Method for the quantitative detection of Vibrio parahaemolyticus, Vibrio vulnificus and Vibrio cholerae

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• 3. The detection method of Vibrio cholerae Vibrio parahaemolyticus Vibrio vulnificus [P] . 韩国专利： KR100659157B1 . 2006-12-19

  机译： 霍乱弧菌副溶血弧菌的检测方法

• 4. THE DETECTION METHOD OF VIBRIO CHOLERAE, VIBRIO PARAHAEMOLYTICUS amp; VIBRIO VULNIFICUS [P] . 韩国专利： KR20060097748A . 2006-09-15

  机译： 霍乱弧菌，副弧菌和外伤弧菌的检测方法

• 5. Process for producing a vibrio cholerae thy a- strain, vibrio cholerae thy a- strain, nucleotide sequences of a vibrio cholerae thy a gene and a 5 'and 3' flank region of a thy a gene structural gene vibrio cholerae protein and vaccine [P] . BR9910703A . 2001-01-30

  机译： 产生霍乱弧菌α-菌株，霍乱弧菌α-菌株，霍乱弧菌thy基因的核苷酸序列以及基因结构基因霍乱弧菌蛋白和疫苗的5'和3'侧翼区域的方法

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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. 霍乱弧菌溶血素PCR检测方法的建立及序列分析 [C] . 陆群英 ,程苏云 ,叶菊莲 . 2007年浙江省医学病毒、微生物学和免疫学学术会议 . 2007
• 3. 副溶血弧菌和创伤弧菌双重Real-time PCR检测方法的建立及其应用 [A] . 蔡潭溪 . 2006