Ando M

References (6)

Title : Mesial Frontal Lobe Infarction Presenting as Pisa Syndrome - Noda_2020_J.Stroke.Cerebrovasc.Dis__104882
Author(s) : Noda K , Ando M , Jo T , Hattori A , Ogaki K , Sugiyama M , Hattori N , Okuma Y
Ref : J Stroke Cerebrovasc Dis , :104882 , 2020
Abstract : Pisa syndrome is usually seen in patients with Alzheimer's disease treated with a cholinesterase inhibitor, dementia with Lewy bodies, Parkinson's disease, or atypical parkinsonism including multiple system atrophy. An 86-year-old woman presented with an acute onset of lateral flexion of her trunk to the left side, i.e., Pisa syndrome. She also showed left hemiparesis predominantly in her lower extremity. Her diffusion-weighted magnetic resonance images showed acute infarction in the right premotor area and supplementary motor area. Clopidogrel (75 mg daily) was prescribed. After two weeks from the onset of symptoms, her Pisa syndrome improved. The pathophysiology of Pisa syndrome has not yet been fully understood, but different mechanisms have been assumed. In this patient, it is possible that the infarction in her unilateral frontal lobe impaired the information processing from the temporoparietal cortex to the frontal lobe, including the premotor area and supplementary motor area for anticipatory postural control.
ESTHER : Noda_2020_J.Stroke.Cerebrovasc.Dis__104882
PubMedSearch : Noda_2020_J.Stroke.Cerebrovasc.Dis__104882
PubMedID: 32417237

Title : Acetylcholinesterase (AChE) inhibition aggravates fasting-induced triglyceride accumulation in the mouse liver - Yokota_2014_FEBS.Open.Bio_4_905
Author(s) : Yokota S , Nakamura K , Ando M , Kamei H , Hakuno F , Takahashi S , Shibata S
Ref : FEBS Open Bio , 4 :905 , 2014
Abstract : Although fasting induces hepatic triglyceride (TG) accumulation in both rodents and humans, little is known about the underlying mechanism. Because parasympathetic nervous system activity tends to attenuate the secretion of very-low-density-lipoprotein-triglyceride (VLDL-TG) and increase TG stores in the liver, and serum cholinesterase activity is elevated in fatty liver disease, the inhibition of the parasympathetic neurotransmitter acetylcholinesterase (AChE) may have some influence on hepatic lipid metabolism. To assess the influence of AChE inhibition on lipid metabolism, the effect of physostigmine, an AChE inhibitor, on fasting-induced increase in liver TG was investigated in mice. In comparison with ad libitum-fed mice, 30 h fasting increased liver TG accumulation accompanied by a downregulation of sterol regulatory element-binding protein 1 (SREBP-1) and liver-fatty acid binding-protein (L-FABP). Physostigmine promoted the 30 h fasting-induced increase in liver TG levels in a dose-dependent manner, accompanied by a significant fall in plasma insulin levels, without a fall in plasma TG. Furthermore, physostigmine significantly attenuated the fasting-induced decrease of both mRNA and protein levels of SREBP-1 and L-FABP, and increased IRS-2 protein levels in the liver. The muscarinic receptor antagonist atropine blocked these effects of physostigmine on liver TG, serum insulin, and hepatic protein levels of SREBP-1 and L-FABP. These results demonstrate that AChE inhibition facilitated fasting-induced TG accumulation with up regulation of the hepatic L-FABP and SREBP-1 in mice, at least in part via the activation of muscarinic acetylcholine receptors. Our studies highlight the crucial role of parasympathetic regulation in fasting-induced TG accumulation, and may be an important source of information on the mechanism of hepatic disorders of lipid metabolism.
ESTHER : Yokota_2014_FEBS.Open.Bio_4_905
PubMedSearch : Yokota_2014_FEBS.Open.Bio_4_905
PubMedID: 25383314

