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Estrogen Receptor α Roles in Breast Cancer Chemoresistance
Xu, Chao-Yang,Jiang, Zhi-Nong,Zhou, Ying,Li, Jia-Jia,Huang, Li-Ming Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.7
Resistance to chemotherapy treatment, which may lead to limited efficacy of systemic therapy in breast cancer patients, is multifactorial. Among the mechanisms of resistance to chemotherapy treatment, there are those closely related to estrogen receptor ${\alpha}$, P-glycoprotein, multidrug resistance-related protein, glutathione S-transferase pi and topoisomerase-II. $ER{\alpha}$ is ligand-activated transcription factor that regulates gene expression and plays a critical role in endocrine signaling. In previous preclinical and clinical studies, positive $ER{\alpha}$ expression in breast cancer cells was correlated with decreased sensitivity to chemotherapy. This article reviews current knowledge on the predictive value of $ER{\alpha}$ with regard to response to chemotherapy. Better understanding of its role may facilitate patient selection of therapeutic regimens and lead to optimal clinical outcomes.
CHAO-PING CHEN,Li,Xu,LI LI,YAN-QIN XU 장전수학회 2010 Proceedings of the Jangjeon mathematical society Vol.13 No.3
The Ioachimescu's constant I = 0.539645.... is defined as the limit of the sequence In = [수식] (n ∈ N). In this paper, we establish the asymptotic representation of the sequence (In)n∈N, and obtain the upper and lower bounds for In- and I.
( Li-yang Sun ),( Jiong-jie Yu ),( Ju-dong Li ),( Xin-fei Xu ),( Jia-he Wang ),( Bing Quan ),( Wen-tao Yan ),( Feng Shen ),( Chao Li ),( Lei Liang ),( Tian Yang ) 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
Aims: Surgical site infection (SSI) is a common postoperative complication and associated with an increased morbidity, hospital stay, and overall cost. The aim of the present study was to identify risk factors for SSIs after hepatic resection based on a large single-center cohort. Methods: A retrospective study was conducted of 6,132 patients who underwent liver resection without concomitant biliary reconstruction or gastrointestinal procedures between 2014 and 2016 at the largest hepatic center in China. The occurrences of SSI, classified as incisional SSI and organ/space SSI within 30 days after operation were investigated. Patient- and surgical-related risk variables were collected using standardized data collection form. A likelihood ratio forward regression model was used to assess the independent association of risk factors with SSI. Results: SSI developed in 587 patients (9.6%), including superficial/deep incisional SSI in 357 patients (5.8 %), and organ/ space SSI in 304 patients (5.0 %). Multivariate logistic regression analysis showed that obesity, diabetes mellitus, ASA score ≥ 2, liver cirrhosis, re-hepatectomy, hepatoliathiasis, and intraoperative blood transfusion were independent risk factors of overall SSI. However, incisional and organ/space SSI differed from each other with respect to risk factors. Among a variety of risk factors, hepatolithiasis, liver cirrhosis, and intraoperative blood transfusion were consistently associated with both incisional and organ/space SSI. Conclusions: SSI is a common complication after liver resection, and more caution should be taken in patients with hepatolithiasis or liver cirrhosis. Prevention strategies focusing on factors associated with SSI is necessary in order to reduce SSI after liver resection.
