兔绿脓假单胞菌性肺炎的诊断与防治

本文报道近年来我省某试验养兔场兔群中流行一种生前以呼吸困难、口鼻出现血样分泌物症状,死后剖检以肺组织变性坏死为特征的疫情,经临床观察、实验诊断、病理剖检和病理组织学检查、流行病学调查及动物致病性实验研究,鉴定为绿脓假单胞菌(Ps.aeruginosa)引起的肺炎,该病特点传染快、死亡率高。通过流行病学调查,探索该病发病流行规律,为防治本病提供科学依据。     

HPLC法测定盐酸氯苯胍原粉含量

目的：采用高效液相色谱法测定盐酸氯苯胍的含量。方法：样品经1％盐酸甲醇萃取．以SHIMADZUC8色谱柱（250mm×4．6mm,5μm）分离,甲醇和2．5％的磷酸溶液以体积比75比25的混合液为流动相,在检测波长为317nm处测定。结果：峰面积与盐酸氯苯胍的质量浓度在1—100．0mg·L^-1范围内呈线性关系。标准加入回收率为（n=6）95．2％,相对标准偏差（n=5）小于0．5％。     

抗菌素在犬病治疗过程中的合理应用

在各类细菌感染性犬病的治疗过程中,抗菌素是临床上最为广泛应用的药物之一,它在抗菌消炎、控制感染、促进康复方面发挥着重要作用.合理的抗菌素治疗,应根据犬病和个体的差异而选择不同抗菌素,从而达到有效的抑制或杀灭特异的病原体,并避免出现耐药性及药物副作用,使病犬治愈康复.     

乳酸恩诺沙星可溶性粉在鸡体内的药动学研究

24只苏禽黄羽肉鸡随机分成2组,分别按10 mg/kg体重剂量静注和内服乳酸恩诺沙星。测定乳酸恩诺沙星在鸡体内的药动学参数和生物利用度。恩诺沙星血药浓度数据用3p87计算机软件处理。静注乳酸恩诺沙星后的血药浓度-时间数据符合二室开放模型,主要动力学参数:t1/2α(0.45±0.16)h,t1/2β(7.02±1.42)h,CL(s)(0.38±0.10)L/kg/h,AUC(23.69±5.56)(mg/L)×h。内服乳酸恩诺沙星的血药浓度时间数据,符合有吸收因素二室模型,主要动力学参数:t1/2ka(0.60±0.01)h,t1/2ke(8.25±1.73)h,tpeak(2.44±0.17)h,Cmax(1.44±0.30)mg/L,AUC(20.74±3.80)(mg/L)×h,F 87.54%。结果表明,乳酸恩诺沙星可溶性粉在鸡体内具有吸收快、分布广、消除较慢以及内服生物利用度高的药动学特征。     

鸡球虫耐药性的机理检测方法及其延缓措施

文章对鸡球虫耐药性的产生机制、检测方法及其延缓措施的研究进展进行了概述。     

Bio—G除臭剂对蛋鸡舍内氨气及产蛋性能的影响

在面积相等，饲养密度相近的2栋蛋鸡舍内连续15d喷洒Bio-G除臭剂，每天1次，每次5L，结果表明，喷洒Bio-G后，鸡舍氨气含量明显下降，但对蛋鸡产蛋性能无明显影响。     

生物纤维饲料在蛋鸡生产中的应用研究

生物纤维饲料是对玉米淀粉湿磨国工过程中的浸泡液，黄浆和玉米皮渣等副产品经生物发酵方法而形成的一种新型饲料。本文研究了生物纤维饲料在蛋鸡饲养中的饲喂效果。试验表明，半风干生物纤维饲料（含水分26．68％）以5％比例添加蛋鸡日粮中的饲喂效果与对照组相比，日均产蛋量提高6．4％，平均产蛋率提高6．05％，料蛋比下降13．01％，毛利润提高90．70％，而风干生物纤维饲料（含水分15．44％），则以10％比添加于蛋鸡日粮时，表现出较明显的增产效果，其与对照组相比，日均产蛋量提高4．04％，平均产蛋率提高4．18％，料蛋比下降4．09％，毛利润提高25．74％。     

利用风险分析原理完善动物源性食品安全标准体系

近年来，一些危害人类生命健康的重大动物源性食品安全事件不断发生，如发生在比利时的二恶英事件，英国的疯牛病事件，日本的大肠杆菌0157污染事件以及禽流感疫情等。食品安全已成为一个日益引起关注的全球性热点问题。建立以风险分析为基础的标准体系，推行动物源性食品安全科学的管理模式。     

警犬技术工作执法资格等级考试考核制度研究

2008年开始,公安部警犬技术学校希望通过警犬技术工作执法资格等级考试考核制度的研究,以进一步促进警犬技术工作的正规化、规范化、标准化.     

Calcium homeostasis and its relationship to superoxide production in blood and milk neutrophils of lactating goats

Polymorphonuclear neutrophils (PMN), which comprise over 70% of the somatic cells in goat milk, are a major cellular component of innate immunity in the goat mammary gland. However, the function of milk PMNs is modified after diapedesis compared to PMNs in blood. As many aspects of PMN activity depend directly on intracellular Ca²⁺ concentration ((Ca²⁺)_i), the present study aimed to determine the changes in Ca²⁺ homeostasis of milk PMNs from lactating goats compared to autologous blood PMNs, and to examine the significance of these variations to the immuno-competency of milk PMNs. The intracellular Ca²⁺ store of freshly prepared milk cells was estimated from the elevation of (Ca²⁺)_i after ionomycin treatment, which was found to be significantly less than blood PMNs. Replenishment of the intracellular Ca²⁺ store in milk cells after intracellular Ca²⁺ depletion by Bapta-AM followed by spiking with 2.5 mM Ca²⁺ for 20 min was also compared to that of blood PMNs, showing that after depletion/spiking the intracellular Ca²⁺ store in milk cells was much less than blood PMNs. The production of superoxide anion (O₂^?) in vitro in response to (Ca²⁺)_i-dependent or (Ca²⁺)_i-independent modulators was used to evaluate the relevance of altered Ca²⁺ homeostasis on the immuno-competency of milk cells compared to blood PMNs. The results indicated that milk cells produced similarly low levels of O₂^? as blood PMNs when treated with ionomycin. However, the amount of O₂^? produced by milk cells in response to phorbol 12-myristate 13-acetate (PMA) stimulation, although greater than ionomycin treatment, was significantly less than that of blood PMNs. The capacity for O₂^? production by both cell types in response to PMA reverted to the resting state with use of the protein kinase C (PKC) inhibitor, staurosporine. In conclusion, the current study demonstrated an irreversible shortage of intracellular Ca²⁺ in the milk PMNs of lactating goats compared to blood PMNs. It also showed that preliminary O₂^–production, primed by ionomycin treatment, remained unchanged in milk PMNs, despite the shortage in intracellular Ca²⁺, but decreased O₂^? production capacity, mediated via the PKC pathway, in milk PMN. It is suggested that the defects in Ca²⁺ homeostasis in milk PMNs of lactating goats is partially attributable for the post-diapedesis functionality modifications.