MOVING ON RIGHT AND LEFT MECHANISM FOR TILLER

• 1. 一种促进人体肿瘤发生、发展的新机制 [P] . 中国专利： CN105902528A . 2016-08-31
• 2. 一种与浆液性卵巢癌发生发展机制相关的microRNA分子及其应用 [P] . 中国专利： CN104830858A . 2015-08-12
• 3. MOVING ON RIGHT AND LEFT MECHANISM FOR TILLER [P] . 日本专利： JPS56106505A . 1981-08-24

  机译： 耕作者左右机制的发展

• 4. MOVING ON RIGHT AND LEFT MECHANISM FOR TILLER [P] . 日本专利： JPS56111150U . 1981-08-27

  机译： 耕作者左右机制的发展

• 5. Principle of interpreting system for language written right to left - has carriage moving right to left and print mechanism shift to back at end of line [P] . NL7406427A . 1975-11-17

  机译： 从右到左书写的语言的解释系统的原理-使行从右向左移动，并且打印机制在行尾移至后退

• 1. The moving mechanisms of LNAPL in unsaturated zone and aquifer [J] . 世界地质：英文版 . 1998,第001期
• 2. Neuroendocrine mechanisms of left ventricular dysfunction stimulated by anger stress in rats with atherosclerosis-a putative role of natriuretic peptide [J] . Lin Chen, Xian-Zhi He, Qi-Ming Liu 亚太热带医药杂志（英文版） . 2014,第001期
• 3. Study on proton transport mechanism in a polymer electrolyte membrane by 1{sup left}H/2{sup left}D replace MRI under fuel cell operation [C] . TERANISHI Kazuhiro, TSUSHIMA Shohji, NISHIDA Kosuke, 日本伝熱シンポジウム . 2005
• 4. Molecular Mechanisms of Angiodysplasia and Non-surgical Bleeding in Human Patients with Continuous-Flow Left Ventricular Assist Devices [D] . Tabit, Corey Emil. 2018
• 5. De novo assembly and transcriptome analysis of two contrary tillering mutants to learn the mechanisms of tillers outgrowth in switchgrass (Panicum virgatum L.) [O] . Kaijie Xu, Fengli Sun, Guaiqiang Chai, 2015
• 6. De novo assembly and transcriptome analysis of two contrary tillering mutants to learn the mechanisms of tillers outgrowth in switchgrass (Panicum virgatum L.) [O] . Kaijie eXu, Fengli eSun, Yongfeng Wang eWang, 2015

• 1. Effect of exercise training on left ventricular remodeling in patients with myocardial infarction and possible mechanisms [J] . Meng Cai ,Lei Wang ,Yan-Long Ren . 世界临床病例杂志 . 2021,第022期
• 2. Stem cell mechanisms during left ventricular remodeling post-myocardial infarction:Repair and regeneration [J] . Rogelio Zamilpa ,Mary M Navarro ,Iris Flores . 世界心脏病学杂志：英文版（电子版） . 2014,第7期
• 3. BACKGROUND： Vibrio vulnifi cus inside the body could activate the NF-!B signaling pathwayand initiate the inflammatory cascade. The lung is one of the earliest organs affected by sepsisassociated with acute lung injury. High mobility group protein B1 （HMGB1） is an important late-actingpro-infl ammatory cytokine involving in the pathophysiology of sepsis. It is also involved in the injuryprocess in the lung, liver and intestine. There has been no report on the involvement of HMGB1 inVibrio vulnifi cus sepsis-induced lung injury.METHODS： Sixty rats were randomly divided into a normal control group （group A, n=10） anda Vibrio vulnificus sepsis group （group B, n=50）. Sepsis was induced in the rats by subcutaneousinjection of Vibrio vulnificus （concentration 6×108 cfu/mL, volume 0.1 mL/100g）） into the left lowerlimbs. The rats in group B were sacrifi ced separately 1, 6, 12, 24, and 48 hours after the infection.Their lungs were stored as specimens, lung water content was measured, and lung pathology wasobserved under a light microscope. The expressions of the HMGB1 gene and protein in the lungswere detected by RT-PCR and Western blot. Data were analyzed with one-way analysis of variance（ANOVA） and the LSD method for pair-wise comparison between the two groups. P〈0.05 wasconsidered statistically signifi cant.RESULTS： Compared to group A （0.652±0.177）, HMGB1 mRNA expression in the lungs ofgroup B was signifi cantly higher at 0 hour （1.161±0.358, P=0.013）, 24 hours （1.679±0.235, P=0.000）,and 48 hours （1.258±0.274, P=0.004） （P〈0.05）, and peaked at 24 hours. Compared to group A（0.594±0.190）, HMGB1 protein expression at 6 hours （1.408±0.567, P=0.026） after infection wassignificantly increased （P〈0. 05）, and peaked at 24 hours （2.415±1.064, P=0.000） after infection.Compared to group A （0.699±0.054）, lung water content was significantly increased at 6 hours（0.759±0.030, P=0.001）,12 hours （0.767±0.023, P=0.000）, 24 hours （0.771±0.043, P=0.000） and 48hours （0.789±0.137, P=0.000） after infection （P〈0.05）. Compared to group A, pathological changesat 12 hours in group B indicate marked pulmonary vascular congestion, interstitial edema andinfl ammatory infi ltration. Alveolar cavity collapse and boundaries of the alveolar septum could not beclearly identifi ed.CONCLUSION： Vibrio vulnifi cus sepsis can lead to injury in rat lungs, and increased HMGB1expression in lung tissue may be one of the mechanisms for injury from Vibrio vulnifi cus sepsis. [J] . Qiao-meng Qiu ,Zhong-wang Li ,Lu-ming Tang . 世界急诊医学杂志(英文) . 2011,第4期
• 4. 从大鼠血清E2、子宫ERαmRNA水平探讨左右归丸逆转化疗致POF的时效机制 [C] . 肖新春 ,崔晓萍 . 中华中医药学会第15次全国中医妇科学术年会 . 2015
• 5. 医务社会工作者与志愿者的服务联动机制构建与发展策略研究 [A] . 卫燕青 . 2020