H5N1亚型禽流感灭活疫苗免疫鸵鸟后抗体消长规律及免疫程序的研究

为了探讨鸵鸟对H5亚型禽流感灭活疫苗的免疫原性,做好鸵鸟禽流感的防控工作,采用哈尔滨兽医研究所研制的重组H5N1亚型禽流感疫苗,不同剂量免疫鸵鸟,用HI方法检测母源抗体和免疫抗体,根据母源抗体的衰减和免疫抗体的消长规律确定首免和再免日龄.结果表明,雏鸵鸟母源抗体能维持约3周～8周;8周龄时分组首免,C1组产生的免疫反应优于C2组,抗体峰值能达到7.50 log2,维持时间为9周左右;17周龄时C1组以3.0 mL/羽进行二免,2周后抗体达到7.40log2,3周～7周抗体维持在高峰值,最高达8.80log2,以后逐渐下降,有效抗体水平能维持至接种后25周左右.二免后25周进行三免,以5 mL/羽三免后2周抗体可达到9.80log2,2周～4周抗体维持在最高峰,以后缓慢下降,期间抗体时有起伏,但有效抗体水平约可维持1年时间.三免后45周内抗体水平合格率均在70%以上.根据抗体消长规律,初步推荐了鸵鸟的免疫程序.     

小白菜新品种京绿7号的选育

京绿7号是由来源于上海和北京的两个地方品种选择的自交不亲和系Y134和Y105杂交而成。植株半直立,株高24cm,开展度37cm;叶深绿色、有光泽,叶面稍皱,叶柄绿色、有光泽、宽5.7cm、厚1.0cm;单株质量0.25kg左右,每667m2产量2400kg左右;高抗黑腐病,抗病毒病、黑斑病,晚抽薹性极强,适宜北方地区冬春季栽培。     

The latent gene expression of Epstein-Barr virus in nasopharyngeal carcinoma

AIM: To examine the latent membrane protein 1(LMP1)-DNA sequence in nasopharyngeal carcinoma(NPC) and detect mRNA expression of LMP1,EBNA1,EBNA2,and to explore the relationship between EBV infectious status,expression products and NPC carcinogenesis.METHODS: LMP1 DNA was detected in NPC by PCR.Direct sequence was applied to analyze the difference between NPC-LMP1-DNA and B95-8- LMP1-DNA.mRNA expressions of LMP1,EBNA1,EBNA2 in NPC were detected by nested RT-PCR.RESULTS: LMP1 DNA existed in all 47 NPC tissues.Several single nucleotide variations were found between NPC-LMP1-DNA and B95-8- LMP1-DNA.The notable variation was the lost of XhoⅠrestriction site in NPC.Direct sequence showed 30 bp deletion in NPC.The mRNA expressions of LMP1,EBNA1 and EBNA2 in NPC were 76.6%,80.0% and 74.5% respectively by nested RT-PCR.The expression of EBNA1 in NPC was promoted by Q promoter while the expression of EBNA1 in B95-8 was promoted by C promoter.CONCLUSION: The way of EBV involved in NPC is complex.Latent genes such as LMP1,EBNA1 and EBNA2 as well as early lytic gene BARF1 may all play certain roles in NPC carcinogenesis.     

Histamine receptor antagonist prevent and ameliorate airway remodeling and acid-base imbalance in asthma of guinea pig

AIM:To investigate the effect of histamine receptor antagonist on airway remodeling and acid-base imbalance in asthma of guinea pig. METHODS:Guinea pigs were divided into 5 groups: the normal control group, the asthma model group, the continued asthma model group, histamine group and histamine receptor antagonist group. For each group, the content of histamine, Na+, Cl-, PaO2, PaCO2, pH, AB, SB in serum, and thickness of airway mucosa and smooth muscle cell layer were measured and compared with each other. RESULTS:(1) According to the content of histamine in serum and thickness of airway mucosa and smooth muscle, the order was: the histamine group>continued asthma model group>the asthma model group>the normal control group (P<0.01), and the histamine receptor antagonist groupthe continued asthma model group (P<0.01), but for PaCO2, the order was conversed. Airway remodeling, increase in histamine in serum, respiratory acidosis and metabolic acidosis in asthmatic guinea pig were observed. Exogenous histamine accentuated the change, however, histamine receptor antagonist attenuated it. CONCLUSION:Histamine may take part in the airway remodeling of asthma. Histamine receptor antagonist can prevent and ameliorate airway remodeling and acid-base imbalance in asthma of guinea pig.     

