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Search Results: 1 - 10 of 462 matches for " Maki Mizogami "
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Comparative Interactions of Anesthetic Alkylphenols with Lipid Membranes  [PDF]
Hironori Tsuchiya, Maki Mizogami
Open Journal of Anesthesiology (OJAnes) , 2014, DOI: 10.4236/ojanes.2014.412044
Abstract: Objective: While substituted phenols have a variety of pharmacological activity, the mechanism underlying their anesthetic effects remains uncertain especially about the critical target. We characterized the lipid membrane-interacting properties of different phenols by comparing with general anesthetic propofol and local anesthetics. Based on the results, we also studied the pharmacological effects possibly associated with their membrane interactivities. Methods: 1,6-Diphenyl-1,3,5-hexatriene-labeled lipid bilayer membranes were prepared with 1,2-dipalmitoyl-phosphatidylcholine as model membranes and with different phospholipids and cholesterol to mimic neuronal membranes. These membrane preparations were treated with phenols and anesthetics at 1 - 200 μM, followed by measuring the fluorescence polarization to determine the membrane interactivities to change membrane fluidity. Antioxidant effects were fluorometrically determined using diphenyl-1-pyrenylphosphine-incorporated liposomes which were treated with 10 - 100 μM phenols, and then peroxidized with 10 μM peroxynitrite. Results: Several phenols interacted with the model membranes and the neuronal mimetic membranes to increase their fluidity at 1 - 10 μM as well as lidocaine and bupivacaine did at 50 - 200 μM. Their comparative potencies were propofol > thymol > isothymol > guaiacol > phenol > eugenol, and bupivacaine > lidocaine, consistent with the rank order of neuro-activity. These phenols inhibited membrane lipid peroxidation at 10 and 100 μM with the potencies correlating to their membrane interactivities. Conclusion: The structure-specific membrane interaction is at least in part responsible for the pharmacology of anesthetic alkylphenols. Membrane-interacting antioxidant alkylphenols may be protective against the peroxynitrite-relating ischemia/reperfusion injury.
Membrane interactivity of charged local anesthetic derivative and stereoselectivity in membrane interaction of local anesthetic enantiomers
Hironori Tsuchiya, Maki Mizogami
Local and Regional Anesthesia , 2008, DOI: http://dx.doi.org/10.2147/LRA.S3876
Abstract: rane interactivity of charged local anesthetic derivative and stereoselectivity in membrane interaction of local anesthetic enantiomers Original Research (6022) Total Article Views Authors: Hironori Tsuchiya, Maki Mizogami Published Date August 2008 Volume 2008:1 Pages 1 - 9 DOI: http://dx.doi.org/10.2147/LRA.S3876 Hironori Tsuchiya1, Maki Mizogami2 1Department of Dental Basic Education; 2Department of Anesthesiology, Asahi University School of Dentistry, Mizuho, Gifu, Japan Abstract: With respect to the membrane lipid theory as a molecular mechanism for local anesthetics, two critical subjects, the negligible effects of charged drugs when applied extracellularly and the stereoselective effects of enantiomers, were verified by paying particular attention to membrane components, phospholipids with the anionic property, and cholesterol with several chiral carbons. The membrane interactivities of structurally-different anesthetics were determined by their induced fluidity changes of liposomal membranes. Lidocaine (3.0 μmol/mL) fluidized phosphatidylcholine membranes, but not its quaternary derivative QX-314 (3.0 μmol/mL). Similarly to the mother molecule lidocaine, however, QX-314 fluidized phosphatidylserine-containing nerve cell model membranes and acidic phospholipids-constituting membranes depending on the acidity of membrane lipids. Positively charged local anesthetics are able to act on lipid bilayers by ion-pairing with anionic (acidic) phospholipids. Bupivacaine (0.75 mol/mL) and ropivacaine (0.75 and 1.0 μmol/mL) fluidized nerve cell model membranes with the potency being S( )-enantiomer < racemate < R(+)-enantiomer (P < 0.01, vs antipode and racemate) and cardiac cell model membranes with the potency being S( )-ropivacaine < S( )-bupivacaine < R(+)-bupivacaine (P < 0.01). However, their membrane effects were not different when removing cholesterol from the model membranes. Stereoselectivity is producible by cholesterol which increases the chirality of lipid bilayers and enables to discriminate anesthetic enantiomers. The membrane lipid interaction should be reevaluated as the mode of action of local anesthetics.
