亚油酸体系脂质过氧化引起的DNA损伤研究

用含两个双键的不饱和脂肪酸-亚油酸作为模型化合物,分析其过氧化程度,同时检测了由于脂质过氧化而引起的DNA损伤,结果表明:在脂质过氧化过程中,DNA与亚油酸过氧化产物反应生成一种荧光物质、其最大激发波长315nm最大发射波长410nm并随着氧化时间增加而增加,与此同时,双链DNA百分含量明显下降,DNA-溴乙锭复合物荧光显著降低,反映了DNA二级结构受到破坏.上述结果揭示了脂质过氧化产物在自由基引起DNA的损伤中可能起重要作用     

侧脑室注射促甲状腺激素释放激素对大鼠睡眠—觉醒的影响

采用多导睡眠描记术研究了例脑室注射促甲状腺激素释放激素(TRH)对正常大鼠和去甲状腺大鼠睡眠-觉醒的影响。在正常大鼠,TRH引起觉醒增加,浅慢波睡眠(SWS_1)、深慢波睡眠(SWS_2)和总睡眠时间(TST)均减少,异相睡眠(PS)消失,SWS_1、SWS_2和PS的潜伏期均显著延长,给药后立即产生效应并在1h内达高峰。去甲状腺对大鼠的睡眠-觉醒无明显影响,注射TRH后引起的效应与正常大鼠相似。结果提示TRH有促进大鼠觉醒的作用,对各睡眠时相均有抑制作用,其作用部位可能在下丘脑以外的中枢结构。     

生长抑素在糖尿病大鼠胰腺外分泌功能降低中的作用

本实验观察到,用链佐霉素造成大鼠糖尿病模型,其胰腺组织中生长抑素含量明显升高。大鼠皮下注射生长抑素(100μg·kg~(-1)·d~(-1))5d,其胰腺组织中淀粉酶的含量明显降低。体外胰腺灌流也表明,生长抑素能抑制CCK—8刺激引起的胰腺淀粉酶释放。以上结果提示,糖尿病时胰腺组织中生长抑素含量的增加可能在胰腺外分泌功能降低中有一定的作用。     

镇海棘螈产卵场微生境选择

镇海棘螈(Echinotriton chinhaiensis)为国家一级重点保护野生动物,其种群面临着生境退化及丧失的重要威胁。产卵是决定镇海棘螈种群数量增长的关键环节之一,了解其产卵选择的微生境偏好可以更有针对性地保护该物种。本研究旨在确定影响镇海棘螈产卵场微生境选择的关键环境变量,同时为该物种的产卵生境保护、改造和重建提供科学基础。本文于2021年3-5月(繁殖期)在浙江省宁波市北仑区林场对镇海棘螈产卵位点(n=105)与非产卵位点(n=70)处的18个微生境变量进行调查。采用拟合优度卡方检验判断3种无序分类变量的差异性,并利用生境喜好系数对生境选择性进行分析。采用二元逻辑斯蒂回归模型对15个数值型变量进行分析,确定影响镇海棘螈产卵微生境选择的关键变量。结果显示镇海棘螈繁殖期间对产卵场微生境有明显偏好,通常产卵于朝向水坑、落叶层较厚(5.19±0.18 cm)、坡度较陡(18.64°±1.18°)和土壤含水量较低(33.51%±1.87%)的土壤基质上。此外,在大型遮蔽物中,镇海棘螈偏好选择体积较小的石块和乔木(2,994.63±316.17 cm³)作为遮蔽...     

含人口迁移的性传染病模型

本文研究一类含人口迁移的性传染病模型,应用摄动方法和定性方法研究平衡点的稳定性和迁移率的影响。普举例说明。     

环境温度影响蟾蜍卵母细胞成熟能力的机制之实验分析

长年饲养在高温(28—30℃)环境中雌性中华大蟾蜍,它们的卵母细胞可以长足,但经激素处理时,生发泡不破裂,仅显示成熟过程早期阶段的变化。值得注意的是,在孕酮刺激后的高温卵卵质中,出观了一种能诱发低温卵恢复减数分裂的物质,称作为“依赖冬眠因子的促成熟物质”(HF-MPS)。HF-MPS 与MPF 有不少相似之处,如孕酮处理后,它们在卵质中出现的时间相仿,它们的形成均不依赖于转录水平,而是依赖于翻译水平的蛋白质合成活动;但亦存在不同之处,如MPF 诱发低温卵GVBD 时程不受温度影响,而HF-MPS 在10℃环境中,诱发低温卵GVBD 的时间明显延缓;MPF 不仅能诱发低温卵GVBD,而且同样能诱发高温卵GVBD,然而,HF-MPS 只能诱发低温卵GVBD。由此表明,MPF 和HF-MPS 似乎是截然不同的两类活性蛋白质。高温卵缺少低温诱发产生的“冬眠因子”,所以不能恢复cdc 2基因的转录活动,不能实现MPF 自身催化扩增作用,不能保证孕酮处理后的卵母细胞完成正常成熟的全过程变化。足见,低温是中华大蟾蜍卵母细胞恢复减数分裂过程中的必要条件,是导致中华大蟾蜍现有区域分布的内在原因之一。     

Differences between migrasome,a ‘new organelle’, and exosome

The migrasome is a new organelle discovered by Professor Yu Li in 2015. When cells migrate, the membranous organelles that appear at the end of the retraction fibres are migrasomes. With the migration of cells, the retraction fibres which connect migrasomes and cells finally break. The migrasomes detach from the cell and are released into the extracellular space or directly absorbed by the recipient cell. The cytoplasmic contents are first transported to the migrasome and then released from the cell through the migrasome. This release mechanism, which depends on cell migration, is named ‘migracytosis’. The main components of the migrasome are extracellular vesicles after they leave the cell, which are easy to remind people of the current hot topic of exosomes. Exosomes are extracellular vesicles wrapped by the lipid bimolecular layer. With extensive research, exosomes have solved many disease problems. This review summarizes the differences between migrasomes and exosomes in size, composition, property and function, extraction method and regulation mechanism for generation and release. At the same time, it also prospects for the current hotspot of migrasomes, hoping to provide literature support for further research on the generation and release mechanism of migrasomes and their clinical application in the future.     

The Puccinia striiformis effector Hasp98 facilitates pathogenicity by blocking the kinase activity of wheat TaMAPK4

The obligate biotrophic fungus Puccinia striiformis f. sp. tritici (Pst) employs virulence effectors to disturb host immunity and causes devastating stripe rust disease. However, our understanding of how Pst effectors regulate host defense responses remains limited. In this study, we determined that the Pst effector Hasp98, which is highly expressed in Pst haustoria, inhibits plant immune responses triggered by flg22 or nonpathogenic bacteria. Overexpression of Hasp98 in wheat (Triticum aestivum) suppressed avirulent Pst-triggered immunity, leading to decreased H₂O₂ accumulation and promoting P. striiformis infection, whereas stable silencing of Hasp98 impaired P. striiformis pathogenicity. Hasp98 interacts with the wheat mitogen-activated protein kinase TaMAPK4, a positive regulator of plant resistance to stripe rust. The conserved TEY motif of TaMAPK4 is important for its kinase activity, which is required for the resistance function. We demonstrate that Hasp98 inhibits the kinase activity of TaMAPK4 and that the stable silencing of TaMAPK4 compromises wheat resistance against P. striiformis. These results suggest that Hasp98 acts as a virulence effector to interfere with the MAPK signaling pathway in wheat, thereby promoting P. striiformis infection.