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| 1 | Function of apoptosis and expression of the proteins Bcl-2,p53 and C-myc in the development of gastric cancer显示文摘INTRODUCTIONIn China ,the incidence and mortality of gastric cancer rank the second among all cancers. Recent development of cancer [1-20].The aim of this study was investigat the insight of apoptosis and bcl-2, p53 and C-myc protein expression in the development of gastric cancer . | An Gao Xu Shao Guang Li Ji Hong Liu Ai Hua Gan Research Laboratory of Digestive Disease,Huizhou Central People’s Hospital,Huizhou 516001,Guangdong Province,ChinaDr.An Gao Xu graduated from Guangdong Medical College in 1984.He is an associate physician-in-chief,specializing in the research and treatment of gastrointestinal and liver tumors.He has published 24 papers and 1 book. | 2001 | World Journal of Gastroenterology2001，7，3： | 91 |
| 2 | Advanced characterization of pores and fractures in coals by nuclear magnetic resonance and X-ray computed tomography显示文摘This paper demonstrates capabilities of low-field nuclear magnetic resonance (NMR) and microfocus X-ray computed tomography (μCT) in advanced, nondestructive, and quantitative characterization of pore types, producible porosity, pore structure, and spatial disposition of pore-fractures in coals. Results show that the NMR transverse relaxation time (T2) at 0.5–2.5, 20–50, and >100 ms correspond to pores of <0.1 μm, >0.1 μm, and fractures, respectively. A much higher T2 spectrum peak reflects a much better development of pores (or fractures) corresponding to the T2, and vice versa. Three basic components in coals, i.e., the pores (or fractures), coal matrix, and minerals have their distinctive range of CT numbers. Among these, the CT number of pores is commonly less than 600 HU. The producible porosity, which is a determination of permeability, can be calculated by T2 cutoff value (T2C) of coal NMR. The coal pore structure can be efficiently estimated by the newly proposed 'T2C based model'. Finally, μCT scan was proven capable of modeling and spatial visualization of pores and fractures. | YAO YanBin, LIU DaMeng, CAI YiDong & LI JunQian School of Energy Resources, China University of Geosciences, Beijing 100083, China | 2010 | Science China Earth Sciences2010，53，6： | 61 |
| 3 | Biomolecular basis of the role of diabetes mellitus in osteoporosis and bone fractures显示文摘Osteoporosis has become a serious health problem throughout the world which is associated with an increased risk of bone fractures and mortality among the people of middle to old ages.Diabetes is also a major health problem among the people of all age ranges and the sufferers due to this abnormality increasing day by day.The aim of this review is to summarize the possible mechanisms through which diabetes may induce osteoporosis.Diabetes mellitus generally exerts its effect on different parts of the body including bone cells specially the osteoblast and osteoclast,muscles,retina of the eyes,adipose tissue,endocrine system specially parathyroid hormone(PTH) and estrogen,cytokines,nervous system and digestive system.Diabetes negatively regulates osteoblast differentiation and function while positively regulates osteoclast differentiation and function through the regulation of different intermediate factors and thereby decreases bone formation while increases bone resorption.Some factors such as diabetic neuropathy,reactive oxygen species,Vitamin D,PTH have their effects on muscle cells.Diabetes decreases the muscle strength through regulating these factors in various ways and ultimately increases the risk of fall that may cause bone fractures. | Bipradas Roy | 2013 | World Journal of Diabetes2013，4，4： | 41 |