Title : Anti-Alzheimer's drug, donepezil, markedly improves long-term survival after chronic heart failure in mice - Handa_2009_J.Card.Fail_15_805
Author(s) : Handa T , Katare RG , Kakinuma Y , Arikawa M , Ando M , Sasaguri S , Yamasaki F , Sato T
Ref : J Card Fail , 15 :805 , 2009
Abstract : BACKGROUND: We previously reported that chronic vagal nerve stimulation markedly improved long-term survival after chronic heart failure (CHF) in rats through cardioprotective effects of acetylcholine, independent of the heart rate-slowing mechanism. However, such an approach is invasive and its safety is unknown in clinical settings. To develop an alternative therapy with a clinically available drug, we examined the chronic effect of oral donepezil, an acetylcholinesterase inhibitor against Alzheimer's disease, on cardiac remodeling and survival with a murine model of volume-overloaded CHF. METHODS AND RESULTS: Four weeks after surgery of aortocaval shunt, CHF mice were randomized into untreated and donepezil-treated groups. Donepezil was orally given at a dosage of 5 mgxkg(-1)xday(-1). After 4 weeks of treatment, we evaluated in situ left ventricular (LV) pressure, ex vivo LV pressure-volume relationships, and LV expression of brain natriuretic peptides (BNP). We also observed survival for 50 days. When compared with the untreated group, the donepezil-treated group had significantly low LV end-diastolic pressure, high LV contractility, and low LV expression of BNP. Donepezil significantly reduced the heart weight and markedly improved the survival rate during the 50-day treatment period (54% versus 81%, P < .05). CONCLUSIONS: Oral donepezil improves survival of CHF mice through prevention of pumping failure and cardiac remodeling.
ESTHER : Handa_2009_J.Card.Fail_15_805
PubMedSearch : Handa_2009_J.Card.Fail_15_805
PubMedID: 19879468

Title : Genetic polymorphisms of the multidrug resistance-associated protein 2 gene (ABCC2) and Irinotecan toxicity - Kitagawa_2004_J.Clin.Oncol_22_2009
Author(s) : Kitagawa C , Ando M , Ando Y , Sekido Y , Usui M , Takahashi K , Shimokata K , Hasegawa Y
Ref : J Clin Oncol , 22 :2009 , 2004
Abstract : 2009 Background: Irinotecan unexpectedly causes severe, occasionally fatal, toxicity of leukopenia or diarrhea. Irinotecan is metabolized by carboxylesterase to form an active SN-38, which is further conjugated and detoxified by UDP-glucuronosyltransferase (UGT) 1A1 to yield its b-glucuronide. Multidrug resistance-assocciated protein 2 (MRP2, ABCC2) transports SN-38-glucuronide from hepatocytes to the bile, as it transports bilirubin in the body.
METHODS: We examined the polymorphisms of ABCC2 gene, -24C>T, 1249G>A, 2366C>T, 2302C>T, 2375A>G, 2439+2 T>C, 3449 G>A, and 3517A>T, in 120 Japanese cancer patients who had been treated with irinotecan, including 27 patients who experienced severe toxicity of G4 leukopenia and/or G3 or worse diarrhea. Our hypothesis was that patients with the variant ABCC2 allele would have an increased risk of severe toxicity.
RESULTS: We detected the four variant alleles, -24C>T, 1249G>A, 2366C>T, and 2375A>G. The association between ABCC2 variants, -24C>T or 1249G>A, and severe toxicity was investigated (Table). Neither univariate analysis (odds ratio, 0.78; 95% confidential interval (CI), 0.21-2.35; odds ratio, 1.05; 95% CI, 0.41-2.56) nor multivariate logistic regression analysis (odds ratio, 0.98; 95% CI, 0.23-3.44; odds ratio, 1.17; 95% CI, 0.40-3.26) found any significant association between severe toxicity and the ABCC2 variants in 1249G>A or -24C>T, respectively. We detected a heterozygote for 2366C>T in one patient and a new heterozygote for 2375A>G in one patient. Severe toxicity was not occurred in these patients. There were no apparent associations between the ABCC2 variants and pharmacokinetics of irinotecan, SN-38 and SN-38 glucuronide.
CONCLUSIONS: This pharmacogenetic study did not find any evidence that determination of ABCC2 genotypes would be useful for predicting severe toxicity by irinotecan. [Figure: see text] No significant financial relationships to disclose.
ESTHER : Kitagawa_2004_J.Clin.Oncol_22_2009
PubMedSearch : Kitagawa_2004_J.Clin.Oncol_22_2009
PubMedID: 28015787

