检索结果-南通市图书馆

Neural Regeneration Research 2023年第2期18卷 322-323页

作者： Hannah Musco julie A.wixey UQ Centre for Clinical Research Faculty of MedicineUniversity of QueenslandQueenslandAustralia

Fetal growth restriction(FGR)is one of the most common contributors to increased risk of mortality in the fetal/neonatal period and long-term morbidity in the infant(Malhotra et al.,2019).FGR can arise from many pathophysiological processes associated with maternal,fetal,genetic,or placental compromise;however,placental insufficiency is the most common cause of FGR.Placental insufficiency during pregnancy results in chronic fetal hypoxia where a lack of oxygen and nutrients supply to the developing fetus impacts normal development of the fetus.

关键词： fetal fetus insufficiency

Could serotonin play a role in abnormal brain outcomes in fetal growth restriction?

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2023年第3期18卷 543-544页

作者： Kate Beecher julie A.wixey UQ Centre for Clinical Research Faculty of MedicineThe University of QueenslandHerstonQLDAustralia

Fetal growth restriction(FGR)describes a fetus that has not grown to its expected biological potential in utero.FGR can result from maternal,fetal,or placental complications,though it is commonly caused by placental insufficiency.The prolonged hypoxic environment the FGR fetus is exposed to has detrimental effects on the newborn,which extends to adverse long-term neurological outcomes in a significant proportion of FGR infants(Malhotra et al.,2019).Unfortunately,there are currently no therapies to reduce the adverse neurological outcomes in FGR.Neuronal injury is evident in the FGR brain,and therefore understanding which neurons are lost and how they are lost will aid in the selection of treatment options for FGR.

关键词： fetal fetus insufficiency

Improving brain outcomes in the growth restricted newborn: treating after birth

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2021年第5期16卷 978-979页

作者： julie A.wixey Stella Tracey Bjorkman UQ Centre for Clinical Research Faculty of MedicineThe University of QueenslandHerstonQueenslandAustralia

Intrauterine growth restriction(IUGR)occurs when a baby is unable to grow normally due to receiving inadequate nutrients while developing in the womb.IUGR is a leading cause of perinatal death and longterm disability.The fetal brain is particularly vulnerable to IUGR conditions and adverse outcomes range from learning,attention and behavioral difficulties,to cerebral palsy.Due to medical advancements,more IUGR babies now survive,resulting in an even greater burden of disability.

关键词： restricted IUGR advancement

Targeting inflammation to reduce brain injury in growth restricted newborns:a potential treatment?

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2017年第11期12卷 1804-1806页

作者： julie a wixey Paul B Colditz Stella Tracey Bjorkman Centre for Clinical Research Faculty of MedicineThe University of QueenslandHerstonQueenslandAustralia

Introduction： Intrauterine growth restriction （IUGR） is commonly caused by placental insufficiency, resulting in a chronic hypoxic environment and subsequent abnormal fetal development. The developing brain is particularly vulnerable to IUGR conditions. Multiple causal factors associated with brain injury in fetal growth restriction include the timing of placental insufficiency, onset and subsequent severity of fetal compromise, fetal cerebrovascular response and the redistribution of brain blood flow. Although a significant proportion of IUGR infants exhibit adverse long-term neu- rological outcomes, relatively few studies have focused on the mechanisms of brain injury in the IUGR neonate. Clini- cal imaging studies of IUGR infants demonstrate alterations in grey matter and white matter volume and structure （Tolsa et al., 2004; Esteban et al., 2010; Padilla et al., 2015）. Cortical grey matter volume is reduced by up to 28% compared with control infants （Tolsa et al., 2004） and both white and grey matter show structural changes （Esteban et al., 2010）. These structural changes persist at 1 year of age and are associated with significant developmental disabilities （Tolsa et al., 2004;

关键词： Targeting inflammation brain injury

Hypoxia-ischemia in the immature rodent brain impairs serotonergic neuronal function in certain dorsal raphé nuclei

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2020年第3期15卷 457-463页

作者： Hanna E.Reinebrant julie A.wixey Kathryn M.Buller UQ Centre for Clinical Research Faculty of Medicine The University of Queensland

Neonatal hypoxia-ischemia(HI)results in losses of serotonergic neurons in specific dorsal raphe nuclei.However,not all serotonergic raphe neurons are lost and it is therefore important to assess the function of remaining neurons in order to understand their potential to contribute to neurological disorders in the HI-affected neonate.The main objective of this study was to determine how serotonergic neurons,remaining in the dorsal raphe nuclei after neonatal HI,respond to an external stimulus(restraint stress).On postnatal day 3(P3),male rat pups were randomly allocated to one of the following groups:(i)control+no restraint(n=5),(ii)control+restraint(n=6),(iii)P3 HI+no restraint(n=5)or(iv)P3 HI+restraint(n=7).In the two HI groups,rat pups underwent surgery to ligate the common carotid artery and were then exposed to 6%O2 for 30 minutes.Six weeks after P3 HI,on P45,rats were subjected to restraint stress for 30 minutes.Using dual immunolabeling for Fos protein,a marker for neuronal activity,and serotonin(5-hydroxytrypamine;5-HT),numbers of Fos-positive 5-HT neurons were determined in five dorsal raphe nuclei.We found that restraint stress alone increased numbers of Fos-positive 5-HT neurons in all five dorsal raphe nuclei compared to control animals.However,following P3 HI,the number of stress-induced Fos-positive 5-HT neurons was decreased significantly in the dorsal raphe ventrolateral,interfascicular and ventral nuclei compared with control animals exposed to restraint stress.In contrast,numbers of stress-induced Fos-positive 5-HT neurons in the dorsal raphe dorsal and caudal nuclei were not affected by P3 HI.These data indicate that not only are dorsal raphe serotonergic neurons lost after neonatal HI,but also remaining dorsal raphe serotonergic neurons have reduced differential functional viability in response to an external stimulus.Procedures were approved by the University of Queensland Animal Ethics Committee(UQCCR958/08/NHMRC)on February 27,2009.

关键词： dorsal raphe nuclei Fos hypoxia-ischemia neonate newborn brain injury preterm restraint stress serotonin