Saito M

References (20)

Title : Salivary leukocyte esterase activity by SillHa is a risk indicator of periodontal disease - Ishii_2023_BMC.Oral.Health_23_187
Author(s) : Ishii K , Venkataiah VS , Kajiwara T , Umezawa K , Suzuki S , Nakano M , Sawaguchi M , Yahata Y , Saito M
Ref : BMC Oral Health , 23 :187 , 2023
Abstract : BACKGROUND: There is increasing evidence that diagnostic salivary tests measuring inflammatory biomarkers are being developed to assess inflammatory status for early detection, prevention, and progression of periodontal disease. Therefore, the aim of the present study was to investigate and identify the salivary biomarker that can predict the inflammatory status of periodontal disease. METHODS: A total of 36 patients (28 women and 8 men) with an average age of 57 years were investigated. Unstimulated saliva was collected from the recruited subjects and analyzed using SillHa, a saliva-testing device that measures bacteria count, saliva buffer capacity, acidity, leukocyte esterase, protein, and ammonia. Periodontal parameters were then obtained by clinical examination and initial periodontal therapy was performed. Data obtained with SillHa were compared with clinical periodontal parameters at baseline, re-examination (three months from baseline), and final examination (six months from re-examination). RESULTS: Leukocyte esterase activity in saliva measured by SillHa; BOP and PCR measured by clinical examination showed a significant difference between baseline and final examination and between re-examination and final examination. Patients in the lower median group (group 1) had a significant difference in leukocyte esterase activity between baseline and final examination and re-examination and final examination. In addition, patients in Group 1 had significantly lower BOP between baseline and final examination. While patients in the higher median group (group 2) showed a modest decrease in leukocyte esterase activity, which was significant only between baseline and final examination, no significant changes were observed concerning BOP. Furthermore, the associated systemic disease was observed in 30% and 81.2% of group 1 and 2 patients, respectively. CONCLUSION: The results suggest that leukocyte esterase activity in saliva measured by SillHa could serve as a reliable diagnostic marker for monitoring inflammatory status in periodontal disease.
ESTHER : Ishii_2023_BMC.Oral.Health_23_187
PubMedSearch : Ishii_2023_BMC.Oral.Health_23_187
PubMedID: 36998066

Title : A Method for Isolation of Extracellular Vesicles and Characterization of Exosomes from Brain Extracellular Space - Perez-Gonzalez_2017_Methods.Mol.Biol_1545_139
Author(s) : Perez-Gonzalez R , Gauthier SA , Kumar A , Saito M , Levy E
Ref : Methods Mol Biol , 1545 :139 , 2017
Abstract : Extracellular vesicles (EV), including exosomes, secreted vesicles of endocytic origin, and microvesicles derived from the plasma membrane, have been widely isolated and characterized from conditioned culture media and bodily fluids. The difficulty in isolating EV from tissues, however, has hindered their study in vivo. Here, we describe a novel method designed to isolate EV and characterize exosomes from the extracellular space of brain tissues. The purification of EV is achieved by gentle dissociation of the tissue to free the brain extracellular space, followed by sequential low-speed centrifugations, filtration, and ultracentrifugations. To further purify EV from other extracellular components, they are separated on a sucrose step gradient. Characterization of the sucrose step gradient fractions by electron microscopy demonstrates that this method yields pure EV preparations free of large vesicles, subcellular organelles, or debris. The level of EV secretion and content are determined by assays for acetylcholinesterase activity and total protein estimation, and exosomal identification and protein content are analyzed by Western blot and immuno-electron microscopy. Additionally, we present here a method to delipidate EV in order to improve the resolution of downstream electrophoretic analysis of EV proteins.
ESTHER : Perez-Gonzalez_2017_Methods.Mol.Biol_1545_139
PubMedSearch : Perez-Gonzalez_2017_Methods.Mol.Biol_1545_139
PubMedID: 27943212

Title : Add-on therapy with anagliptin in Japanese patients with type-2 diabetes mellitus treated with metformin and miglitol can maintain higher concentrations of biologically active GLP-1\/total GIP and a lower concentration of leptin - Osonoi_2016_Peptides_86_118
Author(s) : Osonoi T , Saito M , Hariya N , Goto M , Mochizuki K
Ref : Peptides , 86 :118 , 2016
Abstract : Metformin, alpha-glucosidase inhibitors (alpha-GIs), and dipeptidyl peptidase 4 inhibitors (DPP-4Is) reduce hyperglycemia without excessive insulin secretion, and enhance postprandial plasma concentration of glucagon-like peptide-1 (GLP-1) in type-2 diabetes mellitus (T2DM) patients. We assessed add-on therapeutic effects of DPP-4I anagliptin in Japanese T2DM patients treated with metformin, an alpha-GI miglitol, or both drugs on postprandial responses of GLP-1 and glucose-dependent insulinotropic polypeptide (GIP), and on plasma concentration of the appetite-suppressing hormone leptin. Forty-two Japanese T2DM patients with inadequately controlled disease (HbA1c: 6.5%-8.0%) treated with metformin (n=14), miglitol (n=14) or a combination of the two drugs (n=14) received additional treatment with anagliptin (100mg, p.o., b.i.d.) for 52 weeks. We assessed glycemic control, postprandial responses of GLP-1 and glucose-dependent insulinotropic polypeptide (GIP), and on plasma concentration of leptin in those patients. Add-on therapy with anagliptin for 52 weeks improved glycemic control and increased the area under the curve of biologically active GLP-1 concentration without altering obesity indicators. Total GIP concentration at 52 weeks was reduced by add-on therapy in groups treated with miglitol compared with those treated with metformin. Add-on therapy reduced leptin concentrations. Add-on therapy with anagliptin in Japanese T2DM patients treated with metformin and miglitol for 52 weeks improved glycemic control and enhanced postprandial concentrations of active GLP-1/total GIP, and reduce the leptin concentration.
ESTHER : Osonoi_2016_Peptides_86_118
PubMedSearch : Osonoi_2016_Peptides_86_118
PubMedID: 27780736

