限制人工杉木林生长的土壤因子

福建省来舟林业试验场３６个固定标准地的杉木林分生长与林下土壤的调查分析结果显示，制约传统模式培育的杉木林的生长的主要土壤因子是土壤原有全氮、速效磷、土层厚度和腐殖质层厚度．其中土壤氮磷属较易人工控制因子，为进一步提高人工杉木林生产力，调节土壤氮磷水平可能为其重要途径之一．     

管道输量对柴油蜡沉积作用的试验分析

针对流速对油品结蜡的影响,柴油管壁的结蜡规律与管内流速的关系还尚未明确的问题,在理论推导的基础上进行了室内环道试验,通过分别模拟柴油在有温差段和恒温段时管内流速对管壁结蜡规律的影响,得出了相应的规律,对于指导反季节输送柴油,减少蜡沉积有一定的参考价值。     

畜牧系统灰关联度分析

本文利用灰色系统理论,对影响畜产品产量的主要因素作了灰关联度分析。结果表明,猪出栏率、粮食产量是影响猪肉产量的关键因子（ｒ（ｙ１,ｘ５）＝０．８９４,ｒ（ｙ１,ｘ２）＝０．８２４;禽肉比重、粮食产量是禽肉产量的主控因素（ｒ（ｙ２,ｘ６）＝０．９０５,ｒ（ｙ２,ｘ２）＝０．８４８）;禽出栏率、粮食产量是影响禽蛋产量主要因素（ｒ（ｙ３,ｘ８）＝０．９９８,ｒ（ｙ３,ｘ２）＝０．９９１）;草杂肉比（草食动物和杂食动物肉类比率）与非农业人口率分别是影响草食动物肉类产量与奶产量的关键因素（ｒ（ｙ４,ｘ１０）＝０．８５２,ｒ（ｙ５,ｘ１２）＝０．８３２）,文中所建立的ＧＭ（Ｏ,Ｎ）静态模型具有较高的拟合度（平均误差皆在－１～１％之间）。     

马尾松采脂量的相关因子分析

根据6年来的马尾松收脂量，结合生态因子、树体因子、采脂间隔期、采脂负荷等因素进行分析，结果表明：马尾松产脂量与温度、树高、胸径等呈显著或极显著的相关关系，生态因子中以气温对马尾松产脂量的影响最大，树体因子中以树龄的影响最大，降雨、土壤、地形等因子对采脂量也有影响，这些因子对马尾松产脂量的影响作用是综合的。     

太子参ISSR反应体系的优化

通过单因子试验和正交设计,对影响太子参ISSR-PCR扩增效果的因素,如模板DNA浓度、Taq酶浓度、dNTPs浓度、引物浓度、退火温度、延伸时间和循环数进行优化。确立了可用于太子参ISSR-PCR分析最适宜的反应体系:20μL反应体系中含80 ng模板DNA,0.5U Taq酶,0.4μmol·L~(-1)引物,0.18 mmol·L~(-1)dNTPs;PCR扩增延伸时间为70 s,循环数为35。稳定性试验表明,该体系能在不同太子参品种中扩增出清晰明亮、稳定性、多态性好的条带。     

一种分析边坡稳定性的新型方法

本文对人工神经网络即BP模型做了简要的介绍，并用BP网络的非线性映射能力计算了边坡稳定性的安全系数。结果表明利用BP网络求得的安全系数满足工程要求，并且其方法是合理、简单、可行的，值得推广。     

上海郊区农民居住集中现状分析与对策

基于青浦区推进农民居住集中工作的调查资料,分析了整个居住集中过程中农民的意愿水平、推动和制约因素政策的有效性及其相关性等因素,并针对性地提出相关的政策建议和措施。     

Protective role of heat-shock protein 70 in gastric mucosal lesion induced by endotoxin in cirrhotic rats with portal hypertensive gastropathy