| 4 | Immunohistochemical study on p53,H-rasp21,c-erbB-2 protein and PCNA expression in HCC tissues of Hart and minority ethnic patients显示文摘AIM To find out the difference of humanprimary liver carcinogenesis between Han andminority ethnic patients in Xinjiang.METHODS Expression of p53,c-erbB-2,H-rasp21 protein and proliferating cell nuclearantigen(PCNA)in tumor tissues of 50 patients(Han 38,minority 12)with primary hepaticcarcinoma was detected byimmunohistochemistry(LSAB).RESULTS The positive frequency of p53,c-erbB-2,H-rasp21 and PCNA expression was46.0%(23/50),70.0%(35/50),68.0%(34/50)and 82.0%(41/50)in tumor tissues;4.0%(2/50),22.0%(11/50),64.0%(32/50)and 52.0%(26/ 50)in peritumors respectively and asignificant difference,except for H-rasp21,ofoncogene alteration was found(P<0.05)between tumor and non-tumorous tissues.Combined the three oncogenes alteration,26%(13/50)tumor tissues had positiveimmunoreactivity,but in peritumor and normallivers it was negative.The positive rate of p53,c-erbB-2 and H-rasp21 protein expression was39.5%(15/38),60.5%(23/38)and 39.5%(15/38)in tumors of Han patients;66.7%(8/12),100%(12/12)and 75.0%(9/12)in minoritiesrespectively,with statistical difference (P<0.05).CONCLUSION Overexpression of p53,c-erbB-2and H-rasp21 in human primary liver carcinoma isan important biomarker of genetic alteration.The different frequency of these oncogeneticchanges may reflect some environmental or/andethnic hereditary factors affecting the livercarcinogenesis.The special life style of Han,Uygur,Kazak and Mongolia nationalities inXinjiang may also be related to theetiopathogenesis of this disease. | Guo Yue Lin Zhao Lun Chen Cai Mo Lu Ying Li Xiao Jia Ping Rong Huang Department of Laboratory Medicine,Chinese PLA 474 Hospital,Urumqi 830011,Xinjiang Uygur Autonomic Region,China Department of Pathology,the 1st Teaching Hospital,Xinjiang Medical University,Urumqi 830054,Xinjiang Uygur Autonomic Region,China | 2000 | World Journal of Gastroenterology2000，6，2： | 40 |
| 5 | Androgen receptor: structure, role in prostate cancer and drug discovery显示文摘Androgens and androgen receptors (AR) play a pivotal role in expression of the male phenotype. Several diseases, such as androgen insensitivity syndrome (AIS) and prostate cancer, are associated with alterations in AR functions. Indeed, androgen blockade by drugs that prevent the production of androgens and/or block the action of the AR inhibits prostate cancer growth. However, resistance to these drugs often occurs after 2-3 years as the patients develop castration-resistant prostate cancer (CRPC). In CRPC, a functional AR remains a key regulator. Early studies focused on the functional domains of the AR and its crucial role in the pathology. The elucidation of the structures of the AR DNA binding domain (DBD) and ligand binding domain (LBD) provides a new framework for understanding the functions of this receptor and leads to the development of rational drug design for the treatment of prostate cancer. An overview of androgen receptor structure and activity, its actions in prostate cancer, and how structural information and high-throughput screening have been or can be used for drug discovery are provided herein. | MH Eileen TAN Jun LI H Eric XU Karsten MELCHER Eu-leong YONG | 2015 | Acta Pharmacologica Sinica2015，36，1： | 39 |
| 6 | Delayed hepatocarcinogenesis through antiangiogenic intervention in the nuclear factor-kappa B activation pathway in rats显示文摘BACKGROUND:The active form of nuclear factor-kappa B(NF- κB)is involved in the initiation,generation,and development of hepatocellular carcinoma(HCC),and is up-regulated in inflammation-associated malignancies.We investigated the dynamic expression of NF-κB and its influences on the occurrence of HCC through antiangiogenic(thalidomide) intervention in NF-κB activation. METHODS:Hepatoma models were induced with 2-fluorenyl- acetamide(2-FAA,0.05%)in male Sprague-Dawley rats,and thalidomide(100 mg/kg body weight)was administered intragastrically to intervene in NF-κB activation.The pathological changes in the liver of sacrificed rats were assessed after hematoxylin and eosin staining.NF-κB mRNA was amplified by RT-nested PCR.The alterations of NF-κB and vascular endothelial growth factor(VEGF)expression were analyzed by enzyme-linked immunosorbent assay,immunohistochemistry,and Western blotting. RESULTS:Rat hepatocytes showed denatured,precancerous,and cancerous stages in hepatocarcinogenesis,with an increasing tendency of hepatic NF-κB,NF-κB mRNA,and VEGF expression,and their values in the HCC group were higher than those in controls(P<0.001).In the thalidomide- treated group,the morphologic changes generated only punctiform denaturation and necrosis at the early or middle stages,and nodular hyperplasia or a little atypical hyperplasia at the final stages,with the expression of NF-κB (χ2=9.93,P<0.001)and VEGF(χ2=8.024,P<0.001)lower than that in the 2-FAA group. CONCLUSION:NF-κB is overexpressed in hepatocarcinogenesis and antiangiogenic treatment down-regulates the expression of NF-κB and VEGF,and delays the occurrence of HCC. | Dong, Zhi-Zhen Yao, Deng-Fu Wu, Wei Yao, Min Yu, Hong-Bo Shen, Jun-Jun Qiu, Li-Wei Yao, Ning-Hua Sai, Wen-Li Yang, Jun-Ling | 2010 | Hepatobiliary & Pancreatic Diseases International2010，9，2： | 31 |
