20 results on '"Mari Matsumoto"'
Search Results
2. Role of ATP-binding cassette transporter A1 in suppressing lipid accumulation by glucagon-like peptide-1 agonist in hepatocytes
- Author
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Jingya Lyu, Hitomi Imachi, Kensaku Fukunaga, Seisuke Sato, Toshihiro Kobayashi, Tao Dong, Takanobu Saheki, Mari Matsumoto, Hisakazu Iwama, Huanxiang Zhang, and Koji Murao
- Subjects
Internal medicine ,RC31-1245 - Abstract
Objective: Adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1) influences hepatic cholesterol transportation. Accumulation of hepatic cholesterol leads to fatty liver disease, which is improved by glucagon-like peptide 1 (GLP-1) in diabetes. Therefore, we analyzed the molecular mechanism in the regulation of hepatic ABCA1 by GLP-1 analogue exendin-4. Methods: Hepatic ABCA1 expression and transcription were checked by western blotting, real-time polymerase chain reaction (PCR), and luciferase assay in HepG2 cells. Chromatin immunoprecipitation (ChIP) and site-directed mutagenesis were employed to determine transcriptional regulation of the ABCA1 gene. Prolactin regulatory element-binding (PREB)-transgenic mice were generated to access the effect of exendin-4 on improving lipid accumulation caused by a high-fat diet (HFD). Results: Exendin-4 stimulated hepatic ABCA1 expression and transcription via the Ca2+/calmodulin (CaM)-dependent protein kinase kinase/CaM-dependent protein kinase IV (CaMKK/CaMKIV) pathway, whereas GLP-1 receptor antagonist exendin9-39 cancelled this effect. Therefore, exendin-4 decreased hepatic lipid content. ChIP showed that PREB could directly bind to the ABCA1 promoter, which was enhanced by exendin-4. Moreover, PREB stimulated ABCA1 promoter activity, and mutation of PREB-binding site in ABCA1 promoter cancelled exendin-4-enhanced ABCA1 promoter activity. Silencing of PREB attenuated the effect of exendin-4 and induced hepatic cholesterol accumulation. Blockade of CaMKK by STO-609 or siRNA cancelled the upregulation of ABCA1 and PREB induced by exendin-4. In vivo, exendin-4 or overexpression of PREB increased hepatic ABCA1 expression and decreased hepatic lipid accumulation and high plasma cholesterol caused by a HFD. Conclusions: Our data shows that exendin-4 stimulates hepatic ABCA1 expression and decreases lipid accumulation by the CaMKK/CaMKIV/PREB pathway, suggesting that ABCA1 and PREB might be the therapeutic targets in fatty liver disease. Keywords: Prolactin regulatory element-binding, Lipid accumulation, Non-alcoholic steatohepatitis, Fatty liver, Cell signaling
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- 2020
- Full Text
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3. Identification of Novel GCK and HNF4α Gene Variants in Japanese Pediatric Patients with Onset of Diabetes before 17 Years of Age
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Rumi Katashima, Mari Matsumoto, Yuka Watanabe, Maki Moritani, and Ichiro Yokota
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Diseases of the endocrine glands. Clinical endocrinology ,RC648-665 - Abstract
Background. Maturity-onset diabetes of the young (MODY) is commonly misdiagnosed as type 1 or type 2 diabetes. Common reasons for misdiagnosis are related to limitations in genetic testing. A precise molecular diagnosis is essential for the optimal treatment of patients and allows for early diagnosis of their asymptomatic family members. Objective. The aim of this study was to identify rare monogenic variants of common MODY genes in Japanese pediatric patients. Methods. We investigated 45 Japanese pediatric patients based on the following clinical criteria: development of diabetes before 17 years of age, a family history of diabetes, testing negative for glutamate decarboxylase-65 (GAD 65) antibodies and insulinoma-2-associated autoantibodies (IA-2A), no significant obesity, and evidence of endogenous insulin production. Genetic screening for MODY1 (HNF4α), MODY2 (GCK), MODY3 (HNF1α), and MODY5 (HNF1β) was performed by direct sequencing followed by multiplex ligation amplification assays. Results. We identified 22 missense variants (3 novel variants) in 27 patients (60.0%) in the GCK, HNF4α, and HNF1α genes. We also detected a whole exon deletion in the HNF1β gene and an exon 5–6 aberration in the GCK gene, each in one proband (4.4%). There were a total of 29 variations (64.4%), giving a relative frequency of 53.3% (24/45) for GCK, 2.2% (1/45) for HNF4α, 6.7% (3/45) for HNF1α, and 2.2% (1/45) for HNF1β genes. Conclusions. Clinicians should consider collecting and assessing detailed clinical information, especially regarding GCK gene variants, in young antibody-negative patients with diabetes. Correct molecular diagnosis of MODY better predicts the clinical course of diabetes and facilitates individualized management.
