Murakami T

References (8)

Title : Clinical impact of diarrhea during enteral feeding after esophagectomy - Haneda_2023_Int.J.Clin.Oncol__
Author(s) : Haneda R , Hiramatsu Y , Kawata S , Soneda W , Booka E , Murakami T , Matsumoto T , Morita Y , Kikuchi H , Takeuchi H
Ref : Int J Clin Oncol , : , 2023
Abstract : BACKGROUND: Enteral feeding (EF) is recommended to enhance nutritional status after esophagectomy; however, diarrhea is a common complication of EF. We investigated the clinical and prognostic impact of diarrhea during EF after esophagectomy. METHODS: One hundred and fifty-two patients who underwent transthoracic esophagectomy were enrolled. The King's stool chart was used for stool characterization. The short- and long-term outcomes were compared between a non-diarrhea (Group N) and diarrhea group (Group D). RESULTS: A higher dysphagia score (<= 1) was observed more frequently in Group D than in Group N (45.7% vs. 19.8%, p = 0.002). Deterioration of serum total protein, serum albumin, serum cholinesterase, and the prognostic nutritional index after esophagectomy was greater in Group D than in Group N (p = 0.003, 0.004, 0.014, and 0.001, respectively). Patients in Group D had significantly worse overall survival (OS) and recurrence-free survival (RFS) than those in Group N (median survival time (MST): OS, 21.9 vs. 30.6 months, p = 0.001; RFS, 12.4 vs. 27.7 months, p < 0.001). In stratified analysis due to age, although there was no difference in OS with or without diarrhea in young patients (MST: 24.1 months in a diarrhea group vs. 33.6 months in a non-diarrhea group, p = 0.218), patients in a diarrhea group had significantly worse OS than those in a non-diarrhea group in elderly patients (MST: 17.8 months vs. 27.9 months, p < 0.001). CONCLUSIONS: Diarrhea during EF can put elderly patients at risk of postoperative malnutrition and a poor prognosis after esophagectomy.
ESTHER : Haneda_2023_Int.J.Clin.Oncol__
PubMedSearch : Haneda_2023_Int.J.Clin.Oncol__
PubMedID: 37994975

Title : Identification of PSD-95 Depalmitoylating Enzymes - Yokoi_2016_J.Neurosci_36_6431
Author(s) : Yokoi N , Fukata Y , Sekiya A , Murakami T , Kobayashi K , Fukata M
Ref : Journal of Neuroscience , 36 :6431 , 2016
Abstract : Postsynaptic density (PSD)-95, the most abundant postsynaptic scaffolding protein, plays a pivotal role in synapse development and function. Continuous palmitoylation cycles on PSD-95 are essential for its synaptic clustering and regulation of AMPA receptor function. However, molecular mechanisms for palmitate cycling on PSD-95 remain incompletely understood, as PSD-95 depalmitoylating enzymes remain unknown. Here, we isolated 38 mouse or rat serine hydrolases and found that a subset specifically depalmitoylated PSD-95 in heterologous cells. These enzymes showed distinct substrate specificity. alpha/beta-Hydrolase domain-containing protein 17 members (ABHD17A, 17B, and 17C), showing the strongest depalmitoylating activity to PSD-95, showed different localization from other candidates in rat hippocampal neurons, and were distributed to recycling endosomes, the dendritic plasma membrane, and the synaptic fraction. Expression of ABHD17 in neurons selectively reduced PSD-95 palmitoylation and synaptic clustering of PSD-95 and AMPA receptors. Furthermore, taking advantage of the acyl-PEGyl exchange gel shift (APEGS) method, we quantitatively monitored the palmitoylation stoichiometry and the depalmitoylation kinetics of representative synaptic proteins, PSD-95, GluA1, GluN2A, mGluR5, Galphaq, and HRas. Unexpectedly, palmitate on all of them did not turn over in neurons. Uniquely, most of the PSD-95 population underwent rapid palmitoylation cycles, and palmitate cycling on PSD-95 decelerated accompanied by its increased stoichiometry as synapses developed, probably contributing to postsynaptic receptor consolidation. Finally, inhibition of ABHD17 expression dramatically delayed the kinetics of PSD-95 depalmitoylation. This study suggests that local palmitoylation machinery composed of synaptic DHHC palmitoylating enzymes and ABHD17 finely controls the amount of synaptic PSD-95 and synaptic function. SIGNIFICANCE STATEMENT: Protein palmitoylation, the most common lipid modification, dynamically regulates neuronal protein localization and function. Its unique reversibility is conferred by DHHC-type palmitoyl acyl transferases (palmitoylating enzymes) and still controversial palmitoyl-protein thioesterases (depalmitoylating enzymes). Here, we identified the membrane-anchored serine hydrolases, ABHD17A, 17B, and 17C, as the physiological PSD-95 depalmitoylating enzymes that regulate PSD-95 palmitoylation cycles in neurons. This study describes the first direct evidence for the neuronal depalmitoylating enzyme and provides a new aspect of the dynamic regulatory mechanisms of synaptic development and synaptic plasticity. In addition, our established APEGS assay, which provides unbiased and quantitative information about the palmitoylation state and dynamics, revealed the distinct regulatory mechanisms for synaptic palmitoylation.
ESTHER : Yokoi_2016_J.Neurosci_36_6431
PubMedSearch : Yokoi_2016_J.Neurosci_36_6431
PubMedID: 27307232
Gene_locus related to this paper: human-ABHD17A , human-ABHD17B , human-ABHD17C , rat-ab17c