Title : A new metabolism-related index correlates with the degree of liver fibrosis in hepatitis C virus-positive patients - Enomoto_2015_Gastroenterol.Res.Pract_2015_926169
Author(s) : Enomoto H , Aizawa N , Nakamura H , Takata R , Sakai Y , Iwata Y , Tanaka H , Ikeda N , Aoki T , Hasegawa K , Yoh K , Hashimoto K , Ishii A , Takashima T , Saito M , Imanishi H , Iijima H , Nishiguchi S
Ref : Gastroenterol Res Pract , 2015 :926169 , 2015
Abstract : Background. Only a few biomarkers based on metabolic parameters for evaluating liver fibrosis have been reported. The aim of this study was to investigate the relevance of an index obtained from three metabolic variables (glycated albumin: GA, glycated hemoglobin: HbA1c, and branched-chain amino acids to tyrosine ratio: BTR) to the degree of liver fibrosis in hepatitis C virus virus- (HCV-) positive patients. Methods. A total of 394 HCV-positive patients were assessed based on the values of a new index (GA/HbA1c/BTR). The index findings were used to investigate the relationship with the degree of liver fibrosis. Results. The new index showed an association with the stage of fibrosis (METAVIR scores: F0-1: 0.42 +/- 0.10, F2: 0.48 +/- 0.15, F3: 0.56 +/- 0.22, and F4: 0.71 +/- 0.30). The index was negatively correlated with three variables of liver function: the prothrombin time percentage (P < 0.0001), albumin level (P < 0.0001), and cholinesterase level (P < 0.0001). The new index showed a higher correlation related to liver function than FIB-4 and the APRI did. In addition, the index showed a higher AUROC value than that of FIB-4 and the APRI for prediction of liver cirrhosis. Conclusion. The new metabolism-related index, GA/HbA1c/BTR value, is shown to relate to the degree of liver fibrosis in HCV-positive patients.
ESTHER : Enomoto_2015_Gastroenterol.Res.Pract_2015_926169
PubMedSearch : Enomoto_2015_Gastroenterol.Res.Pract_2015_926169
PubMedID: 25861264

Title : An Increased Ratio of Glycated Albumin to HbA1c Is Associated with the Degree of Liver Fibrosis in Hepatitis B Virus-Positive Patients - Enomoto_2014_Gastroenterol.Res.Pract_2014_351396
Author(s) : Enomoto H , Aizawa N , Nakamura H , Sakai Y , Iwata Y , Tanaka H , Ikeda N , Aoki T , Yuri Y , Yoh K , Hashimoto K , Ishii A , Takashima T , Iwata K , Saito M , Imanishi H , Iijima H , Nishiguchi S
Ref : Gastroenterol Res Pract , 2014 :351396 , 2014
Abstract : Background. In hepatitis B virus- (HBV-) positive patients, the relationship between the metabolic variables and histological degree of liver fibrosis has been poorly investigated. Methods. A total of 176 HBV-positive patients were assessed in whom the ratios of glycated albumin-to-glycated hemoglobin (GA/HbA1c) were calculated in order to investigate the relationship with the degree of liver fibrosis. Results. The GA/HbA1c ratio increased in association with the severity of fibrosis (METAVIR scores: F0-1: 2.61 +/- 0.24, F2: 2.65 +/- 0.24, F3: 2.74 +/- 0.38, and F4: 2.91 +/- 0.63). The GA/HbA1c ratios were inversely correlated with four variables of liver function: the prothrombin time (PT) percentage (P < 0.0001), platelet count (P < 0.0001), albumin value (P < 0.0001), and cholinesterase value (P < 0.0001). The GA/HbA1c ratio was positively correlated with two well-known markers of liver fibrosis, FIB-4 (P < 0.0001) and the AST-to-platelet ratio index (APRI) (P < 0.0001). Furthermore, the GA/HbA1c showed better correlations with two variables of liver function (PT percentage and cholinesterase value) than did FIB-4 and with all four variables than did the APRI. Conclusion. The GA/HbA1c ratio is associated with the degree of liver fibrosis in HBV-positive patients.
ESTHER : Enomoto_2014_Gastroenterol.Res.Pract_2014_351396
PubMedSearch : Enomoto_2014_Gastroenterol.Res.Pract_2014_351396
PubMedID: 24693282