| 7 | Urinary trypsin inhibitor attenuates hepatic ischemia-reperfusion injury by reducing nuclear factor-kappa B activation显示文摘BACKGROUND:Urinary trypsin inhibitor(UTI)inhibits the inflammatory response and protects against ischemia- reperfusion(I/R)injury.The inflammatory response is mediated by nuclear factor-kappa B(NF-κB)and its related target genes and products such as vascular endothelial cell adhesion molecule and CXC chemokines.We aimed to assess the roles of those mediators in a UTI-treated mouse model of hepatic I/R injury. METHODS:Treatment group 1(UTI given 5 minutes prior to liver ischemia),treatment group 2(UTI given 5 minutes after the anhepatic phase)and a control group were investigated.Blood and liver samples were obtained and compared at 1,3,6 and 24 hours after reperfusion. RESULTS:Attenuation of pathological hepatocellular damage was greater in the treatment groups than in the control group(P<0.05).Compared with the control group, the UTI treatment groups showed significantly lower serum alanine aminotransferase and aspartate aminotransferase levels,decreased myeloperoxidase activity,and reduced NF- κB activation.Also downregulated was the expression of tumor necrosis factor-alpha,cytokine-induced neutrophil chemoattractant,and macrophage inflammatory protein-2 at the mRNA level.P-selectin protein and intercellular adhesion molecule-1 protein expression were also downregulated.In addition,the treatment group 1 showed a better protective effect against I/R injury than the treatment group 2.CONCLUSIONS:UTI reduces NF-κB activation and downregulates the expression of its related mediators, followed by the inhibition of neutrophil aggregation and infiltration in hepatic I/R injury.The protective role of UTI is more effective in prevention than in treatment. | Wu, Yi-Jun Ling, Qi Zhou, Xin-Hui Wang, Yan Xie, Hai-Yang Yu, Ji-Ren Zheng, Shu-Sen | 2009 | Hepatobiliary & Pancreatic Diseases International2009，8，1： | 28 |
| 8 | Production of proinflammatory cytokines in the human THP-1 monocyte cell line following induction by Tp0751,a recombinant protein of Treponema pallidum显示文摘The tissue destruction characteristic of syphilis infection may be caused by inflammation due to Treponema pallidum and the ensuing immune responses to the pathogen.T.pallidum membrane proteins are thought to be potent inducers of inflammation during the early stages of infection.However,the actual membrane proteins that induce inflammatory cytokine production are not known,nor are the molecular mechanisms responsible for triggering and sustaining the inflammatory cascades.In the present study,Tp0751 recombinant protein from T.pallidum was found to induce the production of proinflammatory cytokines,including TNF-α,IL-1βand IL-6,in a THP-1 human monocyte cell line.The signal transduction pathways involved in the production of these cytokines were then further investigated.No inhibition of TNF-a,IL-1β,or IL-6 production was observed following treatment with the SAPK/JNK specific inhibitor SP600125 or with an ERK inhibitor PD98059.By contrast,anti-TLR2 mAb,anti-CD14 mAb,and the p38 inhibitor SB203580 significantly inhibited the production of all three cytokines.In addition,pyrrolidine dithiocarbamate (PDTC),a specific inhibitor of NF-κB,profoundly inhibited the production of these cytokines.Tp0751 treatment strongly activated NF-κB,as revealed by Western blotting.However,NF-κB translocation was significantly inhibited by treatment with PDTC.These results indicated that TLR2,CD14,MAPKs/p38,and NF-κB might be implicated in the inflammatory reaction caused by T.pallidum infection. | LIU ShuangQuan1,2,WANG ShiPing1,WU YiMou3,ZHAO FeiJun3,ZENG TieBing3,ZHANG YueJun3,ZHANG QiuGui2 & GAO DongMei1 1 Department of Parasitology,Xiangya School of Medicine,Central South University,Changsha 410078 ,China 2 The First Affiliated Hospital,University of South China,Hengyan 421001,China 3 Department of Microbiology and Immunology,University of South China,Hengyan 421001,China | 2010 | Science China(Life Sciences)2010，53，2： | 28 |
