The effects of hyperbilirubinaemia on synaptic plasticity in the dentate gyrus region of the rat hippocampus in vivo.

INTRODUCTION: The aim of our study is to investigate the effect of hyperbilirubinaemia on synaptic plasticity in the dentate gyrus (DG) region of the rat hippocampus. MATERIAL AND METHODS: Seven-day-old healthy Sprague Dawley (SD) rats were randomly divided into a control group and an experiment group (n = 20 in each group). The input/output (I/O) functions, paired-pulse reactions (PPR), excitatory postsynaptic potential (EPSP), and population spike (PS) amplitude were measured in the DG area of both groups of rats in response to stimulation applied to the lateral perforant path. RESULTS: Compared with that in the control rats, the current-voltage curves of both EPSP slope and PS amplitude in the experimental rats were significantly depressed. The average peak facilitation was 187 ±16% in the control and 164 ±18% in the experiment group (F = 21.054, p < 0.01). The facilitation period duration of PS was 155 ms in the experimental rats, which was less than that of the controls (235 ms). In the control group, the long-term potentiation (LTP) amplitudes were 140 ±3.5% and 242 ±6%, when estimated from the EPSP slope and PS amplitude, respectively, which were significantly depressed to 124 ±3.4% (EPSP slope, F = 70.489, p < 0.01) and 138 ±8.6% (PS amplitude, F = 253.46, p < 0.01), respectively, in the experiment group. CONCLUSIONS: These findings suggest that hyperbilirubinaemia could induce impairment of synaptic plasticity in the rat DG area in vivo, including I/O function, paired-pulse ratio (PPR), and LTP, which may be closely related to cognitive impairment.

The influence of zinc sulfate on neonatal jaundice: a systematic review and meta-analysis.

INTRODUCTION: Zinc sulfate may be a promising approach to treat neonatal jaundice. However, the results remain controversial. We conducted a systematic review and meta-analysis to evaluate the efficacy and safety of zinc sulfate on hyperbilirubinemia among neonates. METHODS: PubMed, EMbase, Web of science, EBSCO, Cochrane library databases, Ovid, BMJ database, and CINAHL were systematically searched. Randomized controlled trials (RCTs) assessing the effect of zinc sulfate versus placebo on the prevention of jaundice in neonates were included. Two investigators independently searched articles, extracted data, and assessed the quality of included studies. The primary outcomes were total serum bilirubin (TSB) on three days and seven days, the incidence of hyperbilirubinemia. Meta-analysis was performed using random- or fixed-effect models. RESULTS: Five RCTs involving 645 patients were included in the meta-analysis. Overall, compared with placebo, zinc sulfate supplementation failed to significantly reduce TSB on three days (mean difference (MD) = 0.09 mg/dL; 95% confidence interval (CI) = -0.49 to 0.67; p = .77), TSB on seven days (MD = -0.37 mg/dL; 95% CI = -98 to 0.25; p = .25) as well as the incidence of hyperbilirubinemia (OR = 1.14; 95% CI = 0.74 to 1.76; p = .56). Zinc sulfate showed no influence on phototherapy requirement (OR = 0.90; 95% CI = 0.41 to 1.98; p = .79), but resulted in significantly decreased duration of phototherapy (MD = -16.69 h; 95% CI = -25.09 to -8.3 h; p < .0001). CONCLUSIONS: Zinc sulfate could not reduce the TSB on three days and seven days, the incidence of hyperbilirubinemia and phototherapy requirement, but lead to significantly decreased duration of phototherapy.

Role of SIRT1/PGC-1α in mitochondrial oxidative stress in autistic spectrum disorder.

Autistic spectrum disorder (ASD) is a neurodevelopmental disorder and has a high prevalence in children. Recently, mitochondrial oxidative stress has been proposed to be associated with ASD. Besides, SIRT1/PGC-1α signaling plays an important role in combating oxidative stress. In this study, we sought to determine the role of SIRT1/PGC-1α signaling in the ASD lymphoblastoid cell lines (LCLs). In this study, the mRNA and protein expressions of SIRT1/PGC-1α axis genes were assessed in 35 children with ASD and 35 healthy controls (matched for age, gender, and IQ). An immortalized LCL was established by transforming lymphocytes with Epstein-Barr virus. Next, we used ASD LCLs and control LCLs to detect SIRT1/PGC-1α axis genes expression and oxidative damage. Finally, the effect of overexpression of PGC-1α on oxidative injury in the ASD LCLs was determined. SIRT1/PGC-1α axis genes expression was downregulated at RNA and protein levels in ASD patients and LCLs. Besides, the translocation of cytochrome c and DIABLO from mitochondria to the cytosol was found in the ASD LCLs. Moreover, the intracellular reactive oxygen species (ROS) and mitochondrial ROS and cell apoptosis were increased in the ASD LCLs. However, overexpression of PGC-1α upregulated the SIRT1/PGC-1α axis genes expression and reduced cytochrome c and DIABLO release in the ASD LCLs. Also, overexpression of PGC-1α reduced the ROS generation and cell apoptosis in the ASD LCLs. Overexpression of PGC-1α could reduce the oxidative injury in the ASD LCLs, and PGC-1α may act as a target for treatment.

NMDA receptor subunit and CaMKII changes in rat hippocampus by congenital HCMV infection: a mechanism for learning and memory impairment.

The aim of this study was to investigate the effects of congenital human cytomegalovirus infection on the expression levels of N-methyl-D-aspartate receptors (NRs) and Ca/calmodulin-dependent protein kinase II (CaMKII) in the hippocampal neurons of neonatal Sprague-Dawley (SD) rats. Pregnant SD rats were divided into an experimental group and a control group (n=10 in each group). Spatial learning and memory of the offspring of SD rats were evaluated using the Morris water-maze test. Pathological studies of hippocampus sections were carried out. The concentration of [Ca] was measured using a dual-wavelength spectrophotometer method. The expression levels of NRs were detected by an immunohistochemical study. Western blot was performed to detect the expression level of CaMKII. In the Morris water-maze test, the rats in the experimental group showed significantly increased escape latency and distance traveled than the control group. Damaged and structural disorders of the dentate granule in the hippocampus were found in the experimental rats. Immunohistochemistry results showed that the expression levels of NR subunits in the hippocampus of the experimental group were significantly decreased. The concentration of [Ca] in the experimental group was significantly increased. In contrast, the level of CaMKII in the experimental group was significantly decreased. The expressions of the NR subunit and CaMKII were decreased in rat hippocampus by human cytomegalovirus congenital infection, which may be associated with the mechanism underlying the impairment of learning and memory function.

Copper-Catalyzed Cross-Coupling Reaction of Allyl Boron Ester with 1°/2°/3°-Halogenated Alkanes.

The cross-coupling reaction of allyl boron ester with 1°/2°/3°-halogenated alkanes in the presence of copper has been developed for the first time, which provides a mild and efficient method for the construction of saturated C(sp(3))-C(sp(3)) bonds. This protocol shows excellent compatibility with the nonactivated primary, secondary, and even tertiary halogenated alkanes under mild conditions.