An animal model of cerebral palsy induced by prenatal exposure to lipopolysaccharide and hypoxia

BACKGROUND： Neonatal cerebral palsy is mainly caused by prenatal factors. At present, an animal model of prenatal infection and early postnatal hypoxia does not exist. OBJECTIVE： To observe morphology and motor performance following prenatal infection and hypoxic insult-induced brain damage of neonatal rats to verify the feasibility to establish a model of cerebral palsy. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Laboratories of Xinjiang Center for Disease Control and Prevention from September 2007 to June 2008. MATERIALS： The hypoxic incubator was purchased from Shanghai Pediatric Medical Institute, China. Lipopolysaccharide （LPS, Escherichia coil, 055： B5） was purchased from Sigma-Aldrich （St. Louis, MO, USA）. METHODS： A total of 27 Wistar rats, aged 7 days, were randomly assigned to sham-surgery group （n = 15） with no carotid artery incision or hypoxia treatment, hypoxia/ischemia （H/I） group （n = 12） undergoing ligature of the right common carotid artery followed by exposure to hypoxia at postnatal day 7 （P7）, and LPS/H group （n = 19）, in which pregnant rats were exposed in utero to LPS followed by prenatal hypoxia at embryonic day 16. MAIN OUTCOME MEASURES： Behavior, compound muscle action potential, and pathological changes were observed in 28-day-old rats. RESULTS： The footprint repeat space showed that left limb footprint repeatability in the H/I and LPS/H groups was lower than in the sham-surgery group （P 〈 0.05）. The space between the footprints was larger and unstable. Hind limb quadricep compound muscle action potential in the H/I and LPS/H groups showed lower wave amplitude compared with the sham-surgery group （P〈 0.05） Hematoxylin and eosin staining showed irregular cells around the ventricle, as well as periventricular leukomalacia. CONCLUSION： An animal model of cerebral palsy was established, which simulated the human condition most likely associated with occurrence of this disease. This model could be used for experimental studies related to cerebral palsy.

抗组织转谷氨酰胺酶抗体滴度与成人乳糜泻十二指肠组织病理学的相关性

评估血清抗组织转谷氨酰胺酶抗体(抗tTG抗体)滴度与十二指肠黏膜损伤严重程度的相关性,预测国内人群抗tTG抗体滴度诊断乳糜泻及绒毛萎缩的最佳临界值。回顾性分析2017年7月至2022年1月就诊于新疆维吾尔自治区人民医院的76例抗tTG抗体阳性同时行十二指肠活检的成年乳糜泻患者临床及病理资料,统计分析血清抗tTG抗体滴度与十二指肠黏膜损伤严重程度的相关性,预测抗tTG抗体滴度诊断乳糜泻及绒毛萎缩的最佳临界值。在76例患者中,10例被认为是潜在乳糜泻,66例有十二指肠组织病理学改变的患者中,4例为MarshⅠ级,6例为MarshⅡ级,56例为MarshⅢa-c级。统计分析显示,成人乳糜泻的抗tTG抗体滴度与十二指肠黏膜组织病理学损伤的严重程度有关。抗tTG抗体滴度≥5倍正常值上限(ULN)时,诊断乳糜泻的敏感度为83.9%、特异度为92.9%;抗tTG抗体滴度≥8倍ULN时,诊断绒毛萎缩的敏感度为67.9%、特异度为90.0%。超过10倍ULN的抗tTG抗体滴度对诊断成年人乳糜泻具有很强的预测价值。该临界值可与临床判断相结合来诊断乳糜泻,这可能有助于避免侵入性内窥镜检查。