ABSTRACT
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 term-born 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.
ABSTRACT
The present study aimed to assess the effects and mechanisms of genistin in the rat model of myocardial ischemia reperfusion injury. The rat hearts were exposed to the left anterior descending coronary artery (LAD) ligation for 30 min followed by 1 h of reperfusion. In the rat of myocardial ischemia/reperfusion (MI/R), it was found that genistin pretreatment reduced myocardial infarct size, improved the heart rate, and decreased creatine kinase (CK) and lactate dehydrogenase (LDH) levels in coronary flow. This pretreatment also increased catalase (CAT), superoxide dismutase (SOD) activities but decreased glutathione (GSH), malondialdehyde (MDA) levels. Furthermore, we determined that genistin can ameliorate the impaired mitochondrial morphology and oxidation system; interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), and tumor necrosis factor-α (TNF-α) levels were also recovered. Besides, related-proteins of nuclear factor kappa-B (NF-κB) signal pathway activated by P2X7 were investigated to determine the molecular mechanism of genistin and their expressions were measured by western blot. These results presented here demonstrated that genistin enhanced the protective effect on the rats with myocardial ischemia reperfusion injury. Therefore, the cardioprotective effects of genistin may rely on its antioxidant and anti-inflammatory activities via suppression of P2X7/NF-κB pathways.
ABSTRACT
OBJECTIVE: To explore the pathophysiological changes in the functional connectivity of posterior cingulate cortex (PCC) with other brain regions in children with attention-deficit or hyperactivity disorder (ADHD) on resting-state functional magnetic resonance imaging(fMRI) and explore the neural mechanisms of ADHD at the point of relationships between brain regions. METHODS: Thirty children with ADHD from the Third Affiliated Hospital of Soochow University from June 2008 to April 2010 and another 30 age-and-gender-matched controls from a normal primary school over the same period underwent resting-state fMRI scans. And blood oxygenation level dependent (BOLD) signal was acquired to calculate the functional connectivity of PCC with other brain regions controls. Significant differences of connectivity between groups were analyzed with REST software. RESULTS: The pattern of functional connectivity of PCC for the ADHD group was similar to that of the control group. Significant positive functional connectivity with PCC was observed in the default mode of network (DMN) while negative functional connectivity was present in dorsolateral prefrontal cortex, anterior cingulate, parietal cortex and basal ganglia(all P < 0.05, corrected). Compared to the controls, the ADHD group exhibited decreased positive connectivity with PCC in bilateral medial prefrontal cortex (0.07 ± 0.20 vs 0.33 ± 0.23, t = -5.47), right posterior cingulate gyrus(0.25 ± 0.28 vs 0.48 ± 0.30, t = -3.44), right inferior temporal gyrus (-0.05 ± 0.19 vs 0.22 ± 0.22, t = -4.61) and cerebellar posterior lobe (-0.04 ± 0.21 vs 0.17 ± 0.16, t = -3.99), while decreased negative functional connectivity with PCC was observed in left insula (-0.10 ± 0.26 vs -0.30 ± 0.19, t = 3.71), right inferior parietal lobule (0.02 ± 0.18 vs -0.23 ± 0.17, t = 5.20), left postcentral gyrus (0.08 ± 0.26 vs -0.17 ± 0.25, t = 4.06), left superior temporal gyrus (-0.04 ± 0.25 vs -0.27 ± 0.17, t = 4.27), right superior temporal gyrus (-0.08 ± 0.25 vs -0.31 ± 0.21, t = 3.80) and left fusiform gyrus (-0.01 ± 0.25 vs -0.18 ± 0.17, t = 3.57)(all P < 0.05, corrected). CONCLUSIONS: The connectivity of DMN between brain regions is abnormal in ADHD group. And the strengthen of negative relationship between DMN and task activated network becomes reduced. It is surmised that the decreased internal synchronization of default network and disrupted balance between DMN and prefrontal-parietal attentional networks may be important neural mechanisms of ADHD.
