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Search Results: 1 - 10 of 3795 matches for " Masuo Sato "
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Serum Chlorine Level as a Possible Predictive Factor for Oxaliplatin-Induced Peripheral Neuropathy  [PDF]
Satoshi Tanaka, Naoto Suzuki, Akira Mimura, Kaho Kurosawa, Yuriko Murai, Daisuke Saigusa, Makio Gamoh, Masuo Sato, Yoshihisa Tomioka
Pharmacology & Pharmacy (PP) , 2012, DOI: 10.4236/pp.2012.31007
Abstract: Peripheral neuropathy is a major adverse event associated with oxaliplatin-based chemotherapy and is a major dose-limiting adverse event in clinical practice. However, some patients treated with oxaliplatin may show no or minimal peripheral neuropathy. These differences are still poorly understood. The data on patients with colorectal cancer who received oxaliplatin-based regimens between January 2005 and June 2010 at South Miyagi Medical Center were retrospectively retrieved from the medical records. We selected 51 patients, and factor analysis was performed. The serum chlorine (Cl) level at baseline was significantly higher in patients with a high frequency of peripheral neuropathy (106; range 104 - 107 vs. 104; range 101 - 104 mEq/L, p = 0.02). Principal component analysis showed the variables Cl, body mass index, status of liver metastasis, and status of lymph node metastasis were related to the incidence of peripheral neuropathy. Discriminant analysis showed the model had predicted 72.5% of peripheral neuropathy. An understanding of the patient’s characteristics could be useful for preventing or predicting oxaliplatin-induced peripheral neuropathy.
A new mouse model for renal lesions produced by intravenous injection of diphtheria toxin A-chain expression plasmid
Shingo Nakamura, Masuo Terashima, Natsuko Kikuchi, Minoru Kimura, Tadaaki Maehara, Akira Saito, Masahiro Sato
BMC Nephrology , 2004, DOI: 10.1186/1471-2369-5-4
Abstract: An expression plasmid carrying the cytomegalovirus enhancer/chicken β-actin promoter linked to a DT-A gene was mixed with lipid (FuGENE?6) and the resulting complexes were intravenously injected into adult male B6C3F1 mice every day for up to 6 days. After final injection, the kidneys of these mice were sampled on day 4 and weeks 3 and 5.H-E staining of the kidney specimens sampled on day 4 revealed remarkable alterations in glomerular compartments, as exemplified by mesangial cell proliferation and formation of extensive deposits in glomerular basement membrane. At weeks 3 and 5, gradual recovery of these tissues was observed. These mice exhibited proteinuria and disease resembling sub-acute glomerulonephritis.Repeated intravenous injections of DT-A expression plasmid DNA/lipid complex caused temporary abnormalities mainly in glomeruli of mouse kidney. The disease in these mice resembles sub-acute glomerulonephritis. These DT-A gene-incorporated mice will be useful as animal models in the fields of nephrology and regenerative medicine.Glomerular injury has been thought to play an important role in progression to renal failure. To search for therapeutic drugs for renal failure, it is of importance to use renal disease models in animals. There are several experimentally-induced models in animals, including subtotal nephrectomized animals, [1,2] snake venom-induced glomerulonephritis models, [3] and glomerulonephritis models produced by tail-vein injection of antiserum [4-7]. Transgenic mice overexpressing megsin, a novel protein of Kunitz-type plasminogen activator inhibitor, under a ubiquitous promoter system CAG [8] (composed of cytomegalovirus enhancer and chicken β-actin promoter) are reported to exhibit glomerular nephritis associated with mesangial proliferation, accumulation of extracellular matrix and deposits of IgG [9]. Experimentally induced models are always accompanied by fluctuation in degree of manifestation of disease among individuals, and much time
Roles of Beta2- and Beta3-Adrenoceptor Polymorphisms in Hypertension and Metabolic Syndrome
Kazuko Masuo
International Journal of Hypertension , 2010, DOI: 10.4061/2010/832821
Abstract: Hypertension, diabetes mellitus (especially type 2 diabetes mellitus), metabolic syndrome and obesity are rapidly growingpublic health problems. Sympathetic nerve activation is observed in obesity, hypertension and diabetes mellitus, which have strong genetic as well as environmental determinants. Reduced energy expenditure and resting metabolic rate are predictive of weightgain, and the sympathetic nervous system participates in regulating energy balance through thermogenesis. The thermogenic effects of catecholamines in obesity have been mainly mediated via the 2- and 3-adrenergic receptors in humans. Further, 2-adrenoceptors importantly influence vascular reactivity and may regulate blood pressure. Genetic polymorphistns of the -adrenoceptor gene have been shown to alter the function of several adrenoceptor subtypes and thus to modify the response to catecholamine. 2-adrenoceptor polymorphisms (Arg16Gly, Gln27Glu, and Thr164Ile) have been studied in relation to hypertension. Genetic variations in the 3-adrenoceptor (i.e. Try64Arg variant) are also associated with both obesity and hypertension. However, the precise relationships of the polymorphisms of 2- and 3-adrenoceptor genes with sympathetic nervous system activity, hypertension, and metabolic syndrome have not been fully clarified. This paper will discuss the current topics involving the influence of the sympathetic nervous system and 2- and 3- adrenoceptor polymorphisms in hypertension and metabolic syndrome.
