Differential effects of dexamethasone and clenbuterol on rat growth and on beta2-adrenoceptors in lung and skeletal muscle

Beta-adrenergic agonists increase growth rate, but their efficacy is reduced over time as the number of beta2-adrenoceptors in muscle decreases. Dexamethasone increases beta2-adrenoceptor density in many tissues, but this effect has not been reported in skeletal muscle. In this study, male rats were treated daily for 10 d with either clenbuterol (4 mg/kg of feed), dexamethasone (.2 mg/kg BW, s.c.), or clenbuterol plus dexamethasone. Untreated rats served as controls. Dexamethasone caused a marked suppression of growth rate, which resulted in decreased (P < .001) body weight (-29%), carcass weight (-30%), hind-limb muscles (-22%), omental fat (-22%), and heart weight (-10%). Feed intake was reduced (-26%), but feed conversion efficiency was also impaired (P < .001). Clenbuterol caused a small increase in growth rate (+6%; P < .05), with an increase in leg muscle (+7%; P < .01) and heart mass (+8%; P < .05). Feed efficiency was improved (P < .001) by clenbuterol. Rats given the combined treatment still showed a reduction in growth rate (-81%). Clenbuterol caused only a mild attenuation of the effects of dexamethasone on feed intake, BW, and carcass weight, but reduced the catabolic effect of dexamethasone on hind-limb muscle to only -8%. Clenbuterol caused a slight increase in the affinity beta2-adrenoceptors in lung for binding to the radioligand (-)[125I]iodocyanopindolol. Relative to control values, the density of beta2-adrenoceptors in lung was +31% with dexamethasone treatment, -45% with clenbuterol, and -23% with the combined treatment. Clenbuterol also decreased beta2-adrenoceptors in skeletal muscle (-35%), but so did dexamethasone (-13%), so the effects of the beta-adrenergic agonist were not attenuated through use of the combined treatment (-40%). The results show that the inductive effect of glucocorticoids on beta2-adrenoceptors is tissue-specific and that glucocorticoid treatment is not a useful adjunct to beta-adrenergic agonist treatment in animal production.     

猪生殖--呼吸道综合征(PRRS)的诊断与防制

1987年在美国北卡罗来纳州、明尼苏达州以及衣阿华州等地的猪群中爆发了一系列令人震惊的"流产风暴",特征是妊娠母猪发生晚期流产、早产、死胎和木乃伊胎,以及仔猪出现呼吸道病和高死亡率.由于该病前所未闻且病原不明,故被称为"猪神秘病"(MSD)[1-4].其后,加拿大报道了类似的病症[5].1990年冬,欧洲开始流行MSD,首先在德国出现[6].继而,在荷兰、西班牙、比利时、英国、法国等养猪业较发达的欧洲国家陆续爆发了本病[7-10].     

芡欧鼠尾草的组织培养和快速繁殖

以芡欧鼠尾草(Salvia hispanica)成熟种子为外植体,1/2MS为基本培养基,研究不同浓度的外源激素对愈伤组织的诱导、增殖和生根的影响,从而初步建立了芡欧鼠尾草组织培养的快速繁殖体系。结果表明,诱导种子愈伤组织的最适宜培养基为1/2MS+10.0mg·L~(-1) 6-BA+1.0mg·L~(-1) NAA+0.4mg·L~(-1) ZT,诱导率为66.5%;不定芽增殖的最适培养基为1/2MS+3.0mg·L~(-1) 6-BA+0.5mg·L~(-1) NAA,增殖倍数为7.69;生根的最适培养基为1/2MS+0.5mg·L~(-1) NAA,生根率达100%,平均生根数为5.68;移栽后植株生长良好,成活率较高,达97%。     

美国国家动物卫生实验室网络组建与发展现状

2002年,为提升动物外来病入侵和生物恐怖袭击的应对能力,美国以联邦、州立和大学动物卫生诊断实验室为基础,组建了国家动物卫生实验室网络(NAHLN)。十多年来,NAHLN几乎覆盖了美国所有公立动物疫病诊断实验室,网络体系趋于完善;通过联邦和各州持续投资,NAHLN实验室强化了生物安全设施、标准化快检技术、质量体系、电子报告系统、人员素质和应急监测预案等6方面建设,能力大幅提升;按照早发现、快反应、有序恢复(无疫)的理念,设置了风险监测、应急监测、无疫监测3种模式,对10余种优先防范和控制病种实施分类监测,在发现疫情和证实无疫方面发挥了重要作用,HANLN的名字由此得到了美国政府、国会和行业的认可。同时,HANLN也面临着经费支持不足、被动监测组织性不够等问题。     

2019年我国部分地区屠宰生猪旋毛虫和弓形虫检测

为了解我国部分地区屠宰生猪旋毛虫和弓形虫感染情况,2019年在广东（5个）、山东（4个）、云南（6个）等省份的15个大型、中小型生猪屠宰场,采集猪膈肌样品315份,用PCR方法进行旋毛虫和弓形虫病原学检测;在以上3省15个大型、中小型生猪屠宰场（每省5个）,采集血清样品254份,用ELISA方法进行旋毛虫和弓形虫血清学检测。结果显示：经PCR检测,采样地区所有膈肌样品均为旋毛虫阴性,仅在云南省120份膈肌样品中检出1份弓形虫阳性;经ELISA检测,采样地区血清样品的旋毛虫和弓形虫抗体阳性率分别为1.97%和2.36%,不同省份的阳性率分布不一致,中小型屠宰场阳性率均高于大型屠宰场。结果表明,广东、山东、云南等省份屠宰生猪的旋毛虫和弓形虫携带率极低,基本可以保证猪肉的产品安全;部分地区屠宰生猪存在一定的弓形虫感染抗体,尤其是中小型屠宰场,表明此类猪群需要加强饲养环节的弓形虫感染控制。本研究为保障猪肉食品安全及饲养环节的猪旋毛虫和弓形虫感染控制提供了依据和指导。     