Title : Klebsormidium flaccidum genome reveals primary factors for plant terrestrial adaptation - Hori_2014_Nat.Commun_5_3978
Author(s) : Hori K , Maruyama F , Fujisawa T , Togashi T , Yamamoto N , Seo M , Sato S , Yamada T , Mori H , Tajima N , Moriyama T , Ikeuchi M , Watanabe M , Wada H , Kobayashi K , Saito M , Masuda T , Sasaki-Sekimoto Y , Mashiguchi K , Awai K , Shimojima M , Masuda S , Iwai M , Nobusawa T , Narise T , Kondo S , Saito H , Sato R , Murakawa M , Ihara Y , Oshima-Yamada Y , Ohtaka K , Satoh M , Sonobe K , Ishii M , Ohtani R , Kanamori-Sato M , Honoki R , Miyazaki D , Mochizuki H , Umetsu J , Higashi K , Shibata D , Kamiya Y , Sato N , Nakamura Y , Tabata S , Ida S , Kurokawa K , Ohta H
Ref : Nat Commun , 5 :3978 , 2014
Abstract : The colonization of land by plants was a key event in the evolution of life. Here we report the draft genome sequence of the filamentous terrestrial alga Klebsormidium flaccidum (Division Charophyta, Order Klebsormidiales) to elucidate the early transition step from aquatic algae to land plants. Comparison of the genome sequence with that of other algae and land plants demonstrate that K. flaccidum acquired many genes specific to land plants. We demonstrate that K. flaccidum indeed produces several plant hormones and homologues of some of the signalling intermediates required for hormone actions in higher plants. The K. flaccidum genome also encodes a primitive system to protect against the harmful effects of high-intensity light. The presence of these plant-related systems in K. flaccidum suggests that, during evolution, this alga acquired the fundamental machinery required for adaptation to terrestrial environments.
ESTHER : Hori_2014_Nat.Commun_5_3978
PubMedSearch : Hori_2014_Nat.Commun_5_3978
PubMedID: 24865297
Gene_locus related to this paper: kleni-a0a1y1i5c5 , kleni-a0a1y1i3f9 , kleni-a0a1y1hnk2 , kleni-a0a1y1hsz2 , kleni-a0a1y1hva2 , kleni-a0a1y1i2g3 , kleni-a0a1y1i4h5 , kleni-a0a1y1i9h9

Title : Possible involvement of brain prostaglandin E2 and prostanoid EP3 receptors in prostaglandin E2 glycerol ester-induced activation of central sympathetic outflow in the rat - Shimizu_2014_Neuropharmacol_82_19
Author(s) : Shimizu T , Tanaka K , Nakamura K , Taniuchi K , Yawata T , Higashi Y , Ueba T , Dimitriadis F , Shimizu S , Yokotani K , Saito M
Ref : Neuropharmacology , 82 :19 , 2014
Abstract : We recently reported that intracerebroventricularly administered 2-arachidonoylglycerol elevated plasma noradrenaline and adrenaline by brain monoacylglycerol lipase- (MGL) and cyclooxygenase-mediated mechanisms in the rat. These results suggest that 2-arachidonoylglycerol is hydrolyzed by MGL to free arachidonic acid, which is further metabolized to prostaglandins (PGs) by cyclooxygenase in the brain, thereby elevating plasma noradrenaline and adrenaline. On the other hand, 2-arachidonoylglycerol can be also metabolized by cyclooxygenase to PG glycerol esters (PG-Gs), which seems to be hydrolyzed by MGL to free PGs. Here, we examined the involvement of brain PG-Gs in the elevation of plasma noradrenaline and adrenaline regarding PGE2-G and prostanoid EP receptors using anesthetized male Wistar rats. Intracerebroventricularly administered PGE2-G (1.5 and 3 nmol/animal) dose-dependently elevated plasma noradrenaline but not adrenaline. PGE2-G also elevated systolic, mean and diastolic blood pressure and heart rate. The PGE2-G-induced elevation of plasma noradrenaline was attenuated by JZL184 (MGL inhibitor). Intracerebroventricularly administered PGE2 (0.3 and 1.5 nmol/animal) and sulprostone (0.1 and 0.3 nmol/animal) (EP1/EP3 agonist) also elevated plasma noradrenaline but not adrenaline in a dose-dependent manner. The sulprostone-induced elevation was attenuated by L-798,106 (EP3 antagonist), but not by SC-51322 (EP1 antagonist). L-798,106 also attenuated the PGE2-G- and PGE2-induced elevation of plasma noradrenaline, while PF-04418948 (EP2 antagonist) and L-161,982 (EP4 antagonist) had no effect on the PGE2-G-induced response. These results suggest a possibility that brain PGE2-G produced from 2-arachidonoylglycerol can be hydrolyzed to free PGE2, thereby activating central sympathetic outflow by brain prostanoid EP3 receptor-mediated mechanisms in the rat.
ESTHER : Shimizu_2014_Neuropharmacol_82_19
PubMedSearch : Shimizu_2014_Neuropharmacol_82_19
PubMedID: 24657150

