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| 1 | Effect of intravenous transplantation of bone marrow mesenchymal stem cells on neurotransmitters and synapsins in rats with spinal cord injury显示文摘Bone marrow mesenchymal stem cells were isolated, purified and cultured in vitro by Percoll density gradient centrifugation combined with the cell adherence method. Passages 3-5 bone marrow mesenchymal stem cells were transplanted into rats with traumatic spinal cord injury via the caudal vein. Basso-Beattie-Bresnahan scores indicate that neurological function of experimental rats was significantly improved over transplantation time (1-5 weeks). Expressions of choline acetyltransferase, glutamic acid decarboxylase and synapsins in the damaged spinal cord of rats was significantly increased after transplantation, determined by immunofluorescence staining and laser confocal scanning microscopy. Bone marrow mesenchymal stem cells that had migrated into the damaged area of rats in the experimental group began to express choline acetyltransferase, glutamic acid decarboxylase and synapsins, 3 weeks after transplantation. The Basso-Beattie- Bresnahan scores positively correlated with expression of choline acetyltransferase and synapsins. Experimental findings indicate that intravenously transplanted bone marrow mesenchymal stem cells traverse into the damaged spinal cord of rats, promote expression of choline acetyltransferase, glutamic acid decarboxylase and synapsins, and improve nerve function in rats with spinal cord injury. | Shaoqiang Chen Bilian Wu Jianhua Lin | 2012 | Neural Regeneration Research2012，7，19： | 5 |
| 2 | Nuclear Aurora kinase A switches m^(6)A reader YTHDC1 to enhance an oncogenic RNA splicing of tumor suppressor RBM4显示文摘Aberrant RNA splicing produces alternative isoforms of genes to facilitate tumor progression,yet how this process is regulated by oncogenic signal remains largely unknown.Here,we unveil that non-canonical activation of nuclear AURKA promotes an oncogenic RNA splicing of tumor suppressor RBM4 directed by m^(6)A reader YTHDC1 in lung cancer.Nuclear translocation of AURKA is a prerequisite for RNA aberrant splicing,specifically triggering RBM4 splicing from the full isoform(RBM4-FL)to the short isoform(RBM4-S)in a kinase-independent manner. | SiSi Li YangFan Qi JiaChuan Yu YuChao Hao Bin He MengJuan Zhang ZhenWei Dai TongHui Jiang SuYi Li Fang Huang Ning Chen Jing Wang MengYing Yang DaPeng Liang Fan An JinYao Zhao WenJun Fan YuJia Pan ZiQian Deng YuanYuan Luo Tao Guo Fei Peng ZhiJie Hou ChunLi Wang FeiMeng Zheng LingZhi Xu Jie Xu QingPing Wen BiLian Jin Yang Wang Quentin Liu | 2022 | Signal Transduction and Targeted Therapy2022，7，5： | 4 |
| 3 | Rheb promotes brown fat thermogenesis by Notch-dependent activation of the PKA signaling pathway显示文摘Increasing brown and beige fat thermogenesis have an anti-obesity effect and thus great metabolic benefits.However,the molecular mechanisms regulating brown and beige fat thermogenesis remain to be further elucidated.We recently found that fat-specific knockout of Rheb promoted beige fat thermogenesis.In the current study,we show that Rheb has distinct effects on thermogenic gene expression in brown and beige fat.Fat-specific knockout of Rheb decreased protein kinase A(PKA)activity and thermogenic gene expression in brown adipose tissue of high-fat diet-fed mice.On the other hand,overexpression of Rheb activated PKA and increased uncoupling protein 1 expression in brown adipocytes.Mechanistically,Rheb overexpression in brown adipocytes increased Notch expression,leading to disassociation of the regulatory subunit from the catalytic subunit of PKA and subsequent PKA activation.Our study demonstrates that Rheb,by selectively modulating thermogenic gene expression in brown and beige adipose tissues,plays an important role in regulating energy homeostasis. | Wen Meng Xiuci Liang Ting Xiao Jing Wang Jie Wen Hairong Luo Jianhui Teng Yanquan Fei Qinghai Zhang Bilian Liu Fang Hu juli Bai Meilian Liu Zhiguang Zhou Feng Liu | 2019 | Journal of Molecular Cell Biology2019，11，9： | 2 |
