马铃薯蛋白粉对断奶仔猪的应用效果研究

选择30日龄断奶体重为(6.94±0.69)kg的二元杂种商品仔猪184头,按照窝别、性别、体重相近的原则分为5组,饲喂不含马铃薯蛋白粉的基础饲粮和以2%、4%、6%的马铃薯蛋白粉及4%的血浆蛋白粉等氮替代基础饲粮中豆粕的饲粮,每组4～5个重复,每个重复8头仔猪,进行28d的饲养试验。试验第15d称重后,每个重复选择1头体重接近该圈平均体重的仔猪前腔静脉采血,测定血液生化指标;试验第15～18d,以圈为单位,收集粪样,测定蛋白质表观消化率。研究马铃薯蛋白粉在断奶仔猪上的应用效果,确定其适宜添加量。结果表明,饲粮中添加2%马铃薯蛋白粉组,与基础饲粮组相比,试验全期可以提高日增重6.14%(P>0.05)、降低料重比10%(P<0.01),降低腹泻率6.24个百分点(P>0.05),效果相当于甚至优于4%血浆蛋白粉。饲粮中添加4%和6%马铃薯蛋白粉,仔猪生长性能显著或极显著低于基础饲粮组。但6%马铃薯蛋白粉组蛋白质表观消化率高于基础饲粮组和2%马铃薯蛋白粉组(P<0.05),血浆蛋白粉组蛋白质表观消化率略高于基础饲粮组(P>0.05);2%马铃薯蛋白粉组血清总蛋白、白蛋白、球蛋白、胆碱酯酶含量最高;4%血浆蛋白粉组血清尿素氮显著低于基础饲粮组,极显著低于马铃薯蛋白粉组;6%马铃薯蛋白粉组谷丙转氨酶活性高于4%、2%马铃薯蛋白粉组(P<0.05);各个处理血液谷氨酰胺、谷氨酸含量以及谷草转氨酶活性差异不显著。由此结论,马铃薯蛋白粉在断奶仔猪饲粮中的适宜添加量为2%。     

草地早熟禾愈伤组织遗传转化受体系统的建立

以草地早熟禾成熟胚为外植体，并去除部分胚乳，或用浓盐酸处理，选择NB＋2，4-D2mg／L为诱导培养基，NB＋6-BA2mg／L为分化培养基，1／2NB＋IAA0．5mg／L＋NAA0．5mg／L为生根培养基，建立了这些品种的胚性愈伤组织高频诱导与再生系统，确定了G418（40-50mg／L）Hpt（50mg／L）的筛选临界浓度，确定了最佳分化时间，探讨了建立草地早熟禾转化受体系统的必要条件。     

饲料的不同形态与状态对早期断奶仔猪生产性能的影响

试验采用2×2因子设计,共分4个处理,即粉料和颗粒料2种类型,每种类型2种状态(液态和固态)。试验选用96头(21±1)d断奶的三元(D×L×Y)杂交仔猪,试验期21 d。其中液态料按12∶.5的料水比进行浸泡。试验期间考察仔猪的耗料量、增重、腹泻情况、粪便pH值及木糖吸收情况等,并测定饲料的pH值和淀粉糊化度。结果表明:①与粉料组相比,颗粒料组仔猪平均日增重提高了9.7%(P<0.05),平均日采食量提高了13.5%(P<0.10)。②颗粒料的淀粉糊化度比粉料高15%-16%。③液态组仔猪全期平均日采食量和日增重均高于固态组(P<0.05),分别提高了10.3%和12.9%。④液态料组仔猪血清木糖含量比固态料组高52%(P<0.05),且腹泻程度显著(P<0.05)降低。     

食蟹猴骨髓采集穿刺方法及其骨髓象测定

为探索采集食蟹猴骨髓的操作方法及其正常骨髓象指标,试验采集了60只食蟹猴的髂骨骨髓,并测定其骨髓象、测得的骨髓象及采集过程中的注意事项.结果表明,可以顺利的采出骨髓,雌雄之间晚幼红细胞、粒红比有显著性差异(P＜0.05),其余无显著差异.     