Title : Brain RVD-haemopressin, a haemoglobin-derived peptide, inhibits bombesin-induced central activation of adrenomedullary outflow in the rat - Tanaka_2014_Br.J.Pharmacol_171_202
Author(s) : Tanaka K , Shimizu T , Yanagita T , Nemoto T , Nakamura K , Taniuchi K , Dimitriadis F , Yokotani K , Saito M
Ref : British Journal of Pharmacology , 171 :202 , 2014
Abstract : BACKGROUND AND PURPOSE: Haemopressin and RVD-haemopressin, derived from the haemoglobin alpha-chain, are bioactive peptides found in brain and are ligands for cannabinoid CB1 receptors. Activation of brain CB1 receptors inhibited the secretion of adrenal catecholamines (noradrenaline and adrenaline) induced by i.c.v. bombesin in the rat. Here, we investigated the effects of two haemoglobin-derived peptides on this bombesin-induced response EXPERIMENTAL APPROACH: Anaesthetised male Wistar rats were pretreated with either haemoglobin-derived peptide, given i.c.v., 30 min before i.c.v. bombesin and plasma catecholamines were subsequently measured electrochemically after HPLC. Direct effects of bombesin on secretion of adrenal catecholamines were examined using bovine adrenal chromaffin cells. Furthermore, activation of haemoglobin alpha-positive spinally projecting neurons in the rat hypothalamic paraventricular nucleus (PVN, a regulatory centre of central adrenomedullary outflow) after i.c.v. bombesin was assessed by immunohistochemical techniques. KEY
RESULTS: Bombesin given i.c.v. dose-dependently elevated plasma catecholamines whereas incubation with bombesin had no effect on spontaneous and nicotine-induced secretion of catecholamines from chromaffin cells. The bombesin-induced increase in catecholamines was inhibited by pretreatment with i.c.v. RVD-haemopressin (CB1 receptor agonist) but not after pretreatment with haemopressin (CB1 receptor inverse agonist). Bombesin activated haemoglobin alpha-positive spinally projecting neurons in the PVN. CONCLUSIONS AND IMPLICATIONS: The haemoglobin-derived peptide RVD-haemopressin in the brain plays an inhibitory role in bombesin-induced activation of central adrenomedullary outflow via brain CB1 receptors in the rat. These findings provide basic information for the therapeutic use of haemoglobin-derived peptides in the modulation of central adrenomedullary outflow.
ESTHER : Tanaka_2014_Br.J.Pharmacol_171_202
PubMedSearch : Tanaka_2014_Br.J.Pharmacol_171_202
PubMedID: 24138638

Title : Short-term effect of combined drug therapy and cognitive stimulation therapy on the cognitive function of Alzheimer's disease - Matsuda_2010_Psychogeriatrics_10_167
Author(s) : Matsuda O , Shido E , Hashikai A , Shibuya H , Kouno M , Hara C , Saito M
Ref : Psychogeriatrics , 10 :167 , 2010
Abstract : BACKGROUND: Acetylcholinesterase inhibitors (i.e. donepezil) are known to benefit Alzheimer's disease (AD) patients. However, the combined effects of acetylcholinesterase and cognitive stimulation therapy (CST) are still debated. The present study examined their combined effects on the progression of cognitive decline in AD. METHODS: The present study was a non-randomized controlled study and included two groups of patients with AD (i.e. CST group and control group). The CST group consisted of 31 patients with AD who received donepezil and weekly, 30-min CST sessions over the course of 7 weeks. The control group consisted of 18 patients who received only donepezil. Changes in cognitive abilities were assessed with Hasegawa's Dementia Scale-Revised (HDS-R) and were statistically analyzed by repeated-measure analysis of variance (anova). RESULTS: ANOVA showed a significant group x time interaction effect on the HDS-R score. HDS-R scores for the CST group increased significantly during the intervention period, whereas the scores for the control group did not increase. Differences between the means of pre- and post-test HDS-R scores were significantly different between the groups; scores were significantly higher for the CST group than the control group. The groups differed significantly in the proportion of subjects whose score increased by more than four points on the HDS-R (Fisher's exact test, P < 0.05; 8 patients (25.8%) in the CST group and none (0.0%) in the control group). CONCLUSIONS: These results suggest that CST is one of the important non-pharmacological treatment strategies for patients with AD.
ESTHER : Matsuda_2010_Psychogeriatrics_10_167
PubMedSearch : Matsuda_2010_Psychogeriatrics_10_167
PubMedID: 21159050

Title : Human carboxymethylenebutenolidase as a bioactivating hydrolase of olmesartan medoxomil in liver and intestine - Ishizuka_2010_J.Biol.Chem_285_11892
Author(s) : Ishizuka T , Fujimori I , Kato M , Noji-Sakikawa C , Saito M , Yoshigae Y , Kubota K , Kurihara A , Izumi T , Ikeda T , Okazaki O
Ref : Journal of Biological Chemistry , 285 :11892 , 2010
Abstract : Olmesartan medoxomil (OM) is a prodrug type angiotensin II type 1 receptor antagonist widely prescribed as an antihypertensive agent. Herein, we describe the identification and characterization of the OM bioactivating enzyme that hydrolyzes the prodrug and converts to its pharmacologically active metabolite olmesartan in human liver and intestine. The protein was purified from human liver cytosol by successive column chromatography and was identified by mass spectrometry to be a carboxymethylenebutenolidase (CMBL) homolog. Human CMBL, whose endogenous function has still not been reported, is a human homolog of Pseudomonas dienelactone hydrolase involved in the bacterial halocatechol degradation pathway. The ubiquitous expression of human CMBL gene transcript in various tissues was observed. The recombinant human CMBL expressed in mammalian cells was clearly shown to activate OM. By comparing the enzyme kinetics and chemical inhibition properties between the recombinant protein and human tissue preparations, CMBL was demonstrated to be the primary OM bioactivating enzyme in the liver and intestine. The recombinant CMBL also converted other prodrugs having the same ester structure as OM, faropenem medoxomil and lenampicillin, to their active metabolites. CMBL exhibited a unique sensitivity to chemical inhibitors, thus, being distinguishable from other known esterases. Site-directed mutagenesis on the putative active residue Cys(132) of the recombinant CMBL caused a drastic reduction of the OM-hydrolyzing activity. We report for the first time that CMBL serves as a key enzyme in the bioactivation of OM, hydrolyzing the ester bond of the prodrug type xenobiotics.
ESTHER : Ishizuka_2010_J.Biol.Chem_285_11892
PubMedSearch : Ishizuka_2010_J.Biol.Chem_285_11892
PubMedID: 20177059
Gene_locus related to this paper: human-CMBL

