and related metabolic disorders have become leading causes of adult morbidity and mortality. KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule, however, its physiological roles remain unknown. Here we demonstrate that KRAP-deficient (KRAP?/?) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP?/? mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. Notably, glucose uptake in the brown adipose tissue (BAT) in KRAP?/? mice is enhanced in an insulin-independent manner, suggesting that BAT is involved in altered energy homeostasis in KRAP?/? mice, although UCP (Uncoupling protein) expressions are not altered. Of interest is the down-regulation of fatty acid metabolism-related molecules, including acetyl-CoA carboxylase (ACC)-1, ACC-2 and fatty acid synthase in the liver of KRAP?/? mice, which could in part account for the metabolic phenotype in KRAP?/? mice. Thus, KRAP is a novel regulator in whole-body energy homeostasis and may be a therapeutic target in obesity and related diseases.
Impact of Isoniazid Resistance-Conferring Mutations on the Clinical Presentation of Isoniazid Monoresistant Tuberculosis
Raymund Dantes, John Metcalfe, Elizabeth Kim, Midori Kato-Maeda, Philip C. Hopewell, Masae Kawamura, Payam Nahid, Adithya Cattamanchi
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037956
Abstract: Background Specific isoniazid (INH) resistance conferring mutations have been shown to impact the likelihood of tuberculosis (TB) transmission. However, their role in the clinical presentation and outcomes of TB has not been evaluated. Methods We included all cases of culture-confirmed, INH monoresistant tuberculosis reported to the San Francisco Department of Public Health Tuberculosis Control Section from October 1992 through October 2005. For cases with stored culture isolates, we used polymerase chain reaction (PCR) testing and gene sequencing to identify INH resistance-conferring mutations, and compared genotypic and phenotypic characteristics. Results Among 101 consecutive cases of INH monoresistant TB in San Francisco 19 (19%) had isolates with a katG mutation other than S315T; 38 (38%) had isolates with the katG S315T mutation, 29 (29%) had isolates with a inhA-15;c-t promoter mutation, and 15 (15%) had isolates with other mutations. The katG S315T mutation was independently associated with high-level INH resistance (risk ratio [RR] 1.56, 95% confidence interval [CI] 1.07–2.27), and the inhA-15;c-t promoter mutation was inversely associated with high-level INH resistance (RR 0.43, 95% CI 0.21–0.89). However, specific INH resistance-conferring mutations were not associated with the clinical severity or outcomes of INH monoresistant TB cases. Conclusion These data suggest that INH resistance-conferring mutations do not impact the clinical presentation of TB.
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