2017—2018年原料及饲料中霉菌毒素变化趋势

霉菌毒素在原料及饲料中处于不断变化中。为了解国内市场上原料及饲料中霉菌毒素污染情况,2018年度从市场上收集124份样品,经前处理后按照酶联免疫法测定3种霉菌毒素含量并对数据进行分析。结果表明:与2017年相比,呕吐毒素污染范围依然广泛,黄曲霉毒素和玉米赤霉烯酮污染范围有所缩小,但玉米赤霉烯酮超标率呈上升趋势。此外,还对新版饲料卫生标准中玉米赤霉烯酮限量进行了详细的阐述。     

不同灌水施肥条件对苹果生长发育及产量品质的影响

为筛选苹果生长发育所需的最佳灌水施肥组合,选取长势一致的11年生岩富10/M26为试验材料,设置2个施肥量：F1(0 kg/hm²)、F2(施肥量1 050 kg/hm²:20-20-20平衡型水溶肥);设置4个灌水量：零灌水W1(0 m³/hm²)、低水W2(74.4 m³/hm²)、中水W3(148.8 m³/hm²)、高水W4(223.2 m³/hm²),共8个处理,灌水施肥方式为条施,在苹果生长发育过程中进行3次灌水施肥。结果表明,F2W4的产量最高,为14 237.71 kg/hm²,较F1W1(对照)的产量增加了26.68%,F2W4处理收益最高,纯收益为8.02万元/hm²,较F1W1(对照)处理纯收益净增1.04万元/hm²。灌水施肥对果实品质有显著的影响,表现为：果实红绿指数a^...     

土壤局部改良对陕北山地果园苹果生长发育及果实品质的影响

选用4种材料对山地果园土壤进行局部改良,探究不同的改良材料对树体营养、果实产量和果实品质的影响。选用陕北地区主栽的富士系10年生烟富6号/八棱海棠为试验材料,在每棵树两侧距离树干1 m处挖条沟,取羊粪、椰壳、草炭、秸秆4种材料各50L,与150L园土混合后进行土壤局部改良处理,以不进行土壤改良的果树作为对照,测定苹果树生长发育、叶片以及果实指标,比较不同处理的改良效果。用羊粪进行土壤局部改良可显著增加叶片干鲜质量、叶绿素含量和果实品质,其中总叶绿素含量和可溶性固形物含量分别较CK增加23.82%,14.36%;用草炭进行土壤局部改良可显著提高叶片光合特性和果实产量,其中光合速率和果实总产量分别较CK增加53.74%,14.76%;椰壳处理叶片干质量、叶片鲜质量、总叶绿素含量、果实产量分别较CK显著增加了16.65%,18.84%,20.19%,18.19%;秸秆处理的果实明亮度与果实产量较CK显著提高了8.09%,5.40%。4种改良材料均提高了果实品质和产量,均可作为陕北地区土壤局部改良的材料,且以施用椰壳的处理效果最好。     

酪啡肽及其酪蛋白水解肽对早期断奶仔猪分泌型免疫球蛋白A和细胞因子水平的影响

本文旨在研究酪啡肽及其酪蛋白水解肽对早期断奶仔猪分泌型免疫球蛋白A(SIgA)和细胞因子水平的影响。24头仔公猪随机分为对照组(正常哺乳28d断奶)、试验Ⅰ组(添加β-酪啡肽-7)和试验Ⅱ组(添加酪蛋白酶解物)。试验组于21d断奶,再连续添加酪蛋白胃蛋白酶解液或β-酪啡肽-710d,每天2次(共20mL),至32d,3组动物各随机取6头同时剖杀,取血、胃食糜和空肠食糜。观察其血清IL-2、TNF-α和胃肠内容物中SIgA的含量变化。结果表明:添加酪蛋白水解液组仔猪血清中IL-2的水平比对照组高75.9%,差异极显著(P<0.01);试验Ⅰ组血清中IL-2水平比对照组高35.7%,差异显著(P<0.05)。血清中TNF-α水平试验组略低于对照组。在对照组、试验Ⅰ和Ⅱ组仔猪的空肠食糜中均检测到SIgA,平均含量分别为(6.48±0.85)ng/g、(6.30±0.85)ng/g和(8.71±0.54)ng/g。与对照组相比,试验Ⅱ组差异极显著(P<0.05);胃食糜中未检测到SIgA。提示乳源活性肽对早期断奶仔猪细胞免疫和黏膜免疫活性具有一定的促进作用。     

土壤脲酶活性两种测定方法的比较

利用比色法和扩散法对金强河地区和甘肃农业大学校园内的土壤脲酶活性进行了分析。结果表明：比色法和扩散法测定的土壤脲酶活性平均值分别为（0．531±0．207）mg／g和（0．446±0．204）mg／g,两种测定方法的结果和变异系数差异均不显著（P〉0．05）。但从试验操作方面考虑,扩散法操作比较简单、所用药品种类少、时间短,是一种比较可行的土壤脲酶活性测定方法。     

Antitumor activity of Paecilomyces tenuipes polysaccharide and its mechanism in vitro