Title : Influence of carboxylesterase 2 genetic polymorphisms on mycophenolic acid pharmacokinetics in Japanese renal transplant recipients - Fujiyama_2009_Xenobiotica_39_407
Author(s) : Fujiyama N , Miura M , Satoh S , Inoue K , Kagaya H , Saito M , Habuchi T , Suzuki T
Ref : Xenobiotica , 39 :407 , 2009
Abstract : Mycophenolic acid (MPA), converted from the prodrug mycophenolate mofetil (MMF), is generated by intestinal and hepatic esterases. The role of carboxylesterase (CES) in MMF hydrolysis was examined in vitro using human liver microsomes. V(max) and K(m) values of MMF hydrolysis in pooled human liver microsomes were 1368 +/- 44 nmol min(-1) mg(-1) protein and 1030 +/- 65 microM, respectively. Hydrolytic activity was inhibited by the CES inhibitors phenylmethylsulfonylfluoride, bis-p-nitorophenylphosphate and diisopropylfluorophosphate, with IC(50) values of 77.1, 3.59 and 0.0312 microM, respectively. Eighty Japanese renal transplant recipients that received repeated-doses of MMF, tacrolimus and prednisolone,were evaluated for MPA pharmacokinetics 28 days after transplantation to investigate the relationship between MPA pharmacokinetics and CES2 genetic polymorphisms. No significant differences in MPA pharmacokinetics were observed between CES2 A4595G, C8721T orA-1548G genotype groups. CES2 allelic variants also did not appear to affect plasma MPA concentrations between individuals. In conclusion, the study demonstrated that while CES1 and/or CES2 are involved in the hydrolysis of MMF to MPA, CES2 allelic variants appeared to make only a minor contribution to inter-personal differences in MPA pharmacokinetics.
ESTHER : Fujiyama_2009_Xenobiotica_39_407
PubMedSearch : Fujiyama_2009_Xenobiotica_39_407
PubMedID: 19274604

Title : Saponins (Ginsenosides) from stems and leaves of Panax quinquefolium prevented high-fat diet-induced obesity in mice - Liu_2008_Phytomedicine_15_1140
Author(s) : Liu W , Zheng Y , Han L , Wang H , Saito M , Ling M , Kimura Y , Feng Y
Ref : Phytomedicine , 15 :1140 , 2008
Abstract : The present study was performed to clarify whether the crude saponins from stems and leaves of Panax quinquefolium inhibited lipase activity in vitro, and prevented obesity induced in mice by feeding a high-fat diet for 8 weeks. For in vitro experiments, assay for the inhibitory effects of saponins from stems and leaves of Panax quinquefolium on pancreatic lipase activity was performed by measuring the rate of release of oleic acid from triolein. For in vivo experiments, female ICR mice were fed a high-fat diet with or without saponins from stems and leaves of Panax quinquefolium for 8 weeks. The crude saponins inhibited pancreatic lipase activity in vitro. Furthermore, crude saponins (lg/kg body weight) inhibited the elevations of plasma triacylglycerol in rats administered the oral lipid emulsion tolerance test. In addition, long-term administration of crude saponins, the parametrial adipose tissue weight was decreased by feeding a high-fat diet containing l% or 3% crude saponins compared to those of high-fat diet group. It is demonstrated that the anti-obesity effects of the crude saponins from stems and leaves of Panax quinquefolium in high-fat diet-treated mice may be due to the inhibition of intestinal absorption of dietary fat by ginsenosides Rc, Rb(1) and Rb(2).
ESTHER : Liu_2008_Phytomedicine_15_1140
PubMedSearch : Liu_2008_Phytomedicine_15_1140
PubMedID: 18768305