| 9 | Nuclear factor kappa B role in inflammation associated gastrointestinal malignancies显示文摘Nuclear factor kappa B(NF-κB) has an established role in the regulation of innate immunity and inflammation.NF-κB is also involved in critical mechanisms connecting inflammation and cancer development.Recent investigations suggest that the NF-κB signaling cascade may be the central mediator of gastrointestinal malignancies including esophageal,gastric and colorectal cancers.This review will explore NF-κB's function in inflammation-associated gastrointestinal malignancies,highlighting its oncogenic contribution to each step of carcinogenesis.NF-κB's role in the inflammation-to-carcinoma sequence in gastrointestinal malignancies warrants stronger emphasis upon targeting this pathway in achieving greater therapeutic efficacy. | Sahil Gambhir Dinesh Vyas Michael Hollis Apporva Aekka Arpita Vyas | 2015 | World Journal of Gastroenterology2015，21，11： | 24 |
| 10 | Effects of interventions on oxidative stress and inflammation of cardiovascular diseases显示文摘Excessive oxidative stress and low-grade chronic inflammation are major pathophysiological factors contributing to the development of cardiovascular diseases (CVD) such as hypertension, diabetes and atherosclerosis. Accumulating evidence suggests that a compromised antioxidant system can lead to excessive oxidative stress in cardiovascular related organs, resulting in cell damage and death. In addition, increased circulating levels of pro-inflammatory cytokines, such as tumor necrosis factor α, interleukin-6 and C-reactive protein, are closely related to morbidity and mortality of cardiovascular complications. Emerging evidence suggests that interventions including nutrition, pharmacology and exercise may activate expression of cellular anti-oxidant systems via the nuclear factor erythroid 2-related factor 2-Kelchlike ECH-associated protein 1 signaling pathway and play a role in preventing inflammatory processes in CVD. The focus of the present review is to summarize recent evidence showing the role of these anti-oxidant and anti-inflammatory interventions in cardiovascular disease. We believe that these findings may prompt new effective pathogenesis-oriented interventions, based on the exercise-induced protection from disease in the cardiovascular system, aimed at targeting oxidant stress and inflammation. | Sewon Lee Yoonjung Park Mozow Yusof Zuidema Mark Hannink | 2011 | World Journal of Cardiology2011，3，1： | 23 |
| 11 | RANKL,a necessary chance for clinical application to osteoporosis and cancer-related bone diseases显示文摘Osteoporosis is a common bone disease characterized by reduced bone and increased risk of fracture. In postmenopausal women, osteoporosis results from bone loss attributable to estrogen deficiency. Osteoclast differentiation and activation is mediated by receptor activator of nuclear factor-κB ligand(RANKL), its receptor receptor activator of nuclear factor-κB(RANK), and a decoy receptor for RANKL, osteoprotegerin(OPG). The OPG/RANKL/RANK system plays a pivotal role in osteoclast biology. Currently, a fully human antiRANKL monoclonal antibody named denosumab is being clinically used for the treatment of osteoporosis and cancer-related bone disorders. This review describes recent advances in RANKL-related research, a story from bench to bedside. First, the discovery of the key factors, OPG/RANKL/RANK, revealed the molecular mechanism of osteoclastogenesis. Second, we established three animal models:(1) a novel and rapid bone loss model by administration of glutathione-S transferase-RANKL fusion protein to mice;(2) a novel mouse model of hypercalcemia with anorexia by overexpression of soluble RANKL using an adenovirus vector; and(3) a novel mouse model of osteopetrosis by administration of a denosumab-like anti-mouse RANKL neutralizing monoclonal antibody. Lastly, anti-human RANKL monoclonal antibody has been successfully applied to the treatment of osteoporosis and cancer-related bone disorders in many countries. This is a real example of applying basic science to clinical practice. | Hisataka Yasuda | 2013 | World Journal of Orthopedics2013，4，4： | 22 |
