膜式氧合器不同解吸方式对水产养殖水体中氨氮去除效果的影响

研究了膜式氧合器3种不同解吸方式，即：O2对流法、真空抽取法和酸吸收法去除水产养殖水体中氨氮的影响因素，并比较对其氨氮的去除效果。结果表明，氨氮初始浓度和pH是氨氮去除率的主要影响因素；当pH＞9时，O2对流法和真空抽取法对氨氮去除效果比pH＜9时要高，而酸吸收法不论pH高低时比其它2种方法都能获得较高的氨氮去除率。     

蛋氨酸铜和硫酸铜在凡纳对虾饲料中的应用效果比较

通过在饲料中分别加入不同浓度(铜元素的添加浓度分别为0、7.5、15、30、45mg·kg-1饲料)的硫酸铜和蛋氨酸铜,比较了硫酸铜和蛋氨酸铜对凡纳对虾生长、血液免疫因子及虾体铜的影响。添加蛋氨酸铜的各实验组生长速度同对照组之间没有显著差异;而添加硫酸铜的各组,只有铜添加量为30mg·kg-1饲料的试验组生长速度显著高于对照组(P<0.05),其它组同对照组之间差异不显著;成活率各组间无显著差异。除了铜添加量为15mg·kg-1饲料的试验组,各试验组对虾血清的酚氧化酶(PO)活力都高于对照组,其中当铜添加量为30mg·kg-1时最强,在此时蛋氨酸铜添加组的PO活力高于硫酸铜;随着铜添加浓度的提高,超氧化物歧化酶(SOD)活力增强,在添加量达到30mg·kg-1饲料时达到最大,此时硫酸铜组和蛋氨酸铜组间无差异,都为507。对虾肌肉中铜的含量各组间无显著差异,为(4.07±1.80)mg·kg-1,个体间差异非常大;肝胰脏中铜的最高含量为210.36mg·kg-1,最低为33.78mg·kg-1(空白对照组),明显高于肌肉中的含量。结果表明,在试验条件下,同硫酸铜相比,蛋氨酸铜没有显著的促生长效果,对肌肉、肝铜含量以及SOD活性没有显著影响。     

海巴戟DNA提取方法及SRAP分子标记聚类分析

应用SRAP分子标记技术开展海巴戟(Morinda citrifolia Linn,又名Noni)种质资源遗传多样性研究。结果表明,采用改良DNA提取方法能获得质量好,纯度高的海巴戟DNA。应用12对引物对78份海巴戟种质的SRAP分子标记扩增,共获得11 154条带,其中多态性条带有3 792条,多态性为33.99%,种质间具有很好的多态性。聚类分析结果表明,遗传距离为0.66时,78份海巴戟种质可归为2类,即海南本地种和西沙群岛种聚为一类,其余种质则聚为另一类;以0.86为阈值,78份海巴戟种质材料可聚为6类,从上至下依次是:万维2号种、新加坡种、大溪地种、万维1号种、海南本地种、西沙群岛种。其中,大溪地种和万维1号种的相似度较高,可以推断这2个种质亲缘关系较近,新加坡种与万维2号种的亲缘关系次之。     

苯基含氢硅树脂的制备及固化性能研究

以苯基三甲氧基硅烷(Phenyltrimethoxysilane,PTMS)、1,1,3,3-四甲基二硅氧烷(1,1,3,3-Tetramethyldisiloxane,HTMS)和六甲基二硅氧烷(Hexamethyldisiloxane,HMDSO)为主要原料,酸性阳离子交换树脂为催化剂,采用水解缩聚的方法制备了苯基含氢硅树脂(Hydrogen containing phenyl silicone resin,PHMT树脂),采用傅里叶转换红外线光谱(Fourier Transform Infrared Spectroscopy,FTIS)和核磁共振氢谱(1H Nuclear Magnetic Resonance Spectroscopy,1HNMR)对其结构进行了表征,并对其制备工艺、固化性能进行了研究.结果表明,甲氧基的水解程度达99.9%,但羟基缩聚不完全,其残留量约为质量分数0.57%.采用含氢量为体积分数0.37%,黏度为722 mPa·s的苯基含氢硅树脂为交联剂,其固化物机械性能较好.     

