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1.
《园艺学报》2005,32(5):904-904
中国园艺学会第九届第8次常务理事扩大会决定,“中国园艺学会第七届青年学术讨论会”由山东农业大学园艺科学与工程学院和山东省园艺学会承办,将于2006年7月或8月在山东泰安举行。会议交流主题:(1)园艺作物种质资源、遗传育种与生物技术;(2)园艺作物有机、无公害及标准化安全生  相似文献   

2.
为促进园艺作物采后科学技术的发展,由小国园艺学会、美国园艺学会及亚蔬亚洲区域中心联合主办,农业部国际合作司、科技司与农业司协力、的“园艺作物产后技术国际学术讨论会于1995年6月27日~7月1日在北京中国农科院蔬菜花卉所园艺培训中心隆重召开。中国园艺学会相重扬理事长、美国园艺学会D.J.坎特利夫会长。联合国粮农组织(FAO)驻华代表库瑞希先生,亚蔬亚洲区域中心主任杨又迪博士、农业部科技刊  相似文献   

3.
由中国园艺学会热带南亚热带果树分会主办,福建省农业科学院果树研究所、福建省龙眼枇杷育种工程技术研究中心与福建省农业科学院“特色园艺作物育种与技术创新”科技创新团队共同承办的中国园艺学会热带南亚热带果树分会第二届学术研讨会暨全国龙眼产业发展论坛于2008年9月19日至21日至福州召开。  相似文献   

4.
由中国园艺学会热带南亚热带果树分会主办,福建省农业科学院果树研究所、福建省龙眼枇杷育种工程技术研究中心与福建省农业科学院“特色园艺作物育种与技术创新”科技创新团队共同承办的中国园艺学会热带南亚热带果树分会第二届学术研讨会暨全国龙眼产业发展论坛于2008年9月19日至21日在福州召开。  相似文献   

5.
《园艺学报》2013,(3):478
由国际园艺学会和澳大利亚园艺学会和新西兰农业及园艺研究所共同主办的第29届国际园艺大会将于2014年8月17—22日在素有"阳光之城"之称的澳大利亚布里斯班召开(同期举办展览)。会议主题是"园艺——维持生活、生计与园林美化"。会议议题:果树生理及生产体系、葡萄生产、本土蔬菜、高产值蔬菜作物、观赏植物、园艺作物机械化精细化管理、创新性植物保护技术、采后技术、园艺作物育种、园艺作物分子生物学技术、组织快繁技  相似文献   

6.
<正>2014年8月28—30日,由中国园艺学会南瓜研究分会主办,云南省园艺学会、云南省农业科学院园艺作物研究所承办的"中国园艺学会南瓜研究分会2014年南瓜种质资源展示及产业发展研讨会"在美丽的云南省昆明市召开。云南省园艺学会理事长、云南省农业科学院副院长李学林研究员,云南省农业科学院园艺作物研究所所长孔令明研究员等领导应邀出席了开幕式。中国园艺学会南瓜研究分会名誉会长崔崇士教授参加了本次会议。来自全国22个省、  相似文献   

7.
中国园艺学会第九届第8次常务理事扩大会决定,“中国园艺学会第七届青年学术讨论会”由山东农业大学园艺科学与工程学院和山东省园艺学会承办,将于2006年7月或8月在山东泰安举行。  相似文献   

8.
<正>由中国园艺学会主办,山东农业大学、山东省园艺学会承办,山东省农业科学院蔬菜研究所和莱阳农学院共同协办的“中国园艺学会第七届青年学术讨论会”于2006年7月18—20日在山东泰安(山东农业大学)成功召开。来自全国25个省市的60多个大专院校、科研院所和新闻出版单位的160多名代表参加了会议。本次会议出版了《园艺学进展》(第七辑)。  相似文献   

9.
为加强各地青年园艺工作者间的学术交流与合作,促进中国园艺事业的发展,由中国园艺学会主办、浙江省和湖南省园艺学会承办的“中国园艺学会首届青年科技工作者学术讨论会”拟于1994年11月份在杭州举行。征文范围:未在国内外公开发表或全国性学术会议上宣读过的园艺作物(含果树,蔬菜,西、甜瓜,观赏园艺)遗传育种、生物技术,种质资源、生理、栽培和贮藏加工等有关研究报告(限3000—3500字),综述性文章(限5000-7000字)。第一作者年龄限于45周岁以下。截止日期1994年8月30日。征  相似文献   

10.
<正>2016年7月15—18日,由中国园艺学会主办,中国园艺学会西甜瓜专业委员会、新疆维吾尔自治区葡萄瓜果研究所、新疆农科院哈密瓜研究中心与新疆哈密第13届哈密瓜节组委会共同承办,新疆园艺学会、哈密市伊州区农业局、林业局等协办的"2016丝绸之路特色瓜果(哈密)高端论坛"在新疆哈密市举行。来自北京、浙江、湖北、广西、河  相似文献   

