Yamauchi T

References (12)

Title : A novel homozygous nonsense variant of LMF1 in pregnancy-induced hypertriglyceridemia with acute pancreatitis - Tanaka_2023_J.Clin.Lipidol__
Author(s) : Tanaka M , Takase S , Ishiura H , Yamauchi T , Okazaki S , Okazaki H
Ref : J Clin Lipidol , : , 2023
Abstract : Hypertriglyceridemia (HTG)-induced pancreatitis during pregnancy could lead to maternal and fetal death. However, its genetic bases are not fully understood, and its treatment strategies are yet to be established. Here we report a case with a novel homozygous nonsense variant of LMF1 in pregnancy-associated HTG with acute pancreatitis. Our patient had childhood-onset severe HTG that had been well-controlled by dietary management in the non-pregnant period with plasma triglyceride (TG) levels at around 200 mg/dL. Milky plasma was noted at the first-trimester pregnancy checkup, followed by a severe increase in plasma TG (10,500 mg/dL) that resulted in pancreatitis in the last trimester. The implementation of strict dietary fat restriction (less than 4 grams per day) reduced plasma TG levels and led to successful delivery. Exome sequencing revealed a novel homozygous nonsense variant in LMF1 (c.697C>T, p.Arg233Ter). The activities of lipoprotein lipase (LPL) and hepatic lipase in post-heparin plasma were not abolished but reduced. The use of pemafibrate decreased plasma TG levels with a concomitant increase in LPL activity. HTG in childhood or early pregnancy is commonly assumed to be polygenic in origin but should be regarded as a feature suggestive of monogenic hyperchylomicronemia. Adequate TG monitoring and dietary fat restriction should be implemented to prevent potentially lethal events of pancreatitis.
ESTHER : Tanaka_2023_J.Clin.Lipidol__
PubMedSearch : Tanaka_2023_J.Clin.Lipidol__
PubMedID: 37005154

Title : First genomic insights into members of a candidate bacterial phylum responsible for wastewater bulking - Sekiguchi_2015_PeerJ_3_e740
Author(s) : Sekiguchi Y , Ohashi A , Parks DH , Yamauchi T , Tyson GW , Hugenholtz P
Ref : PeerJ , 3 :e740 , 2015
Abstract : Filamentous cells belonging to the candidate bacterial phylum KSB3 were previously identified as the causative agent of fatal filament overgrowth (bulking) in a high-rate industrial anaerobic wastewater treatment bioreactor. Here, we obtained near complete genomes from two KSB3 populations in the bioreactor, including the dominant bulking filament, using differential coverage binning of metagenomic data. Fluorescence in situ hybridization with 16S rRNA-targeted probes specific for the two populations confirmed that both are filamentous organisms. Genome-based metabolic reconstruction and microscopic observation of the KSB3 filaments in the presence of sugar gradients indicate that both filament types are Gram-negative, strictly anaerobic fermenters capable of non-flagellar based gliding motility, and have a strikingly large number of sensory and response regulator genes. We propose that the KSB3 filaments are highly sensitive to their surroundings and that cellular processes, including those causing bulking, are controlled by external stimuli. The obtained genomes lay the foundation for a more detailed understanding of environmental cues used by KSB3 filaments, which may lead to more robust treatment options to prevent bulking.
ESTHER : Sekiguchi_2015_PeerJ_3_e740
PubMedSearch : Sekiguchi_2015_PeerJ_3_e740
PubMedID: 25650158
Gene_locus related to this paper: 9bact-a0a0s6vpc9 , 9bact-a0a0s6vvt4 , 9bact-a0a0s6vpf3