| 4 | Soluble CD163 and CD163 Expression on Monocytes Associated with Chronic Hepatitis B Inflammation and HBsAg Loss显示文摘Background and Aims:Monocyte/macrophage-associat-ed CD163 is an indicator of the severity of liver inflam-mation and cirrhosis,but the difference of soluble CD163(sCD163)levels in chronic hepatitis B(CHB)patients and hepatitis B surface antigen(HBsAg)-loss patients is un-clear.Herein,we aimed to compare the sCD163 levels in CHB patients and HBsAg-loss patients with or without an-tiviral treatment.Methods:sCD163 and CD163 expres-sion on monocytes were compared among four groups,healthy subjects,treatment-naïve CHB patients,sponta-neous HBsAg-loss patients,and treatment-related HBsAg-loss patients.The correlation between sCD163 levels and clinical parameters in CHB patients was analyzed.A group of 80 patients with hepatitis B virus(HBV)infection and liver biopsy were recruited.Results:sCD163 levels were higher in the CHB group than in the other three groups.sCD163 levels were higher in treatment-related HBsAg-loss patients than in spontaneous HBsAg-loss patients.sCD163 levels were negatively correlated with hepatitis B e-antigen(HBeAg)and HBsAg levels in HBeAg-positive patients.Liv-er biopsy results further demonstrated that sCD163 levels were elevated in CHB patients with substantial inflamma-tion(A≥2)or fibrosis(F≥2).The sCD163 model was more sensitive in predicting inflammation than other noninvasive models.Its levels were higher in patients with normal ala-nine aminotransferase levels and significant inflammation(A≥2)than in patients with no or mild inflammation.Con-clusions:sCD163 and CD163 expression on monocytes were associated with CHB inflammation and HBsAg loss,and may be used as markers to predict HBV-specific im-mune activation. | Peilin Xie Bilian Yao Dao Huang Yongyan Chen Qiming Gong Xinxin Zhang | 2022 | Journal of Clinical and Translational Hepatology2022，10，6： | 2 |
| 5 | Postprandial lipemia in children and adolescents显示文摘 | Kolovou GD Bilianou H Mikhailidis DP | 2011 | Curr Vasc Pharmacol2011，9，3： | 1 |
| 6 | Effects of pretreatment with an oral contraceptive on the time required to achieve: pituitary suppression with gonadotropin-releasing hormone analogues And on subsequent implantation and pregnancy rates 显示文摘 | Bilian MM Mahutte NG Dean N | 1998 | Fertil Steril1998，70，： | 1 |
| 7 | Ultrasound effects on the antioxidative defense systems of Porphyridium cruentum显示文摘 | Bilian Chen Jian Huang Juan Wang | 2008 | Colloids and Surfaces B: Biointerfaces2008，61，1： | 1 |
| 8 | Protective effects of Ginkgo biloba extract (EGb761) and its constituents quercetin and ginkgolide B against β-amyloid peptide-induced toxicity in SH-SY5Y cells显示文摘 | Chun Shi Lina Zhao Bilian Zhu Qianxi Li David T. Yew Zhibin Yao Jie Xu | 2009 | Chemico-Biological Interactions2009，，1： | 1 |
| 9 | Optimization of culturing conditions of Porphyridium cruentum using uniform design显示文摘 | Wang Juan Chen Bilian Ran Xiaozhen | 2007 | World Journal of Microbiology & Biotechnology2007，23，10： | 1 |
| 10 | Isolation and antioxidant property of the extracellular polysaccharide from Rhodella reticulata 显示文摘 | Bilian Chen Wenlang You Jian Huang | 2010 | World Joumal of Microbiol- ogy and Biotechnology2010，26，5： | 1 |
| 11 | The factor of intra- abdominal pressure in patients with morbid obesity显示文摘 | Todurov IM Bilians'ky LS Perekhristenko OV | 2013 | Klin Khir2013，5，： | 1 |