Effect of Ganoderma lucidum spores powder on the expression of IGF-1, NF-κB and apoptosis of nerve cells in the brain from epileptic rat

AIM: To investigate the effect of Ganoderma lucidum spores powder on the expression of insulin-like growth factor-1 (IGF-1), nuclear factor-κB (NF-κB) and apoptosis of nerve cells in rats with epilepsy established by pentetrazole. METHODS: The sub-eclampsia dosage of pentetrazole (PTZ) was used to make epilepsy model. Ganoderma lucidum spores powder group was given from stomach. The enduring time and latent period were recorded. The immune reactivity of IGF-1, NF-κB/P65 and apoptosis of nerve cells were measured with immunohistochemical staining and TUNEL method. RESULTS: In high power sight (×400), there were much more apoptosis cells in hippocampus and brain cortex of model group (18.80±2.13, 16.87±2.00) than those in control group (0.97±0.52, 0.58±0.25). The expressions of IGF-1, NF-κB in model group were higher than those in control group. Compared with model group, the latent period of Ganoderma lucidum spores powder group at the 17th, 21th, 25th days were longer (P<0.05, P<0.05, P<0.01, respectively).There were less apoptosis cells in hippocampus and brain cortex of Ganoderma lucidum spores powder group (12.30±2.46, 10.48±1.33) than those in model group. The expression of NF-κB/P65 in Ganoderma lucidum spores powder group was lower than that in model group, but the immune reactivity of IGF-1 increased more distinctly in Ganoderma lucidum spores powder group than that in model group. CONCLUSION: IGF-1, NF-κB and apoptosis of nerve cells may have play a role in occurrence and development of PTZ-induced epilepsy. Ganoderma lucidum spores powder can suppress expression of NF-κB strongly, and facilitate the immune reactivity of IGF-1, which may be one of the mechanisms by which Ganoderma lucidum spores powder restrains the apoptosis of nerve cells caused by epilepsy to prevent the damages of nerve cells.     

Pretreatment of hypertonic saline attenuates the hepatic ischemia reperfusion injury induced by neutrophils

AIM: To explore the effect of the pretreatment of hypertonic saline (HTS) in hepatic ischemia reperfusion (I/R) injury.METHODS: The rats were divided into sham group (sham group), ischemia reperfusion group (IR group) and pretreatment of hypertonic saline group (HTS group). Partial hepatic ischemia reperfusion model was used. The rats were sacrificed at the time of 1 h, 3 h, 6 h, 12 h and 24 h after reperfusion in each group, respectively. Blood samples were obtained to examine ALT. The expression of the CD11b/CD18 (Mac-1) on the neutrophils was analyzed by flow cytometry. RT-PCR and Western blotting were used to examine the expression of intercellular adhesion molecule-1 (ICAM-1) in livers and chromatometry was performed to detect the activity of myeloperoxidase (MPO) in livers. The morphology of hepatocytes and the structure of sinusoid were observed by histological examinations. RESULTS: ① HTS pretreatment decreased the level of ALT at the time points of 3 h, 6 h and 12 h after reperfusion (P<0.05). ② Mac-1 expression in HTS group was lower at 6 h and 12 h after reperfusion compared with IR group (P<0.05). ③ MPO activity in HTS group was lower at 6 h, 12 h and 24 h compared with IR group (P<0.05). ④ RT-PCR and Western blotting analysis indicated that the pretreatment of HTS inhibited the expression of ICAM-1 in livers after reperfusion. ⑤ Moderate hepatocyte swelling and few neutrophil infiltration were observed in HTS group.CONCLUSION: Pretreatment with HTS has the effect on hepatic ischemia reperfusion injury by inhibiting the expression of Mac-1 on circulating neutrophils and the expression of ICAM-1 in the liver.     