Effects of pituitary adenylate cyclase-activating polypeptide on cardiac remodeling in coronary atherosclerotic rabbits

AIM:To study the intervention effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on cardiac remodeling during the development of rabbit coronary atherosclerosis. METHODS:60 male New Zealand rabbits were equally divided into 3 groups randomly: control group (C group), atherosclerosis model group (A group) and PACAP intervention group (P group). At the 4th, 8th and 12th week, 5-6 cases of rabbits in each group were sacrificed, cardiac tissue with coronary arteries were harvested to make paraffin sections. The sections were stained with hematoxylin-eosin and van Gieson separately. The qualitative observation and/or quantitative analysis were made by light microscope. RESULTS:（1）There was no lesion in C group. For A group and P group, there were plaques in large epicardial coronary arteries and small coronary arteries; an impressive accumulation of collagen was also observed in myocardium. In P group, the lesions of small coronary arteries were less serious, and the degrees of perivascular and myocardial fibrosis also appeared to be less.（2）For A group, the wall-to-lumen ratios in small coronary arteries were significantly greater at the 12th week (2.58±1.54) than C group (1.34±0.58) and P group (1.39±0.48) （P<0.05）； and the width of cardiomyocyte (13.85 μm±2.27 μm) was already remarkably narrower than C group (14.68 μm±2.40 μm) at the 8th week (P<0.05) and narrower significantly than C group and P group at the 12th week. （3）There were not difference significantly between the above-related parameters of P group and C group (P>0.05). CONCLUSION:Structure changes exist in coronary arteries and myocardium during the development of rabbit coronary atherosclerosis, PACAP can inhibit the cardiac remodeling.     

The levels of 2′, 5′ oligoadenylate synthetase,interleukin 2 and interleukin 12 in hepatitis B virus infection

AIM: In order to study the effect of endogenous interferon system and Th1 response modes on hepatitis B virus infection, the 2′, 5′ oligoadenylate synthetase (2-5OAS), IL-2 and IL-12 were selected as the research parameters. METHODS: The activity of 2-5OAS in peripheral blood mononeuclear cells was determined by sensitive radioenzymatic assay. IL-2 and IL-12 were determined by ELISA. RESULTS: Compared to normal control, the 2-5OAS, IL-2 or IL-12 were not significantly changed (P>0.05) in the asymptomatic HBsAg carricer group. The 2-5OAS, IL-2 and IL-12 were significantly up-regulated (P<0.01) in the group of acute hepatitis, but in the groups of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma, the 2-5OAS, IL-2, IL-12 were significantly down-regulated (P<0.05). Moreover, with the progression of patient′s conditions and with the complications of liver cirrhosis and hepatocellular carcinoma, the 2-5OAS, IL-2 and IL-12 decreased progressively, the 2-5OAS, IL-2, IL-12 were the lowest in guoups of liver cirrhosis and hepatocellular carcinoma (vs each groups of chronic hepatitis, P<0.05). CONCLUSION: The endogenous interferon system and Th1 response are significantly alterable in the different period of hepatitis B virus infection and among the different clinical types. The cellular immunity plays an important role in recovery from HBV infection.     