Title : Donepezil, an acetylcholinesterase inhibitor, enhances adult hippocampal neurogenesis - Kotani_2008_Chem.Biol.Interact_175_227
Author(s) : Kotani S , Yamauchi T , Teramoto T , Ogura H
Ref : Chemico-Biological Interactions , 175 :227 , 2008
Abstract : Donepezil hydrochloride is a potent and selective acetylcholinesterase inhibitor and has been treated for Alzheimer's disease, in which the cholinergic dysfunction is observed. Recently, the degeneration of medial septal cholinergic nuclei in adult rat suppressed the neurogenesis in hippocampal dentate gyrus (DG) was reported. Then, we determined whether donepezil which activated the brain cholinergic system could modulate hippocampal neurogenesis in normal rats. After the injection of 5'-bromo-2'-deoxyuridine (BrdU) to label dividing cells, we orally treated with donepezil (0.5 or 2mg/kg) once a day for 4 weeks. In the other group, we performed 4-week subcutaneous infusion of scopolamine (0.75 or 3mg/day), a muscarinic acetylcholine receptor blocker. The doses of donepezil and scopolamine we used in this study were reported to activate and inhibit cholinergic activity in rats, respectively. One day after the completion of drug treatment, the animals were sacrificed, and immunohistochemical analysis was performed. Donepezil increased, but scopolamine decreased, the number of BrdU-positive cells in the DG as compared with the vehicle-treated control. Neither drug had any effects on the percentage of BrdU-positive cells that were also positive for a neuronal marker NeuN, nor the number of proliferating cell nuclear antigen-positive cells in the DG. These results indicate that donepezil enhances and scopolamine suppresses the survival of newborn neurons in the DG without affecting the proliferation of neural progenitor cell and the neuronal differentiation. We also found that chronic treatment of donepezil enhanced, and scopolamine suppressed phosphorylation of cAMP response element binding protein (CREB), which was involved in cell survival, in the DG. These results suggest that donepezil activates the central cholinergic transmission and enhances the survival of newborn neurons in the DG via CREB signaling.
ESTHER : Kotani_2008_Chem.Biol.Interact_175_227
PubMedSearch : Kotani_2008_Chem.Biol.Interact_175_227
PubMedID: 18501884

Title : Pharmacological evidence of cholinergic involvement in adult hippocampal neurogenesis in rats - Kotani_2006_Neurosci_142_505
Author(s) : Kotani S , Yamauchi T , Teramoto T , Ogura H
Ref : Neuroscience , 142 :505 , 2006
Abstract : In adult hippocampus, neural progenitor cells give rise to neurons throughout life, and the neurogenesis is modulated by various intrinsic and extrinsic factors. Recent reports showed that lesion of septal cholinergic nuclei projecting to hippocampus suppressed the survival of newborn cells in the dentate gyrus (DG) of hippocampus. Here, we studied whether pharmacological treatment to activate or inhibit the cholinergic system could modulate adult hippocampal neurogenesis. 5'-Bromo-2'-deoxyuridine (BrdU) was injected to label dividing cells before the drug treatment. Immunohistochemical analysis was performed in normal rats chronically treated with an acetylcholinesterase inhibitor donepezil or a muscarinic acetylcholine receptor blocker scopolamine for four weeks. Donepezil increased, but scopolamine decreased, the number of BrdU-positive cells in the DG as compared with the control. Neither drug altered the percentage of BrdU-positive cells that were also positive for a neuronal marker neuronal nuclei, nor net population of proliferative cells labeled with proliferating cell nuclear antigen. We also found that donepezil enhanced, and scopolamine suppressed, the expression level of phosphorylated cAMP response element binding protein (CREB), which is related to cell survival, in the DG. These results indicate that donepezil enhances and scopolamine suppresses the survival of newborn cells in the DG via CREB signaling without affecting neural progenitor cell proliferation and the neuronal differentiation. This is the first evidence that pharmacological manipulation of the cholinergic system can modulate adult hippocampal neurogenesis.
ESTHER : Kotani_2006_Neurosci_142_505
PubMedSearch : Kotani_2006_Neurosci_142_505
PubMedID: 16889901