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- 2021
- Full Text
- View/download PDF
4. Identification of Novel GCK and HNF4α Gene Variants in Japanese Pediatric Patients with Onset of Diabetes before 17 Years of Age
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Ichiro Yokota, Maki Moritani, Rumi Katashima, Yuka Watanabe, and Mari Matsumoto
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Proband ,Oncology ,medicine.medical_specialty ,Article Subject ,medicine.diagnostic_test ,business.industry ,Endocrinology, Diabetes and Metabolism ,Type 2 diabetes ,RC648-665 ,medicine.disease ,Asymptomatic ,Diseases of the endocrine glands. Clinical endocrinology ,Exon ,Endocrinology ,Internal medicine ,Diabetes mellitus ,medicine ,Missense mutation ,medicine.symptom ,Family history ,business ,Genetic testing - Abstract
Background. Maturity-onset diabetes of the young (MODY) is commonly misdiagnosed as type 1 or type 2 diabetes. Common reasons for misdiagnosis are related to limitations in genetic testing. A precise molecular diagnosis is essential for the optimal treatment of patients and allows for early diagnosis of their asymptomatic family members. Objective. The aim of this study was to identify rare monogenic variants of common MODY genes in Japanese pediatric patients. Methods. We investigated 45 Japanese pediatric patients based on the following clinical criteria: development of diabetes before 17 years of age, a family history of diabetes, testing negative for glutamate decarboxylase-65 (GAD 65) antibodies and insulinoma-2-associated autoantibodies (IA-2A), no significant obesity, and evidence of endogenous insulin production. Genetic screening for MODY1 (HNF4α), MODY2 (GCK), MODY3 (HNF1α), and MODY5 (HNF1β) was performed by direct sequencing followed by multiplex ligation amplification assays. Results. We identified 22 missense variants (3 novel variants) in 27 patients (60.0%) in the GCK, HNF4α, and HNF1α genes. We also detected a whole exon deletion in the HNF1β gene and an exon 5–6 aberration in the GCK gene, each in one proband (4.4%). There were a total of 29 variations (64.4%), giving a relative frequency of 53.3% (24/45) for GCK, 2.2% (1/45) for HNF4α, 6.7% (3/45) for HNF1α, and 2.2% (1/45) for HNF1β genes. Conclusions. Clinicians should consider collecting and assessing detailed clinical information, especially regarding GCK gene variants, in young antibody-negative patients with diabetes. Correct molecular diagnosis of MODY better predicts the clinical course of diabetes and facilitates individualized management.
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- 2021
5. Excess intracellular ATP causes neuropathic pain following spinal cord injury
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Nobuhiko Nakajima, Yuichiro Ohnishi, Masamichi Yamamoto, Daiki Setoyama, Hirohiko Imai, Tomofumi Takenaka, Mari Matsumoto, Koichi Hosomi, Yoichi Saitoh, Hidemasa Furue, and Haruhiko Kishima
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Pharmacology ,Spinal Cord Dorsal Horn ,Cell Biology ,Cellular and Molecular Neuroscience ,Mice ,Adenosine Triphosphate ,Spinal Cord ,Hyperalgesia ,Quality of Life ,Molecular Medicine ,Animals ,Neuralgia ,Molecular Biology ,Spinal Cord Injuries - Abstract
Intractable neuropathic pain following spinal cord injury (NP-SCI) reduces a patient's quality of life. Excessive release of ATP into the extracellular space evokes neuroinflammation via purinergic receptor. Neuroinflammation plays an important role in the initiation and maintenance of NP. However, little is known about whether or not extracellular ATP cause NP-SCI. We found in the present study that excess of intracellular ATP at the lesion site evokes at-level NP-SCI. No significant differences in the body weight, locomotor function, or motor behaviors were found in groups that were negative and positive for at-level allodynia. The intracellular ATP level at the lesion site was significantly higher in the allodynia-positive mice than in the allodynia-negative mice. A metabolome analysis revealed that there were no significant differences in the ATP production or degradation between allodynia-negative and allodynia-positive mice. Dorsal horn neurons in allodynia mice were found to be inactivated in the resting state, suggesting that decreased ATP consumption due to neural inactivity leads to a build-up of intracellular ATP. In contrast to the findings in the resting state, mechanical stimulation increased the neural activity of dorsal horn and extracellular ATP release at lesion site. The forced production of intracellular ATP at the lesion site in non-allodynia mice induced allodynia. The inhibition of P2X4 receptors in allodynia mice reduced allodynia. These results suggest that an excess buildup of intracellular ATP in the resting state causes at-level NP-SCI as a result of the extracellular release of ATP with mechanical stimulation.
