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이범주,이익수,Chau Ha Pham,정순규,Sulhae Lee,홍광원,유희민 한국미생물·생명공학회 2020 Journal of microbiology and biotechnology Vol.30 No.8
Esculetin 6-O-β-D-arabinofuranosyl-(1 →6)-β-D-glucopyranoside (EAG) is a coumarin glycoside isolated from the stem bark of Fraxinus rhynchophylla. This study scrutinized the anti-proliferative activity of EAG on blood cancer-derived Jurkat leukemic cells. Cell viability assays in leukemic cancer cells determined that EAG possesses potent anti-proliferative effects. Moreover, treatment with EAG increased the proportion of apoptotic cells, resulted in cell cycle arrest being induced at the subG0/ G1 phase, and reduced the proportion of cells present in the S phase. In addition, mitochondrial membrane potential was reduced by EAG in Jurkat cells. Additionally, EAG triggered apoptosis that was mediated by the downregulation of BCL-XL, p-IκBα, and p-p65 expressions in addition to the upregulation of cleaved Caspase 3 and BAX expressions. These findings revealed that the toxic effect of EAG was mediated by intracellular signal transduction pathways that involved a mechanism in which reactive oxygen species (ROS) were upregulated. Thus, this study concludes that EAG could potentially serve as a therapeutic agent for leukemia.
Management of malignant central airway obstruction in a tertiary hospital in viet nam
( Giap Vu Van ),( Chau Ngo Quy ),( Ha Pham Ngoc ),( Du Nguyen Ngoc ),( Duc Hoang Anh ) 대한결핵 및 호흡기학회 2019 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.127 No.-
Objective: To evaluate the causes and treatments of patients with malignant central airway obstruction (CAO). Subjects: 37 patients were diagnosed with malignant CAO at Respiratory Center of Bach Mai Hospital. Methods: Retrospective and Prospective, descriptive study. Results: Average age was 53.8 ± 13.1 years. CAO occurred mainly in the 45-59 age group and in men more than women. No significant differences between the number of patients with cancer originated from in (group 1) and out (group 2) of the airway with regard to the number of patients, degree of stenosis and location of stenosis. In group 1, NSCLC accounted for the majority. In group 2, squamous-cell esophageal carcinoma had the highest proportion. The prevalence of patient having treatment was higher than not having treatment statistically. In the treatment group, the number of participants undergoing a combination of airway stent insertion and balloon dilatation was predominant. There were no significant differences in causes or locations or degrees of stenosis respecting treatment modalities. Participants having comfort after treatment accounted for the majority. In no treatment group and treatment group, cumulative proportions surviving were 0% (at 11th month) and 44.3% (at 9th month), respectively. The survival time in the treatment group (15.1 ± 3.4 months) was statistically longer than in no treatment group (4.4 ± 1.9 months) (p = 0.031). Conclusions: Causes of malignant CAO are varied and induce a variety of location and degree of stenosis, thereby leading to diverse treatments. Clinicians need to consider having appropriate treatments for patients to increase their comfort and survival time.
( Phil Jun Lee ),( Chau Ha Pham ),( Nguyen Thi Thanh Thuy ),( Hye-jin Park ),( Sung Hoon Lee ),( Hee Min Yoo ),( Namki Cho ) 한국미생물생명공학회(구 한국산업미생물학회) 2021 Journal of microbiology and biotechnology Vol.31 No.2
This study aimed to investigate the neuroprotective effects of 1-methoxylespeflorin G11 (MLG), a pterocarpan, against glutamate-induced neurotoxicity in neuronal HT22 hippocampal cells. The protective effects of MLG were evaluated using MTT assay and microscopic analysis. The extent of apoptosis was studied using flow cytometric analysis performed on the damaged cells probed with annexin V/propidium iodide. Moreover, mitochondrial reactive oxygen species (ROS) were assessed using flow cytometry through MitoSOXTM Red staining. To determine mitochondrial membrane potential, staining with tetramethylrhodamine and JC-1 was performed followed by flow cytometry. The results demonstrated that MLG attenuates glutamate-induced apoptosis in HT22 cells by inhibiting intracellular ROS generation and mitochondrial dysfunction. Additionally, MLG prevented glutamate-induced apoptotic pathway in HT22 cells through upregulation of Bcl-2 and downregulation of cleaved PARP-1, AIF, and phosphorylated MAPK cascades. In addition, MLG treatment induced HO-1 expression in HT22 cells. These results suggested that MLG exhibits neuroprotective effects against glutamate-induced neurotoxicity in neuronal HT22 cells by inhibiting oxidative stress and apoptosis.