国内外蔬菜保险的发展及对天津的启示

介绍了国内外蔬菜保险的现状及典型案例,并阐述了天津蔬菜保险发展的现状及政策性建议,如加大蔬菜保险推广宣传工作的力度,拓展蔬菜保险的有效需求;采取培养蔬菜保险专业人员、创新蔬菜保险产品设计、完善蔬菜保险业务管理制度等措施来壮大蔬菜保险的供给能力;通过完善蔬菜保险条例、构建蔬菜信息平台、探索财政补贴方式、建立应对巨灾风险机制等措施,建立健全蔬菜保险的保障措施。     

环保型蔬菜专题讲座之一环保型蔬菜类型及产销要求

环保型蔬菜即通常所说的生态蔬菜、无污染蔬菜、卫生蔬菜、安全蔬菜、营养蔬菜等.广义上讲,环保型蔬菜应集安全、卫生、优质、营养于一体.环保型蔬菜在产销过程中不能受环境的污染,也不污染生态环境,能保持生态平衡,能保持或发展优良的生态环境,并使蔬菜生产获得持续发展的可能.     

重庆市蔬菜农药残留动态变化及质量安全风险评估

对重庆市大型蔬菜批发市场、农贸市场、超市、生产基地7大类蔬菜中9种农药残留情况进行了定点跟踪监测。结果表明,2006年蔬菜农药总残留量具有先上升后下降的动态变化;其中农药残留超标率为豆类、茄果类和绿叶菜类蔬菜高于其它种类蔬菜,市场蔬菜高于基地蔬菜,外地蔬菜高于本地蔬菜;第二、三季度的蔬菜质量安全指数大于1,安全状态存在一定风险;从农药污染综合值评价,甲胺磷、氧化乐果是影响重庆市蔬菜质量安全的主要因素。     

蔬菜产业培育对我国农民人均收入的影响效应研究——基于1990—2016年全国数据

家庭是社会最基本的单元。增加农村家庭收入是"三农"工作的核心,是乡村振兴的促进剂。如何提高农民人均收入,是我国全面建成小康社会的重点。加快蔬菜产业培育是提高农民人均收入的有效途径。从影响蔬菜产业培育的多个因素中选取蔬菜播种面积、蔬菜产量、蔬菜出口量、蔬菜出口额、蔬菜平均商品率这5个因子,采用全国1990—2016年相关数据,运用多元回归分析的方法,研究蔬菜产业培育对农民人均收入的影响效应。结果表明,蔬菜产量和蔬菜出口额对农民人均收入的影响显著,而蔬菜播种面积、蔬菜出口量和蔬菜平均商品率对农民人均收入的影响并不显著。基于此,应充分利用科技力量,提高蔬菜产量,加快蔬菜流通效率,以增加农民收入;应继续增大蔬菜出口额,实现更大的蔬菜贸易顺差,以促进农民持续增收。     

实施品牌提升战略,推动寿光蔬菜产业转型升级

作为中国"蔬菜之乡",寿光蔬菜的发展在全国起到了积极引领作用。目前普通蔬菜供应基本满足社会需要,甚至出现局部滞销的情况,消费者对蔬菜品质越来越高的要求,对营养、安全、绿色的高端品牌蔬菜需求增加。笔者从寿光蔬菜现状、寿光蔬菜走高端品牌化发展的必要性、寿光蔬菜高端品牌化发展的措施等方面进行了分析。寿光要在蔬菜生产方面继续发挥"领头羊"的作用,就要在营养、安全、绿色的高端品牌蔬菜生产方面走在前列,做出特色,推动寿光蔬菜产业转型升级,促进寿光蔬菜品牌的健康成长。     

多吃五色果蔬利于五脏养生

中医理论中的＂五行＂讲究五色与五脏相对,平时生活中多吃五色的果蔬是利于五脏养生的。我们按照颜色的由浅到深,把蔬菜分为白色蔬菜、黄色蔬菜、红色蔬菜、绿色蔬菜、紫色蔬菜和黑色蔬菜。一般来说,蔬菜的颜色深浅与它的营养含量成正比,即颜色越深营养价值越高。白色蔬菜：常见的白色蔬菜有莲藕、白萝卜、竹笋、茭白、花菜、冬瓜等。食用白色蔬菜能起到缓解情绪.     