Title : A novel complex deletion-insertion mutation mediated by Alu repetitive elements leads to lipoprotein lipase deficiency - Okubo_2007_Mol.Genet.Metab_92_229
Author(s) : Okubo M , Horinishi A , Saito M , Ebara T , Endo Y , Kaku K , Murase T , Eto M
Ref : Mol Genet Metab , 92 :229 , 2007
Abstract : Lipoprotein lipase (LPL) deficiency is a rare autosomal recessive inherited disorder, characterized by marked hypertriglyceridemia, eruptive xanthoma, hepatosplenomegaly, recurrent attacks of pancreatitis, and markedly low or absent LPL activity in postheparin plasma. A majority of LPL deficient patients have been reported to have point mutations in the LPL gene; however, we find a complex deletion-insertion mutation by Alu elements, mobile retrotransposons, in a patient with LPL deficiency. This patient suffered from acute pancreatitis, showed chylomicronemia and lacked detectable LPL activity or mass in her postheparin plasma. Southern blot analysis and long-range PCR of the patient's DNA demonstrated a 2.2-kb deletion encompassing exon 2. Sequence analysis revealed (1) a 2.3-kb deletion between an AT-rich region adjacent to an Alu element in intron 1 and another Alu element in intron 2; (2) an insertion of approximately 150bp 5'-truncated Alu sequence with a poly (A) tail at the deletion point. The inserted sequence belongs to Alu Yb9, the youngest subfamily of Alu elements. The deletion occurred at the consensus cleavage site (3'-A|TTTT-5') without target site duplication. These findings indicated that Alu retrotransposition caused the complex deletion-insertion. The patient was homozygous for this complex mutation, which eliminates exon 2 and leads to LPL deficiency. To our knowledge, the patient is the first case with LPL deficiency due to a complex deletion-insertion mediated by Alu repetitive elements.
ESTHER : Okubo_2007_Mol.Genet.Metab_92_229
PubMedSearch : Okubo_2007_Mol.Genet.Metab_92_229
PubMedID: 17706445

Title : Sequence analysis of three plasmids harboured in Rhodococcus erythropolis strain PR4 - Sekine_2006_Environ.Microbiol_8_334
Author(s) : Sekine M , Tanikawa S , Omata S , Saito M , Fujisawa T , Tsukatani N , Tajima T , Sekigawa T , Kosugi H , Matsuo Y , Nishiko R , Imamura K , Ito M , Narita H , Tago S , Fujita N , Harayama S
Ref : Environ Microbiol , 8 :334 , 2006
Abstract : Rhodococcus erythropolis strain PR4 has been isolated as an alkane-degrading bacterium. The strain harbours one linear plasmid, pREL1 (271 577 bp) and two circular plasmids, pREC1 (104 014 bp) and pREC2 (3637 bp), all with some sequence similarities to other Rhodococcus plasmids. For pREL1, pREC1 and pREC2, 298, 102 and 3 open reading frames, respectively, were predicted. Linear plasmid pREL1 has several regions homologous to plasmid pBD2 found in R. erythropolis BD2. Sequence analysis of pREL1 and pBD2 identified common metal-resistance genes on both, but pREL1 also encodes alkane-degradation genes not found on pBD2, with enzyme constituents some of which are quite different from those of other organisms. The alkane hydroxylase consisted of a cytochrome P450 monooxygenase, a 2Fe-2S ferredoxin, and a ferredoxin reductase. The ferredoxin reductase amino acid sequence resembles the AlkT (rubredoxin reductase) sequence. A zinc-containing alcohol dehydrogenase further oxydizes alkanols, alkane oxidation products catalysed by alkane hydroxylase. Of the circular plasmids, the pREC1 sequence is partially similar to the sequence of pREAT701, the virulence plasmid found in Rhodococcus equi. pREC1 has no pREAT701 virulence genes and encodes genes for beta-oxidation of fatty acids. Thus, joint actions of enzymes encoded by pREL1 and pREC1 may enable efficient mineralization of alkanes.
ESTHER : Sekine_2006_Environ.Microbiol_8_334
PubMedSearch : Sekine_2006_Environ.Microbiol_8_334
PubMedID: 16423019
Gene_locus related to this paper: rhosp-AHY95170 , rhoe4-c0zm41 , rhoe4-c0zny8 , rhoe4-c0zp51 , rhoe4-c0zp80 , rhoe4-c0zpm5 , rhoe4-c0zq56 , rhoe4-c0zq93 , rhoe4-c0zri5 , rhoe4-c0zse4 , rhoe4-c0ztk5 , rhoe4-c0ztv6 , rhoe4-c0ztz5 , rhoe4-c0zw14 , rhoe4-c0zyp1 , rhoe4-c1a1s7 , rhoe4-c1a149 , rhoe4-c1a168 , rhoe4-q3l9i4 , rhoe4-q3l9v3 , rhoe4-q3l9y4 , rhoe4-q3l922 , rhoe4-q3la05 , rhoer-c3jd87 , rhoer-c3jdh1 , rhoer-c3jfg3 , rhoer-c3jfu1 , rhoer-c3jfv6 , rhoer-c3jfw7 , rhoer-c3jg26 , rhoer-c3jgc0 , rhoer-c3jgr8 , rhoer-c3ji24 , rhoer-c3jif3 , rhoer-c3jif5 , rhoer-c3jif6 , rhoer-c3jiw5 , rhoer-c3jl72 , rhoer-c3jle6 , rhoer-c3jmu4 , rhoer-c3jqd8 , rhoer-c3jqd9 , rhoer-c3jqg3 , rhoer-c3jqn9 , rhoer-c3jqs1 , rhoer-c3jr01 , rhoer-c3jrb8 , rhoer-c3jt01 , rhoer-c3jtx3 , rhoer-c3jtx4 , rhoer-c3jvx6 , rhoer-c3jwe1 , rhoer-c3jwn8 , rhosp-bphD2 , rhoe4-c0zua7