Roles of Beta2- and Beta3-Adrenoceptor Polymorphisms in Hypertension and Metabolic Syndrome
Kazuko Masuo
International Journal of Hypertension , 2010, DOI: 10.4061/2010/832821
Abstract: Hypertension, diabetes mellitus (especially type 2 diabetes mellitus), metabolic syndrome and obesity are rapidly growing public health problems. Sympathetic nerve activation is observed in obesity, hypertension and diabetes mellitus, which have strong genetic as well as environmental determinants. Reduced energy expenditure and resting metabolic rate are predictive of weight gain, and the sympathetic nervous system participates in regulating energy balance through thermogenesis. The thermogenic effects of catecholamines in obesity have been mainly mediated via the 2- and 3-adrenergic receptors in humans. Further, 2-adrenoceptors importantly influence vascular reactivity and may regulate blood pressure. Genetic polymorphistns of the -adrenoceptor gene have been shown to alter the function of several adrenoceptor subtypes and thus to modify the response to catecholamine. 2-adrenoceptor polymorphisms (Arg16Gly, Gln27Glu, and Thr164Ile) have been studied in relation to hypertension. Genetic variations in the 3-adrenoceptor (i.e. Try64Arg variant) are also associated with both obesity and hypertension. However, the precise relationships of the polymorphisms of 2- and 3-adrenoceptor genes with sympathetic nervous system activity, hypertension, and metabolic syndrome have not been fully clarified. This paper will discuss the current topics involving the influence of the sympathetic nervous system and 2- and 3- adrenoceptor polymorphisms in hypertension and metabolic syndrome. 1. Introduction Obesity, hypertension, and metabolic syndrome (type 2 diabetes mellitus) are major and growing health problems and are known as high-risk factors for subsequent cardiovascular and renal complications [1–3]. Obesity, hypertension, diabetes, and metabolic syndrome are intimately associated [4–6], and sympathetic nervous activation is frequently observed in those conditions. Thus, sympathetic nerve activation may play a major role in the onset and development of hypertension, obesity, and metabolic syndrome (diabetes mellitus) as well as cardiovascular complications in patients with hypertension, diabetes and obesity [2, 7]. The sympathetic nervous system plays an important role in the regulation of energy expenditure. Reduced energy expenditure and resting metabolic rate are predictive of weight gain (obesity). The sympathetic nervous system participates in regulating energy balance through thermogenesis [8]. A large part of the sympathetic nervous system-mediated energy expenditure takes place in skeletal muscle, via the coupling of catecholamines with β2-adrenoceptors.
Roles of eIF2α kinases in the pathogenesis of Alzheimer’s disease
Masuo Ohno
Frontiers in Molecular Neuroscience , 2014, DOI: 10.3389/fnmol.2014.00022
Abstract: Cell signaling in response to an array of diverse stress stimuli converges on the phosphorylation of eukaryotic initiation factor-2α (eIF2α). Evidence is accumulating that persistent eIF2α phosphorylation at Ser51 through prolonged overactivation of regulatory kinases occurs in neurodegenerative diseases such as Alzheimer’s disease (AD), leading to shutdown of general translation and translational activation of a subset of mRNAs. Recent advances in the development of gene-based strategies and bioavailable inhibitors, which specifically target one of the eIF2α kinases, have enabled us to investigate pathogenic roles of dysregulated eIF2α phosphorylation pathways. This review provides an overview of animal model studies in this field, focusing particularly on molecular mechanisms by which the dysregulation of eIF2α kinases may account for synaptic and memory deficits associated with AD. A growing body of evidence suggests that correcting aberrant eIF2α kinase activities may serve as disease-modifying therapeutic interventions to treat AD and related cognitive disorders.
Quantum Analysis and Nonequilibrium Response
Masuo Suzuki
Physics , 1998, DOI: 10.1143/PTP.100.475
Abstract: The quantum derivatives of $e^{-A}, A^{-1}$ and $\log A$, which play a basic role in quantum statistical physics, are derived and their convergence is proven for an unbounded positive operator $A$ in a Hilbert space. Using the quantum analysis based on these quantum derivatives, a basic equation for the entropy operator in nonequilibrium systems is derived, and Zubarev's theory is extended to infinite order with respect to a perturbation. Using the first-order term of this general perturbational expansion of the entropy operator, Kubo's linear response is rederived and expressed in terms of the inner derivation $\delta_{{\cal H}}$ for the relevant Hamiltonian ${\cal H}$. Some remarks on the conductivity $\sigma (\omega)$ are given.