AIM: To investigate the protective role of heat-shock protein 70 (HSP70) in the pathogenesis of gastric mucosal damage in cirrhotic rats with portal hypertensive gastropathy (PHG).METHODS: The rat model of liver cirrhosis with PHG was established by injection with tetrachloride.The animals were divided into normal control group, PHG group, PHG+heat treatment group, PHG+BPI21 group and PHG+endotoxin groups.The endotoxin used in the experiment was at the dose of 3 mg/kg and endotoxin antagonist BPI21 was at the dose of 2 mg/kg.HSP70 was induced by pre-treating the animals with mild whole-body heating.The levels of HSP70 and tumor necrosis factor alpha (TNF-α) in the gastric mucosa were measured by ELISA.Furthermore, the pathological changes of the gastric mucosa were observed under microscope with HE staining.RESULTS: Compared with the normal control rats, the rats in PHG group showed obvious gastric pathological lesion, decrease in HSP70 production and increase in TNF-α level in the gastric mucosa, and increased endotoxin concentration in the plasma.Compared with PHG+endotoxin group, the gastric mucosal lesion in PHG+BPI21 group was significantly attenuated, accompanied by the increase in HSP70 production and decrease in TNF-α level in the gastric mucosa.Heat treatment increased HSP70 production and decreased TNF-α concentration in the PHG rats, thus attenuating the gastric mucosal damage.CONCLUSION: HSP70 alleviates the gastric mucosal lesion induced by endotoxin in cirrhotic rats with PHG and decreases the concentration of TNF-α in gastric mucosa, indicating a protective role of HSP70 in the pathogenesis of gastric mucosal damage in PHG.     

Proliferative effect of PDGF and anti-proliferative activity of AMPK on vascular smooth muscle cells

AIM: To investigate the proliferative effect of platelet-derived growth factor (PDGF) and anti-proliferative activity of AMP-activated protein kinase (AMPK) on vascular smooth muscle cells (VSMCs). METHODS: The proliferation of VSMCs cultured with PDGF and activation of AMPK were observed. VSMCs were divided in 4 groups: control group; PDGF group; 5-aminoimidazole-4 -carboxamide-1-β-D-riboside (AICAR) group and AICAR+PDGF group. The time course of AMPK activation was determined. The protein level of mTOR was also measured. RESULTS: Compared with control group, the proliferative rate in PDGF group was significantly increased. The growth of VSMCs was inhibited in a time-dependent manner and the activity of p-mTOR was significantly decreased in AICAR group. Compared with control group, the expression of p-AMPK in PDGF group was significantly decreased, and that in AICAR group and AICAR+PDGF group was significantly increased. The expression of p-AMPK in AICAR+PDGF group was higher than that in PDGF group. The activity of p-mTOR in PDGF group was significantly higher than that in control group, while that of AICAR group and AICAR+PDGF group was significantly decreased. The expression of p-mTOR in AICAR+PDGF group was lower than that in PDGF group. CONCLUSION: Stimulation of VSMCs with PDGF promotes the cell proliferation, which can be inhibited by AICAR. The proliferation of VSMCs activated by AMPK is probably correlated with the down-regulation of mTOR expression.     

Effect of all-trans-retinoic acid on the proliferation and expression of α-SMA in human embryonic lung fibroblasts

AIM: To investigate the effects of all-trans-retinoic acid (ATRA) on the proliferation and differentiation of transforming growth factor β₁(TGF-β₁)-stimulated human embryonic lung fibroblasts (HFL-I).METHODS: The HFL-I cells were cultured in vitro and were pretreated with ATRA for 3 days at the concentrations of 0.1 μmol/L, 1 μmol/L and 10 μmol/L. The proliferation of HFL-1 cells was detected by MTT method. The mRNA expression of α-smooth muscle actin(α-SMA) in HFL-I cells stimulated with TGF-β₁ for 0 h, 6 h, 12 h, 24 h, 48 h and 72 h was detected by RT-PCR and the protein expression of α-SMA at the time points of 1,3 and 5 days was detected by Western blotting. The mRNA expression of α-SMA in HFL-I cells pretreated with different concentrations of ATRA for 24 h was detected the by RT-PCR and the protein expression at time point of 3rd day was detected by Western blotting. RESULTS: Different concentration of ATRA inhibited the proliferation of HFL-I in a dose-dependent manner (P<0.05). Both mRNA and protein expression of α-SMA in HFL-I cells pretreated with TGF-β₁ was up-regulated (P<0.05). ATRA down-regulated the mRNA and protein expression of α-SMA induced by TGF-β₁ in a dose-dependent manner (P<0.05). CONCLUSION: ATRA inhibits the proliferation and TGF-β₁-stimulated differentiation in HFL-I cells by down-regulating the mRNA and protein expression of α-SMA.