Etoposide induces apoptosis via mitochondrial signaling pathway with cytochrome c release in Jurkat leukemia cells

AIM:To investigate the molecular mechanisms of apoptosis and to elucidate the apoptosis signaling pathway triggered by etoposide in Jurkat human leukemia cells. METHODS:Apoptosis was detected using annexin V-FITC and propidium iodide (PI) staining, respectively, and annexin V-FITC positive cells and hypodiploid cells were analyzed by flow cytometry. Mitochondrial membrane potential (△Ψm) was detected using 3, 3-dihexyloxycarbocyanine iodide ［DiOC6(3)］ staining and △Ψm low cells were analyzed by flow cytometry. Preparation of cytosolic extracts and isolation of mitochondria were completed by centrifugation. Western blotting analysis was used to evaluate the level of cytochrome c, caspase-3, and poly (ADP-ribose) polymerase (PARP) expression. RESULTS:Etoposide induced apoptosis showing phosphatidylserine externalization and DNA fragmentation in a time-dependent manner and the apoptosis could be inhibited by a broad caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD.fmk). Collapse of △Ψm induced by etoposide preceded DNA fragmentation and phosphatidylserine externalization. In contrast, it was not blocked by zVAD.fmk. Etoposide caused cytochrome c release from mitochondria into cytosol, subsequent activation of caspase-3 (32 kD) presented with an intermediate (20 kD) and its active product (17 kD), and cleavage of full-length PARP (116 kD) into the so-called apoptotic 85 kD fragment. CONCLUSION:Etoposide-induced Jurkat cell apoptosis is initiated through mitochondria signaling pathway with cytochrome c release into cytoplasm and caspase is the ultimate executioner of cell apoptosis.     

Effects of immune-enhancing parenteral nutrition on nutritional status,immunity and inflammatory responses in postoperative patients with portal hypertension surgery

AIM:This study was conducted to evaluate the effects of postoperative immune-enhancing parenteral nutrition on the nutritional statue,immune function,and inflammatory responses in patients undergoing portal hypertension surgery. METHODS: This study was designed as a prospective,randomized and controlled clinical trial. Forty-two patients undergoing portal hypertension surgery were randomly assigned to receive either an immune-enhancing parenteral nutrition(adding glutamine and recombinant human growth hormone,n=22) or an isocaloric and isonitrogenous control standard parenteral nutrition(n=20) for seven days. Parenteral nutrition was initiated 3 days after surgery. Blood samples were obtained on day 0,3,and 10. Host nutritional statue was evaluated by measuring levels of prealbumin and transferrin,immunity was observed by measuring levels of CD4+ cells,CD8+ cells,CD4+/CD8+,IgG,IgM and IgA,and the inflammatory responses was determined by assessing IL-2,TNF-α and C-reactive protein(CRP) levels. RESULTS:On postoperative day 10,among patients receiving an immune-enhancing parenteral nutrition,prealbumin,transferrin,CD4+ cells,CD4+/CD8+,IgG and IL-2 levels were significantly higher than those in control group,and TNF-α and CRP concentrations were significantly decreased（P<0.05）. CONCLUSION:Postoperative administration of immune-enhancing parenteral nutrition in patients undergoing portal hypertension surgery can improve postoperative nutritional statue and immune function,and relieve inflammatory response.     

Overexpressed human FAT10 protein induces the apoptosis in the starved HEK293 cells

AIM: To study the effect of human FAT10 on the apopotosis of HEK293 cells using flag-tagged human FAT10 protein.METHODS: The fragment of FAT10 gene was cloned into the pcDNA3-flag vector,which was identified by PCR,enzyme digestion and sequencing.The reconstructed plasmids were transfected into HEK293 cells.The expression of introduced FAT10 in the normal cultured and starved cells was detected respectively by Western blotting.XTT assay and DNA ladder method were used to analyze the effect of FAT10 on the apoptosis of starved HEK293 cells.RESULTS: The reconstructed plasmids were highly expressed in HEK293 cells with different expression mode at the mormal cultured and starved state.The livability of starved FAT10 overexpressed HEK293 cells was significantly lower than that of normal cultured cells.DNA ladder was observed in the starved FAT10 overexpressed cells,but not in the normal cultured cells.CONCLUSION: The eukaryotic expressed plasmids of flag-tagged FAT10 were constructed successfully,and highly expressed in HEK293.Overexpressed FAT10 enhances the apoptosis in the starved HEK293 cells.