中国玉米国际竞争力的分析及启示

采用相关最新数据,对中国玉米的生产要素、贸易竞争力指数、国际市场占有率和显示性比较优势指数进行实证分析,并与国际相关指标进行对比解析。结果表明,近10年来中国玉米的国际竞争力虽有一定的竞争能力,但呈下降趋势。中国玉米竞争力存在价格和非价格两个方面主要因素,通过分析中国玉米竞争力发展的优劣势,未来中国玉米竞争能力的提高应注重发展特色玉米农业、降低成本、拓展市场多元化、完善政策扶持和保障等。     

低氮胁迫下我国不同年代玉米品种产量及产量构成因子变化趋势研究

试验以我国不同年代的35个玉米品种为材料,在施氮肥和不施氮肥两个水平下对产量、穗长、穗粗、穗粒数、秃尖长、轴粗、百粒重共7个农艺性状进行考查比较。结果表明,除轴粗以外,其余几个农艺性状不同年代间差异均达到显著或极显著水平,随年代变化玉米品种产量显著提高,氮胁迫压力下不同年代玉米品种产量均下降。正常施氮条件下,各年代玉米品种的穗长、穗粗、穗粒数呈上升趋势,低氮胁迫降低了穗长、穗粗、穗粒数及百粒重,而对轴粗无明显影响。研究还表明,1950年以来我国玉米品种的耐低氮能力没有明显提高。育种工作要在自交系选育中重视低氮条件,为进一步培育耐低氮杂交种奠定基础。     

寄生虫细胞因子免疫的研究进展（一）

寄生虫在入侵机体时必须具备逃避机体免疫,破坏宿主免疫屏障才能感染,这种入侵过程必然和宿主机体的免疫系统发生联系,不但使宿主的先天免疫细胞功能缺失,而且获得性免疫也受到抑制。寄生虫感染均不同程度地伴随免疫损伤,宿主在感染寄生虫后产生的免疫应答中,细胞因子作为免疫过程中的介质起到关键作用,主要是调节机体细胞免疫抗虫,保护机体不被感染,其中巨噬细胞是主要功能的承担者。本文将阐述细胞因子在寄生虫感染过程中所发挥的免疫作用,为解决寄生虫感染的防控问题奠定基础,同时为寄生虫的研究提供新的思路。     

黄秆乌哺鸡竹个体结构因子相关性研究

以黄秆乌哺鸡竹为试验材料,研究了竹子个体结构因子之间的相关性,建立了黄秆乌哺鸡竹各个相关结构因子之间的线性方程模型.结果显示,竹子各个结构因子之间具有较好的相关性,其中胸径是影响竹子其他生物量因子的决定因子;单株竹秆质量、竹壁厚以靠近竹基部表现最为明显,是竹材具可利用性的有效段位.研究结果可为估算竹子的生物量与生产力、描述竹子的秆形特征、量化各结构因子之间的关系提供依据.     

Platelet-Rich Plasma as an Adjunctive Therapy for the Management of a Severe Chronic Distal Limb Wound in a Foal

Distal limb wounds are frequent in horses after traumatic events. The use of platelet-rich plasma (PRP) represents a simple method of treating wounds in equines. A case of a chronic severely contaminated distal limb wound in an 8-month-old foal is presented. The patient was managed with the combination of standard wound therapy (debridement and bandages), surgery, and PRP obtained by a manual tube protocol. No complications were observed with the PRP treatment, and the foal was fully recovered 2 months later. The results from this case report indicate that PRP and its by-products (platelet-poor plasma) could be used as an adjunctive treatment in severe distal limb wounds in horses. A clinical controlled study should be performed to test this hypothesis.     

