首页> 外国专利> Method of detecting ineffective prionic proteins (prpless thanspgreater thanscless than/spgreater than) by means of raman-laser spectroscopy

Method of detecting ineffective prionic proteins (prpless thanspgreater thanscless than/spgreater than) by means of raman-laser spectroscopy

机译：通过拉曼激光光谱法检测无效的普里宁蛋白的方法（无精制比精制比精制/比精制比）

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摘要

Method for detecting infectious prion protein (PrP Sc {}) laser-Raman spectroscopy.; The present invention provides a method, by Raman spectroscopy-laser, for detecting infectious prion protein (PrP {Sc}) in biological samples of animals infected with a TSE, and its application is extensible blood, among others, bovine , goats, humans and birds. The process of this invention, qualitative and quantitative, includes a first step aimed at obtaining the fraction of the blood where the infective prion proteins are more concentrated. The results obtained by the method described in this invention on the analysis of prions have agreed 100% with the test biodiagnosis postmortem brain samples made by the relevant animals from which Blood samples were taken.

机译：检测传染性病毒蛋白（PrP Sc {}）的激光拉曼光谱法。本发明提供了一种通过拉曼光谱仪-激光检测被TSE感染的动物的生物样品中的感染性ion病毒蛋白（PrP {Sc}）的方法，其应用是可扩展的血液，尤其是牛，山羊，人和人。鸟类。本发明的方法在定性和定量上包括第一步，该步骤旨在获得感染性pr病毒蛋白更浓缩的血液部分。通过本发明中描述的方法对analysis病毒的分析获得的结果与由采集血样的相关动物制成的测试生物诊断死后脑样品100％一致。 展开▼

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公开/公告号AU2003281571A8

专利类型

公开/公告日2004-02-09

原文格式PDF

申请/专利权人 CONSEJO SUPERIOR DE INVESTIGACIONES CIENTIFICAS;UNIVERSIDAD DE ZARAGOZA;
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申请/专利号AU20030281571

发明设计人 EVA MONLEON MOSCARDO;PEDRO CARMONA HERNANDEZ;JAIME MONREAL LLOP;MARTA MONZON GARCES;JUAN JOSE BADIOLA DIEZ;
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申请日2003-07-10

分类号G01N21/65;G01N33/68;

国家 AU

入库时间 2022-08-21 23:02:09

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1. 可转动精制盘中的精制分段和包括一具有这种精制分段的精制盘的精制装置 [P] . 中国专利： CN1308083C . 2007.04.04

2. 可转动精制盘中的精制分段和包括一具有这种精制分段的精制盘的精制装置 [P] . 中国专利： CN1434747A . 2003-08-06

3. METHOD OF DETECTING INEFFECTIVE PRIONIC PROTEINS (PRPLESS THANSPGREATER THANSCLESS THAN/SPGREATER THAN) BY MEANS OF RAMAN-LASER SPECTROSCOPY [P] . AU2003281571A1 . 2004-02-09

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机译：用拉曼激光光谱法检测无效的PR蛋白（PRP ）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

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