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‘玉绿’是以白梨品种‘莱阳茌梨’为母本。砂梨系统‘太白’为父本杂交选育而成的优质早熟砂梨品种．在武汉地区7月底到8月上旬成熟。该品种果形端正,果实近圆形,果皮绿色,果点较小,果面光滑;平均单果质量270．0g,最大单果质量433．9g,可溶性固形物含量10．5％～12．2％．总酸含量0．28％,维生素C含量42．7mg/kg。果肉白色,肉质细嫩、汁多,酸甜可口。早果,丰产,稳产,抗病性强。2009年通过湖北省农作物品种审定委员会审定（鄂审果2009002）,定名为‘玉绿’。 相似文献
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‘红宝石’海棠的枝叶颜色是紫红色。以具有柱型特性的98—1和M9×63—2—19为母本、‘红宝石’海棠为父本进行杂交,其1年生苗颜色90．63％～94．92％呈现彩色表现型。另外5．09％-9．38％为绿色表现型。培育1年后彩色的遗传特性表现稳定。调查认为,‘红宝石’海棠枝叶颜色的彩色是由显性基因控制的。同时,在以选择彩色基因型为目标的选育中,在杂交苗真叶二三叶期,对颜色为绿色的杂种类型进行淘汰是有效措施。‘红宝石’海棠是培育彩色观赏苹果树种的良好育种亲本。‘寒富’（母本）ב舞美’（父本）和‘舞美’（母本）×小苹果（父本）的杂交后代中,有50％的类型出现彩色类型,符合柱型单显性基因的遗传规律特性。 相似文献
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小苹果新品种‘紫香’是以‘红海棠’为母本,‘赤阳’为父本人工杂交选育而成.2012年2月通过了黑龙江省农作物品种审定委员会的审定并命名.果实呈短圆锥形,平均果重45 g,最大果重74 g,8月下旬至9月初果实成熟,果实整齐度好,较耐贮藏和运输,丰产性好.可溶性固形物含量12.7％,可溶性糖含量11.94％,抗坏血酸含量37.0 mg/kg,可滴定酸含量0.46％.近4 a区域试验点平均每公顷产量25 860 kg,比对照品种‘金红’增产6.5％,生产试验点2a平均每公顷产量28 510 kg,比对照品种‘金红’增产6.41％.植株抗寒、抗病性强,适应性好,易栽培管理,适宜黑龙江省东南部地区栽培. 相似文献
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<正>‘粉红公主’草莓由‘章姬’与‘给维塔’杂交育成。2014年12月通过北京市林木品种审定委员会审定并命名。1品种特征特性果实圆锥形或楔形,一、二级序果平均单果质量20.5 g,最大单果质量43 g。果面粉红色,有光泽。甜多酸少,有香味。可溶性固形物含量10.4%,维生素C含量58.9 mg/100 g,还原糖含量为4.25%,可滴定酸含量 相似文献
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建平县一些山地梨园存在品种杂、管理粗放、产量低、经济效益差的情况。为了扭转这种局面。做到品种适应市场需求。我们于2003年在建平县小塘镇小塘村北山的李振彬梨园。通过高接将其改造成‘南果梨’试验园，面积0．4hm^2。试验园属丘陵山地，阳坡，土壤为褐土，肥力较差，有机质含量低。现有梨树117株，35年生，品种以‘苹果梨’为主， 相似文献
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<正>‘红露’苹果是由韩国园艺研究所用短枝型‘早艳’ב金矮生’杂交育成~([1]),具有早产、丰产、色艳、果个大、极耐贮运和抗逆性强等特性~([2]),发展前景良好。2013年从烟台引进接穗嫁接繁殖,2014年在大连市农业科学研究院苹果试验园试栽。试栽园为老梨园更新,土壤碱解氮含量为57.8 mg/kg、有效磷29.2 mg/kg、速效钾132.5 mg/kg、pH值6.38。苗木为一年生‘红露’嫁接苗,砧 相似文献
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AIM: The study was undertaken to explore the dynamic changes of the concentration of nitric oxide(NO) in ischemic myocardium and its mechanism.METHODS: In vivo myocardial ischemia of mice and in vitro perfused isolated heart of rat were used in the experiment. The effects of severity and time of ischemia on NO production, NOS activity and mRNA were examined, respectively. RESULTS: There was a considerable difference (P<0.01) in the concentration of NO between ischemia group [(9.12±1.40) μmol/L] and control group [(20.16±1.67) μmol/L] after Pit(30 U/kg) administration, and the concentration of NO of ischemic group significantly decreased [(9.17±1.33) μmol/L] compared with control group [(19.90±1.95) μmol/L] after 30 minutes of ischemia. Also, the concentration of NO after Pit(20 U/L) administration in K-H and 15 min of ischemia was (15.41±2.00) μmol/L and (15.09±2.00) μmol/L respectively in vitro, significantly lower than control group [(23.83±2.33) μmol/L and (23.63±2.52) μmol/L]. In addition, compared with control group, the number of NOS positive cells, NOS activity as well as mRNA expression in atrial muscle and ventricular muscle of ischemic group were markedly reduced, respectively. CONCLUSION: Myocardial ischemia could reduced the NO level in myocardium, down-regulation of NOS mRNA could be the possible mechanism. 相似文献
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AIM: To observe the direct effect of lipopolysaccharide (LPS) on secretion of endothelin-1 (ET-1) and nitric oxide by human umbilical vein endothelial cell and cell viability of the secretor. METHODS: The third passage of human umbilical vein endothelial cells were incubated with different concentrations of LPS (1 g/L, 100 mg/L, 10 mg/L, 1 mg/L, 100 μg/L, 10 μg/L, 1 μg/L) for 6 hours, and the culture supernatants were collected. The concentrations of ET-1 were determined by radioimmunoassay, the concentrations