A METHOD OF DETECTING ARGYROPHILIC PROTEIN OF NUCLEOLUS ORGANIZER REGIONS (Ag-NORs) IN THE T LYMPHOCYTES

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  机译： 一种检测t淋巴细胞核仁组织区（ag-nors）嗜银蛋白的方法

• 4. METHODS FOR DETECTING, IDENTIFYING , ISOLATING AND SELECTIVELY LABELING AND TARGETING TH1 LYMPHOCYTES BY MEANS OF THE LAG-3 PROTEIN [P] . IL122832B . 2006-08-20

  机译： 通过lag-3蛋白手段检测，鉴定，分离和选择性标记和靶向TH1淋巴细胞的方法

• 5. METHODS FOR DETECTING, IDENTIFYING , ISOLATING AND SELECTIVELY LABELING AND TARGETING TH1 LYMPHOCYTES BY MEANS OF THE LAG-3 PROTEIN [P] . IL122832A . 2006-08-20

  机译： 通过lag-3蛋白手段检测，鉴定，分离和选择性标记和靶向TH1淋巴细胞的方法

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• 1. 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
• 2. 类风湿性关节炎患者外周血T淋巴细胞Ag-NORs及T亚群的变化 [C] . 周晖 ,江楚文 ,石蕴珍 . 第二届全国现代免疫诊断技术学术研讨会 . 2005
• 3. 正常人、肿瘤及肺结核患者外周血T淋巴细胞核仁形成区嗜银蛋白（Ag-NORs）含量的对比分析 [A] . 李恂 . 2003