11.
AIM: To study the mechanism of berberine on the adhesion between human pulmonary carcinoma cells (PG cells) and HUVECs. METHODS: The effect of berberine (2.5-40 mg/L) on the proliferation of HUVECs was detected by MTT method. Further, PG cells were treated with berberine at doses of 2.5, 5, 10 mg/L for 6, 12, 24 h. The adhesion between PG cells and HUVECs was determined by rose bengal staining. The expression of CD44s on PG cells were determined by fluorescence antibody staining. Fluorescence anisotropy imaging system was used to assay the fluidity of PG cell membrane. RESULTS: Berberine at concentrations of 2.5, 5, 10 mg/L were the safety doses to the proliferation of HUVECs treated for 6, 12, 24 h. Berberine inhibited the adhesion between PG cells and HUVECs significantly in a dose-dependent manner (P<0.05 or P<0.01). Meanwhile, berberine increased the expression of CD44s on PG cells (P<0.05 or P<0.01). Berberine decreased the fluidity of PG cell membrane in a dose-dependent manner after 24 h incubation. CONCLUSION: Berberine inhibits the adhesion between PG cells and HUVECs by regulating the expression of adhesion molecules and the fluidity of cell membrane on PG cells.  相似文献   

12.
AIM: To study the effect of berberine on the proliferation of human pulmonary carcinoma cells (PG cells). METHODS: The proliferation of PG cells was determined by using MTT assay. Cell cycle and apoptosis of PG cells were determined by using flow cytometry. Confocal scanning imaging system was used to assay the ROS-releasing level of PG cells. RESULTS: Berberine was shown to inhibit proliferation of PG cells directly and in a concentration-dependent manner (P<0.05,P<0.01). Berberine blocked the cell cycle of PG cells, and beberine at concentration of 40 mg/L induced the apoptosis of PG cells. After 6 or 12 h incubation, berberine began to induce ROS-releasing in PG cells at 10 mg/L. While incubated with berberine for 24 h, PG cells were induced to release ROS at lower concentration. CONCLUSION: Berberine has an inhibitory effect on the proliferation of PG cells, and these effect may be carried out by regulating the production of intracellular ROS and the process of cell cycle.  相似文献   

13.
AIM: To investigate the effects of rapamycin on apoptosis, proliferation, migration ability and tumor related apoptosis inducing ligand(TRAIL) in cultured human umbilical vein endothelial cells(HUVECs). METHODS: Cultured HUVECs were treated with rapamycin at the concentrations of 0, 1, 10 and 100 μg/L for 24 h. The cell proliferation was measured by CCK-8 method. The cell migration ability was detected by Transwell chambers and wound healing test. The apoptotic index of HUVECs was quantitatively determined by measuring the activation of caspase-3. The morphological changes of the apoptotic cells were observed by DAPI staining. The expression of TRAIL was detected by Western blotting. RESULTS: A 24 h-incubation with rapamycin(1-100 μg/L) caused significant cell loss associated with the increase in apoptosis, as quantified by the determination of caspase-3 activity(P<0.01) in HUVECs. Obvious apoptotic morphology was observed by DAPI staining in HUVECs incubated with rapamycin. Rapamycin at the concentrations of 1-100 μg/L also impaired the migration ability of HUVECs(P<0.01). In addition, rapamycin(10-100 μg/L) inhibited the proliferation of HUVECs, whereas rapamycin at 1 μg/L had no such effect(P<0.01). Rapamycin(10-100 μg/L) also induced TRAIL expression in a dose-dependent manner(P<0.01). CONCLUSION: Rapamycin induces apoptosis, and inhibits the proliferation and migration of HUVECs. The up-regulation of TRAIL might be related to the injury of vascular endothelial cells caused by rapamycin.  相似文献   

14.
AIM:To study the effect of activated protein C (APC) at different concentrations on apoptosis of human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS).METHODS:The HUVECs were induced by LPS (1.0 mg/L) as apoptotic model that was administered by different concentration of APC (10 μg/L or 50 μg/L). Meanwhile, the control group and induced apoptosis group induced by LPS (1.0 mg/L) stimulation were also set up. The changes of cellular ultrastructures were observed under electron microscope. The DNA ladder and TUNEL fluorescent staining were measured in cells. Annexin-Ⅴ/PI double staining was used to measure the cell apoptosis rate by flow cytometry. Cell survival rate was measured by MTT assay. The proliferating cell nuclear antigen (PCNA) expression levels in cells were also measured by Western blotting to reflect the proliferation of the cells.RESULTS:There were significant apoptotic changes in the cells induced by LPS, but the apoptotic changes were reduced and apoptosis rates were decreased in the cells treated with APC. Meanwhile, cell survival rate and the protein levels of PCNA were increased after APC treatment, particularly at the concentration of 50 μg/L, which showed difference when compared with those induced apoptosis group by LPS (P<0.05).CONCLUSION:APC can inhibit HUVECs apoptosis induced by LPS and promote cell proliferation, thus protect the cells from injury.  相似文献   