of nitric oxide were determined using Greiss's method. The viabilities of cells were measured by MTT method. RESULTS: The concentration of ET-1 (pg/L) of normal control group was 251.64±10.90. The concentrations of ET-1 (pg/L) of LPS treated groups were 220.85±19.14, 278.67±15.45, 306.40±11.60, 312.87±33.50, 324.38±17.02, 291.49±14.30, 282.11±13.38, respectively (each group compared with normal control group, P<0.05 or P<0.01). The concentration of NOx (μmol/L) of normal control group was 629.46±13.36. The concentrations of NOx (μmol/L) of LPS treated groups were 732.58±23.21, 669.87±9.32, 661.24±16.80, 650.33±13.24, 606.59±12.94, 626.75±9.83, 627.61±5.61, respectively (each group compared with normal control group, P<0.05 or P<0.01). The viabilities of endothelial cells of LPS treated groups were 74%, 81%, 86%, 88%,91%, 93%, 93%, respectively. CONCLUSION: LPS of lower concentrations had no significantly lethal effect on human umbilical vein endothelial cells, but enhanced secretion of ET-1 and inhibited NO production. LPS in higher concentrations showed significant lethal effect on human umbilical vein endothelial cells, inhibited secretion of ET-1 and enhanced NO production. 相似文献
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AIM: To approach the changes of endostatin levels in BALB/c nude mice bearing human nasopharyngeal carcinoma(NPC) in different period (5, 10, 20, 30 and 40 days) and the relationship between endostatin and tumor's development. METHODS: BALB/c nude mice bearing NPC was reproduced by hypodermic implantation of human CNE-2 cells into right-side of axillary fossa. The level of plasma endostation was detected, and the weight of isolated tumors was measured. On the basis of the regulation of these changes, their relationships were explored. RESULTS: At 5 days [(137.61±53.41) μg/L] or 10 days [(103.06±17.33) μg/L] endostatin level had no apparent alternation in comparison with control group [(113.56±21.74) μg/L, P>0.05]. At 20, 30 and 40 days concentration of endostatin[(212.80±85.91) μg/L,(293.63±62.53) μg/L, (271.57±32.45) μg/L, respectively] were higher than that of the control group (P<0.05). Along with the development of the tumors, both the levels of endostatin and tumors weight increased. There was a positive correlation between the level of endostatin and tumor weight (r=0.687, P<0.05). CONCLUSION:These results suggested that endostatin links with the development of NPC. 相似文献
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GONG Ya-jun LAI Kun-bei LI Long-hui HUANG Chuang-xin XU Fa-bao ZHOU Li-jun JIN Chen-jin 《园艺学报》2020,36(1):104-111
AIM: To investigate the role of macrophages in the process of nicotine aggravating choroidal neovascularization (CNV). METHODS: After administration of nicotine (100 mg/L in drinking water) for 4 weeks, the mice were used to induce CNV by laser photocoagulation. Seven days after laser injury, the mice were perfused with fluorescein isothiocyanate-labeled dextran through the left ventricle, and areas of CNV were measured. At the 1st, 3rd, 7th and 14th days after laser injury, the spatial and temporal distribution of macrophages was detected by immunofluorescence staining. The mRNA expression of macrophage-related markers were detected by RT-qPCR. Moreover, vascular endothelial growth factor (VEGF) and inflammation-related molecules including intercellular adhesion molecule (ICAM)-1, tumor necrosis factor (TNF)-α and interleukin (IL)-6 in the retinal pigment epithelium-choroid-sclera complexes were detected at the 1st and 3rd days after laser photocoagulation. RESULTS: The degree of leakage and areas of CNV were significantly increased by nicotine exposure compared with