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- 2022
6. Role of ATP-binding cassette transporter A1 in suppressing lipid accumulation by glucagon-like peptide-1 agonist in hepatocytes
- Author
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Hitomi Imachi, Koji Murao, Tao Dong, Seisuke Sato, Huanxiang Zhang, Jingya Lyu, Toshihiro Kobayashi, Mari Matsumoto, Kensaku Fukunaga, Takanobu Saheki, and Hisakazu Iwama
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0301 basic medicine ,Cell signaling ,Prolactin regulatory element-binding ,Lipid accumulation ,Mice ,chemistry.chemical_compound ,0302 clinical medicine ,ChIP, Chromatin immunoprecipitation ,ERK, extracellular signal-regulated kinase ,Glucagon-Like Peptide 1 ,Tumor Cells, Cultured ,Transcriptional regulation ,Non-alcoholic steatohepatitis ,biology ,TG, triglyceride ,Kinase ,CaMKK, Ca2+/calmodulin-dependent protein kinase ,digestive, oral, and skin physiology ,GLP-1, glucagon-like peptide-1 ,Hep G2 Cells ,Cell biology ,GLP-1R, GLP-1 receptor ,HCV, hepatitis C virus ,CREB, cAMP-responsive element binding ,Original Article ,lipids (amino acids, peptides, and proteins) ,NASH, nonalcoholic steatohepatitis ,LDL-C, low density lipoprotein cholesterol ,hormones, hormone substitutes, and hormone antagonists ,ATP Binding Cassette Transporter 1 ,endocrine system ,lcsh:Internal medicine ,Calmodulin ,Mice, Transgenic ,030209 endocrinology & metabolism ,03 medical and health sciences ,Downregulation and upregulation ,PI3K, phosphatidylinositol 3 kinase ,Fatty liver ,PKC, protein kinase C ,Animals ,Humans ,Protein kinase A ,lcsh:RC31-1245 ,Molecular Biology ,PREB, prolactin regulatory element-binding protein ,Cell Biology ,Lipid Metabolism ,HDL, high density lipoprotein ,ABCA1, ATP-binding cassette transporter A1 ,030104 developmental biology ,HDL-C, HDL cholesterol ,chemistry ,ABCA1 ,Hepatocytes ,biology.protein ,Exenatide ,PKA, protein kinase A ,NAFLD, nonalcoholic fatty liver disease ,Chromatin immunoprecipitation ,Adenosine triphosphate - Abstract
Objective Adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1) influences hepatic cholesterol transportation. Accumulation of hepatic cholesterol leads to fatty liver disease, which is improved by glucagon-like peptide 1 (GLP-1) in diabetes. Therefore, we analyzed the molecular mechanism in the regulation of hepatic ABCA1 by GLP-1 analogue exendin-4. Methods Hepatic ABCA1 expression and transcription were checked by western blotting, real-time polymerase chain reaction (PCR), and luciferase assay in HepG2 cells. Chromatin immunoprecipitation (ChIP) and site-directed mutagenesis were employed to determine transcriptional regulation of the ABCA1 gene. Prolactin regulatory element-binding (PREB)-transgenic mice were generated to access the effect of exendin-4 on improving lipid accumulation caused by a high-fat diet (HFD). Results Exendin-4 stimulated hepatic ABCA1 expression and transcription via the Ca2+/calmodulin (CaM)-dependent protein kinase kinase/CaM-dependent protein kinase IV (CaMKK/CaMKIV) pathway, whereas GLP-1 receptor antagonist exendin9-39 cancelled this effect. Therefore, exendin-4 decreased hepatic lipid content. ChIP showed that PREB could directly bind to the ABCA1 promoter, which was enhanced by exendin-4. Moreover, PREB stimulated ABCA1 promoter activity, and mutation of PREB-binding site in ABCA1 promoter cancelled exendin-4-enhanced ABCA1 promoter activity. Silencing of PREB attenuated the effect of exendin-4 and induced hepatic cholesterol accumulation. Blockade of CaMKK by STO-609 or siRNA cancelled the upregulation of ABCA1 and PREB induced by exendin-4. In vivo, exendin-4 or overexpression of PREB increased hepatic ABCA1 expression and decreased hepatic lipid accumulation and high plasma cholesterol caused by a HFD. Conclusions Our data shows that exendin-4 stimulates hepatic ABCA1 expression and decreases lipid accumulation by the CaMKK/CaMKIV/PREB pathway, suggesting that ABCA1 and PREB might be the therapeutic targets in fatty liver disease., Graphical abstract Image 1, Highlights • The GLP-1R agonist exendin-4 suppressed lipid accumulation by upregulating ABCA1 expression in hepatocytes. • Exendin-4 regulated the expression and transcription of hepatic ABCA1 via the CaMKK/CaMKIV/PREB pathway. • Overexpression of PREB or exendin-4 protected mouse liver from fatty liver by upregulation of ABCA1.
