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Osteosarcoma cybrids에서 미토콘드리아 tRNA^(Leu(UUR)) A3243G 점돌연변이에 의한 인슐린 저항성의 발생
지미홍,이완 동국대학교 의학연구소 2009 東國醫學 Vol.16 No.1
미토콘드리아의 산화적 인산화 능력과 ATP 합성 능력은 말초 조직에서 인슐린 감수성과 밀접한 관계가 있으며, 미토콘드리아 DNA (mitochondrial DNA, mtDNA) 변이는 당뇨병 발병의 중요한 요인으로 알려져 있다. 이와 더불어 MELAS 증후군 환자와 미토콘드리아성 당뇨병 환자에게서 mtDNA tRNA^(Leu(UUR))유전자의 뉴클레오티드 3243부분이 adenine (A)에서 guanine (G)으로 치환된 A3243G 점돌연변이가 관찰된다. 본 연구팀은 mtDNA A3243G 점돌연변이와 인슐린 저항성의 상관성을 밝히기 위해, mtDNA A3243G 점돌연변이 osteosarcoma cybrids에서 인슐린 유도에 의한 인슐린 신호전달 분자들의 발현과 인산화를 살펴보았다. mtDNA A3243G 점돌연변이가 있는 mutant cybrid는 단백질 합성이 감소한다는 보고가 있으나,적어도 인슐린 신호전달 분자들인 insulin receptor (IR), insulin receptor substrate-1 (IRS- I) , phosphatidylinositide 3 kinase (PI3K) , phosphatidylinositide dependent protein kinase-1 (PDK- I) 그리고 Akt의 발현에는 영향을 미치지 않았다. 흥미롭게도, 인슐린에 의해 유도되는 IRS-1과 Akt의 인산화는 A3243G 점돌연변이가 있는 mutant cybrid에서 유의하게 감소하므로, 인슐린 저항성의 발생과 관련이 있다는 것을 증명할 수 있었다. 따라서 본 연구결과 mtDNA A3243G 점돌연변이가 인슐린에 의해 유도되는 IRS-1의 인산화를 감소시켜 인슐린 저항성을 유발한다고 사료된다. Mitochondrial oxidative phosphorylation and the ATP production are closely correlated with the insulin sensitivity in peripheral tissues, and the mutations of mitochondrial DNA (mtDNA) are regarded as factors in the pathogenesis of diabetes. An adenine (A) to guanine (G) mutation in the tRNA^(Leu(UUR)) gene at nucleotide position 3243 (A3243G) of mitochondrial DNA (mtDNA) has been observed in patients with MELAS syndrome and mitochondrial diabetes. To elucidate the association of the mtDNA A3243G point mutation and insulin resistance, we investigated the expression and insulin-sensitive phosphorylation of insulin signaling intermediates in A3243G osteosarcoma cybrids. Although A3243G mutant cybrid reduced in protein synthesis rate, the expressions of insulin signaling intermediates such as insulin receptor (IR), insulin receptor substrate-1 (IRS-1), phosphatidylinositide 3 kinase (PI3K), phosphatidylinositide dependent protein kinase (PDK-1) and Akt were not affected by A3243G mutation. Interestingly, insulin-stimulated phosphorylations of IRS-1 and Akt were significantly reduced in A3243G mutant cybrid, clearly demonstrating that mtDNA A3243G mutation developed insulin resistance. We thus suggest that point mutation in mtDNA A3243G point mutation causes insulin resistance by reducing the insulin-stimulated tyrosine phosphorylation of IRS-1 in osteosarcoma cybrids.
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최형수,지미홍,김성진,안효섭 대한혈액학회 2016 Blood Research Vol.51 No.2
BackgroundChildhood immune thrombocytopenic purpura (ITP) is a common acquired bleeding disorder. Even though most children recover, either spontaneously or with therapy, 10‒20% of newly diagnosed ITP cases have a chronic course beyond 12 months. This study evaluated whether clinical and laboratory findings can predict the response to intravenous immunoglobulin (IVIG) and progression to persistent or chronic ITP in children.MethodsDuring the period between March 2003 and June 2015, we retrospectively analyzed 72 children, newly diagnosed with ITP, who received IVIG treatment. Peripheral blood counts were obtained at diagnosis and at 1, 3, 6, and 12 months after IVIG treatment.ResultsAfter 6 months of IVIG treatment, 14 of 72 patients (19.4%) had persistent ITP, and after 12 months, 7 of 40 patients (17.5%) had chronic ITP. Age at diagnosis, gender, history of viral infection, or vaccination before disease onset were not statistically correlated with platelet recovery at 6 and 12 months. However, a platelet count recovery of ≥100×103/L at 1 and 3 months was significantly correlated with platelet recovery at 6 (P<0.001 and P<0.001, respectively) and 12 (P=0.007 and P=0.004, respectively) months.ConclusionThis study demonstrated that early platelet count recovery, at 1 and 3 months after IVIG treatment, predicts a short disease duration and a favorable outcome in children with new-ly diagnosed ITP. Further investigation in a larger group of patients is warranted to validate these findings.
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최준표,Losol Purevsuren,Ayoub Ghazal,지미홍,김세훈,조상헌,장윤석 대한면역학회 2022 Immune Network Vol.22 No.2
Foreign molecules, including viruses and bacteria-derived toxins, can also induce airway inflammation. However, to the best of our knowledge, the roles of these molecules in the development of airway inflammation have not been fully elucidated. Herein, we investigated the precise role and synergistic effect of virus-mimicking double-stranded RNA (dsRNA) and staphylococcal enterotoxin B (SEB) in macrophages and epithelial cells. To identify cytokine expression profiles, both the THP-1-derived macrophages and BEAS-2B epithelial cells were stimulated with dsRNA or SEB. A total of 21 cytokines were evaluated in the culture supernatants. We observed that stimulation with dsRNA induced cytokine production in both cell types. However, cytokine production was not induced in SEB-stimulated epithelial cells, compared to the macrophages. The synergistic effect of dsRNA and SEB was evaluated observing cytokine level and intracellular phospho-signaling. Fifteen different types were detected in high-dose dsRNA-stimulated epithelial cells, and 12 distinct types were detected in macrophages; those found in macrophages lacked interferon production compared to the epithelial cells. Notably, a synergistic effect of cytokine induction by co-stimulation of dsRNA and SEB was observed mainly in epithelial cells, via activation of most intracellular phosphor-signaling. However, macrophages only showed an accumulative effect. This study showed that the type and severity of cytokine productions from the epithelium or macrophages could be affected by different intensities and a combination of dsRNA and SEB. Further studies with this approach may improve our understanding of the development and exacerbation of airway inflammation and asthma.
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