Title : Effects of ketamine on neostigmine-induced contractile and phosphatidylinositol responses of the rat trachea - Saito_2003_J.Anesth_17_104
Author(s) : Saito M , Shibata O , Yamaguchi M , Miyoshi H , Makita T , Sumikawa K
Ref : J Anesth , 17 :104 , 2003
Abstract : PURPOSE: Neostigmine causes airway smooth muscle contraction through the direct stimulation of muscarinic receptors and the activation of phosphatidylinositol (PI) responses. Ketamine attenuates airway smooth muscle contraction. It is not clear whether ketamine attenuates neostigmine-induced airway smooth muscle contraction by inhibiting the PI response. This study was designed to examine the effects of ketamine on neostigmine-induced contractile and PI responses of the rat trachea.
METHODS: Thirty male Wistar rats weighing 250-350 g were used. In the experiment on the contractile response, active contraction was induced with 1 microM neostigmine in the presence or absence of ketamine. In the experiment on the phosphatidylinositol response, the trachea slices were incubated with [3H]myo-inositol, 1 microM neostigmine, or 100 microM aluminum fluoride, and ketamine. The formation of [3H]inositol monophosphate (IP1), a degradation product of the phosphatidylinositol response, was measured with a liquid scintillation counter. Statistical significance (P < 0.05) was determined by analysis of variance.
RESULTS: Neostigmine 1 microM caused tracheal ring contraction. This contraction was attenuated by ketamine dose-dependently and reached resting tension at 100 microM. Neostigmine- and aluminum fluoride-induced IP1, accumulation was also attenuated by ketamine. CONCLUSION: The results suggest that ketamine attenuates neostigmine-induced contractile responses, at least in part, through the inhibition of phospholipase C coupled with G protein in the PI response.
ESTHER : Saito_2003_J.Anesth_17_104
PubMedSearch : Saito_2003_J.Anesth_17_104
PubMedID: 12903921

Title : Differences in incision shape based on the keratome bevel - Akura_2001_J.Cataract.Refract.Surg_27_761
Author(s) : Akura J , Funakoshi T , Kadonosono K , Saito M
Ref : J Cataract Refract Surg , 27 :761 , 2001
Abstract : PURPOSE: To evaluate differences in incision shape due to the bevel of the keratome. SETTING: Kushimoto Rehabilitation Center, Kushimoto, Japan.
METHODS: Three types of keratomes (bibevel, bevel up, and bevel down) were inserted into soft polyvinyl chloride sheets and polyurethane sheets, and the incision shapes in the blade entrance and exit planes were evaluated. The experiments were repeated using soft polyvinyl chloride domes and silicone domes.
RESULTS: In the experiments using artificial sheets, the incisions in the blade entrance and exit planes using the bibevel keratome had a linear shape, those using the bevel-up keratome had an inverse-V shape, and those using the bevel-down keratome had a V shape. In the experiments using artificial domes, the incision shapes were the same as those in the artificial sheets.
CONCLUSIONS: The incision shape differed according to the direction of the keratome bevel. These experiments and results may provide useful data when new knives are developed or when incision shapes following intended specifications are stably made.
ESTHER : Akura_2001_J.Cataract.Refract.Surg_27_761
PubMedSearch : Akura_2001_J.Cataract.Refract.Surg_27_761
PubMedID: 11377909

Title : Toluene inhalation induced epididymal sperm dysfunction in rats - Ono_1999_Toxicology_139_193
Author(s) : Ono A , Kawashima K , Sekita K , Hirose A , Ogawa Y , Saito M , Naito K , Yasuhara K , Kaneko T , Furuya T , Inoue T , Kurokawa Y
Ref : Toxicology , 139 :193 , 1999
Abstract : Toluene is a widely abused inhaled solvent. This study was designed to determine whether toluene abuse affects the reproductive functions or general health of males. Seven-week-old male Sprague-Dawley rats were exposed to toluene vapor inhalation (0, 4000, or 6000 ppm; 2 h/day) daily for 5 weeks. Exposure-related suppression of body weight gain and food consumption were observed. Salivation and lacrimation were observed during exposure periods and intensified with repeated exposure. Rats exposed to 6000 ppm toluene had decreased spleen and thymus weights, as well as suppressed lymphocyte counts. In 6000 ppm group, the epididymal sperm counts, sperm motility, sperm quality and in vitro penetrating ability to zona-free hamster eggs were significantly reduced, while no exposure-related changes in the testes weight or spermatogenesis within testes were detected. Tail-less sperm heads were seen within zona-free eggs incubated with sperm from rats exposed to 6000 ppm toluene, but not control rats. No significant changes were observed in serum luteinizing hormone, follicle-stimulating hormone, or testosterone levels following 1 month of exposure to 6000 ppm toluene. These results indicate that high concentrations of toluene may directly target sperm in the epididymis and disrupt sperm maturation.
ESTHER : Ono_1999_Toxicology_139_193
PubMedSearch : Ono_1999_Toxicology_139_193
PubMedID: 10647920