- Published
- 2020
7. HDL promotes adiponectin gene expression via the CAMKK/CAMKIV pathway
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Jingya Lyu, Kensaku Fukunaga, Koji Murao, Hitomi Imachi, Mari Matsumoto, Takanobu Saheki, Tomohiro Ibata, Toshihiro Kobayashi, Seisuke Sato, and Japar B Salimah
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CD36 Antigens ,medicine.medical_specialty ,animal structures ,Gene Expression ,Calcium-Calmodulin-Dependent Protein Kinase Kinase ,Mice ,Endocrinology ,Internal medicine ,3T3-L1 Cells ,Gene expression ,medicine ,Animals ,Scavenger receptor ,Phosphorylation ,Molecular Biology ,CAMKK2 ,Gene knockdown ,Adiponectin ,Chemistry ,Reverse cholesterol transport ,lipids (amino acids, peptides, and proteins) ,Signal transduction ,Lipoproteins, HDL ,hormones, hormone substitutes, and hormone antagonists ,Lipoprotein - Abstract
Adiponectin (APN) is an adipokine that protects against diabetes and atherosclerosis. High-density lipoprotein (HDL) mediates reverse cholesterol transport, which also protects against atherosclerosis. In this process, the human homolog of the B class type I scavenger receptor (SR-BI/CLA-1) facilitates the cellular uptake of cholesterol from HDL. The level of circulating APN is positively correlated with the serum level of HDL-cholesterol. In this study, we investigated whether HDL stimulates the gene expression of APN through the Ca2+/calmodulin (CaM)-dependent protein kinase IV (CaMKIV) cascade. APN expression was examined using real-time PCR and western blot analysis in 3T3-L1 cells incubated with HDL. CaMKIV activity was assessed by the detection of activation loop phosphorylation (at Thr196 residue), and the effect of the constitutively active form, CaMKIVc, on APN promoter activity was investigated. Our results showed that HDL stimulated APN gene expression via hSR-BI/CLA-1. Furthermore, we explored the signaling pathways by which HDL stimulated APN expression in 3T3-L1 cells. The stimulation of APN gene expression by HDL appears to be mediated by CaMKK, as STO-609, a specific inhibitor of CaMKK2, prevents this effect. We revealed that CaMKIVc increased APN gene transcriptional activity, and the CaMKIV-dominant negative mutant blocked the effect of HDL on APN promoter activity. Finally, knockdown of hSR-BI/CLA-1 also canceled the effect of HDL on APN gene expression. These results suggest that HDL has an important role to improve the function of adipocytes by activating hSR-BI/CLA-1, and CaMKK/CaMKIV pathway is conceivable as one of the signaling pathways of this activation mechanism.
- Published
- 2021
8. Identification of Novel
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Rumi, Katashima, Mari, Matsumoto, Yuka, Watanabe, Maki, Moritani, and Ichiro, Yokota
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Male ,Adolescent ,Diabetes Mellitus, Type 2 ,Hepatocyte Nuclear Factor 4 ,Japan ,Genetic Variation ,Humans ,Female ,Child ,Pediatrics ,Germinal Center Kinases ,Research Article - Abstract
Background Maturity-onset diabetes of the young (MODY) is commonly misdiagnosed as type 1 or type 2 diabetes. Common reasons for misdiagnosis are related to limitations in genetic testing. A precise molecular diagnosis is essential for the optimal treatment of patients and allows for early diagnosis of their asymptomatic family members. Objective The aim of this study was to identify rare monogenic variants of common MODY genes in Japanese pediatric patients. Methods We investigated 45 Japanese pediatric patients based on the following clinical criteria: development of diabetes before 17 years of age, a family history of diabetes, testing negative for glutamate decarboxylase-65 (GAD 65) antibodies and insulinoma-2-associated autoantibodies (IA-2A), no significant obesity, and evidence of endogenous insulin production. Genetic screening for MODY1 (HNF4α), MODY2 (GCK), MODY3 (HNF1α), and MODY5 (HNF1β) was performed by direct sequencing followed by multiplex ligation amplification assays. Results We identified 22 missense variants (3 novel variants) in 27 patients (60.0%) in the GCK, HNF4α, and HNF1α genes. We also detected a whole exon deletion in the HNF1β gene and an exon 5–6 aberration in the GCK gene, each in one proband (4.4%). There were a total of 29 variations (64.4%), giving a relative frequency of 53.3% (24/45) for GCK, 2.2% (1/45) for HNF4α, 6.7% (3/45) for HNF1α, and 2.2% (1/45) for HNF1β genes. Conclusions Clinicians should consider collecting and assessing detailed clinical information, especially regarding GCK gene variants, in young antibody-negative patients with diabetes. Correct molecular diagnosis of MODY better predicts the clinical course of diabetes and facilitates individualized management.