Interaction of Local Anesthetics with Biomembranes Consisting of Phospholipids and Cholesterol: Mechanistic and Clinical Implications for Anesthetic and Cardiotoxic Effects
Hironori Tsuchiya,Maki Mizogami
Anesthesiology Research and Practice , 2013, DOI: 10.1155/2013/297141
Abstract: Despite a long history in medical and dental application, the molecular mechanism and precise site of action are still arguable for local anesthetics. Their effects are considered to be induced by acting on functional proteins, on membrane lipids, or on both. Local anesthetics primarily interact with sodium channels embedded in cell membranes to reduce the excitability of nerve cells and cardiomyocytes or produce a malfunction of the cardiovascular system. However, the membrane protein-interacting theory cannot explain all of the pharmacological and toxicological features of local anesthetics. The administered drug molecules must diffuse through the lipid barriers of nerve sheaths and penetrate into or across the lipid bilayers of cell membranes to reach the acting site on transmembrane proteins. Amphiphilic local anesthetics interact hydrophobically and electrostatically with lipid bilayers and modify their physicochemical property, with the direct inhibition of membrane functions, and with the resultant alteration of the membrane lipid environments surrounding transmembrane proteins and the subsequent protein conformational change, leading to the inhibition of channel functions. We review recent studies on the interaction of local anesthetics with biomembranes consisting of phospholipids and cholesterol. Understanding the membrane interactivity of local anesthetics would provide novel insights into their anesthetic and cardiotoxic effects. 1. Introduction Local anesthetics clinically used so far have the common chemical structure that is composed of three portions: the hydrophobic moiety consisting of an aromatic ring, the intermediate chain, and the hydrophilic moiety consisting of an amino terminus. The aromatic residue confers lipid solubility on a drug molecule, whereas the ionizable amino group confers, water solubility. The intermediate portion provides the spatial separation between hydrophobic and hydrophilic end and structurally classifies local anesthetics into amide type and ester type (Figure 1). Figure 1: Representative amide and ester local anesthetics. Because of the presence of substituted amino groups, local anesthetics are referred to as the bases with pKa values ranging from 7.7 to 8.1 at 37°C for the amide type and from 8.4 to 8.9 at 37°C for the ester type [1], so they exist in uncharged and positively charged form. After injected, local anesthetics show an in vivo equilibrium between the uncharged and the charged fraction of molecules. According to the Henderson-Hasselbalch equation, the percentage of uncharged molecules depends
Direct Vasocontractile Activities of Bupivacaine Enantiomers on the Isolated Rat Thoracic Aorta
Mai Mukozawa,Ko Takakura,Maki Mizogami
Anesthesiology Research and Practice , 2010, DOI: 10.1155/2010/820186
Abstract: Background. In vitro studies with isolated arteries have shown direct vasoactivity of racemic bupivacaine. However, there is little information on the direct vasoactivities of bupivacaine enantiomers, S(?)- and R(+)-bupivacaine. Methods. We performed functional examinations using isolated intact thoracic aortic rings from male Wistar rats. Changes in ring tension produced by S(?)-, R(+)-, or racemic bupivacaine were measured in Krebs solution. Results. S(?)-bupivacaine produced the strongest contraction of the three agents. R(+)-bupivacaine showed limited vasoconstriction. The effects of racemic bupivacaine were located between these two. Conclusion. Each bupivacaine enantiomer showed specific vasocontractile activity, which affects the activity of racemic bupivacaine. 1. Introduction The local anesthetic bupivacaine is a racemic mixture of S(?)