盐池半荒漠风沙区土地沙漠化发生发展规律的研究

本文耐盐池半荒漠风沙区土地沙漠化发生发展规律进行了探讨，主要分析了在土地沙漠化的过程中土壤和植被的变化过程及其成因。     

丝兰属植物提取物降低鸡舍氨气浓度的效果试验

通过在21日龄的肉用仔鸡饲料中添加丝兰属植物提取物(其有效成分为丝兰皂角苷)，研究丝兰属植物提取物对降低鸡舍中氨气浓度和提高肉仔鸡生产性能的效果。试验结果表明，试验组鸡舍内氨气平均浓度为4．75mg／L，对照组鸡舍内氨气平均浓度为13．80mgl／L，试验组比对照组鸡舍内氨气平均浓度降低了9．05mg／L，经t检验，两鸡舍内氨气平均浓度差异显著(P＜0．05)，并且试验组比对照组饲料报酬提高了8.92％。     

代乳粉用于早期断奶犊牛的效果研究

犊牛使用代乳品可以节省鲜奶，降低饲养成本，控制疾病的发生，促进消化系统的发育。试验用24头犊牛做试验，60日龄断奶。结果表明，代乳品组犊牛增重47．55千克；对照组增重41．72千克；吃代乳品的犊牛在30-60日龄的日增重达到1026克，高于对照组103克。吃代乳品的犊牛每增重1千克的直接饲料成本为15．13元，比鲜奶组犊牛低2．14元／千克。     

中药穿心莲对新城疫HI抗体滴度的影响

1日龄肉仔鸡随机分为A、B、C、D、E、F、G7个试验组,每组组内设2个重复小组,每个重复小组35只鸡。A、B、C、D、E、F试验组添加穿心莲,G组不添加。各组均对新城疫进行首免和二免。结果发现,穿心莲能显著提高肉鸡的新城疫HI抗体滴度水平。另外,穿心莲的抗体滴度水平有一定的剂量依赖性,随着剂量的上升效果有提高的趋势。     

养殖小区防疫问题及改进措施

随着畜牧业的发展，全国各地养殖小区雨后春笋般建立起来。养殖小区是一种新型的畜牧业生产形式，它是在一定范围内按照集约化养殖的要求，建立的有一定规模的较为规范、严格管理的养殖园区。它是我国畜牧养殖从农村庭院养殖的小规模状态向大型现代化养殖的一种过渡型。是符合我国目前畜牧业发展状况的一种养殖模式，对推     

茶薪菇原生质体制备及诱变的研究

对茶薪菇原生质体的分离及再生进行研究 ,结果表明以溶壁酶的去壁效果最好 ,不同酶组合可提高去壁效果 ,酶解液在 2 0 %时原生质体释放量很高。酶解适宜温度为 30℃ ,培养 4～ 5d的菌丝酶解 3h释放的原生质体最多。以甘露醇作为渗透压稳定剂 ,原生质体的释放量及再生率均较高 ,再生率达到 5 %左右 ,经紫外线照射 2 0s,致死率即达 70 %以上     

旱作条件下转甜菜碱醛脱氢酶基因水稻籽粒灌浆特性的研究

在旱作条件下,对转甜菜碱醛脱氢酶(BADH)基因水稻的3个品系(52-7、51-15、51-22)、受体亲本中花8号(ck1)和当地推广的以色列陆稻白珍珠(ck2)的籽粒灌浆特性进行了比较分析。结果表明:5个品种(系)的强、弱势粒灌浆过程均符合Richards模型,强、弱势粒灌浆为异步灌浆型。三个转BADH基因品系与其受体亲本相比,强、弱势粒的灌浆速率提高,活跃灌浆期延长,灌浆高峰期的籽粒重增加;籽粒灌浆中、后期,强势粒的灌浆天数缩短,强、弱势粒的平均灌浆速率提高,且不同粒位籽粒灌浆速率差异减小,最终使不同粒位籽粒大小的差异缩小和粒重增加。最大灌浆速率、平均灌浆速率和灌浆高峰期的粒重与千粒重存在显著正相关。     

Model establishment and biological behaviour observation of mouse blastocyst co-cultured with hepatocarcinoma cell lines with differently invasive and metastatic potential in vitro