海南水生蔬菜产业发展现状

海南发展耐湿热水生蔬菜可缓解夏秋蔬菜淡季需求压力,弥补大陆冬季蔬菜供应空缺,拉长水生蔬菜供应时间。海南现有12类水生蔬菜,本文对海南现有的水生蔬菜种类及其生产、分布状况作了调查,阐明了海南发展水生蔬菜的优势和劣势,并提出应搜集整理水生蔬菜资源,开展水生蔬菜育种,水生蔬菜温、光及生理生态,水生蔬菜特殊病虫害,提早或延后上市时间等多项研究,力争将海南水生蔬菜做出特色。     

广西农科院蔬菜研究所“丰成”蔬菜新品种简介

<正>广西农业科学院蔬菜研究所蔬菜新品种专栏广西农业科学院蔬菜研究所是从事蔬菜优良新品种选育、蔬菜高新栽培技术研究、蔬菜病虫害综合防治技术研究以及蔬菜贮藏加工技术研究的省级科研单位,在瓜类、茄果类新品种选育及推广、无土栽培技     

我国蔬菜市场预测预警研究浅析

在探讨蔬菜预测、预警理论发展情况的基础上,介绍了蔬菜市场预测预警的核心内容即蔬菜价格监测和蔬菜价格预警理论体系的概况,着重从蔬菜价格监测的概念、蔬菜价格监测的品种及范围、蔬菜价格监测体系3个方面介绍了蔬菜价格监测的主要内容;并分别从数量供应、需求、贮藏库、市场价格4个角度总结蔬菜预测预警现状,最后进行了展望。     

基于消费者的购买意愿建设蔬菜质量安全追溯体制所需的外部条件分析

可追溯体系是保障蔬菜质量安全的有效途径,消费者是实施蔬菜可追溯体系的最终推动者.现通过对河北蔬菜质量追溯体制建设现状的调查,以河北省石家庄市的消费者为例,分析消费者对可追溯性蔬菜的购买意愿.结果表明:消费者重视蔬菜质量安全、对可追溯蔬菜了解不够、价格是影响消费者购买意愿的主要因素.基于以上分析结合河北省蔬菜生产实际,阐述了建立蔬菜质量追溯体制需要具备的外部条件包括:蔬菜市场准入门槛建设、批发市场成为蔬菜责任的第一承担者、减少蔬菜流通环节、加强蔬菜质量安全检测、广泛开展社会监督,最后提出了蔬菜质量追溯体制框架的初步设想.     

Effect of non-alcoholic fatty liver disease on metabolic syndrome-rela-ted type 2 diabetes

AIM: To investigate the effect of non-alcoholic fatty liver disease (NAFLD) on metabolic syndrome (MS)- related type 2 diabetes. METHODS: Sixty-four rats were randomly divided into 8 groups: normal control groups of 3 months (3NC), 6 months (6NC), 9 months (9NC) and 12 months (12NC), and high-sucrose and high-fat groups of 3 months (3H), 6 months (6H), 9 months (9H) and 12 months (12H). The serum levels of alanine transaminase (ALT), free fatty acid (FFA), endotoxin (LPS), tumor necrosis factor alpha (TNFα), C-reactive protein (CRP), monocyte chemotactic protein-1 (MCP-1), fasting plasma glucose (FPG) and fasting plasma insulin (FINS) were measured. The insulin resistance index (HOMA-IR) and beta cell function index(HOMA-β) were also calculated. The specimens of liver and pancreas were prepared for microscopic observation with HE and Sudan Ⅳ staining. The visceral adipose specimens were also prepared with HE staining. The apoptosis of islet cells was detected by TUNEL.RESULTS: Compared with normal control groups, the levels of ALT, FFA, LPS, TNFα, CRP, MCP-1, FPG, FINS and HOMA-IR in high-sucrose and high-fat groups of every phase were higher, but the level of HOMA-β in 6H group showed a compensatory increase first and then progressively decreased. Compared with normal control groups, TUNEL results showed that the number of apoptotic islet cells in high-sucrose and high-fat groups gradually increased from the 3rd to the 12th month. CONCLUSION: The NAFLD plays a trigger role in the start of MS-related type 2 diabetes.     

Role of glucose-regulated protein 78 in pulmonary microvascular remodeling during development of rat hepatopulmonary syndrome