- and R(+)-enantiomers. Racemic bupivacaine has biphasic vasoactivities, namely, vasoconstriction at a low concentration and vasodilatation at a high concentration [1]. Since 1976, when Aps and Reynolds showed this vasoactivity in a double-blind trial with forearm skin color changes of 31 volunteers [1], these vasoactivities have been further demonstrated using various in vivo methods with various animals or humans, such as television microscopy in rat cremaster muscle microvasculatures [2], intravital microscopy through a spinal window in dog pial vasculatures [3], laser Doppler imaging in human skin [4], as well as other techniques. Although inhibition of sympathetic nerves innervating arteries by racemic bupivacaine could not be ignored in in vivo studies, some in vitro studies with isolated preparations from human umbilical arteries [5–7], rat uterine arteries [8], and human uterine arteries [9] have confirmed that the vasoactivities are produced by direct actions of racemic bupivacaine itself on the arteries. S(?)-bupivacaine was developed as an alternative long-acting local anesthetic with a clinical profile similar to that of racemic bupivacaine but with a lower potential for producing systemic toxicity [10]. S(?)-bupivacaine also has biphasic vasoactivities similar to those of racemic bupivacaine, which has been shown in in vivo studies [4, 11–13]. Furthermore, some of the in vivo studies have shown that R(+)-bupivacaine produced a dose-dependent vasodilatation [11, 13]. However, there is little information on the direct vasoactivities of S(?)- and R(+)-bupivacaine based on in vitro study. In this study, we investigated the vasocontractile activities of these agents using isolated rat aorta. 2. Methods
Local anesthetic failure associated with inflammation: verification of the acidosis mechanism and the hypothetic participation of inflammatory peroxynitrite
Takahiro Ueno, Hironori Tsuchiya, Maki Mizogami, Ko Takakura
Journal of Inflammation Research , 2008, DOI: http://dx.doi.org/10.2147/JIR.S3982
Abstract: cal anesthetic failure associated with inflammation: verification of the acidosis mechanism and the hypothetic participation of inflammatory peroxynitrite Original Research (15641) Total Article Views Authors: Takahiro Ueno, Hironori Tsuchiya, Maki Mizogami, Ko Takakura Published Date November 2008 Volume 2008:1 Pages 41 - 48 DOI: http://dx.doi.org/10.2147/JIR.S3982 Takahiro Ueno1, Hironori Tsuchiya2, Maki Mizogami1, Ko Takakura1 1Department of Anesthesiology, Asahi University School of Dentistry, Mizuho, Gifu, Japan; 2Department of Dental Basic Education, Asahi University School of Dentistry, Mizuho, Gifu, Japan Abstract: The presence of inflammation decreases local anesthetic efficacy, especially in dental anesthesia. Although inflammatory acidosis is most frequently cited as the cause of such clinical phenomena, this has not been experimentally proved. We verified the acidosis mechanism by studying the drug and membrane lipid interaction under acidic conditions together with proposing an alternative hypothesis. Liposomes and nerve cell model membranes consisting of phospholipids and cholesterol were treated at different pH with lidocaine, prilocaine and bupivacaine (0.05%–0.2%, w/v). Their membrane-interactive potencies were compared by the induced-changes in membrane fluidity. Local anesthetics fluidized phosphatidylcholine membranes with the potency being significantly lower at pH 6.4 than at pH 7.4 (p < 0.01), supporting the acidosis theory. However, they greatly fluidized nerve cell model membranes even at pH 6.4 corresponding to inflamed tissues, challenging the conventional mechanism. Local anesthetics acted on phosphatidylserine liposomes, as well as nerve cell model membranes, at pH 6.4 with almost the same potency as that at pH 7.4, but not on phosphatidylcholine, phosphatidylethanolamine and sphingomyelin liposomes. Since the positively charged anesthetic molecules are able to interact with nerve cell membranes by ion-paring with anionic components like phosphatidylserine, tissue acidosis is not essentially responsible for the local anesthetic failure associated with inflammation. The effects of local anesthetics on nerve cell model membranes were inhibited by treating with peroxynitrite (50 μM), suggesting that inflammatory cells producing peroxynitrite may affect local anesthesia.