| 12 | Acacetin protects against cerebral ischemia-reperfusion injury via the NLRP3 signaling pathway显示文摘Acacetin(5,7-dihydroxy-4′-methoxyflavone), a potential neuroprotective agent, has an inhibitory effect on lipopolysaccharide-induced neuroinflammatory reactions. However, whether acacetin has an effect on inflammatory corpuscle 3(NLRP3) after cerebral ischemia-reperfusion injury has not been fully determined. This study used an improved suture method to establish a cerebral ischemia-reperfusion injury model in C57BL/6 mice. After ischemia with middle cerebral artery occlusion for 1 hour, reperfusion with intraperitoneal injection of 25 mg/kg of acacetin(acacetin group) or an equal volume of saline(0.1 mL/10 g, middle cerebral artery occlusion group) was used to investigate the effect of acacetin on cerebral ischemia-reperfusion injury. Infarct volume and neurological function scores were determined by 2,3,5-triphenyltetrazolium chloride staining and the Zea-Longa scoring method. Compared with the middle cerebral artery occlusion group, neurological function scores and cerebral infarction volumes were significantly reduced in the acacetin group. To understand the effect of acacetin on microglia-mediated inflammatory response after cerebral ischemia-reperfusion injury, immunohistochemistry for the microglia marker calcium adapter protein ionized calcium-binding adaptor molecule 1(Iba1) was examined in the hippocampus of ischemic brain tissue. In addition, tumor necrosis factor-α, interleukin-1β, and interleukin-6 expression in ischemic brain tissue of mice was quantified by enzyme-linked immunosorbent assay. Expression of Iba1, tumor necrosis factor-α, interleukin-1β and interleukin-6 was significantly lower in the acacetin group compared with the middle cerebral artery occlusion group. Western blot assay results showed that expression of Toll-like receptor 4, nuclear factor kappa B, NLRP3, procaspase-1, caspase-1, pro-interleukin-1β, and interleukin-1β were significantly lower in the acacetin group compared with the middle cerebral artery occlusion group. Our findings indicate that acacetin has a protective effect on cerebral ischemia-reperfusion injury, and its mechanism of action is associated with inhibition of microglia-mediated inflammation and the NLRP3 signaling pathway. | Juan Bu Shen Shi Hui-Qin Wang Xiao-Shan Niu Zong-Feng Zhao Wei-Dong Wu Xiao-Ling Zhang Zhi Ma Yan-Jun Zhang Hui Zhang Yi Zhu | 2019 | Neural Regeneration Research2019，14，4： | 22 |
| 13 | Modified Da-chai-hu Decoction regulates the expression of occludin and NF-κB to alleviate organ injury in severe acute pancreatitis rats显示文摘Modified Da-chai-hu Decoction(MDD), a traditional Chinese medicinal formulation, which was empirically generated from Da-chai-hu decoction, has been utilized to treat severe acute pancreatitis(SAP) for decades. The aim of the present study was to explore its potential organprotective mechanism in SAP. In the present study, rat SAP model was induced by retrograde injection of 3.5% sodium taurocholate into the biliopancreatic duct, MDD(23.35 g/kg body weight, twelve times the clinical dose) were orally given at 2 h before and 10 h after injection. At 12 h after model induction, blood was taken from vena cava for analysis of amylase, diamine oxidase(DAO), pulmonary surfactant protein-A(SP-A), and C-reactive protein(CRP). Histopathological change of pancreas, ileum and lung was assayed by H&E staining, myeloperoxidase(MPO) activity were determinated using colorimetric assay, and the expressions of occludin and nuclear factor-κB(NF-κB) were detected by real-time RT-PCR and western blot, respectively. In addition, the tissue concentrations of tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), and monocyte chemoattractant protein-1(MCP-1) were measured by enzyme-linked immunosorbent assay(ELISA). The results showed that in SAP rats, MDD significantly alleviated histopathological damage, depressed the MPO activity and the concentrations of TNF-α, IL-1β, and MCP-1 of pancreas, ileum and lung, and reduced the serum levels of amylase [(3283.4±585.5) U·L^(-1) vs(5626.4±795.1) U·L^(-1)], DAO[(1100.1±334.3) U·L^(-1) vs(1666.4±525.3) U·L^(-1)] and