半胱胺盐酸盐对高温季节奶牛生产性能的影响

本文旨在研究半胱胺盐酸盐对高温季节奶牛产奶性能的影响,并探讨其可能的作用机理。试验选用30头泌乳中期荷斯坦牛,多胎,年单产约7500kg。根据试验前1周平均产奶量将牛群配对分组,随机分为对照(n=15)和半胱胺盐酸盐处理(n=15)2个组。试验期内牛舍平均气温高于27℃,温湿指数(THI)值高于79,形成严重热应激环境;两组奶牛采食同等水平日粮,试验组给予30g/d包被的半胱胺盐酸盐(含量30%)。结果显示:与对照相比,半胱胺盐酸盐提高平均产奶量17.1%(P<0.05)、增加平均乳脂率12.6%(P<0.05);血清中T3、T4水平分别降低18.9%(P<0.05)和13.1%(0.05相似文献   

Effects of experimental hypo- and hyperthyroidism on iodothyronine deiodinases in Nile tilapia, Oreochromis niloticus

In the present study, we examined the effects of experimentally-induced increases or decreases in plasma concentrations of thyroid hormones on iodothyronine deiodinases in tilapia, Oreochromis niloticus. To obtain hyperthyroid tilapia, fish were injected with porcine follicle stimulating hormone (pFSH) 36 hours before sampling or fed on demand for 11 days with tilapia pellets containing 12 ppm T3. Tilapias were made hypothyroid by providing them food containing 0.2% methimazole for 11 days. Plasma T4 and T3 and the in vitro deiodinase activity in liver, kidney, brain and gill were measured at the end of the treatment period. Injection with pFSH caused an increase in plasma T4 but had no influence on plasma T3 levels. A small increase in plasma T3 was observed in T3-fed fish. Plasma levels of both T4 and T3 were decreased by methimazole treatment. We observed no changes in kidney type I deiodinase (D1), whereas liver type II deiodinase (D2) was increased during hypothyroidism and decreased during hyperthyroidism. Hypothyroidism resulted in a significant decrease in brain, gill and liver type III deiodinase (D3). An pFSH-induced increase in T4 stimulated brain and gill D3 but not liver D3, whereas the opposite was true in T3-fed fish. We conclude that the regulation of D1 and D3 in tilapia is probably different compared to mammals.     

Eremothecium ashbyii T30过量合成核黄素发酵工艺条件研究

以本室筛得的核黄素同产突变株Ｅ．ａｓｈｂｙｉｉ Ｔ３０为出发株,探讨了发酵工艺条件对核黄素产量的影响。结果表明：不同氮源、碳源、发酵用水、培养基灭菌方式及种子液质量都对核黄素产量有较大的影响,而且在发酵过程中,发酵２４ｈ时添加２５μｍｏｌ／Ｌ的碘乙酸或发酵４０ｈ时补加约２０ｇ／Ｌ的葡萄糖或发酵４８ｈ时补加约１７％（ｖ／ｖ）的新鲜培养基（无油）同对照组相比,分别增产２７．１％,２４．３和２０．９％。     

波兰小麦醇溶蛋白遗传差异及其与新疆稻麦的关系

利用酸性聚丙烯酰胺凝胶电泳（ＡＰＡＧＥ）对９份波兰小麦和２份新疆稻麦进行了醇溶蛋白分析。结果表明：⑴波兰小麦具有明显的醇溶蛋白多态性,９份材料具有７种醇溶蛋白带型,电泳分离出的２７条带中,２３条具有多态性;⑵供试波兰小麦间遗传距离在０－０．７５之间,平均值为０．４９,遗传变异较大。供试波兰小麦在遗传距离０．４９水平上聚为３类,其醇溶蛋白聚类与收集地关系不大;⑶新疆稻麦与波兰小麦的醇溶蛋白电泳图谱具     

南方红豆杉扦插基质配方优化的研究

应用单形重心试验设计对南方红豆杉的扦插生根效果进行了试验, 共选用了４ 种主要基质成份即黄心土、砂子、壤土和珍珠岩按设计要求安排了１５ 种不同的基质配比． 试验分为穗长８ｃｍ 和穗长５ｃｍ 两大组分别进行． 观察了不同组在相同试验条件下各基质配比的扦插生根反应, 并建立了数学模型． 应用现代的模型优化方法得出了最优的配方, 并与实际试验结果进行了比较分析． 导出了以穗长８ｃｍ 与采用基质成分为黄心土５４％ 、珍珠岩４６％ 搭配为最优的组合, 其扦插生根率可达５０．１２％ ． 研究结果为南方红豆杉扦插育苗提供了理论依据和技术参考     