AIM：To explore the mechanisms of pulmonary microvascular remodeling induced by glucose-regulated protein 78 (GRP78) in the development of hepatopulmonary syndrome (HPS) in rats. METHODS：The Wistar rats were randomly divided into HPS groups at the 4th, 6th and 8th weeks, and normal control groups at the corresponding time points. The rat model of HPS produced in the process of liver cirrhosis was induced by employing multiple pathogenic factors to the animals. The rats in normal control group were designed by feeding with standard diet and mineral water. The expression of GRP78, factor Ⅷ- related antigen (FⅧ-RAg), C/EBP homologous protein (CHOP, also called growth arrest and DNA damage-inducible protein 153, GADD153), caspase-12, Bcl-2 and nuclear factor (NF)-κB in the lung tissues were measured by immunohistochemistry. The expression of VEGF at mRNA and protein levels in the lungs was measured by the methods of RT-PCR and Western blotting, respectively. RESULTS：The expression of GRP78, FⅧ-RAg,VEGF and Bcl-2 proteins was gradually increased with the HPS development. The protein expression of NF-κB was also gradually increased, especially in nucleus. GRP78 protein in the lung was positively correlated with the expression of FⅧ-RAg and VEGF, but negatively correlated with the expression of CHOP/GADD153 and caspase-12. The protein levels of GRP78 and FⅧ-RAg, and VEGF at both mRNA and protein levels were higher, and the protein levels of CHOP/GADD153 and caspase-12 were lower in the rats with HPS at every time point than those in normal control rats (P<0.05). CONCLUSION：Overexpression of GRP78 in the lung may be the critical pathogenesis of HPS by promoting cell survival and proliferation, and inhibiting cell apoptosis, thus leading to pulmonary microvascular remodeling.     

Glucose-regulated protein 78 promote cardiomyocyte apoptosis in liver cirrhotic rats

AIM: To explore the cardiomyocyte apoptosis induced by glucose-regulated protein 78/immunoglobulin heavy chain-binding protein (GRP78/BiP) in liver cirrhotic rats and its mechanism. METHODS: The liver cirrhotic rat model was established with multiple pathogenic factors, and sampled at the time points of 4 weeks, 6 weeks and 8 weeks. In experiment 1, the heart was collected and weighed, the thickness of the left ventricular wall was measured, and the ratios of the left ventricular wall thickness to the heart weight, and the heart weight to the body weight were calculated. In experiment 2, TUNEL was used to detect the apoptotic cardiomyocytes,and the protein levels of GRP78/BiP, CCAAT/enhancer-binding protein homologous protein/growth arrest and DNA damage-inducible protein 153 (CHOP/GADD153), caspase-12, nuclear factor-κB p65 (NF-κB p65) and B-cell lymphoma/leukemia-2 (Bcl-2) in the myocar-dium were detected by the method of immunohistochemistry. RESULTS: Compared with the normal myocardium, significant larger ratios of the left ventricular wall thickness to the heart weight and the heart weight to the body weight, a significant increase in the cardiomyocyte apoptosis, and a significant larger positive expression index of GRP78/BiP in the hearts 8 weeks after modeling were observed. The protein levels of CHOP/GADD153 and caspase-12 were gradually increased during the development of liver cirrhosis and were significantly increased at 8 weeks. The positive expression of NF-κB p65 and Bcl-2 showed consistent changes, and were markedly higher at 4 weeks than those at the other time points. The positive expression index of GRP78/BiP was positively correlated with the apoptotic index, and the levels of CHOP/GADD153 and caspase-12. The positive expression index of CHOP/GADD153 was negatively correlated with NF-κB p65 and Bcl-2. CONCLUSION: Elevated expression of GRP78/BiP may play a crucial role in the pathogenesis of liver cirrhotic cardio-myopathy mediated by endoplasmic reticulum stress.     

Expression of cyclooxygenase-2 in IL-1β-stimulated mesangial cells is medicated by NF-κB/IκB signal pathway

AIM: To investigate the role of NF-κB/IκB signal pathway in the regulation of cyclooxygenase-2 (COX-2) expression in human mesangial cells (HMC). METHODS: The PGE₂ concentration in supernatants of HMC was measured by radioimmunoassay. COX-2 mRNA and protein expression were determined by RT-PCR and Western blot. Electrophoretic mobility shift assay (EMSA) and Western blot were used to detect the activity of NF-κB and degradation of IκB. RESULTS: IL-1β significantly upregulated COX-2 expression and PGE₂ production in HMC. Significant up-regulation of NF-κB activation, nuclear translocation of p65 subunit, and degradation of IκB α and IκB β were observed in IL-1β-induced HMC. CONCLUSION: Expression of COX-2 in IL-1β-induced HMC is mediated by NF-κB/IκB signal pathway.     