- Published
- 2021
9. Risk Management and Risk Countermeasure Portfolio of Fog Computing for Improving IoT Security
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Shigeaki Tanimoto, Mari Matsumoto, Teruo Endo, Hiroyuki Sato, and Atsushi Kanai
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- 2022
10. 475-P: Exendin-4 Stimulates eNOS Activation by Upregulation of Scavenger Receptor Type B Class I in Human Endothelial Cells
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Tao Dong, Seisuke Sato, Toshihiro Kobayashi, Mari Matsumoto, Jingya Lyu, Tomohiro Ibata, Hitomi Imachi, Koji Murao, and Kensaku Fukunaga
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endocrine system ,biology ,Chemistry ,Endocrinology, Diabetes and Metabolism ,AMPK ,Promoter ,FOXO1 ,biology.organism_classification ,Molecular biology ,Downregulation and upregulation ,Enos ,Internal Medicine ,Scavenger receptor ,Receptor ,Transcription factor ,hormones, hormone substitutes, and hormone antagonists - Abstract
Exendin-4 (Exenatide), a long-acting agonist of the glucagon-like peptide 1 receptor (GLP-1R), has been confirmed to protect the cardiovascular system from atherosclerosis in type 2 diabetes. However, the detailed mechanism of this process is not clear. Activation of endothelial nitric oxide synthase (eNOS) to produce nitric oxide (NO) plays an important role in endothelial homeostasis. Previous study shows that HDL activates eNOS via its receptor scavenger receptor type B class I (SR-BI). In this study, we checked the effect of exendin-4 on HDL/SR-BI-mediated eNOS activation in HUVECs. Firstly, we demonstrated the expression of GLP-1R in HUVECs and exendin-4 significantly induced HDL-mediated eNOS activation. Next, we found exendin-4 increased the expression and promoter activity of SR-BI, and then blocking of PKA or AMPK by its specific inhibitor cancelled this effect. Consistently, cAMP enhanced SR-BI promoter activity while domain negative AMPK inhibited the effect of exendin-4 on SR-BI promoter activity. Blocking of GLP-1R by exendin 9-39 cancelled exendin-4-induced SR-BI promoter activity and AMPK phosphorylation. As a downstream of AMPK, a transcription factor FoxO1 was confirmed to directly bind to the SR-BI promoter region by Chromatin Immunoprecipitation (ChIP) assay and overexpression of FoxO1 enhanced SR-BI promoter activity. Moreover, exendin-4 markedly increased the expression and nuclear recruitment of FoxO1 by decreasing its phosphorylation. As well as, mutation of FoxO1-binding site in the SR-BI promoter region or silence of FoxO1 cancelled exendin-4-induced SR-BI expression. In summary, our results show that exendin-4 upregulates the expression and transcription of SR-BI via PKA/AMPK/FoxO1 pathway, which contributes to HDL-mediated eNOS activation and NO generation in human endothelial cells. Disclosure J. Lyu: None. H. Imachi: None. K. Fukunaga: None. S. Sato: None. T. Dong: None. T. Ibata: None. T. Kobayashi: None. M. Matsumoto: None. K. Murao: None.
- Published
- 2019
11. Nonvolatile Programmable Switch With Adjacently Integrated Flash Memory and CMOS Logic for Low-Power and High-Speed FPGA
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Mari Matsumoto, Masato Oda, Kosuke Tatsumura, Shinichi Yasuda, and Koichiro Zaitsu
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Dynamic random-access memory ,Hardware_MEMORYSTRUCTURES ,business.industry ,Computer science ,Semiconductor memory ,Programmable logic array ,Flash memory ,Electronic, Optical and Magnetic Materials ,law.invention ,Non-volatile memory ,law ,Hardware_INTEGRATEDCIRCUITS ,Electronic engineering ,Racetrack memory ,Non-volatile random-access memory ,Electrical and Electronic Engineering ,business ,Computer hardware ,Computer memory - Abstract
Novel nonvolatile programmable switch for low-power and high-speed field-programmable gate array (FPGA) where flash memory is adjacently integrated to CMOS logic is demonstrated. The flash memory and the high-speed switching transistor (SwTr) are fabricated close to each other without deteriorating their respective performance. Furthermore, programming schemes to write and erase the flash memory are optimized so that the memory is successfully programmed without any damage to the SwTrs. Flash-based configuration memory in the nonvolatile programmable switch has only half the area of the conventional static random-access memory-based one, and it can be placed in each block in FPGA, enabling efficient power gating that offers low-power FPGA operation.