| 12 | Adoptive transfer of Pfkfb3-disrupted hematopoietic cells to wild-type mice exacerbates diet-induced hepatic steatosis and inflammation显示文摘Background and objectives:Hepatic steatosis and inflammation are key characteristics of non-alcoholic fatty liver disease(NAFLD).However,whether and how hepatic steatosis and liver inflammation are differentially regulated remains to be elucidated.Considering that disruption of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3(Pfkfb3/iPfk2)dissociates fat deposition and inflammation,the present study examined a role for Pfkfb3/iPfk2 in hematopoietic cells in regulating hepatic steatosis and inflammation in mice.Methods:Pfkfb3-disrupted(Pfkfb3^(+/-))mice and wild-type(WT)littermates were fed a high-fat diet(HFD)and examined for NAFLD phenotype.Also,bone marrow cells isolated from Pfkfb3^(+/-)mice andWT mice were differentiated into macrophages for analysis of macrophage activation status and for bone marrow transplantation(BMT)to generate chimeric(WT/BMT-Pfkfb3^(+/-))mice in which Pfkfb3 was disrupted only in hematopoietic cells and control chimeric(WT/BMT-WT)mice.The latter were also fed an HFD and examined for NAFLD phenotype.In vitro,hepatocytes were co-cultured with bone marrowderived macrophages and examined for hepatocyte fat deposition and proinflammatory responses.Results:After the feeding period,HFD-fed Pfkfb3^(+/-)mice displayed increased severity of liver inflammation in the absence of hepatic steatosis compared with HFD-fed WT mice.When inflammatory activation was analyzed,Pfkfb3^(+/-)macrophages revealed increased proinflammatory activation and decreased anti-proinflammatory activation.When NAFLD phenotype was analyzed in the chimeric mice,WT/BMT-Pfkfb3^(+/-) mice displayed increases in the severity of HFD-induced hepatic steatosis and inflammation compared with WT/BMT-WT mice.At the cellular level,hepatocytes co-cultured with Pfkfb3^(+/-) macrophages revealed increased fat deposition and proinflammatory responses compared with hepatocytes co-cultured with WT macrophages.Conclusions:Pfkfb3 disruption only in hematopoietic cells exacerbates HFD-induced hepatic steatosis and inflammation whereas the Pfkfb3/iPfk2 in nonhematopoietic cells appeared to be needed for HFD feeding to induce hepatic steatosis.As such,the Pfkfb3/iPfk2 plays a unique role in regulating NAFLD pathophysiology. | Xin Guo Bilian Zhu Hang Xu Honggui Li Boxiong Jiang Yina Wang Benrong Zheng Shannon Glaser Gianfranco Alpini Chaodong Wu | 2020 | Liver Research2020，4，3： | 1 |
| 13 | Superlinear/quadratic smoothing Broyden-like method for the generalized nonlinear complementarity problem显示文摘 | Chen Bilian Ma Changfeng | 2011 | Nonlinear Anal: Real World Appl2011，12，： | 1 |
| 14 | Influence of aging and menopause on lipids and lipoproteins in women 显示文摘 | Kolovou GD Bilianou HG | 2009 | An- giology2009，59，2： | 1 |
| 15 | Intrauterine devices 显示文摘 | | 2002 | Best Pract Res Clin Obstet Gynaecol2002，16，2： | 1 |
| 16 | A note on modified Householder iterative method free from second derivatives for nonlinear equations显示文摘 | Chen Bilian Ma Changfeng | 2008 | Applied Mathematics and Computation2008，203，2： | 1 |
| 17 | GRB10 regulates β-cell mass by inhibiting β-cell proliferation and stimulating β-cell dedifferentiation显示文摘Decreased functional β-cell mass is the hallmark of diabetes, but the cause of this metabolic defect remains elusive. Here, we show that the levels of the growth factor receptor-bound protein 10(GRB10), a negative regulator of insulin and m TORC1 signaling, are markedly induced in islets of diabetic mice and high glucose-treated insulinoma cell line INS-1 cells. β-cell-specific knockout of Grb10 in mice increased β-cell mass and improved β-cell function. Grb10-deficient β-cells exhibit enhanced m TORC1 signaling and reduced β-cell dedifferentiation, which could be blocked by rapamycin. On the contrary, Grb10 overexpression induced β-cell dedifferentiation in MIN6 cells. Our study identifies GRB10 as a critical regulator of β-cell dedifferentiation and β-cell mass, which exerts its effect by inhibiting m TORC1 signaling. | Zixin Cai Fen Liu Yan Yang Dandan Li Shanbiao Hu Lei Song Shaojie Yu Ting Li Bilian Liu Hairong Luo Weiping Zhang Zhiguang Zhou Jingjing Zhang | 2022 | Journal of Genetics and Genomics2022，49，3： | 1 |