AIM: To explore interaction and biological behaviour changes of two kinds of cells-blastocysts and hepatocarcinoma cells in the same microenvironment. METHODS:The models of mouse blastocysts co-cultured with human hepatocarcinoma cell lines were established, then biological behaviours and mutual effects of the two kinds of cells in co-culture system were observed. RESULTS: Compared with control group, hepatocarcinoma cells with differently invasive and metastatic potential significantly enhanced the rates of blastocyst hatchment , attachment and outgrowth(P＜0.05). There was no significant difference in those among hepatocarcinoma cells co-cultured groups (P＞0.05). The blastocyst hatched and attached to hepatocarcinoma cells with differently invasive and metastatic potential. Then, differential trophoblasts invaded hepatocarcinoma cells. The clear-cut interfaces were gradually formed between both sides. Hepatocarcinoma cells on interface showed changes of growth direction and cell shapes and did not invade blastocysts. CONCLUSIONS: Hepatocarcinoma cells promoted blastocyst development. Blastocysts implanted and invaded hepatocarcinoma cells with differently invasive and metastatic potential in vitro, which indicate that blastocyst implantation in vitro does not relate with the kinds and differential level of interactional cells and the low selectivity maybe relate with high adaptability of early life.     

Nitric oxide-mediated the cardioprotection of tumor necrosis factor-alpha on cultured neonatal rat cardiomyocytes during hypoxia/reoxygenation

AIM: To investigate the role of nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC) and protein kinase C (PKC) signaling in tumor necrosis factor-α (TNF-α)-induced cardioprotection against hypoxia/reoxygenation (H/R) injury. METHODS: Neonatal rat ventricular myocytes were pretreated with TNF-α or sodium nitroprusside (SNP) or L-arginine (L-Arg), respectively, for 12 h and then subjected to continuous hypoxia for 12 h, followed by reoxygenation for 6 h. The manganese superoxide dismutase (Mn-SOD) activity of the cells was measured after H/R. Myocyte injury was determined by the release of lactic dehydrogenase (LDH). RESULTS: TNF-α (10⁵ U/L) significantly increased the Mn-SOD activity and decreased release of LDH from ventricular myocytes. The cardioprotection against H/R injury was induced by the pretreatment with SNP (5 μmol/L) or L-Arg (5 mmol/L), which was blocked by ODQ (10 μmol/L), the specific sGC inhibitor, and Chel (5 μmol/L), the specific PKC inhibitor. Pretreatment with L-NAME (100 μmol/L), ODQ, Chel, antoxidant 2-MPG (400 μmol/L) or tyrosine kinase inhibitor genistein (50 μmol/L) attenuated the increased Mn-SOD activity and reduced LDH level induced by TNF-α. CONCLUSION: The results suggest that NO may play a role in TNF-α-induced cardioprotection, which is mediated by sGC and PKC.     

Effect of atrial natriuretic peptide on acute lung injury induced by lipopolysaccharide

AIM: To investigate effect of atrial natriuretic peptide (ANP) on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in rat. METHODS: Mean arterial blood pressure (MAP) was recorded with model 6280 physiology intelligentialize grapher, nitric oxide (NO) and endothelin (ET) concentrations in plasma were measured after lipopolysaccharide (LPS) or following LPS ,ANP was injected into vein in rats. After experiment,lung water as well as pulmonary histopathological changes was measured and observed, respectively. RESULTS: Administration of LPS elicited a persistence decrease in MAP (8.1 kPa±2.6 kPa,at 4 h,P<0.01 vs control); NO and ET concentration in plasma was evident higher than that in control group, respectively (P<0.01); Wet-dry ratio of lung was higher than that in control group (5.15±0.43,at 4 h) (P<0.05); Alveolus detelectasis was observed and pulmonary mesenchyme was thicker than that in control group. No erythrocyte and leukocytes in alveolus,which show an interstitial pulmonary edema, was observed in LPS+ANP group, ANP maintained MAP at higher levels (13.35 kPa±2.93 kPa, at 4 h, P<0.05 vs LPS) after an transient decline when LPS was injected; NO and ET concentration of plasma had all significantly decrease, respectively (P<0.05 vs LPS, at 4 h); Wet-dry ratio of lung was lower than LPS group (4.57±0.35, P<0.05). Compared with control group the ratio was not evident difference (P>0.05); The histopathological of lung displayed markedly improved. CONCLUSION: ANP attenuates ALI induced by LPS in the rat. The effect of ANP may be via decreasing secretion of ET,NO and regulation arterial blood pressure.