Local anesthetic failure associated with inflammation: verification of the acidosis mechanism and the hypothetic participation of inflammatory peroxynitrite
Takahiro Ueno,Hironori Tsuchiya,Maki Mizogami,Ko Takakura
Journal of Inflammation Research , 2008,
Abstract: Takahiro Ueno1, Hironori Tsuchiya2, Maki Mizogami1, Ko Takakura11Department of Anesthesiology, Asahi University School of Dentistry, Mizuho, Gifu, Japan; 2Department of Dental Basic Education, Asahi University School of Dentistry, Mizuho, Gifu, JapanAbstract: The presence of inflammation decreases local anesthetic efficacy, especially in dental anesthesia. Although inflammatory acidosis is most frequently cited as the cause of such clinical phenomena, this has not been experimentally proved. We verified the acidosis mechanism by studying the drug and membrane lipid interaction under acidic conditions together with proposing an alternative hypothesis. Liposomes and nerve cell model membranes consisting of phospholipids and cholesterol were treated at different pH with lidocaine, prilocaine and bupivacaine (0.05%–0.2%, w/v). Their membrane-interactive potencies were compared by the induced-changes in membrane fluidity. Local anesthetics fluidized phosphatidylcholine membranes with the potency being significantly lower at pH 6.4 than at pH 7.4 (p < 0.01), supporting the acidosis theory. However, they greatly fluidized nerve cell model membranes even at pH 6.4 corresponding to inflamed tissues, challenging the conventional mechanism. Local anesthetics acted on phosphatidylserine liposomes, as well as nerve cell model membranes, at pH 6.4 with almost the same potency as that at pH 7.4, but not on phosphatidylcholine, phosphatidylethanolamine and sphingomyelin liposomes. Since the positively charged anesthetic molecules are able to interact with nerve cell membranes by ion-paring with anionic components like phosphatidylserine, tissue acidosis is not essentially responsible for the local anesthetic failure associated with inflammation. The effects of local anesthetics on nerve cell model membranes were inhibited by treating with peroxynitrite (50 μM), suggesting that inflammatory cells producing peroxynitrite may affect local anesthesia.Keywords: inflammatory acidosis, local anesthetic failure, membrane lipid interaction, hypothetic mechanism, inflammatory peroxynitrite
Properties of Time-Varying Causality Tests in the Presence of Multivariate Stochastic Volatility  [PDF]
Daiki Maki
Open Journal of Statistics (OJS) , 2016, DOI: 10.4236/ojs.2016.65064
Abstract: This paper compares the statistical properties of time-varying causality tests when errors of variables have multivariate stochastic volatility (SV). The time-varying causal-ity tests in this paper are based on a logistic smooth transition autoregressive model. The compared time-varying causality tests include asymptotic tests, heteroskedasticity-robust tests, and tests using wild bootstrap. Our simulation results show that asymptotic tests and heteroskedasticity-robust counterparts have size distortions under multivariate SV, whereas tests using wild bootstrap have better size properties regardless of type of error. In particular, the time-varying causality test with first-order Taylor approximation using wild bootstrap has better statistical properties.