Fibulin2: a negative regulator of BMSC osteogenic differentiation in infected bone fracture healing
Li Shi-Dan,Xing Wei,Wang Shao-Chuan,Li You-Bin,Jiang Hao,Zheng Han-Xuan,Li Xiao-Ming,Yang Jing,Guo De-Bin,Xie Xiao-Yu,Jiang Ren-Qing,Fan Chao,Li Lei,Xu Xiang,Fei Jun 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Bone fracture remains a common occurrence, with a population-weighted incidence of approximately 3.21 per 1000. In addition, approximately 2% to 50% of patients with skeletal fractures will develop an infection, one of the causes of disordered bone healing. Dysfunction of bone marrow mesenchymal stem cells (BMSCs) plays a key role in disordered bone repair. However, the specific mechanisms underlying BMSC dysfunction caused by bone infection are largely unknown. In this study, we discovered that Fibulin2 expression was upregulated in infected bone tissues and that BMSCs were the source of infection-induced Fibulin2. Importantly, Fibulin2 knockout accelerated mineralized bone formation during skeletal development and inhibited inflammatory bone resorption. We demonstrated that Fibulin2 suppressed BMSC osteogenic differentiation by binding to Notch2 and inactivating the Notch2 signaling pathway. Moreover, Fibulin2 knockdown restored Notch2 pathway activation and promoted BMSC osteogenesis; these outcomes were abolished by DAPT, a Notch inhibitor. Furthermore, transplanted Fibulin2 knockdown BMSCs displayed better bone repair potential in vivo. Altogether, Fibulin2 is a negative regulator of BMSC osteogenic differentiation that inhibits osteogenesis by inactivating the Notch2 signaling pathway in infected bone.
RGS2 promotes estradiol biosynthesis by trophoblasts during human pregnancy
Tang Chao,Jin Meiyuan,Ma Bingbing,Cao Bin,Lin Chao,Xu Shouying,Li Jiayong,Xu Qiang 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Production of estradiol (E2) by the placenta during human pregnancy ensures successful maintenance of placental development and fetal growth by stimulating trophoblast proliferation and the differentiation of cytotrophoblasts into syncytiotrophoblasts. Decreased levels of E2 are closely associated with obstetrical diseases such as preeclampsia (PE) in the clinic. However, the mechanisms underlying the inhibition of placental E2 biosynthesis remain poorly understood. Here, we report that regulator of G-protein signaling 2 (RGS2) affects E2 levels by regulating aromatase, a rate-limiting enzyme for E2 biosynthesis, by using human trophoblast-derived JEG-3 cells and human placental villus tissues. RGS2 enhanced the protein degradation of the transcription factor heart and neural crest derivatives expressed 1 (HAND1) by suppressing ubiquitin-specific protease 14 (USP14)-mediated deubiquitination of HAND1, resulting in the restoration of HAND1-induced trans-inactivation of the aromatase gene and subsequent increases in E2 levels. However, aromatase bound to RGS2 and repressed RGS2 GTPase activating protein (GAP) activity. Moreover, we observed a positive correlation between RGS2 and aromatase expression in clinical normal and preeclamptic placental tissues. Our results uncover a hitherto uncharacterized role of the RGS2-aromatase axis in the regulation of E2 production by human placental trophoblasts, which may pinpoint the molecular pathogenesis and highlight potential biomarkers for related obstetrical diseases.
Treatment of Growth Plate Injury with Microencapsulated Chondrocytes
Wen-Chao Li,Rui-Jiang Xu,Yi-Long Xu,Jing-Xiang Huang,Yu-Hong Gao 한국생물공학회 2013 Biotechnology and Bioprocess Engineering Vol.18 No.4
Background: Tissue-engineered cartilage has provided a promising method in the treatment of physeal growth arrest. This study was designed to investigate transplantation of microencapsulated allogeneic chondrocytes to treat the injured growth plate. Methods: Allogeneic chondrocytes were encapsulated within alginate-polylysinealginate semipermeable membranes. Microencapsulated chondrocytes co-cultured with Bone Mesenchymal Stem Cells (BMSCs) were evaluated whether it could promote chondrogenesis of BMSCs. An experiment model of an injured growth plate was made by resecting the lateral half of the right distal femur physis in rabbits. Microencapsulated allogeneic chondrocytes, allogeneic chondrocytes as well as empty microcapsules were grafted into growth plate defects of 6-week-old rabbits. Histological and radiographic examinations were examined after transplantation up to 16 weeks. Results: The histological study showed that BMSCs co-cultured with microencapsulated chondrocytes could produce GAG and II collagen similarly with chondrocytes. Angular deformity and length discrepancy in the group with microencapsulated allogeneic chondrocytes were less than those in other groups (p < 0.001). The histological study confirmed the viability of microencapsulated chondrocytes at 16 weeks postoperatively. The neogenetic chondrocytes of columnar arrangement have been found in the growth plate defect to prevent early ossification and closure of the growth plate. Conclusions: The histological study confirmed the viability of microencapsulated chondrocytes at 16 weeks postoperatively. The neogenetic chondrocytes of columnar arrangement have been found in the growth plate defect to prevent early ossification and closure of the growth plate.