15.
AIM: To investigate the effects of constant magnetic field on apoptosis, secretion and expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVEC), and their adhesion rates with THP-1 monocytes induced by angiotensin Ⅱ (AngⅡ).METHODS: The third passage of cultured HUVEC was used.There were six groups: control group, Ang Ⅱ (10-6 mol/L) group, Ang Ⅱ with 1, 5, 10 or 20 gausses of constant magnetic field group.Samples were collected 24 h after incubation with or without magnetic field.Apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and propidinm iodide staining with flow cytometry.Secretion and expression of ICAM-1 and VCAM-1 were detected by ELISA and immunocytochemistry, respectively.Adhesion rate between HUVEC and THP-1 was measured by counting method.RESULTS: Ang Ⅱ at concentration of 10-6mol/L induced apoptosis in HUVECs (P<0.05 vs control), whereas in 1, 5, 10 and 20 gausses group, apoptosis of HUVECs was significantly lower than that in Ang Ⅱ group (P<0.05).Ang Ⅱ at concentration of 10-6 mol/L significantly increased secretion and expression of ICAM-1 and VCAM-1 (P<0.05 vs control), whereas secretion and expression of ICAM-1 and VCAM-1 in 1, 5, 10 and 20 gausses group significantly decreased, compared with Ang Ⅱ group (P<0.05).The adhesion rates between HUVEC and THP-1 significantly increased 24 h after incubation of HUVEC with Ang Ⅱ (P<0.05 vs control), in contrast, the adhesion rates between HUVEC and THP-1 in 1, 5, 10 and 20 gausses group significantly decreased, compaed with Ang Ⅱ group (P<0.05).CONCLUSIONS: One gauss to 20 gausses of constant magnetic field antagonizes the effects of Ang Ⅱ on HUVEC, decreases apoptosis and expression of ICAM-1 and VCAM-1 in HUVEC, and also decreases the adhesion rates between HUVEC and monocytes induced by Ang Ⅱ.  相似文献   

16.
AIM: To observe the effects of some component of Chinese herbs for external use on proliferation of human umbilical vein endothelial cells (HUVEC) and investigate the mechanism of promoting tissue repair. METHODS: The method of MTT was used to examine the effects of Rg1, Rh1, perlolyrine, cinnamyl aldehyde, muscone, astragaluspolysaccharin (APS), velver antler polypeptide (VAP) and soluble extract of boswellia carterii birdw (BCB) on proliferation of HUVEC. RESULTS: APS did not promote proliferation of HUVEC at 9.75 mg/L-2.5 g/L; Rh1 promoted proliferation of HUVEC at 1.94 mg/L-0.5 g/L (P<0.05 or P<0.01), and Rg1 inhibited proliferation of HUVEC at 31 mg/L (P<0.05); VAP promoted proliferation of HUVEC at 1 mg/L-0.5 g/L with optimal dose of 10 mg/L (P<0.01), Cinnamyl aldehyde promoted proliferation of HUVEC at 2 g/L(P<0. 05); Muscone and soluble extract of BCB inhibited proliferation of HUVEC at 1 g/L, 0.5-2.5 kg/L(P<0. 01), respectively; Perlolyrine inhibited proliferation of HUVEC at 0.125 g/L-0.5 g/L(P<0. 01). CONCLUSION: The external herbs for supplementing Qi and warming Yang can promote HUVEC proliferation and improve angiogenesis during tissue repair. The external herbs for promoting blood circulation and accelerating capillary movement may have influence upon other stages of tissue repair.  相似文献   

17.
AIM: To explore the effect of water extract propolis (WEP) from Taishan on apoptosis of human umbilical vascular endothelial cells (HUVECs) induced in vitro by tumor necrosis factor-α (TNF-α). METHODS: HUVECs were collect by digestion-perfusion and cultivated. TNF-α at concentration of 50 μg/L was administrated to induce the apoptosis of HUVECs. After injury, HUVECs were treated with WEP at concentrations of 50, 100, and 200 mg/L, respectively, for 24 h. Apoptosis was evaluated by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) and flow cytometry (FCM). RESULTS: Apoptosis index in injured group was significantly higher than that in control group, and decreased significantly after treating with WEP at concentrations of 50, 100, and 200 mg/L, respectively (P<0.01). CONCLUSION: WEP may be useful for protection of vascular endothelial cells by inhibiting apoptosis.  相似文献   