Title : Non-synonymous single nucleotide alterations in the microsomal epoxide hydrolase gene and their functional effects - Maekawa_2003_Xenobiotica_33_277
Author(s) : Maekawa K , Itoda M , Hanioka N , Saito Y , Murayama N , Nakajima O , Soyama A , Ishida S , Ozawa S , Ando M , Sawada J
Ref : Xenobiotica , 33 :277 , 2003
Abstract : 1. By sequencing genomic DNA from 72 established cell lines derived from Japanese individuals, we detected 25 single nucleotide alterations in the microsomal epoxide hydrolase (EPHX1) gene. Of them, five were exonic alterations resulting in amino acid alterations (77C>G, T26S; 128G>C, R43T; 337T>C, Y113H; 416A>G, H139R; 823A>G, T275A). The T26S, R43T, Y113H and H139R substitutions were found at relatively high frequencies and seemed to be polymorphic, and T26S and T275A were novel. 2. To examine the effects of these amino acid alterations on EPHX1 function, EPHX1 cDNA constructs of wild-type and five variants were transfected into COS-1 cells, and their hydrolytic activities for cis-stilbene oxide were determined in vitro. Although all of the transfectants expressed EPHX1 mRNA and protein at similar levels, the variant H139R protein was expressed at a significantly higher level (128% of the wild-type). K(m) values were not significantly different between the wild-type and variants. 3. Increase (140%) in the enzymatic activity (V(max)) of the variant H139R was accompanied by the increased EPHX1 protein level without any significant change in the intrinsic EPHX1 activity. On the other hand, the variant R43T showed increased values for V(max) and clearance (V(max)/K(m)) (around 130%) both on a microsomal protein basis and on a EPHX1 protein basis. 4. These results suggest that R43T as well as H139R increase epoxide hydrolase activity.
ESTHER : Maekawa_2003_Xenobiotica_33_277
PubMedSearch : Maekawa_2003_Xenobiotica_33_277
PubMedID: 12637245

Title : Inhibitory effect of acephate (N-acetyl O, S-dimethyl thiophosphoramide) on serum cholinesterase--effect of acephate on cholinesterase - Ando_1982_J.Toxicol.Sci_7_185
Author(s) : Ando M , Wakamatsu K
Ref : Journal of Toxicological Sciences , 7 :185 , 1982
Abstract : The Lineweaver-Burk plot of the activity of human serum cholinesterase against the concentration of butyrylthiocholineiodide was shown by two intersecting lines. The Hill plot of cholinesterase activity was linear over the entire range of the substrate concentration. The n value, an interaction coefficient, was less than 1.0 (about 0.8). These results suggest that cholinesterase has multiple substrate binding sites. Acephate, one of the organophosphorous insecticides, inhibited the activity of cholinesterase. Acephate at concentration under 1.25 mM (about 230 ppm in serum) did not inhibit the activity of cholinesterase. The minimum concentration of acephate inhibition of cholinesterase activity was at 2.5 mM. An equilibrium constant(K) can be used as an indicator of inhibitory effect on cholinesterase. The serum cholinesterase activity of workers who were exposed to acephate is not affected when the concentration of acephate in serum is less than 200 ppm. This result suggests that the activity of serum cholinesterase is not an accurate indicator of the exposure of the low toxic insecticides, e.g. acephate. The inhibitory effect of acephate on cholinesterase decreased after the incubation with S-9 mixture. This result suggests that a part of acephate is metabolized to inactive substances in the liver.
ESTHER : Ando_1982_J.Toxicol.Sci_7_185
PubMedSearch : Ando_1982_J.Toxicol.Sci_7_185
PubMedID: 7154130