Protective effect of emodin on lung injury induced by hepatic fibrosis in rats

AIM:To explore the protective effect of emodin on lung injury induced by hepatic fibrosis in rats. METHODS:The hepatic fibrosis rat model was established with multiple pathogenic factors (CCl 4, ethanol, high fat, high cholesterol and low choline) and treated with different doses (20 mg/kg and 40 mg/kg) of emodin for 4 weeks. The hepatic index was measured. The biochemical indexes, endotoxin, homocysteine, albumin, aspartate aminotransferase,alanine aminotransferase, total bilirubin, total cholesterol and triglyceride, and hepatic fibrosis indexes, hyaluronic acid, laminin, collagen IV and procollagen Ⅲ, were detected. The histopathological changes of the liver were observed. The pulmonary index was determined. The histopathological changes of the lungs were observed. The levels of tumor necrosis factor α (TNF-α), malondialdehyde (MDA), nitric oxide (NO) and peroxynitrite (ONOO-) in the lung tissues were analyzed. RESULTS:The rat hepatic fibrosis model was successfully established. In model group, lung edema and inflammation occurred, and the pulmonary index and the levels of TNF-α, MDA, NO and ONOO- in the lung tissues were increased significantly. In emodin treatment groups, the pulmonary indexes were lower than that in model group. The pathological injury of the lung tissues was alleviated. The levels of TNF-α, MDA, NO and ONOO- in the lung tissues were decreased. CONCLUSION:Emodin has a protective effect on lung injury induced by hepatic fibrosis in rats.     

Effect of captopril on AGS nude mouse model of gastric cancer

AIM: To observe the effect of captopril on the genesis and development of gastric cancer, and to explore its clinical treatment feasibility for gastric cancer. METHODS: The human gastric cancer cell line AGS was used to establish a tumor model in nude mice, and the model mice were randomly divided into 3 groups: positive control (5-fluorouracil) group, normal control (saline) group and experimental (captopril) group. After intraperitoneal injection or intragastric administration of the drugs, the tumor growth curve was determined, and the tumor tissues were also sampled to detect the expression of Ki-67, STAT3, Bax and Bcl-2 by real-time quantitative PCR and immunohistochemistry. The apoptosis was detected by TUNEL+DAPI staining. RESULTS: The tumor growth curve showed that the tumor model in the nude mice was successfully established. The tumor volumes among groups showed significantly different after 14 d growth. The increase in the tumor volume in normal control group was significantly faster than that in the other two groups, and that in positive control group was the slowest. The expression of Bax in captopril group increased, and the expression of STAT3, Ki-67 and Bcl-2 was reduced as compared with normal control group and positive control group. Compared with normal control group, the apoptotic rate increased significantly, and the protein expression of p-STAT3 and STAT3 decreased obviously in positive control group and captopril group. CONCLUSION: With better feasibility, angiotensin-converting enzyme inhibitor captopril has a significant effect on treating gastric cancer in the AGS nude mouse model by regulating the expression of STAT3, Bax, Bcl-2 and Ki-67 to accelerate the apoptosis of cancer cells, thus inhibiting tumor growth.     

Aortic expression of HSP22, TNF-α and eNOS in rats with hyperlipidemia and effects of atorvastatin