用RFLP鉴定普通小麦—纤毛鹅观草二体附加系中外源染色体的同源转化性

用小麦族7个部分同源群的40个RFLP探针对小麦——纤毛鹅观草二体附加系进行分析,在证实了原有细胞学鉴定结果的基础上,又进一步提供了纤毛鹅观草染色体部分同源群的分子证据。即96K025,96K026中添加的一对纤毛鹅观草染色体B属于第2部分同源群;96K012, 96K013中添加的一对染色体E属于第5部分同源群。对以上株系的衍生株系     

Effect of microRNA-7 knockdown on ConA-induced acute liver injury in mice

AIM: To study the effect of microRNA-7 (miR-7) knockdown (KD) on concanavalin A (ConA)-induced acute liver injury (ALI) in mice.METHODS: Wild type (WT) mice and miR-7KD mice were received ConA (30 mg/kg) to induced acute liver injury model by intraperitoneal injection, and the morphological changes, liver weight and weight index were measured 48 h later. The pathological changes of the liver tissues were observed by HE staining. The levels of serum alanine aminotransferase (ALT), IL-4 and IFN-γ were detected by ELISA. The proportional changes of CD4⁺ T cells and the relative levels of IL-4 and IFN-γ were analyzed by flow cytometry.RESULTS: The color of the liver tissue became lighter, and the weight and weight index were changed significantly in miR-7KD mice compared with control group (P<0.05). HE staining showed that the inflammatory cell infiltration was increased in the liver of miR-7KD mice. Moreover, the level of serum ALT was significantly increased (P<0.05). The serum level of IFN-γ elevated significantly (P<0.01), while the IL-4 levels decreased significantly (P<0.01) in the serum of miR-7KD mice. Furthermore, the proportion of CD4⁺ T cells and relative IFN-γ cells increased obviously (P<0.01).CONCLUSION: miR-7 knockdown promotes the pathogenesis of the ConA-induced acute liver injury in mice.     

NKT cells inhibit Ang II-induced phenotypic transformation of mouse vascular smooth muscle cells by down-regulating PDGFRβ

AIM To investigate the role of natural killer T (NKT) cells in the phenotypic transformation of vascular smooth muscle cells induced by hypertension in mice. METHODS The hypertension model in wild-type and CD1d gene knockout mice was established by continuous infusion of angiotensin II (Ang II) at a dose of 490 ng·kg^-1·min^-1 for 14 d, and the NKT cell specific agonist α-galactosylceramide (α-GC) was given at a dose of 100 μg/kg in wild-type mice. The blood pressure of the mice was monitored by non-invasive tail cuff method. The thickness of aortic wall was measured by HE staining, and the degree of aortic fibrosis was observed by Masson staining. The expression levels of α-smooth muscle actin (α-SMA), osteopontin (OPN) and platelet-derived growth factor receptor β (PDGFRβ) in aortic tissue were detected by Western blot. RESULTS Compared with control group, the blood pressure, the aortic wall thickness, the degree of aortic fibrosis, the secretory marker protein OPN expression and the PDGFRβ expression were all increased significantly after infusion of Ang II for 14 d (P<0.05), while the expression of contractile marker protein α-SMA was decreased (P<0.05). The above changes were aggravated after CD1d gene knockout (P<0.05), but were attenuated after administration of α-GC (P<0.05). CONCLUSION NKT cells reduces Ang II-induced phenotypic transformation of mouse vascular smooth muscle cells by reducing the expression of PDGFRβ, increasing the expression of contractile protein and decreasing the expression of secretory protein.     

Pathogenesis,prevention and treatment of COVID-19 based on Th17/Treg immune imbalance

The extremely severe epidemic situation of coronavirus disease 2019 （COVID-19） outbreak around the world with high infectiousness and rapid spread has become a public health emergency of international concern. The disease is caused by severe acute respiratory syndrome coronavirus 2 （SARS-CoV-2）, and cytokine storm is an important pathological manifestation. Related studies have shown that cytokine storm and dysregulation of host immune responses characterized by lymphopenia are important mechanisms for the pathogenesis of severe COVID-19. The immune response disorder of COVID-19 is closely related to T helper 17 cell/regulatory T cell （Th17/Treg） immune imbalance. SARS-CoV-2 infection leads to excessive activation of lung immune cells, forming a cytokine storm dominated by interleukin-6 （IL-6）. Then, the Th17/Treg immune balance is broken, forming a vicious circle, which eventually promotes the rapid aggravation of the disease. Finally, COVID-19 progresses into acute respiratory distress syndrome, and even respiratory failure until death. Therefore, it is more important to discuss the prevention and treatment of COVID-19 from the perspective of immune imbalance. On the view of treatment, before effective antiviral drugs and vaccines are successfully developed, we should pay attention to immune regulation for severe and critically ill patients. Treatments with inflammatory factor blockers, glucocorticoids, recovered plasma and traditional Chinese medicine have certain immunomodulatory effect. This article discusses the pathogenesis of COVID-19 based on Th17/Treg immune imbalance, and elaborates on immunomodulatory therapy, aiming to provide reference for the prevention and treatment of COVID-19 and drug development.