CRP [(7.6±1.2) μg·mL^(-1) vs(17.8±3.8) μg·mL^(-1)]. However, the serum SP-A concentration [(106.1±16.6) pg·mL^(-1) vs(90.1±14.9) pg·mL^(-1)] was elevated when treated SAP rats with MDD. Furthermore, MDD increased the occludin expression and reduced the NF-κB expression in pancreas, ileum and lung of SAP rats. Our findings suggested that MDD administration was an effective therapeutic approach for SAP treatment. It could up-regulate occludin expression to protect intercellular tight junction and down-regulate NF-κB expression to inhibit inflammatory reaction of pancreas, ileum and lung. | ZHAO Guang ZHUO Yu-Zhen CUI Li-Hua LI Cai-Xia CHEN Sha-Yan LI Dan LIU Jun-Hong LI Di-Hua CUI Nai-Qiang ZHANG Shu-Kun | 2019 | Chinese Journal of Natural Medicines2019，17，5： | 23 |
| 14 | Therapy of gallstone disease:What it was,what it is,what it will be显示文摘Cholesterol gallstone disease is a common clinical condition influenced by genetic factors,increasing age,female gender,and metabolic factors.Although laparoscopic cholecystectomy is currently considered the gold standard in treating patients with symptomatic gallstones,new perspectives regarding medical therapy of cholelithiasis are currently under discussion,also taking into account the pathogenesis of gallstones,the natural history of the disease and the analysis of the overall costs of therapy.A careful selection of patients may lead to successful nonsurgical therapy in symptomatic subjects with a functioning gallbladder harboring small radiolucent stones.The classical oral litholysis by ursodeoxycholic acid has been recently paralleled by new experimental observations,suggesting that cholesterol-lowering agents which inhibit cholesterol synthesis (statins) or intestinal cholesterol absorption (ezetimibe),or drugs acting on specific nuclear receptors involved in cholesterol and bile acid homeostasis,might be proposed as additional approaches for treating cholesterol gallstones.In this review we discuss old,recent and future perspectives on medical treatment of cholesterol cholelithiasis. | Piero Portincasa Agostino Di Ciaula Leonilde Bonfrate David QH Wang | 2012 | World Journal of Gastrointestinal Pharmacology and Therapeutics2012，3，2： | 21 |
| 15 | Efficient production of omega-3 fatty acid desaturase (sFat-1)-transgenic pigs by somatic cell nuclear transfer显示文摘Omega-3(ω-3) fatty acid desaturase transgenic pigs may improve carcass fatty acid composition. The use of transgenic pigs is also an excellent large animal model for studying the role of ω-3 fatty acids in the prevention and treatment of coronary heart disease and cancer. Transgenic pigs carrying synthesized fatty acid desaturase-1 gene (sFat-1) from Caenorhabditis briggsae by somatic cell nuclear transfer (SCNT) were produced for the first time in China. Porcine fetal fibroblast cells were transfected with a sFat-1 expression cassette by the liposome-mediated method. Transgenic embryos were reconstructed by nuclear transfer of positive cells into enucleated in vitro matured oocytes. A total of 1889 reconstructed embryos were transferred into 10 naturally cycling gilts. Nine early pregnancies were established, 7 of which went to term. Twenty-one piglets were born. The cloning efficiency was 1.1% (born piglets/transferred embryos). The integration of the sFat-1 gene was confirmed in 15 live cloned piglets by PCR and Southern blot except for 2 piglets. Expression of the sFat-1 gene in 12 of 13 piglets was detected with RT-PCR. The data demonstrates that an efficient system for sFat-1 transgenic cloned pigs was developed, which led to the successful production of piglets expressing the sFat-1 gene. | PAN DengKe1, ZHANG Li1, ZHOU YanRong2, FENG Chong1, LONG Chuan1, LIU Xiao1, WAN Rong3, ZHANG Jian3, LIN AiXing3, DONG EnQiu4, WANG ShuChen4, XU HouGang4 & CHEN HongXing2 1 Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, Beijing 100193, China 2 Beijing Institute of Biotechnology, Beijing 100071, China 3 China Agricultural University, Beijing 100193, China 4 Yutian Breeding Swine Farms, Yutian 064104, China | 2010 | Science China(Life Sciences)2010，53，4： | 21 |