uclear factor κB in LPS stimulated rat alveolar macrophages promotes TNF-α secretion

AIM: To investigate the activation of nuclear factor κB (NF-κB) induced by lipopolysaccharides (LPS) in rat alveolar macrophages (AMs) and its regulatory role in tumor necrosis factor (TNF-α) secretion. METHODS: The dynamic activity changes of NF-κB induced by LPS were determined with electrophoretic mobility shift assay (EMSA). Antisense oligonucleotides of NF-κB subunit (p65) were transfected into AMs prior to LPS stimulation. The effect of antisense oligonucleotide transfection on expressions of p65 and TNF-α in supernatant were measured with Western blotting and enzyme linked immunosorbent assay (ELISA), respectively.RESULTS: NF-κB activity increased markedly and reached its peak level at 4 h after LPS stimulation. After transfected with antisense oligonucleotides of NF-κB subunit (p65), expression of p65 and TNF-α in supernatant decreased markedly.CONCLUSION: NF-κB activity has a positive effect on regulating secretion of TNF-α in AMs induced by LPS.     

The effects of 17β-estradiol on cardiomyocyte hypertrophy induced by endothelin

AIM:To investigate the effect of 17β-estradiol (E₂) on myocardial hypertrophy induced by endothelin-1(ET-1) and the related mechanism. METHODS:Myocardial cells from neonate rats were cultured in vitro and myocardial hypertrophy model was established with ET-1.The effects of 17β-estradiol on myocardial hypertrophy were observed. The role of ERK1/2 in the effects of 17β-estradiol was also detected. RESULTS:Compared with control group,ET-1 increased cell protein content,cell surface area and ［³H］^-Leucine ［³H］^-Leu) incorporation. Pretreatment with E₂ for 24 h could inhibit the increase in cell protein content,cell surface area and ［³H］^-Leu incorporation induced by ET-1.ET-1 significantly stimulated ERK1/2 activity,which was prevented by pretreatment with E₂.Tamoxifen,estradiol receptor antagonist,partially inhibited the effect of E₂. The ability of ET-1 to stimulate ［³H］^-Leu incorporation was significantly blocked by PD98059,which could enhance the inhibitory effect of E₂ on the increase of ［³H］^-Leu incorporation in cardiomyocytes induced by ET-1.CONCLUSION:E₂ can inhibit cardiomyocyte hypertrophy induced by ET-1. This effect is mediated by estrogen receptor. ERK1/2 signal pathway is closely correlated with the inhibitory effect of E₂ on cardiomyocyte hypertrophy induced by ET-1.     

Caspase 3 inhibitor Ac-DEVD-CHO attenuates 10-hydroxycamptothecin-induced activation of NF-κB in Bcap37 cells

AIM:To investigate the role of caspase 3 inhibitor Ac-DEVD-CHO in caspase 3 signaling pathway and NF-κB activation induced by 10-hydroxycamptothecin (HCPT) in human breast carcinoma cells. METHODS:The cell growth inhibition was measured by MTT assay. Agarose gel electrophoresis was performed for detecting cell apoptosis. Western blotting was used for determining protein expression. DIG-EMSA was conducted to measure the DNA-binding activation of NF-κB. RESULTS:Caspase 3 inhibitor Ac-DEVD-CHO attenuated HCPT-induced apoptosis in human breast carcinoma. Ac-DEVD-CHO also suppressed the degradation of caspase 3 and IκBα,and arrested the activation of NF-κB. CONCLUSION:Caspase 3 inhibitor Ac-DEVD-CHO regulates the activation of caspase 3 and NF-κB,and attenuates apoptosis in Bcap37 cell line induced by HCPT.