Activation of Akt signal pathway cascades in kidney tissue in murine chronic graft-versus-host disease lupus nephritis and its regulation by prednisone

AIM:To examine whether Akt signal pathway proteins, including Akt, NF-κB and IκBα, are activated in kidney tissue of murine chronic graft-versus-host disease (GvHD) lupus nephritis in vivo, and whether prednisone suppresses activation of them.METHODS:Akt activity and phosphorylated IκBα were detected by Western-blot. Activation of NF-κB was detected by electropheretic mobility shift assay (EMSA). RESULTS:Activity of Akt, NF-κB and phosphorylated IκBα were significantly increased in kidney tissue of murine chronic graft-versus-host disease (GvHD) in 8th week and 12th week after monocell injection, respectively. However, they were no significant elevation in 16th week, when compared with controls. Prednisone treatment significantly prevented the increase in serum anti-dsDNA antibody level, urinary protein excretion and glomerular cell proliferation in GvHD mice, indicating the beneficial effects of prednisone on this model. Prednisone also significantly suppressed the increase in the activities of glomerular Akt, NF-κB and phosphorylated IκBα. CONCLUSION:This study provides the first evidence of marked increase in glomerular Akt-NF-κB signal pathway activities in murine chronic graft-versus-host disease lupus nephritis. The beneficial effect of prednisone on this lupus nephritis model may be partially mediated by the suppression of abnormal Akt- NF-κB activation.     

1,25-dihydroxyvitamin D3 inhibits nuclear factor kappa B signaling pathway in passively sensitized human airway smooth muscle cells

AIM:To investigate the effects of 1,25-dihydroxyvitamin D3 ［1,25-(OH)2D3］ on nuclear factor kappa B (NF-κB) signaling pathway in passively sensitized human airway smooth muscle cells (HASMCs). METHODS:HASMCs were passively sensitized with 10% serum from asthmatic patients. 1,25-(OH)2D3 was used as an interfering factor. Electrophoretic mobility shift assay (EMSA) was used to detect the DNA-binding activity of NF-κB. Immunocytochemical staining was used to observe the nuclear translocation of NF-κB p65. Western blotting was used for IκBα and phosphorylated IκBα protein detection. Real-time fluorescence quantitative PCR was used to determine vitamin D receptor (VDR), vitamin D 24-hydroxylase (CYP24) and IκBα mRNA expression. The mRNA expression of IκBα in HASMCs after actinomycin D treatment was also determined. RESULTS:(1) 1,25-(OH)2D3 significantly attenuated the DNA-binding activity of NF-κB and the nuclear translocation of NF-κB p65 in HASMCs passively sensitized by asthmatic serum. (2) 1,25-(OH)2D3 enhanced IκBα mRNA stability and inhibited IκBα protein phosphorylation in passively sensitized HASMCs, thus increasing IκBα expression in these HASMCs. (3) 1,25-(OH)2D3 up-regulated VDR mRNA level and evoked its functional response in passively sensitized HASMCs. CONCLUSION: 1,25-(OH)2D3 enhanced the expression of IκBα and therefore inhibited NF-κB signaling passway in HASMCs. This effect may be dependent on VDR, and responsible for the inhibitory effect of 1,25-(OH)2D3 on passively sensitized HASMCs.     

Role of GRP78 in alteration of myocardium induced by intestinal endotoxemia in cirrhotic rats

AIM: To explore the role of glucose-regulated protein 78 (GRP78) in the alteration of myocardium induced by intestinal endotoxemia in cirrhotic rats. METHODS: Fifty-one male Wistar rats were randomly divided into liver cirrhosis groups of 4-week, 6-week and 8-week, and normal control groups at corresponding time points. The cardiac functions of the 8-week rats were measured. Tumor necrosis factor α(TNF-α) and malondialdehyde(MDA) in myocardial tissues were detected. The number of myocardial cells and the collagen volume fraction (CVF) were determined with toluidine blue and van Giesan staining, respectively. The expression of GRP78 and hypoxia-inducible facotr 1α(HIF-1α) was analyzed by the method of immnunohistochemistry. RESULTS: Compared with normal control group at corresponding time point, left ventricular end-diastolic pressure(LVEDP) and ±LV dp/dt_max in 8-week group were significantly decreased (P<0.05). The levels of TNF-α, MDA and CVF, the protein expression of GRP78 and HIF-1α in the myocardial tissues were significantly increased in every model group (P<0.05), and the number of myocardial cells was gradually decreased (P<0.05). Elevated levels of endotoxin in plasma were positively correlated with the levels of alanine aminotransferase (ALT),homocysteine (Hcy) and TNF-α in plasma, the levels of TNF-α, MDA and CVF, and protein levels of GRP78 and HIF-1α in the myocardial tissues (P<0.05). Elevated protein expression of GRP78 in the myocardial tissues was positively correlated with the levels of ALT, Hcy in plasma and MDA, CVF, HIF-1α protein in the myocardial tissues (P<0.05). CONCLUSION: Intestinal endotoxemia induced by liver cirrhosis may directly or indirectly lead to endoplasmic reticulum stress and overexpression of GRP78. GRP78 may be a key molecule in the pathogenesis of myocardial remodeling and functional alteration induced by liver cirrhosis.     