18.
AIM: To investigate the effect of oxidized LDL (ox-LDL) on the expression of gap junction protein connexin43 in cultured human umbilical vein endothelial cells (HUVECs) in vitro. METHODS: Human umbilical vein endothelial cells cultured in normal condition were divided into blank control group, 50 mg/L,100 mg/L and 200 mg/L ox-LDL intervention groups. The mRNA expression of connexin43 in cultured HUVECs was detected with RT-PCR method; while the protein level of connexin43 was determined by the method of immunocytochemistry in the control and 100 mg/L ox-LDL intervention groups 24 h after ox-LDL was given. RESULTS: Different concentrations (50 mg/L, 100 mg/L, 200 mg/L) of ox-LDL up-regulated mRNA expression of connexin43 in cultured HUVECs after 24 h intervention (P<0.01). The protein level of connexin43 in cultured HUVECs intervened with 100 mg/L Ox-LDL for 24 h was up-regulated as compared to the control cells (P<0.01).CONCLUSION: Ox-LDL may up-regulate the expression of connexin43 at mRNA and protein levels in cultured human umbilical vein endothelial cells within short time, indicating that connexin43 plays an important role in the pro-atherosclerotic effect of Ox-LDL.  相似文献   

19.
AIM: To investigate the protective effects of berberine against liver injury induced by lipopolysaccharide in mice and the mechanisms underlying its protective effect. METHODS: The male mice were divided randomly into control, berberine group, LPS group and berberine treatment group. Mice were administered intragastrically with distilled water (0.01 mL/g) or 5 g/L neutral sulfate berberine (0.01 mL/g) once a day for 5 days and injected intraperitoneally with normal saline or LPS (0.02 mL/g,28 mg/kg)at 1 h after gavage on day 5. Blood was collected for determining alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, the content of tumor necrosis factors-α (TNF-α) at 10 h and 2 h after LPS or normal saline injection, respectively. Furthermore, the liver tissue was processed, and histological changes and ultrastructure in liver were observed with light and electron microscopy, malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in liver were also detected. RESULTS: Both ALT and AST activities in serum in LPS group were higher than those in control and berberine treatment group. LPS increased the serum TNF-ɑ content at 2 h after injection, which was reversed by berberine pretreatment. The histological examination showed that LPS caused severe hepatic cell edema, degeneration, apoptosis and even necrosis, and ultrastructure observation demonstrated that LPS induced mitochondrial swelling, condensation and margination of chromatin, irregular nuclear envelope in hepatocytes. The above pathological changes produced by LPS were attenuated by berberine pretreatment. Moreover, MDA contents in liver tissue were higher in LPS group than control and berberine treatment group, but there were no significant difference in SOD activity between berberine treatment and LPS group. CONCLUSION: Berberine has a protective effect on LPS-induced liver injury in mice, the mechanisms may be related to its decreasing the production of TNF-α, inhibiting lipid peroxidation and protecting mitochondria.  相似文献   

20.
MENG Xin  ZHANG Jin  WU Wei  BAI Song 《园艺学报》2004,20(4):598-602
AIM: To investigate the effects of advanced glycation end products (AGEs) on protein and mRNA expression of macrophage inflammatory protein-1α (MIP-1α) in cultured human umbilical vein endothelial cells(HUVECs). METHODS: HUVECs were cultured with AGEs at different concentrations for 24 h and at a concentration of 400 mg/L for different time.The levels of mRNA and protein expression of MIP-1α in cultured HUVEC were detected by in situ hybridization and Western blot, respectively. RESULTS: In situ hybridization showed that after exposure of HUVECs to AGEs at different concentrations (100 mg/L, 200 mg/L, 400 mg/L) for 24 h, the average integrated optical density values (18.76±3.17, 26.58±1.61, 34.23±2.25) of MIP-1α mRNA expression in HUVECs were higher than that in control group (13.83±1.24, P0.05). After exposure of HUVECs to AGEs at a concentration of 400 mg/L for 12 h, 24 h and 36 h, the average integrated optical density values of MIP-1α mRNA expression in HUVECs were 22.67±1.46, 34.23±2.25 and 42.28±3.14, higher than that in 0 h group (12.56±1.24, P0.05). Western Blot showed that exposure of HUVECs to AGEs at different concentrations(100 mg/L, 200 mg/L, 400 mg/L) for 24 h resulted in a 1.34-fold, 1.87-fold and 2.46-fold increase in the expression of MIP-1α protein in HUVECs compared with BSA control group (P<0.05). Meanwhile, exposure of HUVECs to AGEs at a concentration of 400 mg/L for 12 h, 24 h and 36 h resulted in a 1.82-fold, 2.71-fold and 3.34-fold increase in MIP-1α protein expression in HUVECs compared with 0 h group (P<0.05). CONCLUSION:These data suggest that AGEs could induce a high expression of MIP-1αmRNA and protein in cultured HUVECs in a dose-dependent and time-dependent manner.  相似文献   

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