Title : Teratogenicity and developmental toxicity of chlorpyrifos. Maternal exposure during organogenesis in mice - Tian_2005_Reprod.Toxicol_20_267
Author(s) : Tian Y , Ishikawa H , Yamaguchi T , Yamauchi T , Yokoyama K
Ref : Reprod Toxicol , 20 :267 , 2005
Abstract : Chlorpyrifos, an organophosphate pesticide, was evaluated for potential teratogenicity and developmental toxicity in mice. Pregnant females were given a single intraperitoneal injection (40 or 80 mg/kg) on day 10 of gestation and fetuses were evaluated on gestation day 17. At 80 mg/kg, chlorpyrifos treatment resulted in a significant reduction in numbers of live fetuses, and increase in resorptions, versus control litters. There was no indication of maternal toxicity. External and skeletal malformations were observed at 80 mg/kg, but not 40 mg/kg. Rates of fetuses with cleft palate increased significantly (p<0.05) following 80 mg/kg chlorpyrifos (5.97%) versus control litters (0.97%). Similarly, the absence of thoracic vertebrae was increased and the number of caudal vertebrae was significantly decreased. It is suggested that chlorpyrifos is teratogenic and embryotoxic in mice at doses below those that cause significant maternal toxicity.
ESTHER : Tian_2005_Reprod.Toxicol_20_267
PubMedSearch : Tian_2005_Reprod.Toxicol_20_267
PubMedID: 15907662

Title : Micronucleus formation in 3-day mouse embryos associated with maternal exposure to chlorpyrifos during the early preimplantation period - Tian_2003_Reprod.Toxicol_17_401
Author(s) : Tian Y , Yamauchi T
Ref : Reprod Toxicol , 17 :401 , 2003
Abstract : Chlorpyrifos, an organophosphate pesticide, was evaluated for its ability to induce cytogenetic damage in preimplantation embryos after maternal exposure. Pregnant female mice were intraperitoneally (i.p.) administered a single dose of chlorpyrifos (40 or 80 mg/kg) at 10:00 h on Day 0 of pregnancy. On Day 3 of gestation, blastocysts were collected and evaluated for gross morphology, micronucleus (MN) frequency, and cell number. A significant increase in MN frequency indicating cytogenetic damage was observed in the treatment groups in comparison to control. The MN frequency revealed a clear dose-dependent increase. There was also a significant decrease in the embryo cell number in the 80 mg/kg treated group. A simultaneous decrease in the cell number and increase in MN frequency may reflect an embryonic developmental disadvantage resulting from maternal treatment with chlorpyrifos.
ESTHER : Tian_2003_Reprod.Toxicol_17_401
PubMedSearch : Tian_2003_Reprod.Toxicol_17_401
PubMedID: 12849850

Title : Purification, characterization, and gene cloning of a novel fluoroacetate dehalogenase from Burkholderia sp. FA1. - Kurihara_2003_J.Mol.Catal.B.Enzym_23_347
Author(s) : Kurihara T , Yamauchi T , Ichiyama S , Takahata H , Esaki N
Ref : J Mol Catal B Enzym , 23 :347 , 2003
Abstract : Fluoroacetate dehalogenase catalyzes the hydrolytic defluorination of fluoroacetate to produce glycolate. The enzyme is unique in that it catalyzes the cleavage of the highly stable carbon-fluorine bond in an aliphatic compound. The bacterial isolate FA1, which was identified as Burkholderia, grew on fluoroacetate as the sole carbon source to produce fluoroacetate dehalogenase (FAc-DEX FA1). The enzyme was purified to homogeneity and characterized. The molecular weights were estimated to be 79,000 and 34,000 by gel filtration and SDS-polyacrylamide gel electrophoresis (PAGE), respectively, suggesting that the enzyme is a dimer. The purified enzyme was specific to haloacetates, and fluoroacetate was the best substrate. The activities toward chloroacetate and bromoacetate were less than 5% of the activity toward fluoroacetate. The Km and Vmax values for the hydrolysis of fluoroacetate were 5.1 mM and 11 umol per minute milligram, respectively. The gene coding for the enzyme was isolated, and the nucleotide sequence was determined. The open reading frame consisted of 912 nucleotides, corresponding to 304 amino acid residues. Although FAc-DEX FA1 showed high sequence similarity to fluoroacetate dehalogenase from Moraxella sp. B (FAc-DEX H1) (61% identity), the substrate specificity of FAc-DEX FA1 was significantly different from that of FAc-DEX H1: FAc-DEX FA1 was more specific to fluoroacetate than FAc-DEX H1.
ESTHER : Kurihara_2003_J.Mol.Catal.B.Enzym_23_347
PubMedSearch : Kurihara_2003_J.Mol.Catal.B.Enzym_23_347
Gene_locus related to this paper: bursp-deha