control group. Heavy leakage rate and areas of CNV of in nicotine group were 56.25% and (17 569.96±1 444.00) μm2, while those in control group were 31.25% and (10 158.63±711.00) μm2 (P < 0.05). Nicotine promoted the infiltration of M2 macrophages and increased the ratio of M2/M1 macrophages (P < 0.05). In addition, nicotine accelerated the mRNA expression of M2 macrophage-related markers and up-regulated protein expression of VEGF, ICAM-1, TNF-α and IL-6 (P < 0.05). CONCLUSION: Nicotine promotes the polarization of M2 macrophages, increases the ratio of M2/M1 macrophages, and ultimately accelerates the development of CNV. 相似文献
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AIM: We hypothesize that peroxisome proliferator-activated receptor α(PPARα) agonists act directly on nitric oxide (NO) production in vascular endothelium. Thus, the purpose of this study is to investigate the effects of fenofibrate on endothelial NO synthase(eNOS) activity and its expression in cultured vascular endothelial cells. METHODS: Bovine aortic endothelial cells (BAECs) were treated with the PPARα activator fenofibrate. The eNOS activity and the expression of eNOS protein and its mRNA were determined. RESULTS: Our data show that fenofibrate increased eNOS activity in a dose-and time-dependent manner. At the concentration of 10 μmol/L or more, fenofibrate treatment caused a significant increase in eNOS activity. The maximal increase in eNOS activity(2.32±0.47 fold of the control) was observed with 50 μmol/L fenofibrate treatment for 48 h. Fenofibrate failed to increase eNOS activity at 1 and 12 h. RT-PCR analysis demonstrated that eNOS mRNA relative to β-actin mRNA significantly increased at concentrations of 5 μmol/L or more. It reached 2.08±0.33 fold of the control with 50 μmol/L fenofibrate. Significant increase in eNOS mRNA levels was observed after 6 h, and lasted for 48 h. The peak increase in eNOS mRNA levels(2.13±0.30 fold of the control,P<0.01) was observed with 50 μmol/L fenofibrate treatment for 12 h. Longer incubation of cells with 50 μmol/L fenofibrate caused no further increase. The treatment of BAECs with fenofibrate for 48 h demonstrated a concentration-dependent increase in eNOS protein levels as measured by Western blot analysis. Densitometric analysis indicated that there was a significant increase in eNOS to β-actin ratios after fenofibrate treatment at concentrations of 10,50 and 100 μmol/L(1.80±0.45, 2.70±0.42 and 2.20±0.32 fold of the control, respectively, P<0.01). The significant increase in eNOS protein levels was observed 12 h after treatment and lasted for 48 h. CONCLUSION: PPARα activator fenofibrate, enhances endothelial NO production by directly upregulating eNOS expression and activity. 相似文献
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ZOU Ying LING Qin-jie LIU Qiu-ying ZHANG Yi-bo GAO DONG-fang LU Qiao-ying LIU Jie ZHENG Wen-jie HUANG Zhi 《园艺学报》2010,26(12):2363-2367
AIM: To investigate the effects of selenium (Se) compounds on the generation of nitric oxide (NO) and reactive oxygen species (ROS), and the activity of nitric oxide synthase (NOS) in umbilical cord mesenchymal stem cells (MSCs). METHODS: MSCs were cultured in the medium of DMEM/F12 containing 10% FBS and exposed to the compounds of selenium , selenocysteine (Se-Cys) or nano-selenium (Nano-Se) at concentrations of 0.1 μmol/L to 0.5 μmol/L. The concentration of NO and the activity of NOS in treated MSCs were detected by the method of nitrate reductase assay. The fluorescent intensity of ROS was determined by DCFH-DA probe. RESULTS: The production of NO was (18.13±6.80) μmol/L in the control MSCs,(20.93±5.68) μmol/L in the MSCs treated with Se(Ⅳ) at concentration