Question

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内质网应激在大鼠煤工尘肺引发认知功能改变中的作用
近年来研究发现内质网功能紊乱引发的内质网应激反应可以导致特异性细胞凋亡，被认为是细胞凋亡的第三条途径。各种影响内质网微环境和功能的刺激均可以引发内质网应激，启动未折叠蛋白质反应，促进细胞恢复常态。但是当各种刺激持续存在，ERS将导致细胞凋亡。GRP78 (78kD glucose regulated protein)和CHOP/GADD153(growth arrest-andDNA damage-inducible gene 153)是内质网应激的两个经典标志物。内质网应激反应启动后,GRP78迅速上调以发挥内质网自稳功能,细胞适应应激而存活,后期则由于应激时间过长导致内质网功能障碍,损伤程度加重,不能通过促进GRP78表达以缓解内质网应激,GRP78蛋白表达下调，并启动包括GADD153依赖通路在内的细胞凋亡途径,导致细胞死亡。临床实践证实，慢阻肺、阻塞性睡眠呼吸暂停综合征等可致机体长期缺氧的疾病均可引起认知功能障碍。煤工尘肺患者由于呼吸功能下降，往往伴有明显缺氧的临床表现。目前对煤工尘肺的研究多侧重于呼吸系统本身和心血管系统方面，是否同时也损害了患者的认知功能？是我们必须关注的重大医学和社会问题。国内外的研究尚属起步阶段，我们导师牛小媛教授领导的团队，做了有意义的探索。发现煤工尘肺患者认知功能障碍的发病率较高，因而对其发病机制的研究有重要的临床价值。本实验旨在建立理想的煤工尘肺大鼠模型，以内质网应激理论为指导，研究煤工尘肺对大鼠海马神经元凋亡和认知功能的影响，为探讨煤工尘肺患者认知功能障碍的发生机制提供必要的实验依据，为临床预防、诊断和治疗提供新思路和新策略。

Answer 1

Endoplasmic reticulum stress in coal worker's pneumoconiosis rats work by cognitive function change in the role

Recently, research has found that the endoplasmic reticulum function disorder caused by the endoplasmic reticulum stress response can lead to specific cell apoptosis, is considered to be the third way cell apoptosis. All sorts of effects endoplasmic reticulum microenvironment and function are the stimulus can trigger the endoplasmic reticulum stress, start not fold protein reaction, promote cells returned to normal. But when various stimuli persist, ERS will result in cell apoptosis. GRP78 (78 kD glucose regulated protein) and CHOP/GADD153 (growth arrest-andDNA damage-inducible gene 153) is the stress of endoplasmic reticulum two classic markers. Endoplasmic reticulum stress response is started, the GRP78 rapid rise to play the endoplasmic reticulum since steady function, the cell, adapt to stress and live, and later due to stress is a long time lead to the endoplasmic reticulum function obstacle, increase the degree of damage, not by promoting GRP78 express to alleviate the endoplasmic reticulum stress, GRP78 protein expression cut, and start GADD153 rely on pathways, including cell apoptosis ways, causing cell death. Clinical practice proof, copd, obstructive sleep apnea syndrome can cause the body's long-term anoxic disease all can cause cognitive dysfunction. Coal worker's pneumoconiosis work patients because respiratory function decline, usually with obvious the clinical manifestations of oxygen. At present the research work of coal worker's pneumoconiosis strong on the respiratory system itself and cardiovascular system, whether also damaged their cognitive functions? Are we must pay more attention to the major medical and social problems. Domestic and foreign research is still in the initial stage, our tutor cow professor of leadership team little gentle, do have the significative exploration. Coal worker's pneumoconiosis found work cognitive function in patients with higher incidence of obstacles, and the pathogenesis of research are important clinical value. This experiment is to establish the ideal of the coal worker's pneumoconiosis work in the rat model, with the endoplasmic reticulum stress theory as the guide, the coal worker's pneumoconiosis work on rat neurons in the hippocampus apoptosis and the influence of cognitive function, to explore the coal worker's pneumoconiosis work cognitive function in patients with obstacles happens to provide necessary experiment basis, for clinical prevention, diagnosis and treatment to provide new ideas and new strategy.