AIM:To investigate the antitumor activity and mechanism of Paecilomyces tenuipes polysaccharide(PTPS).METHODS:PTPS-I was obtained by water extraction and alcohol precipitation, and purified by DEAE-cellulose and Sephadex G-100 chromatography. Human erythroleukemia cell line K562, laryngocarcinoma cell line Hep2 and hepatic carcinoma cell line SMMC-7721were co-cultured with PTPS-I or the conditioned medium which prepared with PTPS-I-stimulated human mononuclear cells (PTPS-I-MNC-CM), and the proliferation of tumor cells was determined. The cell counting kit-8 (CCK-8) was used to determine the proliferation of MNCs. The FQ-RT-PCR was applied to investigate the expression of TNF-α and IL-6 mRNA in MNCs. RESULTS:PTPS-I-MNC-CM inhibited the proliferation of K562, Hep2 and SMMC-7721 cells in vitro (P<0.01). Cytotoxicity of PTPS-I against K562, Hep2 and SMMC-7721 cells was not observed (P<0.01). PTPS-I stimulated the proliferation of MNCs (P<0.01) and significantly enhanced the expression of TNF-α and IL-6 mRNA in MNCs (P<0.05, P<0.01). CONCLUSION:The results suggest that PTPS-I is an immunomodulator and its antitumoral activity is through the immunomodulatory mechanism rather than the direct cytotoxicity against tumor cells.     

Significance of soluble CD40 ligand in the vulnerability of coronary atherosclerotic plaque

AIM: To evaluate the significance of serum soluble CD40 ligand (sCD40L) in the vulnerability of coronary atherosclerotic plaque, the relationship between the level of sCD40L and the stenosis degree of the coronary artery by the coronary angiography (CAG), and other inflammatory factors. METHODS: According to WHO diagnostic criterior of coronary heart disease (CHD) and the results of CAG, 84 cases of CHD and 20 cases of non-CHD (NCHD) were included in this study. 84 cases of CHD were divided into three groups: 30 cases in acute myocardial infarction (AMI) group, 30 cases in unstable angina (UA), 24 cases in stable angina (SA). The sera levels of sCD40L in four groups were detected by the enzyme-linked immunosorbent assay (ELISA) and the results were expressed with μg/L. CAG were all conducted in four cases and the results were further evaluated by Jenkins score. ESR and CRP were detected at the same time. RESULTS: The sera levels of sCD40L in four groups were significantly different (P<0.01). The level of sCD40L in AMI group (8.48±4.13) μg/L was higher than that in SA group (4.36±2.68) μg/L, P<0.01 and NCHD group (4.12±1.96) μg/L, P<0.01. The level of sCD40L in UA group (8.72±4.26) μg/L was higher than that in SA group and NCHD group (P<0.01). The level of sCD40L in UA group was slightly higher than that in AMI group, but the difference of two group is not significant (P>0.05). The level of sCD40L in SA group was slightly higher than that in NCHD group, but the difference of two group is not significant (P>0.05). The sera levels of sCD40L in CHD were significantly and positively correlated with Jenkins score (r=0.524, P<0.01). The sera level of sCD40L was positively correlated with the levels of CRP and ESR. CONCLUSION: The sera levels of sCD40L in the patients with various types of CHD are significantly different. The level of sCD40L in the patients with AMI and UA are significantly higher than those in SA and NCHD groups, which may reflect the vulnerability of coronary atherosclerotic plaque. The sera levels of sCD40L is increased with the increasing number of diseased coronary branches and Jenkins score, suggesting that sCD40L promotes atherosclerosis and also can be used as a parameter to predict pathological severity of coronary atherosclerosis. The level of sCD40L is obviously correlated with the levels of CRP and ESR.     

Oxidative stress plays an important role in acetaldehyde-induced cardiomyocytes apoptosis

AIM: To elucidate the mechanism of alcoholic myocardiopathy (AHMD) by exploring the role of ROS mediated oxidative stress in acetaldehyde-induced cardiomyocytes apoptosis. METHODS: Cultured rat cardiomyocytes were stimulated with acetaldehyde (100 μmol/L) for 24 h, then the cell apoptotic index were examined and compared to that with alcohol (100 μmol/L) stimulation. The changes of ROS levels and SOD activities were explored by a time-dependent model in acetaldehyde-induced cardiomyocytes. Meanwhile, the phosphorylation changes of ROS mediated MAPK signaling pathway correlated proteins were also detected, with which compared that changes both in pre-adding NAC acetaldehyde-induced cardiomyocytes, and in H2O2 (100 μmol/L) induced cardiomyocytes, respectively. RESULTS: Acetaldehyde had more obvious apoptotic effect than alcohol through caspase 3 activating (P<0.05, vs control), both cellular ROS level and SOD activity increased in a time-dependent way, and reached the peak value of (78.84%±4.33%) for ROS and (0.55±0.02) for SOD among 18 to 24 h, respectively. Meanwhile, JNK and ERK protein phosphorylation upregulated in acetaldehyde-induced cardiomyocytes, and was reversed by NAC anti-oxidative effect. However all the phosphorylation levels were weaker than that in H2O2-induced group. CONCLUSION: Acetaldehyde causes oxidative damage in cardiomyocytes through enhancing cellular ROS level, and induces cardiocytes apoptosis by activating ROS mediated JNK pathway. The novel way of depressing cellular ROS level or blocking the special apoptotic pathway may have effects on AHMD preservation and therapy.