Effect of Yiqi Huayu Huatan decoction on expression of KLF15, HMGB1, NF-κB and its downstream inflammatory factors in rats with UUO-induced renal interstitial fibrosis

AIM: To observe the effect of Yiqi Huayu Huatan decoction (YHHD) on unilaterral ureteral obstruction (UUO)-induced renal interstitial fibrosis in rats, and to investigate the possible mechanism. METHODS: Female SD rats (n=48) were randomly divided into sham group, model group, telmisartan group, and low-, middle-and high-dose YHHD groups, with 8 rats in each group. The UUO model rats was established by ligating left ureter. The rats in sham group and model group were treated with equal volume of normal saline, others were treated with the corresponding drugs daily. After 12 weeks, the rats were sacrificed. The serum samples were collected for determining the concentrations of cystatin C (Cys-C) and uric acid (UA). The morphological changes of the renal tissue were observed by PAS staining. The collagen fiber was observed by Masson staining. The mRNA expression of Krüppel-like factor 15 (KLF15), high-mo-bility group box protein 1 (HMGB1), nuclear factor-κB (NF-κB), IκB, monocyte chemotactic protein-1 (MCP-1), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), fibronectin (FN), collagen type I (Col I) and Col-Ⅳ was detected by real-time PCR. The protein expression of KLF15, HMGB1 and NF-κB was detected by Western blot. The protein expression of MCP-1 was determined by the method of immunohistochemistry. RESULTS: Compared with sham group, the deposition rate of collagen fibers and the concentration of Cys-C in model group were significantly increased (P<0.05), the mRNA and protein expression of KLF15 was significantly down-regulated (P<0.05), while the mRNA expression of HMGB1, NF-κB, IκB, MCP-1, IL-1β, TNF-α, FN, Col I and Col Ⅳ and the protein expression of HMGB1, NF-κB and MCP-1 were significantly up-regulated (P<0.05). Compared with model group, the deposition rates of collagen fibers in middle-and high-dose YHHD groups and telmisartan group were significantly decreased (P<0.05), with down-regulated protein expression of HMGB1 and NF-κB and mRNA expression of IL-1β and TNF-α (P<0.05). The protein expression of KLF15 was significantly up-regulated in high-dose YHHD group and telmisartan group (P<0.05), while the protein expression of MCP-1 and the mRNA expression of FN were significantly down-regulated (P<0.05). The mRNA expression of KLF15 was significantly up-regulated in high-dose YHHD group (P<0.05), while the mRNA expression of MCP-1, Col I and Col IV was significantly down-regulated (P<0.05). The mRNA expression of NF-κB and IκB was significantly down-regulated and the concentration of Cys-C was significantly decreased in each dose of YHHD groups and telmisartan group (P<0.05). No significant difference of UA level among the groups was observed. CONCLUSION: YHHD alleviates renal interstitial fibrosis in a dose-dependent manner, and YHHD at high dose shows the most obvious effect. The mechanism may be associated with the up-regulation of KLF15 and the down-regulation of HMGB1, NF-κB and its downstream inflammation-related factors in the renal tissue.     

Expression of MMP-2 and NF-κB in myocardium of mice with viral myocarditis

AIM: To observe the effects of TNF-α/nuclear factor-κB(NF-κB)/matrix metalloproteinase-2(MMP-2) pathway on the expression of MMP-2 in the mice with viral myocarditis. METHODS: Six-week-old inbred male mice were randomly assigned to control and myocarditis group. The mice in myocarditis group and control group were intraperitoneally inoculated with 0.1 mL 10^-5.69 TCID50/mL coxsackievirus B3 and vehicle (PBS), respectively. Ten mice were sacrificed at the 4th and 10th days after injection. The blood and heart specimens were harvested. The serum content of TNF-α was measured by ELISA. The myocardial levels of MMP-2, NF-κB p65 and IκBα were determined by Western blot. RESULTS: Compared with control group, the protein expression of MMP-2 and NF-κB p65 in the myocardium and the serum content of TNF-α were significantly increased in myocarditis group (P<0.05). The protein expression of IκBα was lower in myocarditis group than that in control group (P<0.05).CONCLUSION: TNF-α, NF-κB p65 and MMP-2 were higher in the mice with acute viral myocarditis. The increased expression of them might be involved in the pathogenesis of viral myocarditis.