Title : Degradation of bradykinin in human urine by carboxypeptidase Y-like exopeptidase and neutral endopeptidase and their inhibition by ebelactone B and phosphoramidon - Saito_1995_Int.J.Tissue.React_17_181
Author(s) : Saito M , Majima M , Katori M , Sanjou Y , Suyama I , Shiokawa H , Koshiba K , Aoyagi T
Ref : Int J Tissue React , 17 :181 , 1995
Abstract : Incubation of bradykinin with human urine resulted in a successive degradation of bradykinin-(1-8), bradykinin-(1-7), bradykinin-(1-6), and bradykinin-(1-5). Although D,L-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid (100 microM) and captopril (100 microM) did not have any significant effect on bradykinin degradation in human urine, the neutral endopeptidase inhibitor phosphoramidon (100 microM), a carboxypeptidase Y-like exopeptidase inhibitor ebelactone B (100 microM), and o-phenanthroline (100 microM) significantly inhibited bradykinin degradation by 36%, 38% and 48% respectively. The combination of phosphoramidon and ebelactone B completely (by 95%) inhibited bradykinin degradation in human urine. At pH 5, bradykinin degradation was performed by carboxypeptidase Y-like exopeptidase; at pH 7, this degradation was performed by neutral endopeptidase in addition to carboxypeptidase Y-like exopeptidase. From these results, it can be concluded that carboxypeptidase Y-like exopeptidase and/or neutral endopeptidase certainly have a role in kinin degradation in human urine under neutral and acid pH conditions.
ESTHER : Saito_1995_Int.J.Tissue.React_17_181
PubMedSearch : Saito_1995_Int.J.Tissue.React_17_181
PubMedID: 8835628

Title : Metabolism of choline in brain of the aged CBF-1 mouse - Saito_1986_J.Neurosci.Res_15_197
Author(s) : Saito M , Kindel G , Karczmar AG , Rosenberg A
Ref : Journal of Neuroscience Research , 15 :197 , 1986
Abstract : In order to quantify the changes that occur in the cholinergic central nervous system with aging, we have compared acetylcholine (Ach) formation in brain cortex slice preparations from 2-year-old aged CBF-1 mouse brains and compared the findings with those in 2-4-month-old young adult mouse brain slices. Incorporation of exogenous radioactively labelled choline (31 nM [3H] choline) into acetyl choline in incubated brain slices was linear with time for 90 min. Percentage of total choline label distributed into Ach remained constant from 5 min after starting the incubation to 90 min. In contrast, distribution of label into intracellular free choline (Ch) and phosphorylcholine (Pch) changed continuously over this period suggesting that the Ch pool for Ach synthesis in brain cortex is different from that for Pch synthesis. Incorporation of radioactivity into Ach was not influenced by administration of 10 microM eserine, showing that the increment of radioactivity in Ach reflects rate of Ach formation, independently from degradation by acetylcholine esterases. Under our experimental conditions, slices from cortices of aged 24-month-old mouse brain showed a significantly greater (27%) incorporation of radioactivity into intracellular Ach than those from young, 2-4-month-old, brain cortices. Inhibitors of Ach release, 1 mM ATP or GABA, had no effect. Since concentration of radioactive precursor in the incubation medium was very low (31 nM), the Ch pool for Ach synthesis in slices was labelled without measurably changing the size of the endogenous pool. These data suggest a compensatory acceleration of Ach synthesis or else a smaller precursor pool specific for Ach synthesis into which labelled Ch migrated in aged brain.(ABSTRACT TRUNCATED AT 250 WORDS)
ESTHER : Saito_1986_J.Neurosci.Res_15_197
PubMedSearch : Saito_1986_J.Neurosci.Res_15_197
PubMedID: 3959130

Title : Decreased sodium influx and abnormal red cell membrane lipids in a patient with familial plasma lecithin: cholesterol acyltransferase deficiency - Murayama_1984_Am.J.Hematol_16_129
Author(s) : Murayama N , Asano Y , Hosoda S , Maesawa M , Saito M , Takaku F , Sugihara T , Miyashima K , Yawata Y
Ref : Am J Hematol , 16 :129 , 1984
Abstract : Red cell membrane metabolism in familial lecithin:cholesterol acyltransferase (LCAT) deficiency was investigated. The family presented here is the third case discovered in Japan. An increase of free cholesterol was observed in the red cell membranes, concomitant with increased phosphatidyl choline. Osmotic fragility of the patient's red cells was diminished rather than increased. Red cell survival (51Cr T1/2) was shortened (15 days). Sodium influx was markedly decreased, although sodium efflux, both ouabain-sensitive and ouabain-insensitive, was normal. The activity of acetyl-cholinesterase as a marker of the outer leaflet of the red cell membranes was decreased, while the activity of glyceraldehyde-3-phosphate dehydrogenase as a marker of the inner leaflet was normal. No abnormalities of adenosine triphosphatases in red cell membranes were observed. These results suggest that the alteration of cholesterol metabolism in the plasma of LCAT deficiency increases the red cell membrane cholesterol and affects the functions of the red cell membranes, especially of the outer leaflet, which may result in decreased sodium influx.
ESTHER : Murayama_1984_Am.J.Hematol_16_129
PubMedSearch : Murayama_1984_Am.J.Hematol_16_129
PubMedID: 6695915