Title : Pharmacokinetics and neurotoxicity of dipterex in hens. A comparative study of administration methods - Xie_1998_J.Toxicol.Sci_23_25
Author(s) : Xie X , Piao FY , Tian Y , Yamauchi T
Ref : Journal of Toxicological Sciences , 23 :25 , 1998
Abstract : We compared the tissue concentration of dipterex and the inhibition of the neuropathy target esterase (NTE) activity among groups of hens (n = 8 each) which were intravenously (i.v.), subcutaneously (s.c.) or orally (p.o.) administered the insecticide dipterex. The tissue concentrations of dipterex in the s.c. group were higher than those in the i.v. and p.o. groups. When dosed subcutaneously, the tissue concentration of dipterex was high in the brain, spinal cord and muscle at 3 hr after dosing and then concentrated in the spinal cord and muscle for the subsequent 3 hr. When dosed intravenously or orally, dipterex was evenly dispersed in various tissues. All hens treated with dipterex showed acute neurotoxic signs within 15 min after dosing. The hens dosed intravenously recovered from this acute poisoning within 3 hr, and the hens dosed orally recovered within 6 hr, while the hens dosed subcutaneously recovered within 24 hr after dosing. One hen in the s.c. group exhibited acute neurological sequelae following the acute poisoning. In addition, the loss of body weight was the largest in the s.c. group (157 +/- 49 g), moderate in the i.v. group (133 +/- 91 g), small in the p.o. group (96 +/- 54 g) and the smallest in the PMSF (phenylmethanesulfonyl fluoride, which was dosed to promote delayed neuropathy) group (80 +/- 49 g). In the untreated hens, the activity of NTE in both the cerebrum and cerebellum was higher than that in the midbrain (p < 0.01). There was no difference in NTE activity between the cerebrum and cerebellum. In both the cerebrum and midbrain, the inhibition of NTE activity in the p.o. group was less than that in the i.v. and s.c. groups, and no difference was found between the i.v. and s.c. groups. In the cerebellum, the inhibition of NTE activity in the s.c. group was larger than that in the i.v. and p.o. groups. These results indicate that the s.c. dosing of dipterex results in a stronger neurotoxicity compared to i.v. and p.o. dosing. However, it was difficult to induce the clinical signs of delayed neuropathy with any administration of dipterex in hens, even when the promotion of delayed neurotoxicity of dipterex was attempted with PMSF or double doses of dipterex itself.
ESTHER : Xie_1998_J.Toxicol.Sci_23_25
PubMedSearch : Xie_1998_J.Toxicol.Sci_23_25
PubMedID: 9513919