Irreversibility and Entropy Production in Transport Phenomena II -- Statistical-mechanical Theory on Steady States including Thermal Disturbance and Energy Supply
Masuo Suzuki
Physics , 2011, DOI: 10.1016/j.physa.2011.09.033
Abstract: Some general aspects of nonlinear transport phenomena are discussed on the basis of two kinds of formulations obtained by extending Kubo's perturbational scheme of the density matrix and Zubarev's non-equilibrium statistical operator formulation. Both formulations are extended up to infinite order of an external force in compact forms and their relationship is clarified through a direct transformation.
General Formulation of Quantum Analysis
Masuo Suzuki
Physics , 1998, DOI: 10.1142/S0129055X9900009X
Abstract: A general formulation of noncommutative or quantum derivatives for operators in a Banach space is given on the basis of the Leibniz rule, irrespective of their explicit representations such as the G\^ateaux derivative or commutators. This yields a unified formulation of quantum analysis, namely the invariance of quantum derivatives, which are expressed by multiple integrals of ordinary higher derivatives with hyperoperator variables. Multivariate quantum analysis is also formulated in the present unified scheme by introducing a partial inner derivation and a rearrangement formula. Operator Taylor expansion formulas are also given by introducing the two hyperoperators $ \delta_{A \to B} \equiv -\delta_A^{-1} \delta_B$ and $d_{A \to B} \equiv \delta_{(-\delta_A^{-1}B) ; A}$ with the inner derivation $\delta_A : Q \mapsto [A,Q] \equiv AQ-QA$. Physically the present noncommutative derivatives express quantum fluctuations and responses.
Irreversibility and Entropy Production in Transport Phenomena I
Masuo Suzuki
Physics , 2011, DOI: 10.1016/j.physa.2011.01.008
Abstract: *First-principles derivation of the entropy production in erectric static conduction. *The second-order (symmetric) density matrix contributes to the entropy production. *New schemes of steady states formulated using a relaxation-type von Neumann equation. *Stationary temperature is introduced to characterize steady states. *The mechanism of the entropy production in steady states is also clarified.
Phospho-eIF2α Level Is Important for Determining Abilities of BACE1 Reduction to Rescue Cholinergic Neurodegeneration and Memory Defects in 5XFAD Mice
Latha Devi,Masuo Ohno
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0012974
Abstract: β-Site APP-cleaving enzyme 1 (BACE1) initiates amyloid-β (Aβ) generation and thus represents a prime therapeutic target in treating Alzheimer's disease (AD). Notably, increasing evidence indicates that BACE1 levels become elevated in AD brains as disease progresses; however, it remains unclear how the BACE1 upregulation may affect efficacies of therapeutic interventions including BACE1-inhibiting approaches. Here, we crossed heterozygous BACE1 knockout mice with AD transgenic mice (5XFAD model) and compared the abilities of partial BACE1 reduction to rescue AD-like phenotypes at earlier (6-month-old) and advanced (15–18-month-old) stages of disease, which expressed normal (~100%) and elevated (~200%) levels of BACE1, respectively. BACE1+/? deletion rescued memory deficits as tested by the spontaneous alternation Y-maze task in 5XFAD mice at the earlier stage and prevented their septohippocampal cholinergic deficits associated with significant neuronal loss. Importantly, BACE1+/? deletion was no longer able to rescue memory deficits or cholinergic neurodegeneration in 5XFAD mice at the advanced stage. Moreover, BACE1+/? deletion significantly reduced levels of Aβ42 and the β-secretase-cleaved C-terminal fragment (C99) in 6-month-old 5XFAD mouse brains, while these neurotoxic β-cleavage products dramatically elevated with age and were not affected by BACE1+/? deletion in 15–18-month-old 5XFAD brains. Interestingly, although BACE1+/? deletion lowered BACE1 expression by ~50% in 5XFAD mice irrespective of age in concordance with the reduction in gene copy number, BACE1 equivalent to wild-type controls remained in BACE1+/?·5XFAD mice at the advanced age. In accord, phosphorylation of the translation initiation factor eIF2α, an important mediator of BACE1 elevation, was dramatically increased (~9-fold) in 15–18-month-old 5XFAD mice and remained highly upregulated (~6-fold) in age-matched BACE1+/?·5XFAD mice. Together, our results indicate that partial reduction of BACE1 is not sufficient to block the phospho-eIF2α-dependent BACE1 elevation during the progression of AD, thus limiting its abilities to reduce cerebral Aβ/C99 levels and rescue memory deficits and cholinergic neurodegeneration.
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