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RISS 인기검색어
- 검색키워드
- 저자 : Yi-Juan Ma (검색결과 4 건)
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Xie, Mei-Juan,Ma, Yi-Hua,Miao, Lin,Wang, Yan,Wang, Hai-Zhen,Xing, Ying-Ying,Xi, Tao,Lu, Yuan-Yuan Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.13
Emodin, a natural anthraquinone isolated from the traditional Chinese medicine Radix rhizoma Rhei, can induce apoptosis in many kinds of cancer cells. This study demonstrated that emodin induces apoptosis in human colon cancer HCT116 cells by provoking oxidative stress, which subsequently triggers a p53-mitochondrial apoptotic pathway. Emodin induced mitochondrial transmembrane potential loss, increase in Bax and decrease in Bcl-2 expression and mitochondrial translocation and release of cytochrome c to cytosol in HCT116 cells. In response to emodin-treatment, ROS increased rapidly, and subsequently p53 was overexpressed. Pretreatment with the antioxidant NAC diminished apoptosis and p53 overexpression induced by emodin. Transfecting p53 siRNA also attenuated apoptosis induced by emodin, Bax expression and mitochondrial translocation being reduced compared to treatment with emodin alone. Taken together, these results indicate that ROS is a trigger of emodin-induced apoptosis in HCT116 cells, and p53 expression increases under oxidative stress, leading to Bax-mediated mitochondrial apoptosis.
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Xiao, Yang,Liu, Jun,Huang, Xin-En,Ca, Li-Hua,Ma, Yi-Min,Wei, Wei,Zhang, Rong-Xia,Huang, Xiao-Hong,Chang, Juan,Wu, Yi-Jia Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.23
Objective: To observe treatment effects and safety of fluvoxamine combined with oxycodone prolonged-release tablets in treating patients with moderate to severe cancer pain. Methods: Patients confirmed pathologically with cancer and complicated with moderate to severe pain, were divided into control and experimental groups. Oxycodone prolonged-release tablets, with or without fluvoxamine, were administrated to all study patients until pain relief. Degree of pain relief, dose of oxycodone prolonged-release tablets, side effects and quality of life were compared before and after treatment. Results: In total, 120 patients were recruited. No statistically significant difference was detected regarding age, gender, types of cancer, KPS between two groups of patients (P>0.05). Baseline pain score of patients with moderate pain in treatment and control group was $4.9{\pm}0.8$ and $5.1{\pm}0.8$, respectively; and decreased to $1.8{\pm}1.1$ and $1.2{\pm}1.1$ after treatment, respectively. Pain intensity was significantly reduced in the treatment group (P=0.028). Average daily consumption of oxycodone prolonged-release tablets was ($54.0{\pm}19.6$) mg and ($44.7{\pm}18.7$) mg respectively, which is lower in treatment grpup than in control group, but the difference was not statistically significant (P=0.065). Baseline pain score of patients with severe pain in treatment and control groups were $8.3{\pm}1.1$ and $8.3{\pm}1.1$, respectively; and pain intensity after treatment decreased to $2.9{\pm}1.0$ and $2.3{\pm}1.0$. Pain intensity was significantly reduced in the treatment group, with statistical significance (P=0.026). Average daily consumption of oxycodone prolonged-release tablets was ($132.0{\pm}42.2$) mg and ($110.7{\pm}33.9$) mg, respectively, which is lower in treatment group than in control group, and the difference was statistically significant (P=0.035). In terms of quality of life, patients in treatment group had better performance status, daily activity, mood, and sleep than that in control group (P < 0.05). Patients in two groups had similar side effects, eg., constipation, nausea/vomiting, lethargy, dizziness, itchy skin, dysuria, and ataxia. Lower incidence of nausea/vomiting, lethargy, was obtained from patients in treatment than in control group, while significant low constipation was observed in treatment than in control group (35.0% vs 49.2%, P=0.026). Conclusion: Fluvoxamine combined with oxycodone prolonged-release tablets could be more effective in treating patients with cancer pain, and could reduce the dosage of oxycodone prolonged-release tablets and thus be associated with lower side effects, and improved quality of life.
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Xue-Yong Zhang,Ying-Na Jian,Hong Duo,Xiu-Ying Shen,Yi-Juan Ma,Yong Fu,Zhi-Hong Guo 대한기생충학ㆍ열대의학회 2019 The Korean Journal of Parasitology Vol.57 No.4
Coenurosis is an important zoonotic helminthic disease caused by the larval stage of the tapeworm Taenia multiceps. This parasite typically infects the brain of the intermediate hosts, including sheep, goat, cattle and even hu- mans. We report a case of T. multiceps infection in a yak confirmed by clinical symptoms, morphological characteristics, and molecular and phylogenetic analyses. The coenurus was thin-walled, whitish, and spherical in shape with a diameter of 10 cm. The parasite species was identified as T. multiceps by PCR amplification and sequencing of the 18S rRNA, cox1 and nad1 genes. Three gene sequences all showed high homology (all above 97%) with the reference sequences from different hosts. Moreover, phylogenetic reconstructions with the 3 published Taenia gene sequences confirmed that the Qinghai yak isolate was closely related to T. multiceps. Although there are advanced diagnosis and treatment meth- ods for coenurosis, early infection is difficult to diagnose. Importantly, the findings of yak infection case should not be ig- nored due to its zoonotic potential.
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Li Cui,Weiquan Bu,Jie Song,Liang Feng,Tingting Xu,Dan Liu,Wenbo Ding,Jianhua Wang,Changyang Li,Binge Ma,Yi Luo,Ziyu Jiang,Chengcheng Wang,Juan Chen,Jian Hou,Hong-mei Yan,Lei Yang,Xiao-bin Jia 대한약학회 2018 Archives of Pharmacal Research Vol.41 No.3
Alantolactone is a sesquiterpene lactone isolatedfrom Inula helenium L. Although alantolactone possessesanti-inflammation and apoptosis-induction activities, theunderlying mechanism of anti-cancer effect on humanbreast cancer cells remains largely unknown. In this study,we explored the possibility of alantolactone as an apoptosis-inducing cytotoxic agent using MDA-MB-231 cells asin vitro model. Alantolactone significantly induced itsapoptosis, demonstrated by cell cycle analysis, annexinV-APC/7-AAD double staining and dUTP nick end labeling. Additionally, alantolactone triggered the mitochondrial-mediated caspase cascade apoptotic pathway, whichwas confirmed by increased Bax/Bcl-2 ratio, loss of MMP,release of cytc from mitochondria to cytoplasm, activationof caspase 9/3, and subsequent cleavage of PARP. Z-VADFMKpartially prevented apoptosis induced by alantolactone. Alantolactone provoked the production of ROS, whileNAC (a scavenger of ROS) reversed alantolactone-mediateddepolarization of MMP and apoptosis. Alantolactonemodulated the activities of MAPKs. As expected, cotreatmentwith SB203580, SP600125 or U0126 could reducedthe apoptotic rate. Furthermore, alantolactone decreasedthe protein expressions of p-NF-kB p65 and p-STAT3,increased p-c-Jun level in a dose-dependent manner. Thesefindings suggested that alantolactone possessed anticanceractivity via ROS-mediated mitochondrial dysfunctioninvolving MAPK pathway, and had an effect on the transcriptionfactors of NF-kB, AP-1 and STAT3.
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