Title : Delayed neuropathy and inhibition of soluble neuropathy target esterase following the administration of organophosphorus compounds to hens - Tian_1998_Tohoku.J.Exp.Med_185_161
Author(s) : Tian Y , Xie XK , Piao FY , Yamauchi T
Ref : Tohoku J Exp Med , 185 :161 , 1998
Abstract : Delayed neuropathy and inhibition of soluble neuropathy target esterase (NTE) and acetylcholinesterase (AChE) activities in different regions of brain and spinal cord of adult hens were studied after the intravenous administration of leptophos (30 mg/kg), tri-o-cresyl phosphate (TOCP 40 mg/kg) or dipterex (200 mg/kg). The level of NTE activity varied according to the regions of the central nervous system (CNS) of the control (normal) hen, being higher in the cerebrum (74.1 micromol of phenyl valerate hydrolyzed/10 minutes/mg protein) and in the cerebellum (68.7), and lower in the spinal cord (44.5 in cervical, 55.6 in thoracic and 50.0 in lumbar cord). Hens given leptophos and TOCP demonstrated delayed neuropathy with obvious inhibition of NTE, but the times of onset and the degrees of peak inhibition of NTE activity were different: 6-24 hours after dosing and 73-82% of normal activity for leptophos, and 24-48 hours and 45-80% for TOCP, respectively. Furthermore, the average inhibition of NTE during 6-48 hours after dosing, (called here 'period average inhibition') was also significantly different between the leptophos group (63-73%) and TOCP group (40-64%). Hens given dipterex did not demonstrate delayed neuropathy, and had the least peak inhibition and period average inhibition of NTE activity among the 3 groups. Ratios of NTE inhibition/AChE inhibition were higher in the leptophos group (0.91-1.24) and TOCP group (1.13-2.45) than in the dipterex group (0.25-0.79). These results indicate that the distribution of NTE in the soluble fraction of membrane proteins is different in different regions of the CNS, and that the degree of peak inhibition of NTE activity and the time of onset of peak inhibition induced by organophosphorus compounds (OPs) also differ for different OPs. Thus, practical and useful NTE measurements should identify the peak inhibition and period inhibition in several nervous tissue regions.
ESTHER : Tian_1998_Tohoku.J.Exp.Med_185_161
PubMedSearch : Tian_1998_Tohoku.J.Exp.Med_185_161
PubMedID: 9823777

Title : Protective effect of pretreatment against the acute toxicity of formulated cyanofenphos in hens - Konno_1984_Tohoku.J.Exp.Med_142_155
Author(s) : Konno N , Yamauchi T , Yamaguchi Y , Fukushima M
Ref : Tohoku J Exp Med , 142 :155 , 1984
Abstract : Cyanofenphos (Surecide, O-ethyl O-4-cyanophenyl phenylphosphonothioate) is an organophosphorus pesticide. The protective effect against the near lethal dose, 140% the LD50, of formulated cyanofenphos developed in hens pretreated daily with a small dosage of 1.4% the LD50. The oral LD50 for formulated cyanofenphos was 700 mg/kg in the control hens and 1170 mg/kg in the hens pretreated with 10 mg/kg daily for 8 days. The length of the pretreatment period is important in inducing the protective effect. The protective action against 140% the LD50, 1,000 mg/kg, reached its maximum at approximately 24 hr after the last pretreatment. Pretreatment with 20 mg/kg daily for 8 days also acted as an antagonist for a challenge dose of 1,000 mg/kg. Three hours after a challenge dose of 400 mg/kg, brain acetylcholinesterase (AChE) activity was 0.14% delta pH/hr (17.6% of initial value) in hens pretreated with 10 mg/kg daily for 8 days and was 0.21 delta pH/hr (9.1% of initial value) in control hens, the difference being statistically significant (p less than 0.01). The protective effect of pretreatment against the acute toxicity of formulated cyanofenphos appears to be related to the fact that the formulation produced less inhibition of brain AChE activity in the pretreated hens than in the controls.
ESTHER : Konno_1984_Tohoku.J.Exp.Med_142_155
PubMedSearch : Konno_1984_Tohoku.J.Exp.Med_142_155
PubMedID: 6719451

Title : [Intensifying effect of repeated pretreatment for delayed neurotoxicity from organophosphorus insecticide cyanofenphos in hens] -
Author(s) : Yamauchi T , Konno N , Yamaguchi Y , Fukushima M
Ref : Nihon Eiseigaku Zasshi , 39 :611 , 1984
PubMedID: 6521033

Title : Protective effect of pretreatment against the anticholinesterase action of cyanofenphos -
Author(s) : Konno N , Yamauchi T , Yamaguchi Y , Fukushima M
Ref : Developments in Toxicology & Environmental Sciences , 11 :503 , 1983
PubMedID: 6677495