Xue-Ping Li,Qing-Qing Xu,Wei-Biao Liao,Zhan-Jun Ma,Xiao-Ting Xu,Meng Wang,Peng-Ju Ren,Li-Juan Niu,Xin Jin,Yong-Chao Zhu 한국식물학회 2016 Journal of Plant Biology Vol.59 No.5
Abscisic acid (ABA) and hydrogen peroxide (H2O2) are important regulatory factors involved in plant development under adversity stress. Here, the involvement of H2O2 in ABA-induced adventitious root formation in cucumber (Cucumis sativus L.) under drought stress was determined. The results indicated that exogenous ABA or H2O2 promoted adventitious rooting under drought stress, with a maximal biological response at 0.5 μM ABA or 800 μM H2O2. The promotive effects of ABA-induced adventitious rooting under drought stress were suppressed by CAT or DPI, suggesting that endogenous H2O2 might be involved in ABA-induced adventitious rooting. ABA increased relative water content (RWC), leaf chlorophyll content, chlorophyll fluorescence parameters (Fv/Fm, ΦPS II and qP), water soluble carbohydrate (WSC) and soluble protein content, and peroxidase (POD), polyphenol oxidase (PPO) and indoleacetate oxidase (IAAO) activities, while decreasing transpiration rate. However, the effects of ABA were inhibited by H2O2 scavenger CAT. Therefore, H2O2 may be involved in ABA-induced adventitious root development under drought stress by stimulating water and chlorophyll content, chlorophyll fluorescence, carbohydrate and nitrogen content, as well as some enzyme activities.
( Ju-dong Li ),( Xin-fei Xu ),( Jiong-jie Yu ),( Zhen-li Li ),( Hao Xing ),( Han Wu ),( Han Zhang ),( Chao Li ),( Ming-da Wang ),( Meng-chao Wu ),( Wan-yee Lau ),( Tian Yang ) 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
Aims: A family history of liver cancer is regarded as a risk factor for hepatocellular carcinoma (HCC) development. We investigated the association between family history and cancer recurrence and survival in patients with hepatitis B virus (HBV)- related HCC. Methods: Patients who underwent curative resection of HBV-related HCC between 2003 and 2013 from a tertiary hepatobiliary center in China were enrolled in this study. A family history was defined as a self-reported history of primary liver cancer in the first-degree relatives. Propensity score matching (PSM) and multivariable Cox-regression analyses were performed to compare the overall survival (OS) and recurrence-free survival (RFS) between patients with and without a family history of liver cancer. Results: Of 1,112 patients, 183 patients (16.5%) had a family history of liver cancer. A family history was not associated with OS and RFS (P=0.994 and 0.428) in the entire cohort. Using PSM, 179 pairs of patients with and without a family history but with comparable baseline characteristics and operative variables were created. A family history was associated with decreased OS and RFS (P=0.042 and 0.006) in the PSM cohort. On multivariable Cox-regression analyses, a family history was significantly associated with decreased OS (HR: 1.574, 95% CI: 1.171-2.116, P=0.003) and RFS (HR: 1.534, 95% CI: 1.176-2.002, P=0.002) after adjusting for other prognostic factors. Conclusions: A family history of liver cancer was associated with decreased OS and RFS rates after curative resection in patients with HBV-related HCC.