| 16 | Chemoprevention of tea on colorectal cancer induced by dimethylhydrazine in Wistar rats显示文摘AIM To investigate the chemopreventiveeffects of green tea and tea pigment on 1,2-dimethylhydrazine(DMH)-induced rat colorectalcarcinogenesis.METHODS Male weaning Wistar rats wererandomly allocated into four groups.Rats in thepositive control group were given s.c.injectionof DMH,once a week for ten weeks;rats in tea-treated groups,with the same DMH treatment asin the positive group,received 2% green tea and0.1% tea pigments;rats in the negative controlgroup were given s.c.injection of the samevolume of saline as well as DMH in the positivegroup.Animals were sacrified and necropsied atthe end of week 16 and week 32.RESULTS Aberrant cryptic foci(ACF)wereformed in animals in DMH-treated groups at theend of week 16.Compared to the DMH group,green tea and tea pigments groups had less ACF(148.25 and 204.25,respectively,P<0.01).Atthe end of week 32,all rats in DMH groupdeveloped large intestinal tumors.The resultsalso showed that DMH increased labeling index(LI)of proliferating cell nuclear antigen(PCNA)of intestinal mucosa and the expression of ras-p21.However,in the tea-treated groups,PCNA-LI was significantly reduced as compared withthe positive control group(36.63 and 40.36 inthe green tea group and tea pigment group,respectively,at the end of the experiment,P<0.01).ras-p21 expression was alsosignificantly reduced(2.07 and 2.36 in the colontumors of rats in the green tea group and teapigments group,respectively at the end of theexperiment,P<0.01).Furthermore,green tea and tea pigment inhibited the expression of Bcl-2protein(2,5,1,0 and 2,4,1,0,respectively,at the end of the experiment P<0.01),andinduced expression of Bax protein(0,1,3,4and 0,1,4,3,respectively,P<0.01).CONCLUSION Chinese green tea drinkinginhibited ACF and colonic tumors formation inrats,which showed that tea had a significantchemopreventive effect on DMH-inducedcolorectal carcinogenesis.Such effects may bedue to suppression of cell proliferation andinduction of apoptosis in the intestinal crypts. | Jia XD Han C | 2000 | World Journal of Gastroenterology2000，6，5： | 21 |
| 17 | Historically significant events in the discovery of RANK/RANKL/OPG显示文摘After it was suggested 30 years ago that the osteoblast lineage controlled the formation of osteoclasts, methods were developed that established this to be the case, but the molecular controls were elusive. Over more than a decade much evidence was obtained for signaling mechanisms that regulated the production of a membrane- bound regulator of osteoclastogenesis, in the course of which intercellular communication in bone was revealed in its complexity. The discovery of regulation by tumor necrosis factor ligand and receptor families was made in the last few years of the twentieth century, leading since then to a new physiology of bone, and to exciting drug development. | T John Martin | 2013 | World Journal of Orthopedics2013，4，4： | 21 |
| 18 | Peroxisome proliferator-activated receptors for hypertension显示文摘Peroxisome proliferator-activated receptors(PPARs) are ligand-activated transcription factors belonging to the nuclear receptor superfamily, which is composed of four members encoded by distinct genes(α, β, γ, and δ). The genes undergo transactivation or transrepression under specific mechanisms that lead to the induction or repression of target gene expression. As is the case with other nuclear receptors, all four PPAR isoforms contain five or six structural regions in four functional domains; namely, A/B, C, D, and E/F. PPARs have many functions, particularly functions involving control of vascular tone, inflammation, and energy homeostasis, and are, therefore, important targets for hypertension, obesity, obesity-induced inflammation, and metabolic syndrome in general. Hence, PPARs also represent drug targets, and PPARα and PPARγ agonists are used clinically in the treatment of dyslipidemia and type 2 diabetes mellitus, respectively. Because of their pleiotropic effects, they have been identified as active in a number of diseases and are targets for the development of a broad range of therapies for a variety of diseases. It is likely that the range of PPARγ agonist therapeutic actions will result in novel approaches to lifestyle and other diseases. The combination of PPARs with reagents or with other cardiovascular drugs, such as diuretics and angiotensin Ⅱ receptor blockers, should be studied.This article provides a review of PPAR isoform characteristics, a discussion of progress in our understanding of the biological actions of PPARs, and a summary of PPAR agonist development for patient management. We also include a summary of the experimental and clinical evidence obtained from animal studies and clinical trials conducted to evaluate the usefulness and effectiveness of PPAR agonists in the treatment of lifestyle-related diseases. | Daisuke Usuda Tsugiyasu Kanda | 2014 | World Journal of Cardiology2014，6，8： | 19 |