AIM:To establish a rat hyperlipidemia model for studying the aortic expression of heat shock protein 22 (HSP22), tumor necrosis factor alpha (TNF-α) and endothelial nitric oxide synthase (eNOS) and the effect of atorvastatin intervention. METHODS:Hyperlipidemia model was established in SD rats. Afterwards, the rats were divided into normal control group, high fat group and high fat+atorvastatin intervention group. The expression of HSP22 and TNF-α in the rat aortas was detected by immunohistochemical assay and the expression of eNOS was assessed by Western blotting. RESULTS:No detectable expression of HSP22 and TNF-α in the normal control group was observed. However, the expression of HSP22 and TNF-α was positive in the high fat group and the atorvastatin intervention group. The mean densities of HSP22 and TNF-α positive particles were significant lower in the atorvastatin intervention group as compared with high fat group (both P＜0.05). The expression of eNOS protein in the high fat group and atorvastatin intervention group was significantly lower than that in normal control group (P<0.01). However, no marked difference of eNOS protein expression between high fat group and atorvastatins intervention group was observed. CONCLUSION: The expression of HSP22 and TNF-α in the rat aortas is increased in the hyperlipidemia rat model. This effect can be restored by atorvastatin treatment. The expression of eNOS in the rat aortas is decreased in the hyperlipidemia rat model, but this tendency could not be attenuated by atorvastatin.     

低蛋白日粮对育肥猪养分消化率和排泄量的影响

试验旨在探讨低蛋白日粮对育肥猪养分消化率和排泄量的影响。选用42头初始体重为(91.13±1.64)kg的杜长大育肥猪分为2组,每组3个重复,分别饲喂粗蛋白水平为15.49%(对照组)和12.59%(低蛋白组)的日粮。试验期30d。结果表明:(1)低蛋白组干物质、粗脂肪消化率显著提高(P0.01),粗蛋白、钙、磷消化率无显著变化;(2)低蛋白组精氨酸、天冬氨酸、异亮氨酸消化率比对照组分别低2.02%(P0.05)、5.42%(P0.05)、2.97%(P0.05),苏氨酸、蛋氨酸、脯氨酸消化率较对照组分别提高2.93%(P0.05)、1.43%(P0.05)、1.19%(P0.05);(3)低蛋白组育肥猪每天的氮排泄量比对照组低23.96%(P0.05),而有机物、磷、钙排泄量无显著差异(P0.05)。试验结果显示,日粮蛋白水平降低2.9个百分点可以改善养分的消化率,减少氮排放,但降低了精氨酸的消化率。     

猪繁殖与呼吸综合征病毒基因工程双标记疫苗rHN4-△25+NP49株最小免疫剂量的测定

将35头40日龄猪繁殖与呼吸综合征病毒(Porcine reproductive and respiratory syndrome virus,PRRSV)、猪瘟病毒(Classical swine fever virus,CSFV)、猪圆环病毒(Porcine circovirus type 2,PCV2)抗原及抗体均为阴性的健康仔猪,随机分成7组,每组5头,命名为XJ1~XJ7组。XJ1~XJ6组分别免疫PRRSV基因工程双标记疫苗rHN4-△25+NP49株,接种剂量分别为102TCID50/头、103TCID50/头、104TCID50/头、105TCID50/头、106TCID50/头和107TCID50/头,XJ7组为对照组,按1mL/头剂量接种DMEM。各试验组在免疫后28 d,用3×104.0TCID50/头剂量感染HP-PRRSV HuN4第5代强毒,疫苗免疫和攻毒后观察和检测各组试验猪的免疫效果。结果表明:攻毒前XJ2-XJ6组PRRSV ELISA抗体在免疫后14 d全部转为阳性,XJ1组在免疫后21 d转为阳性,但维持在较低水平;XJ2-XJ6组针对标记基因NP49的特异性抗体在免疫后28 d转阳性。攻毒后对照组全部发病,且死亡2头,XJ1有4头发病,XJ2-XJ6组无发病和死亡,本研究结果表明PRRSV基因工程双标记疫苗rHN4-△25+NP49株对仔猪提供免疫保护的最小免疫剂量为103TCID50/头。     

KC1对中间球海胆幼虫变态的诱导效果

中间球海胆（Strongylocentrotus intermedius)八腕后期幼虫，在KC1添加浓度100mmol/L海水中，分别处理5，10，15min后，均变态为正常稚海胆，中间试验及生产应用结果表明，经KC1处理，幼虫的附着时间缩短了36h，附着率则分别增加了40．4％，27．75％。