Title : [Treatment approach to congenital myasthenic syndrome in a patient with acetylcholine receptor deficiency] - Ishigaki_2009_No.To.Hattatsu_41_37
Author(s) : Ishigaki K , Murakami T , Ito Y , Yanagisawa A , Kodaira K , Shishikura K , Suzuki H , Hirayama Y , Osawa M
Ref : No To Hattatsu , 41 :37 , 2009
Abstract : Congenital myasthenic syndromes (CMS) are rare heterogeneous disorders of neurotransmission caused by genetic defects of neuromuscular junction molecules. While CMS patients have been reported worldwide, in Japan there have been only a few descriptions of adult CMS patients with acetylcholinesterase (AChE) deficiency and slow channel syndrome. Herein, we report a Japanese CMS patient with acetylcholine receptor (AChR) deficiency, diagnosed during childhood, and our treatment approach to the patient. This 13-year-old Japanese boy had had severe myasthenic symptoms since infancy. Ptosis, his first symptom, appeared at 5 months and nasal voice was recognized at 2 years of age. AchR and anti-muscle-specific tyrosine kinase (Musk) antibody remained negative. A positive tensilon test and decremental response on electromyogram supported the diagnosis of sero-negative myasthenia gravis. Despite thymectomy and strong immunosuppressive therapy including steroid pulse and FK 506, he gradually deteriorated and became wheelchair bound. Genetic analyses for AchR, Rapsyn, Musk and AChE were negative. At age 11 years, a muscle biopsy was performed in the deltoid muscle for neuromuscular junction sampling. Electron microscopic and confocal microscopic analysis of endplates showed almost complete loss of AChR and the diagnosis of CMS with AChR deficiency was confirmed. All immunosuppressive therapies were discontinued. Instead, we started Ubretide and 3,4-diaminopyridine (DAP) after obtaining informed consent. Although not approved in Japan for this use, 3,4-DAP is reportedly effective in refractory cases of CMS. The patient experienced no side effects. Despite all of the objective data were improving, his subjective symptoms and ADL remained poor. There are still many challenges in the treatment of the patient.
ESTHER : Ishigaki_2009_No.To.Hattatsu_41_37
PubMedSearch : Ishigaki_2009_No.To.Hattatsu_41_37
PubMedID: 19172815

