METHOD FOR DETECTING SERIOUS CHILDHOOD EARLY-ONSET NEURODEGENERATIVE ENCEPHALOPATHY OR CARRIER THEREOF

• 1. 大脑生理与认知功能及神经退行性疾病的检测系统及方法 [P] . 中国专利： CN112656367A . 2021-04-16
• 2. 检测个体罹患神经退行性疾病风险的方法 [P] . 中国专利： CN110168375A . 2019-08-23
• 3. Severe childhood onset onset neurodegenerative encephalopathy or method of detecting the cause [P] . JP6935890B2 . 2021-09-15

  机译： 严重的儿童发病发病的神经变性脑病或检测原因的方法

• 4. METHOD FOR DETECTING NEONATAL TO CHILDHOOD-ONSET CEREBRAL SMALL BLOOD VESSEL DISEASE OR CARRIERS THEREOF [P] . 日本专利： JP2020061955A . 2020-04-23

  机译： 检测新生儿至小儿脑小血管疾病或载体的方法

• 5. Analyzing samples by measuring light scattering, useful e.g. for detecting bovine spongiform encephalopathy, where scattering particles are formed by reaction in carrier fluid [P] . 德国专利： DE10128978A1 . 2002-12-19

  机译： 通过测量光散射来分析样品，例如用于检测牛海绵状脑病，其中载液中的反应形成散射颗粒

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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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