Method for determining or detecting damage in organ donor then to xenotransplantation based on analytes derived from organ donor

• 1. 基于供体器官衍生的分析物测定或检测在异体移植后供体器官损坏的方法 [P] . 中国专利： CN1205081A . 1999-01-13
• 2. 用于供体器官上的碳水化合物抗原切割的酶促组合物、与其相关的方法和用途 [P] . 中国专利： CN112839512A . 2021-05-25
• 3. METHOD OF DETERMINING OR DETECTING DONOR ORGAN DAMAGE FOLLOWING XENOTRANSPLANTATION BASED ON DONOR ORGAN-DERIVED ANALYTES [P] . CA2239882C . 2003-07-29

  机译： 基于捐赠者器官分析的异种移植后确定或检测捐赠者器官损伤的方法

• 4. Method of determining or detecting donor organ damage following xenotransplantation based on donor organ-derived analytes [P] . CZ288968B6 . 2001-10-17

  机译： 基于供体器官衍生的分析物确定或检测异种移植后供体器官损伤的方法

• 5. METHOD OF DETERMINING OR DETECTING DONOR ORGAN DAMAGE FOLLOWING XENOTRANSPLANTATION BASED ON DONOR ORGAN-DERIVED ANALYTES [P] . HUT78056A . 1999-07-28

  机译： 基于捐赠者器官分析的异种移植后确定或检测捐赠者器官损伤的方法

• 1. Liver transplantation using organs from deceased organ donors：a single organ transplant center experience [J] . Ming Han, Lin-Wei Wu, An-Bin Hu, 国际肝胆胰疾病杂志（英文版） . 2014,第004期
• 2. Personalized Donor-Recipient Matching for Organ Transplantation [C] . Jinsung Yoon, Ahmed M. Alaa, Martin Cadeiras, AAAI Conference on Artificial Intelligence . 2017
• 3. The Influence of Health Locus of Control on Organ Donor Intention and Registration [D] . Pozarnsky, Deborah Jean. 2019
• 4. Brain arrest: the neurological determination of death and organ donor management in Canada: Organ donor management in Canada: recommendations of the forum on Medical Management to Optimize Donor Organ Potential [O] . Sam D. Shemie, Heather Ross, Joe Pagliarello, 2006
• 5. Will donor‐derived neoplasia be problematic after clinical pig organ or cell xenotransplantation? [O] . Abhijit Jagdale, Hayato Iwase, Edwin Klein, 2018

• 1. A Novel Next-Generation Sequencing Approach without Donor-Derived Material for Acute Rejection and Infection Monitoring in Solid Organ Transplantation [J] . Bing Wei ,Liuhong Zeng ,Di Shao . 癌症治疗（英文） . 2018,第9期
• 2. Selecting suitable solid organ transplant donors: Reducing the risk of donor-transmitted infections [J] . Christopher S Kovacs Jr ,Christine E Koval ,David van Duin . 世界移植杂志 . 2014,第2期
• 3. 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
• 4. Pre-emptive live donor kidney transplantation-moving barriers to opportunities:An ethical,legal and psychological aspects of organ transplantation view [J] . David van Dellen ,Lisa Burnapp ,Franco Citterio . 世界移植杂志 . 2021,第4期
• 5. 提高脑死亡供体器官利用率——哈尔滨医科大学附属第一医院案例总结 [C] . 刘宏宇 ,迟超 . 第19届中国南方国际心血管病学术会议 . 2017
• 6. DBCD供体评估及器官保护与其肝肾移植受者术后器官功能恢复的相关性分析 [A] . 王镪 . 2014