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- 2015
12. セイネンキ ノ ユウジン カンケイ ニオケル ドウチョウ コウドウ : ドウチョウ コウドウ シャクド ノ サクセイ
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Makiko, KASAI and Mari, MATSUMOTO
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青年期 ,同調行動 ,education ,友人関係 - Abstract
This study was conducted to examine instances of conformity behavior, anxiety, public self?consciousness, and approval motivation in adolescent friendships. First, a conformity behavior scale was constructed based on 6 ifferent scales that measure conformity motivation, conformity tendency, conformity orientation and conformity behavior. The subjects comprised 83 male and 72 female university students. They were exposed to item analysis and factor analysis exercises, and a twenty?four?items conformity behavior scale was developed. Second, the hypothesis that adolescents with high anxiety, high public consciousness and high approval motivation have a tendency to conform to others was tested. A total of 57 items were tested on 123 male and 171 female high school students. The results showed that both the internal conformity factor and the external conformity factor are related to anxiety and approval motivation. Therefore, a part of the hypothesis that says that high school students tend to conform to others because of their anxiety and motivation to secure the approval of others was verified in this study. Some studies, however, showed that conforming behavior causes stress in adolescents. In our conclusion, with the view to releasing adolescents from such stress, we suggested that they practice self?assertive behavior.
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- 2010
13. Interaction Between Methyl CpG-Binding Protein and Ran GTPase during Cell Division in Tobacco Cultured Cells
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Wada Yuko, Hyun-Jung Kim, Akiko Koike, Yutaka Kodama, Shinjiro Ogita, Hiroshi Sano, Mari Matsumoto, Aiko Yano, Nir Ohad, and Tomotaka Shinya
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Cell division ,Arabidopsis Proteins ,Molecular Sequence Data ,Cell Cycle Proteins ,Original Articles ,Plant Science ,GTPase ,Biology ,Molecular biology ,Transport protein ,Chromatin ,Cell biology ,DNA-Binding Proteins ,Protein Transport ,Bimolecular fluorescence complementation ,Two-Hybrid System Techniques ,Tobacco ,Ran ,Amino Acid Sequence ,Mitosis ,Cell Division ,Cells, Cultured ,Cellular localization - Abstract
� Background and Aims Methyl CpG-binding proteins are considered to play critical roles in epigenetic control of gene expression by recognizing and interacting with 5-methylcytosine (m 5 C) in eukaryotes. However, among 13 corresponding genes in Arabidopsis thaliana, designated as featuring a methyl-binding domain (MBD), only four have so far been shown actually to bind to m 5 C. One example, AtMBD5, was selected here to screen for interacting proteins. � Methods Yeast two-hybrid assays were used for screening, and physical interaction was confirmed by pulldown and bimolecular fluorescence complementation (BiFC) assays. Cellular localization was analysed by fluorescence-tagged fusion proteins using tobacco (Nicotiana tabacum) cultured bright yellow 2 cells. � Key Results A gene finally identified was found to encode AtRAN3, a protein that belongs to the Ran GTPase family, which plays a critical role in nucleocytoplasmic transport and spindle bipolarization during cell division. AtMBD5 and AtRAN3 were clearly shown to interact in the nucleus by BiFC. On co-expression of AtMBD5-cyan fluorescence protein and yellow fluorescence protein-AtRAN3 in tobacco cells, both localized to the nucleus in the resting stage, migrating to the cytoplasm, primarily around chromatin, during mitosis, particularly at metaphase. � Conclusions These results suggest that AtMBD5 becomes localized to the vicinity of chromosomes with the aid of AtRAN3 during cell division, and may play an important role not only in maintenance of chromatin structures by binding to m 5 C, but also in progress through mitosis by detaching from m 5 C. The present findings also shed light on the physiological function of Ran GTPases, direct target proteins of which have not thus far been well defined, suggesting their key role in chromatin movements in plant cells.
- Published
- 2006
14. Threats to Hope in People with Severe Chronic Obstructive Pulmonary Disease
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Yoko Doi and Mari Matsumoto
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medicine.medical_specialty ,business.industry ,Internal medicine ,Physical therapy ,Medicine ,General Medicine ,business ,Severe chronic obstructive pulmonary disease - Abstract
本研究は,重症慢性閉塞性肺疾患(chronic obstructive pulmonary disease,以下COPD)患者の希望を脅かす要素を抽出,記述することを目的とした.10名の研究参加者に対し,半構造化面接を実施し,得られたデータを質的帰納的に分析した.その結果,重症COPD患者の希望を脅かす要素として,《七転八倒の息苦しさの持続》,《衰え・悪化を知る兆しや証拠》,《活動を妨げる感覚》,《個人としての価値や人格を無視した周囲の対応》の4つのカテゴリーが抽出された.COPD患者が絶望に苛まれることのないよう,このような体験にともなう重症COPD患者の苦痛や苦悩に関心を向け,寄り添う看護師の態度は重要である.看護師は希望を脅かす要素の可能な限りの除去や最小化,あるいは適切な対処へと導くこと,また,それが困難な場合に生じた苦痛や苦悩の緩和をはかることにより,重症COPD患者が絶望を回避,希望を維持できるよう助ける必要がある.
