Are you Hua Zou?

Claim your profile

Publications (3)7.9 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Autism spectrum disorder (ASD) is a heterogeneous grouping of neurodevelopmental disorders characterized by impairment in social interaction, verbal communication and repetitive/stereotypic behaviors. Much evidence suggests that ASD is multifactorial with a strong genetic basis, but the underlying mechanisms are far from clear. Recent advances in genetic technologies are beginning to shed light on possible etiologies of ASD. This review discusses current evidence for several widely studied candidate ASD genes, as well as various rare genes that supports their relationship to the etiology of ASD. The majority of the data are based on molecular, cytogenetic, linkage and association studies of autistic subjects, but newer methods, including whole-exome sequencing, are also beginning to make significant contributions to our understanding of autism.
    Brain research bulletin 06/2012; 88(6):543-52. · 2.18 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Preeclampsia is a prevalent and potentially devastating complication of pregnancy. Intercellular adhesion molecule-1 (ICAM-1) was reported to be involved in the pathogenesis of the disease. Therefore we hypothesized anti-ICAM-1 monoclonal antibody (mAb) could be a therapeutic choice for preeclampsia. The objective of this study was to evaluate its therapeutic effects using a rat model of preeclampsia. Timed pregnant Wistar rats were intravenously injected endotoxin and then randomized to receive either anti-ICAM-1 mAb or saline. The effects of antibody on blood pressure, urinary protein, levels of alanine aminotransferase (ALT), blood urea nitrogen (BUN), creatinine, uric acid, weight of placenta were measured. Pregnancy outcomes were evaluated. Anti-ICAM-1 mAb significantly decreased the levels of blood pressure, urinary protein, maternal BUN, creatnine and uric acid comparing with untreated preeclamptic rats. And the antibody therapy significantly improved pregnancy outcomes. After five days of mAb treatment, most of the parameters in mAb-treated group approached normal levels. Our data prove anti-ICAM-1 mAb therapy as a promising choice for preeclampsia.
    The journal of maternal-fetal & neonatal medicine: the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians 08/2011; 25(6):855-9. · 1.36 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Although the cellular mechanisms responsible for the pathogenesis of autism are not understood, a growing number of studies have suggested that localized inflammation of the central nervous system (CNS) may contribute to the development of autism. Recent evidence shows that IL-6 has a crucial role in the development and plasticity of CNS. Immunohistochemistry studies were employed to detect the IL-6 expression in the cerebellum of study subjects. In vitro adenoviral gene delivery approach was used to over-express IL-6 in cultured cerebellar granule cells. Cell adhesion and migration assays, DiI labeling, TO-PRO-3 staining and immunofluorescence were used to examine cell adhesion and migration, dendritic spine morphology, cell apoptosis and synaptic protein expression respectively. In this study, we found that IL-6 was significantly increased in the cerebellum of autistic subjects. We investigated how IL-6 affects neural cell development and function by transfecting cultured mouse cerebellar granule cells with an IL-6 viral expression vector. We demonstrated that IL-6 over-expression in granule cells caused impairments in granule cell adhesion and migration but had little effect on the formation of dendritic spines or granule cell apoptosis. However, IL-6 over-expression stimulated the formation of granule cell excitatory synapses, without affecting inhibitory synapses. Our results provide further evidence that aberrant IL-6 may be associated with autism. In addition, our results suggest that the elevated IL-6 in the autistic brain could alter neural cell adhesion, migration and also cause an imbalance of excitatory and inhibitory circuits. Thus, increased IL-6 expression may be partially responsible for the pathogenesis of autism.
    Journal of Neuroinflammation 01/2011; 8:52. · 4.35 Impact Factor