of 0.1 μmol/L and (16.73±5.03) μmol/L in the MSCs treated with Se(Ⅳ) at concentration of 0.5 μmol/L for 24 h. The production of NO was (17.20±9.11) μmol/L (P<0.05) in the MSCs treated with Se(IV) at concentration of 0.1 μmol/L and (9.98±4.35) μmol/L (P<0.01) in the MSCs treated with Se(IV) at concentration of 0.5 μmol/L for 48 h, which was significantly lower than that in the control MSCs . No inhibitory effect of Nano-Se and Se-Cys on the production of NO in MSCs was observed. Compared with the control MSCs, Se(Ⅳ) at concentrations of 0.1 μmol/L and 0.5 μmol/L significantly inhibited the generation of ROS and the activity of NOS in MSCs at 24 h and 48 h. CONCLUSION: Se(Ⅳ) inhibits NO/ROS production and NOS activity in a dose-dependent manner in MSCs. 相似文献
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LIU Xiu-hua WU Xu-dong CAI Li-rong LIU Feng-ying TANG Chao-shu SU Jing-yi 《园艺学报》2003,19(11):1456-1458
AIM: To investigate the effects of human urotensin II (hUII) on ischemia/reperfusion (I/R) injury in isolated rat hearts. METHODS: In the ischemia/reperfusion (I/R) model of isolated perfused rat hearts, the effects of hUII pretreatment on cardiac function was monitored with cardiac function software of MFL Lab200. ATP, total calcium, and malondialdehyde (MDA) content in myocardium were detected. The coronary perfusion flow (CPF) and lactate dehydrogenase (LDH) activity in coronary effluent were measured during reperfusion. RESULTS: In the hUII pretreated group, the release of LDH from myocardium was lower [(78.3±18.1)U/L] than I/R group [(109.3±23.9) U/L, P< 0.05], with decreased contents of MDA and calcium in myocardium (decreased by 24% and 27%, respectively, P< 0.05) and an increased myocardial ATP content [(3.8±0.4)μmol/g dw vs (2.2±0.4)μmol/g dw, P< 0.05)]. At the same time, hUII pretreatment increased CPF [(5.4±0.7) mL/min vs (3.8±0.8) mL/min in I/R group, P< 0.05], reduced left ventricular end-diastolic pressure (LVEDP) by 20% ( P< 0.05) with increased±d p /d t max [(217±38) kPa/s and (119±18) kPa/s vs (173±29) kPa/s and (82±25) kPa/s in I/R groups, respectively, P< 0.05]. hUII pretreatment also increased natrite/natrate (NO2-/NO3-) content in coronary effluent [(52.2±12.0)μmol/L vs (32.1±10.2)μmol/L in I/R group, P< 0.05)]. CONCLUSION: hUII pretreatment attenuated I/R injury in isolated perfused rat hearts. The protective mechanism might be associated with NO-mediated coronary vasodilation. 相似文献
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TAO Lu-yuan WU Shao-ze WANG Jiao-ni WANG Guo-qiang XUE Yang-jing XU Zhi-qiang WANG Jie TANG Ji-fei JI Kang-ting 《园艺学报》2016,32(12):2168-2176
AIM: To study the role of amifostine on the formation of benzo[a]pyrene (BaP)-induced abdominal aortic aneurysm (AAA) in C57BL/6J mice and the underlying mechanism. METHODS: RAW246.7 mononuclear macrophage in vitro were divided into control group, DMSO group, BaP group, low dose (1 μmol/L) amfostine treated group, middle dose (5 μmol/L) amfostine treated group and high dose (25μmol/L) amfostine treated group. The influence of BaP on the expression of matrix metalloproteinase (MMP)-9, MMP-12, TNF-α, NF-κB in the RAW246.7 mononuclear macrophages in vitro was determined by Western blot. Male C57BL/6J mice (8 months old) were divided into control group, model group (AngII+BaP group), low dose (50 mg/kg) amfostine treated group and high dose (100 mg/kg) amfostine treated group. After 6 weeks, the abdominal aorta were isolated. The aortic tissues were subjected to HE and Masson staining. The vascular wall structure, infiltration of macrophage, the expression of MMP-9, MMP-12, TNF-α, NF-κB were evaluated by Western blot and immunochemistry