- Published
- 2006
15. Pulmonary metastasis from gastric cancer: A case report and review of literature
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Masae Mano, Motohisa Kuwahara, Mari Matsumoto, Takayuki Shirakusa, Koji Inutsuka, Daisuke Hamatake, Akinori Iwasaki, and Kazuya Naritomi
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medicine.medical_specialty ,Lung ,business.industry ,Stomach ,medicine.medical_treatment ,Cancer ,General Medicine ,medicine.disease ,Surgery ,medicine.anatomical_structure ,Carcinoma ,medicine ,Adenocarcinoma ,Lymphadenectomy ,Gastrectomy ,Radiology ,Metastasectomy ,business - Abstract
We present a case report of a 63-year-old male who underwent lung resections for metastases originating from gastric cancer 18-year after total gastrectomy with lymphadenectomy. The gastrectomy was performed in 1994; histological examination of the original tumor revealed stage II poorly differentiated adenocarcinoma [pT2 (MP), N0, M0]. Chest X-ray and computed tomography in 2012 showed a well-defined tumor, 9 mm in size, at the left S3 of the lung. Thoracoscopic partial resection was performed. The tumor was diagnosed as poorly differentiated carcinoma, most likely metastatic gastric adenocarcinoma. Although rarely performed, resection of pulmonary metastases from carcinoma of the stomach was done to improve the patient’s chances for long-term survival.
- Published
- 2013
16. Long-Termed Field Survey of Indoor Air Quality and Health Hazards in Sick House
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Kazuhiko Kakuta, Satoshi Ishikawa, Kentaro Amano, Koji Netsu, Hiroshi Yoshino, Atsuo Nozaki, Koichi Ikeda, Mari Matsumoto, and Sachiko Hojo
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Cultural Studies ,Sick building syndrome ,Indoor air quality ,Arts and Humanities (miscellaneous) ,Waste management ,Order (business) ,Environmental health ,Architecture ,Environmental science ,Building and Construction ,Field survey ,complex mixtures ,Civil and Structural Engineering - Abstract
In order to determine the factors of origin of Sick House Syndrome (SHS), data of indoor air quality in the sick houses and field survey were collected and carried out respectively, over three summ...
- Published
- 2004
17. Abstract TP120: Plasma D-dimer Level and Cerebral Infarction Volume in Patients With Nonvalvular Atrial Fibrillation
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Mari Matsumoto, Manabu Sakaguchi, Shuhei Okazaki, Shigetaka Furukado, Masafumi Tagaya, Hideki Etani, Takeshi Shimazu, Toshiki Yoshimine, Hideki Mochizuki, and Kazuo Kitagawa
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Advanced and Specialized Nursing ,Neurology (clinical) ,Cardiology and Cardiovascular Medicine - Abstract
Introduction and Hypothesis: The purpose of this study was to investigate the association between plasma D-dimer level at admission and infarct size in non-valvular atrial fibrillation (NVAF) patients. Methods: We identified 124 patients with consecutive ischemic stroke and NVAF who were admitted within 48 hours of symptom onset. We measured infarction volume from CT taken after 3±1 days from the onset. Relationships were analysed between infarction volume, risk factors, preadmission medications and admission conditions. We also assessed the functional outcome by tertile of D-dimer level (≦ 0.83, 0.83-2.16, ≧ 2.16 μg/mL) in patients with preadmission modified Rankin Scale (mRS) score of 0-1. Results: Infarction volume significantly correlated with D-dimer level (r=0.309, p < 0.001) (Figure 1), systolic blood pressure (r=0.201, p=0.026), diastolic blood pressure (r=0.283, p=0.002), National Institutes of Health Stroke Scale (NIHSS) score on admission (r=0.546, p < 0.001) and mRS score at discharge (r=0.557, p Conclusions: Plasma D-dimer level on admission is significantly related to infarction volume and functional outcome, following cardioembolic stroke in NVAF patients.