The equine alveolar macrophage: Functional and phenotypic comparisons with peritoneal macrophages

Alveolar macrophages (AMs) constitute the first line of defence in the lung of all species, playing a crucial role in the regulation of immune responses to inhaled pathogens. A detailed understanding of the function and phenotype of AMs is a necessary pre-requisite to both elucidating their role in preventing opportunistic bacterial colonisation of the lower respiratory tract and developing appropriate preventative strategies. The purpose of the study was to characterise this important innate immune cell at the tissue level by making functional and phenotypic comparisons with peritoneal macrophages (PMs). We hypothesised that the tissue of origin determines a unique phenotype of AMs, which may constitute an appropriate therapeutic target for certain equine respiratory diseases. Macrophages isolated from the lung and the peritoneal cavity of 9 horses were stimulated with various toll like receptor (TLR) ligands and the production of nitrite, tumour necrosis factor alpha (TNFα), interleukin (IL) 10 and indoleamine 2,3-dioxygenase (IDO) were measured by the Griess reaction and enzyme linked immunosorbent assay (ELISA) and/or quantitative polymerase chain reaction, respectively. Cells were also compared on the basis of phagocytic-capacity and the expression of several cell surface markers. AMs, but not PMs, demonstrated increased TNFα release following stimulation with LPS, polyinosinic polycytidylic acid (Poly IC) and heat-killed Salmonella typhinurium and increased TNFα and IDO mRNA expression when stimulated with LPS. AMs showed high expression of the specific macrophage markers cluster of differentiation (CD) 14, CD163 and TLR4, whereas PMs showed high expression of TLR4 only. AMs, but not PMs, demonstrated efficient phagocytic activity. Our results demonstrate that AMs are more active than PMs when stimulated with various pro-inflammatory ligands, thus supporting the importance of the local microenvironment in the activation status of the macrophage. This information provides a valuable knowledge base on which to improve our understanding of the role of macrophages and their microenvironment in equine innate immunity.     

桦褐孔菌多糖对急性感染弓形虫小鼠c-Jun、IL-12和IL-1β的影响研究

为了探讨桦褐孔菌多糖对急性感染弓形虫小鼠核转录因子c-Jun、IL-1β和IL-12的影响,本试验在建立急性感染弓形虫小鼠模型后,随机将其分成3组:阴性组、急性感染弓形虫小鼠模型组和桦褐孔菌多糖试验组。采用RT-PCR法检测肝组织中c-Jun及脾组织中IL-1β和IL-12的mRNA表达;Western blot法检测c-Jun蛋白的表达。结果显示:c-Jun、IL-1β和IL-12的mRNA分别在360、736和978 bp处扩增出单一电泳条带,且c-Jun蛋白在39 ku处表达,均呈现出弓形虫感染组表达量最高,桦褐孔菌多糖试验组次之,对照组最弱。说明桦褐孔菌多糖可能通过下调c-Jun过度表达,抑制IL-1β、IL-12的过度表达,部分阻抑了AP-1信号通路转导,从而减轻炎症反应,达到抗弓形虫感染的目的。     

Role of estrogen receptor-α (ESR1) and the type 1 insulin-like growth factor receptor (IGFR1) in estradiol-stimulated proliferation of cultured bovine satellite cells

Although the exact mechanism(s) by which estradiol (E₂) enhances muscle growth in a number of species, including humans and cattle, is not known, E₂ treatment has been shown to stimulate proliferation of cultured bovine satellite cells (BSCs). This is particularly significant because satellite cells are the source of nuclei needed to support postnatal muscle fiber hypertrophy and are thus crucial in determining the rate and extent of muscle growth. The objective of this study was to assess the role of estrogen receptor-α (ESR1) and the type 1 insulin-like growth factor receptor (IGFR1) in E₂-stimulated proliferation of cultured BSCs. To accomplish this, we have used small interfering RNA (siRNA) to silence expression of ESR1 or IGFR1 and assessed the effects on E₂-stimulated proliferation in BSC cultures. In BSCs treated with nonspecific siRNA, E₂ significantly (P < 0.05) stimulates proliferation under conditions in which neither IGF-1 nor IGF-2 expression is increased; however, treatment of ESR1- or IGFR1-silenced cells with E₂ does not significantly stimulate proliferation. These results indicate that both ESR1 and IGFR1 are required for E₂ to stimulate proliferation in BSC cultures. The fact that this occurs under culture conditions in which neither IGF-1 nor IGF-2 mRNA expression is increased strongly suggests that E₂ activates IGFR1 via a mechanism that does not involve increased IGF-1 or IGF-2 binding to the receptor.