staining. RESULTS: Amifostine attenuated BaP-induced expression of TNF-α, MMP-9, MMP-12, NF-κB in the RAW246.7 mononuclear macrophages (P<0.05). The results of animal experiments showed that the incidence of AAA in high dose amifostine treated group were significantly lower than that in low dose amifostine treated group and model group (P<0.05). Immunohistochemistry staining observation showed that amifostine inhibited the aortic macrophage infiltration more obviously in high amifostine treated group compared with model group and low dose amifostine treated group (P<0.05). Compared with model group and low dose amifostine treated group, the MMP-9, MMP-12, TNF-α and NF-κB expression of abdominal aorta in high amifostine treated group was reduced significantly (P<0.05). CONCLUSION: Amifostine inhibits BaP-induced activation of macrophages, and also prevents the formation of abdominal aortic aneurysm in C57BL/6J mice induced by BaP by inhibition of the NF-κB pathway, macrophage infiltration and the expression of TNF-α and MMPs. 相似文献
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AIM:To observe the changes in right atrial myocyte dimensions with myocardial development. METHODS: Cell length, width, length/width and cross-sectional area were measured in right atrial myocytes isolated from 12 weaning , 10 young , 13 adult human hearts. RESULTS: Cell length, width, length/width and cross-sectional area, at weanling group were (70.2±1.3) μm, (8.0±0.2) μm, (9.0±0.2) and (50.9±2.6) μm2, respectively, at young group were (93.5±1.6) μm, (11.7±0.3)μm, 8.1±0.2, (109.7±5.8) μm2, and (100.9±2.2) μm, (12.1±0.3) μm, 8.5±0.2, (119.0±5.5) μm2 for adult group. Clearly, young myocyte lenght, width, cross-sectional area were greater than that of myocytes at weanling group(P＜0.01) but adult myocytes length/width and cross-sectional area increase slightly compared with young group. The length/width ratio has no significant change through myocyte maturity, which is between 8-9. CONCLUSIONS: Our data suggest that myocyte dimensions expect length/width ratio have increased progressively with maturity, the length/width ratio is preserved in atrial myocyte during the period of normal myocyte growth from weanling to adulthood, and these changes in myocyte dimensions are similar with ventricular myocytes changes from other mammalian species. 相似文献
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AIM and METHODS: To study the changes of serum vascular endothelial growth factor (VEGF) levels in a rat model of acute myocardial infarction (MI) and its significance. Eighty-eight male Sprague-Dawley rats were used in this study. MI was produced by left coronary arterial ligation in 80 animals, and eight rats undergoing thoracotomy but not coronary ligation served as controls (sham).Blood samples were drawn from the right atrium before (sham animals) and 1, 3, 6, 12, 24 hours and 2, 3, 5, 7, 14 days after MI(n=8, respectively). Serum VEGF concentrations were measured by a sensitive enzyme-linked immunosorbent assay with a rabbit polyclonal antibody specific for VEGF. RESULTS: In 8 sham animals, the concentration of serum VEGF was (66.99±17.83) pg/mL. Six hours after MI, the level of serum VEGF significantly increased to (125.68±28.07)pg/mL (P＜0.01 vs sham control), and reached a peak (240.61±70.63 pg/mL, P＜0.01 vs sham control) at 24 hours after ligation and then decreased gradually over the remaining 2 weeks. But the level remained significantly elevated for 14 days (107.64±30.31 pg/mL, P＜0.01 vs sham control).CONCLUSION: Serum VEGF levels markedly and permanently increase in the rat model of acute MI may play an important role in the angiogenesis associated with MI 相似文献