Title : Genome sequence of the cat pathogen, Chlamydophila felis - Azuma_2006_DNA.Res_13_15
Author(s) : Azuma Y , Hirakawa H , Yamashita A , Cai Y , Rahman MA , Suzuki H , Mitaku S , Toh H , Goto S , Murakami T , Sugi K , Hayashi H , Fukushi H , Hattori M , Kuhara S , Shirai M
Ref : DNA Research , 13 :15 , 2006
Abstract : Chlamydophila felis (Chlamydia psittaci feline pneumonitis agent) is a worldwide spread pathogen for pneumonia and conjunctivitis in cats. Herein, we determined the entire genomic DNA sequence of the Japanese C. felis strain Fe/C-56 to understand the mechanism of diseases caused by this pathogen. The C. felis genome is composed of a circular 1,166,239 bp chromosome encoding 1005 protein-coding genes and a 7552 bp circular plasmid. Comparison of C. felis gene contents with other Chlamydia species shows that 795 genes are common in the family Chlamydiaceae species and 47 genes are specific to C. felis. Phylogenetic analysis of the common genes reveals that most of the orthologue sets exhibit a similar divergent pattern but 14 C. felis genes accumulate more mutations, implicating that these genes may be involved in the evolutional adaptation to the C. felis-specific niche. Gene distribution and orthologue analyses reveal that two distinctive regions, i.e. the plasticity zone and frequently gene-translocated regions (FGRs), may play important but different roles for chlamydial genome evolution. The genomic DNA sequence of C. felis provides information for comprehension of diseases and elucidation of the chlamydial evolution.
ESTHER : Azuma_2006_DNA.Res_13_15
PubMedSearch : Azuma_2006_DNA.Res_13_15
PubMedID: 16766509
Gene_locus related to this paper: chlff-q253e0 , chlff-q254l8

Title : Measurement of the serum lipoprotein lipase concentration is useful for studying triglyceride metabolism: Comparison with postheparin plasma - Hirano_2004_Metabolism_53_526
Author(s) : Hirano T , Nishioka F , Murakami T
Ref : Metabolism , 53 :526 , 2004
Abstract : The catalytically inactive form of lipoprotein lipase (LPL) is detectable at high levels in serum, although its physiologic role remains unknown. The aim of this study was to elucidate the clinical significance of serum LPL compared with postheparin LPL or the net increment (Delta) of LPL (postheparin - preheparin LPL). We measured the LPL mass before and 15 minutes after the injection of heparin in 164 subjects with hyperlipidemia. LPL mass was measured by a sensitive sandwich enzyme-linked immunosorbent assay (ELISA). Serum LPL was one fifth of the postheparin LPL concentration. There was a weak correlation between the serum LPL and postheparin LPL concentrations (r =.225, P </=.005). The Delta LPL concentration was strongly related to the postheparin LPL concentration (r =.965, P </=.0001), but not to the preheparin LPL mass, suggesting that the weak correlation between serum LPL and postheparin LPL levels was attributable to contamination of postheparin plasma by pre-existing LPL (preheparin LPL). Both serum and postheparin LPL were significantly lower in diabetic patients and in subjects with high levels of triglyceride or low levels of high-density lipoprotein (HDL). Serum LPL was correlated negatively with triglyceride, remnants, and insulin resistance and was positively correlated with HDL cholesterol and low-density lipoprotein (LDL) size. Postheparin LPL was strongly correlated with HDL cholesterol, but not with other parameters, as was serum LPL. Delta LPL mass did not show a closer association with triglyceride metabolism than postheparin LPL or preheparin LPL. In conclusion, serum LPL measurement is simple and seems to be useful for studying triglyceride metabolism.
ESTHER : Hirano_2004_Metabolism_53_526
PubMedSearch : Hirano_2004_Metabolism_53_526
PubMedID: 15045703

Title : Effects of carbamazepine on acetylcholine release and metabolism - Mizuno_2000_Epilepsy.Res_40_187
Author(s) : Mizuno K , Okada M , Murakami T , Kamata A , Zhu G , Kawata Y , Wada K , Kaneko S
Ref : Epilepsy Research , 40 :187 , 2000
Abstract : To clarify the mechanisms of action of carbamazepine (CBZ), we investigated the effects of CBZ on acetylcholine (ACh) release and metabolism in rat striatum and hippocampus. Acute administration of effective dose of CBZ (25 mg/kg) increased both striatal and hippocampal extracellular levels of ACh, whereas a supraeffective dose of CBZ (50 mg/kg) did not affect the levels and a toxic dose of CBZ (100 mg/kg) decreased the extracellular ACh levels in both brain regions. Both acute and chronic administrations of CBZ (25 and 50 mg/kg, mg/kg per day) increased intracellular ACh levels in striatum and hippocampus. The striatal intracellular ACh levels were decreased by both acute and chronic administrations of CBZ (100 mg/kg, mg/kg per day), whereas the hippocampal intracellular ACh levels were not affected. The effective CBZ concentration did not affect cholinesterase activity, whereas supraeffective CBZ concentration reduced it weakly. Effective dose of CBZ enhanced ACh release and synthesis; however, supraeffective doses of CBZ reduced ACh release and synthesis without enhancement of ACh degradation, indicating that CBZ has biphasic effects on ACh release and synthesis. Thus, the present findings, the slight stimulation of ACh function by effective dose of CBZ, are involved, at least partially, in the antiepileptic and mood stabilizing mechanisms of action of CBZ.
ESTHER : Mizuno_2000_Epilepsy.Res_40_187
PubMedSearch : Mizuno_2000_Epilepsy.Res_40_187
PubMedID: 10863146