| 19 | Dense coding scheme using superpositions of Bell-states and its NMR implementation显示文摘Dense coding using superpositions of Bell-states is proposed. The generalized Grover's algorithm is used to prepare the initial entangled states, and the reverse process of the quantum algorithm is used to determine the entangled state in the decoding measurement. Compared with the previous schemes, the superpositions of two Bell-states are exploited. Our scheme is demonstrated using a nuclear magnetic resonance (NMR)quantum computer. The corresponding manipulations are obtained. Experimental results show a good agreement between theory and experiment. We also generalize the scheme to transmit eight messages by introducing an additional two-state system. | ZHANG Jingfu, XIE Jingyi, DENG Zhiwei & LU Zhiheng Key Laboratory for Quantum Information and Measurements, Department of Physics, Tsinghua University, Beijing 100084, China Center for Quantum Information, Tsinghua University, Beijing 100084, China Department of Materials Science and Engineering, Beijing Normal University, Beijing 100875, China Testing and Analytical Center, Beijing Normal University, Beijing 100875, China Department of Physics, Beijing Normal University, Beijing 100875, China | 2005 | Science China(Physics,Mechanics & Astronomy)2005，48，1： | 18 |
| 20 | Production of transgenic blastocyst by nuclear transfer from different types of somatic cells in cattle显示文摘The present study examined the effects of genetic manipulation to the donor cell and different types of transgenic donor cells on developmental potential of bovine nuclear trans-fer (NT) embryos. Four types of bovine somatic cells, including granulosa cells, fetal fibroblasts, fetal oviduct epithelial cells and fetal ovary epithelial cells, were transfected with a plasmid (pCE-EGFP-Ires-Neo-dNdB) containing the enhanced green fluorescent protein (EGFP) and neomycin-resistant (Neor) genes by electroporation. After 14 days selection with 800 mg/mL G418, transgenic cell lines from each type of somatic cells were obtained. Nontransgenic granulosa cells and all 4 types of transgenic somatic cells were used as nuclear donor to produce transgenic embryos by NT. There was no significant difference in development rates to the blas-tocyst stage for NT embryos from transgenic and nontransgenic granulosa cells (44.6% and 42.8%, respectively), and transfer of NT embryos derived from transgenic and nontransgenic granulosa cells to recipients resulted in similar pregnancy rates on day 90 (19% and 25%, re-spectively). The development rates to the blastocyst stage of NT embryos were significantly dif-ferent among different types of transgenic donor cells (P<0.05). Blastocyst rates from fetal ovi-duct epithelial cell and granulosa cell (49.1% and 44.6%, respectively) were higher than those from fetal fibroblast (32.7%) and fetal ovary epithelial cell (22.5%). These results suggest that (i) genetic manipulation to donor cells has no negative effect on in vitro and early in vivo develop-mental competence of bovine NT embryos and (ii) granulosa and fetal oviduct epithelial cells can be used to produce transgenic bovine NT embryos more efficiently. In addition, GFP can be used to select transgenic NT embryos as a non-invasive selective marker. | GONG Guochun1, DAI Yunping1, FAN Baoliang1, ZHU Huabing2, WANG Haiping3, WANG Lili1, FANG Changge1, WAN Rong3, LIU Ying3, LI Rong3 & LI Ning1 1. State Key Laboratory for Agrobiotechnology, China Agricultural University, Beijing 100094, China 2. Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100094, China 3. Gentitan Biotechnology Ltd., Beijing 100084, China | 2004 | Science China(Life Sciences)2004，47，2： | 18 |
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