| 18 | The factor of intra-abdominal pressure in patients with morbid obesity 显示文摘 | Todurov IM Bilians'ky LS Perekhristenko OV | 2013 | Klin Khir2013，，5： | 1 |
| 19 | Linking Marine Protected Areas to Integrated Coastal and Ocean Managemenl: a Review of Theory and Practice显示文摘 | Bilian Cicin-Saina Stefan~) Bclfinre | 2005 | Ocean& Coastal Management2005，，： | 1 |
| 20 | Protective effect of paeonol on beta-amyloid 25-35- induced toxicity in PC12 cells显示文摘BACKGROUND:Paeonol is a primary phenolic component of the Chinese medicinal herb Cortex moutan. Recent studies have shown that paeonol has anti-inflammatory, analgesic, and antioxidative effects as well as a significant cardioprotective effect against myocardial ischemia. OBJECTIVE: To investigate the protective effect of paeonol on β-amyloid 25-35-induced toxicity in PC12 cells and analyze its mechanism of action. DESIGN, TIME AND SETTING: A controlled repeated-measures cell-based study was performed in the Department of Pharmacology of Guangdong Medical College between September 2006 and December 2007. MATERIALS: Paeonol was supplied by Xuancheng Baicao Plant Industry and Trade Company, China. PC12 cells were a kind gift from Dr. Haitao Zhang at Guangdong Medical College. β-amyloid 25-35 was purchased from Sigma Company, USA. Lactate dehydrogenase (LDH) and malondialdehyde (MDA) kits were purchased from Nanjing Jiancheng Bioengineering Research Institute, China. METHODS: PC12 cells were maintained in Dulbecco's modified eagle's medium (DMEM) supplemented with 100 mL/L heat-inactivated horse serum and 50 mL/L fetal bovine serum at 37 ℃ and cultured in an incubator with 5% CO2. The medium was renewed every other day. Batches of cells were assigned into three groups. (1) Paeonol group: cells were preincubated with different concentrations of paeonol (12, 25 or 50 μmol/L) for one hour and β-amyloid 25-35 was added to the medium; (2) control group: cells were cultured in DMEM supplemented with 100 mL/L heat-inactivated horse serum and 50 mL/L fetal bovine serum; and (3) β-amyloid 25-35 group: β-amyloid 25-35 was added to the medium. MAIN OUTCOME MEASURES: When PC12 cells in each group were cultured for 24 hours, the cell viability was determined using the MTT reduction assay, LDH release into the culture media was measured by 2,4-dinitrophenylhydrazine chromatometry and MDA content was measured using a thiobarbituric acid assay. RESULTS: When PC12 cells were treated withβ-amyloid 25-35 (50 μmol/L) for 24 hours, their viability was significantly lower compared with the control group (P < 0.01). When the cells were treated with paeonol for one hour prior to incubation withβ-amyloid 25-35, their viability was significantly increased compared with theβ-amyloid 25-35 group (P < 0.05–0.01). LDH activity and MDA level in the β-amyloid 25-35 group were significantly increased compared with the control group (P < 0.01). When the cells were treated with different concentrations of paeonol, LDH activity and MDA level in PC12 cells were significantly decreased compared with theβ-amyloid 25-35 group (P < 0.01). CONCLUSION: Paeonol protects PC12 cells againstβ-amyloid 25-35-induced toxicity and the protective effect of paeonol is probably achieved through its antioxidative effects. | Daohua Xu Chenhui Zhou Bilian Xu Shiying Luo | 2008 | Neural Regeneration Research2008，3，8： | 1 |
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