18 research outputs found
胎盤由来間葉系幹細胞の胎盤機能検査法としての役割に関する研究
No full textThe cellular and molecular mechanisms responsible for pregnancy-related disorders remain unclear. We investigated the feasibility of using placenta-derived mesenchymal stem cells (MSCs) as a tool to study such pregnancy-related disorders. We isolated and expanded adequate numbers of cells with characteristic features of MSCs from the chorionic plate (CP-MSCs), chorionic villi (CV-MSCs), and decidua basalis (DB-MSCs) of human term placental tissues. All placenta-derived MSCs expressed pregnancy-associated C14MC microRNA (miRNA) (miR-323-3p). Interestingly, the placenta-specific C19MC
miRNAs (miR-518b and miR517a) were clearly expressed in CP-MSCs and CV-MSCs of foetal origin, but were barely expressed in DB-MSCs of maternal origin. Furthermore, expression levels of placenta-specific C19MC miRNAs in CV-MSCs remained stable during the ex vivo expansion process and across different pregnancy phases (first trimester versus third trimester). High-efficiency siRNA transfection was confirmed in twice-passaged CV-MSCs with
little toxicity, and microarray analysis was used to screen for miR-518b target genes. Placenta-derived MSCs, especially CV-MSCs, are a potential tool for investigating the role of placental miRNAs in pregnancy-related disorders.長崎大学学位論文 学位記番号:博(医歯薬)甲第1006号 学位授与年月日:平成30年3月20日Author: Naoki Fuchi, Kiyonori Miura, Hanako Doi, Tao-Sheng Li & Hideaki MasuzakiCitation: Scientific Reports, 7, 46220; 201
Porous tungsten prepared by atmospheric-pressure chemical vapor deposition with WF6 and its characterization
No full text336 Study on the vibratory and acoustic characteristics of automatic performing bell : Discussion on howling and wave form of radiated sound pressure
No full textEstablishment of a novel human T-cell leukemia virus type 1 infection model using cell-free virus
No full textNagasaki University (長崎大学)博士(医学)The primary mode of infection by human T-cell leukemia virus type 1 (HTLV-1) is cell-to-cell transmission during contact between infected cells and target cells. Cell-free HTLV-1 infections are known to be less efficient than infections with other retroviruses, and transmission of free HTLV-1 is considered not to occur in vivo. However, it has been demonstrated that cell-free HTLV-1 virions can infect primary lymphocytes and dendritic cells in vitro, and that virions embedded in biofilms on cell membranes can contribute to transmission. The establishment of an efficient cell-free HTLV-1 infection model would be a useful tool for analyzing the replication process of HTLV-1 and the clonal expansion of infected cells. We first succeeded in obtaining supernatants with high-titer cell-free HTLV-1 using a highly efficient virus-producing cell line. The HTLV-1 virions retained the structural characteristics of retroviruses. Using this cell-free infection model, we confirmed that a variety of cell lines and primary cultured cells can be infected with HTLV-1 and demonstrated that the provirus was randomly integrated into all chromosomes in the target cells. The provirus-integrated cell lines were HTLV-1-productive. Furthermore, we demonstrated for the first time that cell-free HTLV-1 is infectious in vivo using a humanized mouse model. These results indicate that this cell-free infection model recapitulates the HTLV-1 life cycle, including entry, reverse transcription, integration into the host genome, viral replication, and secondary infection. The new cell-free HTLV-1 infection model is promising as a practical resource for studying HTLV-1 infection.長崎大学学位論文 学位記番号:博(医歯薬)甲第1585号 学位授与年月日:令和6年3月19日Author: Koh Nagata, Kenta Tezuka, Madoka Kuramitsu, Naoki Fuchi, Yuri Hasegawa, Isao Hamaguchi, Kiyonori MiuraCitation: Journal of Virology, 98(2), art. no. e01862-23 ; 2024Nagasaki University (長崎大学), 博士(医学) (2024-03-19)doctoral thesi
Establishment of a novel human T-cell leukemia virus type 1 infection model using cell-free virus
No full textThe primary mode of infection by human T-cell leukemia virus type 1 (HTLV-1) is cell-to-cell transmission during contact between infected cells and target cells. Cell-free HTLV-1 infections are known to be less efficient than infections with other retroviruses, and transmission of free HTLV-1 is considered not to occur in vivo. However, it has been demonstrated that cell-free HTLV-1 virions can infect primary lymphocytes and dendritic cells in vitro, and that virions embedded in biofilms on cell membranes can contribute to transmission. The establishment of an efficient cell-free HTLV-1 infection model would be a useful tool for analyzing the replication process of HTLV-1 and the clonal expansion of infected cells. We first succeeded in obtaining supernatants with high-titer cell-free HTLV-1 using a highly efficient virus-producing cell line. The HTLV-1 virions retained the structural characteristics of retroviruses. Using