Chao Chen
Fudan University
37 Papers
253 Citations
Chao Chen is an academic researcher from Fudan University. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 10, co-authored 30 publications. Previous affiliations of Chao Chen include Shanghai Jiao Tong University & Wenzhou Medical College.
Chat about Author
Papers
Long-term cognitive impairment and myelination deficiency in a rat model of perinatal hypoxic-ischemic brain injury
TL;DR: In this neonatal rat model of HI, myelination deficiency induced by activated astrocytes and microglia during the early phase with subsequent glial scarring was associated with long-term spatial learning and memory dysfunction.
115
Epidemiology of group B streptococcal infection in pregnant women and diseased infants in mainland China.
TL;DR: The available data suggest that five GBS serotypes account for the majority of the cases of GBS disease in mainland China, and conjugate vaccines comprising some or all of these serotypes are of potential value in the prevention of GB Streptococcus infection.
41
A case series of 130 neonates with congenital syphilis: preterm neonates had more clinical evidences of infection than term neonates.
TL;DR: Preterm neonates with CS had more clinical evidences and suffered more than term ones, and the rate of withdrawal of care was higher in preterm newborns than in term ones.
33
N-Acetylcysteine Improves Hemodynamics and Reduces Oxidative Stress in the Brains of Newborn Piglets with Hypoxia-Reoxygenation Injury
TL;DR: It is suggested that post-resuscitation administration of NAC reduces cerebral oxidative stress with improved cerebral oxygen delivery, and probably attenuates apoptosis in newborn piglets with H-R insults.
26
Hypoxia-ischemia upregulates TRAIL and TRAIL receptors in the immature rat brain.
TL;DR: The results show that the TNF-α superfamily ligand TRAIL is induced on CD68+ microglia/macrophages after perinatal HI and that one of its receptors, DR5, isinduced on neocortical neurons and glial cells, which supports the conclusion that these signaling molecules are involved in the delayed loss of neurons in the neocortex and in the neurobehavioral deficits that are often seen after per inatal HI.
24