Title : A Japanese patient with lipoprotein lipase deficiency homozygous for the Gly188Glu mutation prevalent worldwide - Yoshida_2000_J.Atheroscler.Thromb_7_45
Author(s) : Yoshida T , Gotoda T , Okubo M , Iizuka Y , Ishibashi S , Kojima T , Murakami T , Murase T , Yamada N
Ref : J Atheroscler Thromb , 7 :45 , 2000
Abstract : We studied the molecular basis of familial lipoprotein lipase (LPL) deficiency in a new Japanese kindred. The proband was a four-month-old infant with severe hyperchylomicronemia. In postheparin plasma, LPL activity was virtually absent, although LPL mass was detectable. Single strand conformational polymorphism (SSCP) analysis showed an abnormal band with exon 5 of the LPL gene that was amplified by PCR from the proband's genomic DNA. DNA sequence analysis of the amplified fragment demonstrated that the proband was homozygous for a G-to-A change at nucleotide position 818 resulting in the substitution of glutamic acid for glycine at codon 188. Although this is among the first Gly188Glu mutations identified in Japanese, the missense mutation has previously been reported as a prevalent cause of familial LPL deficiency worldwide and has been proposed to have a common origin. However, DNA haplotype analysis with either restriction fragment length polymorphism (RFLP) or microsatellite markers revealed that the DNA haplotype of the proband was not identical to the haplotype previously reported as common to the other patients with the Gly188Glu mutation. These results add the Gly188Glu mutation to the growing list of LPL gene mutations underlying familial LPL deficiency in Japanese and indicate that the origin of the Gly188Glu mutation is not necessarily common but would be multicentric at least in part.
ESTHER : Yoshida_2000_J.Atheroscler.Thromb_7_45
PubMedSearch : Yoshida_2000_J.Atheroscler.Thromb_7_45
PubMedID: 11425044
Gene_locus related to this paper: human-LPL

Title : Developmental regulation of zebrafish MyoD in wild-type, no tail and spadetail embryos - Weinberg_1996_Development_122_271
Author(s) : Weinberg ES , Allende ML , Kelly CS , Abdelhamid A , Murakami T , Andermann P , Doerre OG , Grunwald DJ , Riggleman B
Ref : Development , 122 :271 , 1996
Abstract : We describe the isolation of the zebrafish MyoD gene and its expression in wild-type embryos and in two mutants with altered somite development, no tail (ntl) and spadetail (spt). In the wild-type embryo, MyoD expression first occurs in an early phase, extending from mid-gastrula to just prior to somite formation, in which cells directly adjacent to the axial mesoderm express the gene. In subsequent phases, during the anterior-to-posterior wave of somite formation and maturation, expression occurs within particular regions of each somite. In spt embryos, which lack normal paraxial mesoderm due to incorrect cell migration, early MyoD expression is not observed and transcripts are instead first detected in small groups of trunk cells that will develop into aberrant myotomal-like structures. In ntl embryos, which lack notochords and tails, the early phase of MyoD expression is also absent. However, the later phase of expression within the developing somites appears to occur at the normal time in the ntl mutants, indicating that the presomitogenesis and somitogenesis phases of MyoD expression can be uncoupled. In addition, we demonstrate that the entire paraxial mesoderm of wild-type embryos has the potential to express MyoD when Sonic hedgehog is expressed ubiquitously in the embryo, and that this potential is lost in some of the cells of the paraxial mesoderm lineage in no tail and spadetail embryos. We also show that MyoD expression precedes myogenin expression and follows or is coincident with expression of snaill in some regions that express this gene.
ESTHER : Weinberg_1996_Development_122_271
PubMedSearch : Weinberg_1996_Development_122_271
PubMedID: 8565839