National Cheng Kung University

About: National Cheng Kung University is a education organization based out in Tainan City, Taiwan. It is known for research contribution in the topics: Population & Thin film. The organization has 49723 authors who have published 69799 publications receiving 1437420 citations. The organization is also known as: NCKU.

Fundamental Movement Skills in Children Diagnosed with Autism Spectrum Disorders and Attention Deficit Hyperactivity Disorder

Abstract: The purpose of this study was to compare the movement skills of children with autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD), and those without disabilities. Ninety-one children (ASD, n = 28; ADHD, n = 29; control, n = 34), ages 6-10 years, were of average IQ participated. After controlling for age, both ASD and ADHD groups scored significantly lower than controls (p's < .05) on overall gross motor development as well as locomotor and object control subtests, and the ASD group performed more poorly than the ADHD group (p's < .01) on both subtests. Of the children with ASD and ADHD, only 16% had clinical levels of impairment. Potential underlying factors are discussed, with suggestions for future research.

MCP-1, a highly expressed chemokine in dengue haemorrhagic fever/dengue shock syndrome patients, may cause permeability change, possibly through reduced tight junctions of vascular endothelium cells.

Abstract: Vascular leakage, one hallmark of dengue haemorrhagic fever (DHF) and dengue shock syndrome, has been linked to the mediators secreted from cells in the circulatory system. In this study, extremely high expression levels of monocyte chemoattractant protein-1 (MCP-1) were found in the plasma of DHF patients compared with low MCP-1 expression levels in the plasma of enterovirus 71-infected patients. It was also found that MCP-1 expression was induced in dengue virus 2 (DV2)-infected monocytes and lymphocytes, but not in liver or endothelial cells. Exposing monolayers of human umbilical vein endothelial cells (HUVECs) to recombinant human MCP-1 (rhMCP-1) or to the culture supernatant of DV2-infected human monocytes increased the vascular permeability of the cells. MCP-1-neutralizing monoclonal antibody only partially prevented monolayer permeability change. Consistently, the distribution of the tight junction protein ZO-1 on the cellular membranes of HUVECs was disrupted by rhMCP-1 or by the conditioned medium of DV2-infected monocytes. In summary, it was found that the increased permeability and disrupted tight junctions of human vascular endothelium cells were effected through a mechanism partially dependent on MCP-1, which was secreted by DV2-infected monocytes and lymphocytes.