Resting-state network complexity and magnitude changes in neonates with severe hypoxic ischemic encephalopathy

Resting-state functional magnetic resonance imaging has revealed disrupted brain network connectivity in adults and teenagers with cerebral palsy. However, the specific brain networks implicated in neonatal cases remain poorly understood. In this study, we recruited 14 termborn infants with mild hypoxic ischemic encephalopathy and 14 term-born infants with severe hypoxic ischemic encephalopathy from Changzhou Children's Hospital, China. Resting-state functional magnetic resonance imaging data showed efficient small-world organization in whole-brain networks in both the mild and severe hypoxic ischemic encephalopathy groups. However, compared with the mild hypoxic ischemic encephalopathy group, the severe hypoxic ischemic encephalopathy group exhibited decreased local efficiency and a low clustering coefficient. The distribution of hub regions in the functional networks had fewer nodes in the severe hypoxic ischemic encephalopathy group compared with the mild hypoxic ischemic encephalopathy group. Moreover, nodal efficiency was reduced in the left rolandic operculum, left supramarginal gyrus, bilateral superior temporal gyrus, and right middle temporal gyrus. These results suggest that the topological structure of the resting state functional network in children with severe hypoxic ischemic encephalopathy is clearly distinct from that in children with mild hypoxic ischemic encephalopathy, and may be associated with impaired language, motion, and cognition. These data indicate that it may be possible to make early predictions regarding brain development in children with severe hypoxic ischemic encephalopathy, enabling early interventions targeting brain function. This study was approved by the Regional Ethics Review Boards of the Changzhou Children's Hospital(approval No. 2013-001) on January 31, 2013. Informed consent was obtained from the family members of the children. The trial was registered with the Chinese Clinical Trial Registry(registration number: ChiCTR1800016409) and the protocol version is 1.0.

Diffusion tensor imaging assesses white matter injury in neonates with hypoxic-ischemic encephalopathy

With improvements in care of at-risk neonates, more and more children survive. This makes it increasingly important to assess, soon after birth, the prognosis of children with hypoxic-ischemic encephalopathy. Computed tomography, ultrasound, and conventional magnetic resonance imaging are helpful to diagnose brain injury, but cannot quantify white matter damage. In this study, ten full-term infants without brain injury and twenty-two full-term neonates with hypoxic-ischemic encephalopathy （14 moderate cases and 8 severe cases） underwent diffusion tensor imaging to assess its feasibility in evaluating white matter damage in this condition. Results demonstrated that fractional anisotropy, voxel volume, and number of fiber bundles were different in some brain areas between infants with brain injury and those without brain injury. The correlation between fractional anisotropy values and neonatal behavioral neurological assessment scores was closest in the posterior limbs of the internal capsule. We conclude that diffusion tensor imaging can quantify white matter injury in neonates with hypoxic-ischemic encephalopathy.

Effects of urotensin-Ⅱ on cytokines in early acute liver failure in mice

AIM:To investigate urotensin-Ⅱ(UⅡ) and its effects on tumor necrosis factor(TNF)-α and interleukin(IL)-1β in early acute liver failure(ALF).METHODS:We investigated the time-dependent alteration in UⅡ levels and its effects on TNF-αand IL-1β in liver and blood in the early stage of lipopolysaccharide/D-galactosamine-induced ALF.RESULTS:After lipopolysaccharide/D-galactosamine challenge,UⅡ rose very rapidly and reached a maximal level 0.5 h,and the level remained significantly elevated after 2 h(P < 0.05).Six hours after challenge,UⅡ began to degrade,but remained higher than at 0 h(P < 0.05).Pretreatment with urantide,an inhibitor of the UⅡ receptor,suppressed the degree of UⅡ increase in liver and blood at 6 h after challenge(P < 0.05 vs paired controls).In addition,liver and blood TNF-α increased from 1 to 6 h,and reached a peak at 1 and 2 h,respectively; however,IL-1β did not rise until 6 h after challenge.Urantide pretreatment inhibited the degree of TNF-α and IL-1β increase following downregulation of UⅡ post-challenge(all P < 0.05).CONCLUSION:UⅡ plays a role in the pathogenesis and priming of ALF by triggering an inflammatory cascade and driving the early release of cytokines in mice.