this cell-free infection model, we confirmed that a variety of cell lines and primary cultured cells can be infected with HTLV-1 and demonstrated that the provirus was randomly integrated into all chromosomes in the target cells. The provirus-integrated cell lines were HTLV-1-productive. Furthermore, we demonstrated for the first time that cell-free HTLV-1 is infectious in vivo using a humanized mouse model. These results indicate that this cell-free infection model recapitulates the HTLV-1 life cycle, including entry, reverse transcription, integration into the host genome, viral replication, and secondary infection. The new cell-free HTLV-1 infection model is promising as a practical resource for studying HTLV-1 infection.長崎大学学位論文 学位記番号:博(医歯薬)甲第1585号 学位授与年月日:令和6年3月19日Author: Koh Nagata, Kenta Tezuka, Madoka Kuramitsu, Naoki Fuchi, Yuri Hasegawa, Isao Hamaguchi, Kiyonori MiuraCitation: Journal of Virology, 98(2), art. no. e01862-23 ; 2024Nagasaki University (長崎大学), 博士(医学) (2024-03-19
Carbon dioxide angiography and arterial embolization could successfully control postpartum uterine hemorrhage for the patient with hypersensitivity to iodine compound
No full textCorrection: Corrigendum: Feasibility of placenta-derived mesenchymal stem cells as a tool for studying pregnancy-related disorders
No full textScientific Reports 7: Article number: 46220; published online: 12 April 2017; updated: 22 December 2017. The original version of this Article contained an error in Affiliation 1 which was incorrectly listed as ‘Department of Obstetrics and Gynaecology, Nagasaki University Graduate School of Medicine, Nagasaki, Japan’.</jats:p
Mesenchymal stem cell-derived extracellular vesicles as probable triggers of radiation-induced heart disease
No full textAbstract Background Radiation-induced heart disease has been reported, but the underlying mechanisms remain unclear. Mesenchymal stem cells (MSCs), also residing in the heart, are highly susceptible to radiation. We examined the hypothesis that the altered secretion of extracellular vesicles (EVs) from MSCs is the trigger of radiation-induced heart disease. Methods By exposing human placental tissue-derived MSCs to 5 Gy γ-rays, we then isolated EVs from the culture medium 48 h later and evaluated the changes in quantity and quality of EVs from MSCs after radiation exposure. The biological effects of EVs from irradiated MSCs on HUVECs and H9c2 cells were also examined. Results Although the amount and size distribution of EVs did not differ between the nonirradiated and irradiated MSCs, miRNA sequences indicated many upregulated or downregulated miRNAs in irradiated MSCs EVs. In vitro experiments using HUVEC and H9c2 cells showed that irradiated MSC-EVs decreased cell proliferation (P < 0.01), but increased cell apoptosis and DNA damage. Moreover, irradiated MSC-EVs impaired the HUVEC tube formation and induced calcium overload in H9c2 cells. Conclusions EVs released from irradiated MSCs show altered miRNA profiles and harmful effects on heart cells, which provides new insight into the mechanism of radiation-related heart disease risks
Natural Course of Human T-Cell Leukemia Virus Type 1 Proviral DNA Levels in Carriers During Pregnancy
No full text1018-53 Pravastatin Prevents Restenosis After PTCA of High Grade Stenotic Lesions — Results of SHIPS (SHIga Pravastatin Study)
No full textThe Shiga Pravastatin Study (SHIPS) is a 5 center randomized, double blind placebo controlled trial to test whether pravastatin, 10 mg twice daily begun at least 10 days prior to elective PTCA in patients with total cholesterol (T-Chol) hess than 280 mg/dl can decrease restenosis. The endpoint is a between group comparison of frequency of restenosis defined as a more than 50% loss of gain at PTCA site at 3 months follow-up by automated quantitative coronary arteriography. 179 lesions (85 pravastatin. 94 placebo) in 124 patients (62 pravastatin. 62 placebo) were randomized. The two groups were comparable for baseline clinical and angiographic characteristics. T-Chol decreased from 204 to 172 mg/dl in pravastatin group (P<0.001), but not in placebo (201 vs 202 mg/dl). Although restenosis rate was not different in the two groups (29.4% in pravastatin vs 39.4% in placebo. P=0.16) as a whole, it was reduced to about 1/5 (8.B%) in pravastatin group compared to 44.B% in placebo (P=0.0011) when the analysis was restricted to high grade lesions (≥75% diameter stenosis by automated analysis. which is equivalent to ≥90% stenosis by visual analysis; 34 lesions in pravastatin, 29 lesions in placebo). The effect of pravastatin in prevention of restenosis in high grade lesions was equally seen both in the groups with baseline T-Chol of above (10.5 vs 45.5%, P=0.029) and below 200 mg/dl (6.7 vs 44.4%. P=0.015).ConclusionPravastatin prevents restenosis after PTCA of high grade lesions irrespective of baseline T-Chol level