- Published
- 2013
18. High-Speed Magnetoresistive Random-Access Memory Random Number Generator Using Error-Correcting Code
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Sumio Ikegawa, Hiroaki Yoda, Shinobu Fujita, Mari Matsumoto, Naoharu Shimomura, and Tetsufumi Tanamoto
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FOS: Computer and information sciences ,Magnetoresistive random-access memory ,Computer Science - Cryptography and Security ,Number generator ,Physics and Astronomy (miscellaneous) ,Computer science ,Random number generation ,General Engineering ,General Physics and Astronomy ,law.invention ,Computer Science::Hardware Architecture ,law ,Entropy (information theory) ,Resistor ,Error detection and correction ,Cryptography and Security (cs.CR) ,Algorithm ,Randomness - Abstract
A high-speed random number generator (RNG) circuit based on magnetoresistive random-access memory (MRAM) using an error-correcting code (ECC) post processing circuit is presented. ECC post processing increases the quality of randomness by increasing the entropy of random number. { We experimentally show that a small error-correcting capability circuit is sufficient for this post processing. It is shown that the ECC post processing circuit powerfully improves the quality of randomness with minimum overhead, ending up with high-speed random number generation. We also show that coupling with a linear feedback shift resistor is effective for improving randomness, 5 pages, 11 figures
- Published
- 2011
19. Localized, aggregative, and diffuse adherence to HeLa cells, plastic, and human small intestines by Escherichia coli isolated from patients with diarrhea
- Author
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Peter Echeverria, Eri Sonoda, Satomi Nakayama, Masako Uchimura, Wantana Paveenkittiporn, Kazumichi Tamura, Yukiko Koyama, Mari Matsumoto, Tatsuo Yamamoto, and Takeshi Yokota
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Adult ,DNA, Bacterial ,Diarrhea ,Biology ,medicine.disease_cause ,Bacterial Adhesion ,Microbiology ,HeLa ,Peyer's Patches ,Culture Techniques ,Intestine, Small ,medicine ,Escherichia coli ,Immunology and Allergy ,Humans ,Diffusely Adherent Escherichia coli ,Enteropathogenic Escherichia coli ,Serotyping ,Child ,Escherichia coli Infections ,Microfold cell ,Adhesins, Escherichia coli ,Microvilli ,biology.organism_classification ,Mucus ,Enterobacteriaceae ,Epithelium ,Infectious Diseases ,medicine.anatomical_structure ,Microscopy, Electron, Scanning ,Plastics ,Bacterial Outer Membrane Proteins ,HeLa Cells ,Plasmids - Abstract
Adherence of diarrhea-associated Escherichia coli was studied by scanning electron microscopy. Enteropathogenic E. coli (EPEC) adherence factor-positive (EAF+) E. coli of EPEC serotypes (class I EPEC) adhered to plastic and human jejunal and ileal mucosa, similar to case and HeLa cells. Localized adherence, elongation of cell microvilli, and "locking" of the bacterial aggregates by the elongated microvilli were evident after incubation for 20 min. EAF+ E. coli adhered strikingly to mucus but rarely to M cells in Peyer's patch-associated epithelium. Most enteroaggregative E. coli (EAggEC) strains adhered to plastic, similar to HeLa cells. Some diffuse-adhering E. coli (DAEC) strains displayed no adherence to plastic but formed "dimples" on HeLa cells. Both EAggEC and DAEC adhered at lower levels to human small intestines (except M cells) than did EAF+ E. coli. In all cases of EAF+ E. coli, EAggEC, and DAEC, strains were found with atypical characteristics. The data demonstrate the unique adherence characteristics of EAF+ E. coli, EAggEC, and DAEC.
- Published
- 1992
20. HDL promotes adiponectin gene expression via the CAMKK/CAMKIV pathway.
- Author
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Toshihiro Kobayashi, Hitomi Imachi, Kensaku Fukunaga, Jingya Lyu, Seisuke Sato, Takanobu Saheki, Tomohiro Ibata, Mari Matsumoto, Japar, Salimah B., and Koji Murao
- Subjects
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HIGH density lipoproteins , *GENE expression , *ADIPONECTIN , *WESTERN immunoblotting , *HDL cholesterol , *PROTEIN kinases - Abstract
Adiponectin (APN) is an adipokine that protects against diabetes and atherosclerosis. High-density lipoprotein (HDL) mediates reverse cholesterol transport, which also protects against atherosclerosis. In this process, the human homolog of the B class type I scavenger receptor (SR-BI/CLA-1) facilitates the cellular uptake of cholesterol from HDL. The level of circulating APN is positively correlated with the serum level of HDLcholesterol. In this study, we investigated whether HDL stimulates the gene expression of APN through the Ca2+/calmodulin (CaM)-dependent protein kinase IV (CaMKIV) cascade. APN expression was examined using real-time PCR and western blot analysis in 3T3-L1 cells incubated with HDL. CaMKIV activity was assessed by the detection of activation loop phosphorylation (at Thr196 residue), and the effect of the constitutively active form, CaMKIVc, on APN promoter activity was investigated. Our results showed that HDL stimulated APN gene expression via hSR-BI/CLA-1. Furthermore, we explored the signaling pathways by which HDL stimulated APN expression in 3T3-L1 cells. The stimulation of APN gene expression by HDL appears to be mediate d by CaMKK, as STO-609, a specific inhibitor of CaMKK2, prevents this effect. We revealed that CaMKIVc increased APN gene transcriptional activity, and the CaMKIV-dominant negative mutant blocked the effect of HDL on APN promoter activity. Finally, kno ckdown of hSR-BI/CLA-1 also canceled the effect of HDL on APN gene expression. These re sults suggest that HDL has an important role to improve the function of adipocytes by activating hSR-BI/CLA-1, and CaMKK/CaMKIV pathway is conceivable as one of the signaling pathways of this activation mechanism. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
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