METHOD FOR PREVENTION OF ROTA-, CORONAVIRAL INFECTION AND CATTLE COLIBACILLOSIS

• 1. 来源于抗-VP6骆驼科动物抗体的单体VHH结构域、二聚体结构域、免疫方法、轮状病毒检测方法、组合物、用于轮状病毒感染的预防和治疗方法 [P] . 中国专利： CN101878227B . 2014.08.27
• 2. 来源于抗-VP6骆驼科动物抗体的单体VHH结构域、二聚体结构域、免疫方法、轮状病毒检测方法、组合物、用于轮状病毒感染的预防和治疗方法 [P] . 中国专利： CN101878227A . 2010-11-03
• 3. METHOD FOR PREVENTION OF ROTA-, CORONAVIRAL INFECTION AND CATTLE COLIBACILLOSIS [P] . 俄罗斯专利： RU0002723709C1 . 2020.06.17
• 4. VACCINE FOR ROTA-, CORONAVIRAL INFECTION AND CATTLE COLIBACILLOSIS [P] . 俄罗斯专利： RU2708891C1 . 2019-12-12

  机译： 轮状，冠状病毒感染和牛肝炎疫苗

• 5. ASSOCIATED WITH PARAINFLUENZA-3 VACCINE, INFECTIOUS RHINOTRACHEITIS, VIRAL DIARRHEA, ROTA- AND CORONAVIRAL INFECTIONS OF CATTLE INACTIVATED EMULSION [P] . 俄罗斯专利： RU2696007C1 . 2019-07-30

  机译： 与PARAINFLUENZA-3疫苗，感染性鼻气管炎，病毒性腹泻，牛失活的乳状液的轮状和冠状病毒感染相关

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• 2. 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
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