Angiotensinogen Expression Is Enhanced in the Progression of Glomerular Disease  [PDF]
Maki Urushihara, Hiroyuki Kobori
International Journal of Clinical Medicine (IJCM) , 2011, DOI: 10.4236/ijcm.2011.24064
Abstract: Intrarenal renin-angiotensin system (RAS) activation plays a critical role in the development and progression of renal injury. In the kidney, all of the RAS components are present and intrarenal angiotensin II (Ang II) is formed by multiple independent mechanisms. Angiotensinogen (AGT) is the only known substrate for renin that is a rate-limiting enzyme of the RAS. Recently, enhanced intrarenal AGT levels have been shown to reflect the intrarenal RAS status in hypertension, chronic glomerular disease and diabetic nephropathy. In this review, we focus on AGT expression of the diseased glomeruli in the progression of glomerular disease. An anti-glomerular basement membrane nephritis rat model developed progressive proteinuria and glomerular crescent formation, accompanied by increased macrophage infiltration and glomerular expression of AGT and Ang II. The addition of Ang II type 1 receptor blocker to CC-chemokine recaptor 2 antagonist markedly attenuated the induction of macrophage infiltration, AGT and Ang II, and reduced glomerular crescent formation. Next, the levels of glomerular AGT expression and marker of reactive oxygen species in Zucker diabetic fatty (ZDF) obese rats were higher than those in ZDF lean rats. Hydrogen peroxide (H2O2) induced an increase in the AGT expression in primary rat mesangial cells. Furthermore, the H2O2-induced upregulation of AGT was inhibited by a mitogen-activated protein kinase kinase and a c-Jun N-terminal kinase inhibitor. These data suggest the potential contribution of enhanced AGT expression in glomeruli to the intrarenal RAS activation for the development of glomerular disease.
Trends in age distribution of participants in a self-covered and a public expense-covered health check-up programs in Japan  [PDF]
Maki Ogawa, Atsushi Imai
Health (Health) , 2012, DOI: 10.4236/health.2012.49088
Abstract: Objective: In Japan, there are unique facilities (namely Ningen Dock) of health check-up, where asymptomatic participants undergo a medical examination at their own expense. The earlier occurrence of cervical cancer and the concern on screening prompted us compare to the age distribution in the self-covered system with that of free physical check-up programs at public expense. Methods: We analyzed medical records of Japanese women, who underwent gynecological examinations at self-covered expense and at public expense between for the periods 2002-2011 and 2005-2009, respectively, restricting examinee’s age group. Results: For self-covered system, approximately 80% of the overall examinee population was occupied with three age groups 30-39, 40-49 and 50-59. The participants was extremely fewer in the over 60 years age group accounting for 10%, compared to those for the public expense-covered system, the over 60 years age group being 25%. Participant under the age of 30 years seemed to increase in chronological order in both systems. Conclusion: The level of knowledge on sexually transmitted infections may contribute to screening promotion for the younger women, while the elderly over 60 years’ attitudes toward screening may be mainly related to social-economic status and/or public expense support.
Contact Urticaria Syndrome from Tofu  [PDF]
Maki Kitakawa, Tokio Nakada
Case Reports in Clinical Medicine (CRCM) , 2016, DOI: 10.4236/crcm.2016.56038
Abstract: A-52-year-old woman ate dinner after preening roses in her garden. Immediately, she developed oralaryngeal malaise and pruritic rash. Nasal obstruction and increase of cutaneous lesions were seen although she took betamethasone, 2 mg, orally. Physical examination revealed geographic wheal on trunk and extremities, and no overt mucosal lesions. History demonstrated that she had developed such reactions four times before: three of the four were seen shortly after eating soybean. Tofu was examined by prick-by-prick testing, and prick testing was performed with a petal, a piece of stem and rose leaf, positive and negative control. Positive reactions to tofu (wheal, 5 × 7 mm) and positive control (wheal 5 × 5 mm) and negative ones to others were noted. Although sensitization to soybean seemed to antedate pollen allergy on the basis of interview, oral allergy syndrome could be complicated because of various pollens-specific IgE. Since soy-bean specific IgE was class 2, such titer was not an effective predictor of clinical severity. This case should be classified into stage 3 of contact urticaria syndrome (CUS). Since CUS can be fatal, we must be careful in management for such patients.
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