家蚕黑尾病及其防治方法研究

家蚕黑尾病主要是由曲霉菌在蚕尾部寄生引起的一种真菌病 ,从病蚕中分离到病原菌有两种 ,一种孢子表面棘多而长、黄褐色 ,孢子大 ,直径 4～ 6 μm ;一种孢子表面棘短而少、蓝绿色 ,孢子小 ,直径 2～ 3μm。黑尾病在高温多湿条件下多发 ,多发生于 4龄中期至 5龄中期。黑尾病病原菌侵染寄生家蚕的过程是 :病原菌分生孢子附着在蚕尾部背板与节间的三角形节间膜处 ,分生孢子发芽侵入蚕体产生黑色小病斑 ,随病情加重病斑加大 ,甚至在病斑处出现节间断裂 ,直至形成黑尾症状。使用药剂防治黑尾病以 5 %亚迪蚕保最佳     

H9亚型禽流感病毒钦州株HA基因的克隆与遗传进化

采集钦州活禽交易市场的鸡气管和泄殖腔的棉拭予样品,用H9亚型分型引物进行PCR初步筛选,阳性样品经SPF鸡胚尿囊腔接种分离病毒,通过RT-PCR方法扩增HA基因,并将其克隆到pMD—18T载体后进行序列测定和分析。结果表明,获得1株H9亚型禽流感病毒命名为：A／Chicken／Guangxi／qz40／2009（简称qz40）。测序结果表明qz40的HA基因片段全长1683bp,编码560个氨基酸;序列同源性比较结果表明,该毒株与参考毒株的核苷酸序列同源性为82．8％．99．9％,推导氨基酸同源性为87．5％．99．6％;HA基因的裂解位点氨基酸顺序为RSSRIGLF,为低致病性毒株;含有7个潜在的N-糖基化位点,其中5个位于HAl部分、2个位于HA2部分;基于H9亚型HA基因的进化树分析表明,qz40株属于欧亚种系的A／Chicken／Beijing／1／94（Ck／Bei—like）群系。     

新城疫活疫苗对控制鸡大肠杆菌病的效果观察

为了研究鸡新城疫活疫苗紧急免疫控制鸡大肠杆菌病的效果,通过大肠杆菌人工感染30日龄蛋鸡,待出现病症后,紧急免疫新城疫La-sota弱毒苗(Ⅳ系)4羽份.免疫后5～17 d,通过血凝抑制试验测定血清新城疫抗体水平,试验组新城疫抗体水平逐步提高,对照组抗体略有下降,免疫后17 d两组抗体水平差异显著(P＜0.05);对照组...     

黔东南州林下鸡高致病性禽流感免疫程序研究

为了探索林下鸡高致病性禽流感免疫程序,在黔东南州的老寨、龙氏、平寨3个林下鸡场随机选择50只雏鸡,采用血凝抑制试验分别对母源抗体、首次免疫抗体、第2次免疫抗体、第3次免疫抗体的变化规律进行检测,研究出黔东南州林下鸡高致病性禽流感的免疫程序,即15日龄进行首次免疫,42～45日龄进行第2次免疫,135～140日龄进行第3次免疫,以后每隔4个月免疫1次。     

Characterization of porcine circovirus type 2 (PCV2) infection in swine lymphocytes using mitogen-stimulated peripheral blood lymphocytes from healthy PCV2-carrier pigs

Information regarding the susceptibility of swine lymphocytes to PCV2 is rather limited. To further explore and characterize the PCV2 infection in swine lymphocytes, an in vitro model using concanavalin A (Con A)-stimulated peripheral blood lymphocytes (PBLs) obtained from clinically healthy PCV2-carrier pigs was introduced. It was found that the PCV2 antigen-containing rate was below 2% in PBLs from healthy PCV2-free pigs following treated simultaneously with Con A and PCV2. However, significantly higher PCV2 antigen- and nucleic acid-containing rates could be seen in Con A-stimulated PBLs from clinically healthy PCV2-carrier pigs. Prior to Con A treatment, both of the PCV2 antigen- and nucleic acid-containing rates in PBLs from healthy PCV2-carrier pigs were less than 1%; however, they reached 22.1+/-5.7% by flow cytometry and 27.1+/-6.5% by in situ hybridization, respectively, at 4-day post-incubation with Con A. Phenotyping of PCV2 antigen-containing cells revealed that PCV2-positive cells could be detected in both T and B lymphocyte populations within which IgM-positive B lymphocytes appeared to have a relatively higher positive rate. The Con A-stimulated PBLs also displayed a significantly higher viral load by the measurement of either PCV2 DNA copy number or viral titer when compared with the non-treated PBLs from healthy PCV2-carrier pigs. The results indicate that PBLs, especially IgM-bearing B lymphocytes, are indeed susceptible to PCV2 infection and PCV2 is capable of replicating in dividing lymphocytes. This activation-induced replication may explain in part the pathogenesis of lymphoid depletion in PMWS-affected pigs.