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Parents of children with autism often report gastrointestinal problems as well as picky eating and selective eating in their children. The purpose of this study was to evaluate the nutritional status and the nutrient intake in 111 Chinese children with autism, aged between 2 and 9 years. Anthropometric data were expressed as Z scores. A 3-day dietary recall was provided by the parents, and the data were compared with the national Dietary Reference Intakes (DRI) standards for Chinese children. The results showed that only nine of the autistic children (8.1%) were acute or chronically malnourished. From the remaining 102 patients, 67 (60.4%) were eutrophic and 35 (31.5%) had either overweight or obesity. Intakes of both calories and proteins were adequate in the vast majority of these children, but the calories from fat was lower than DRI in the same age group. The average intake of vitamin E and niacin exceeded 100% of DRI, and the intakes of vitamin B1 and B2, magnesium, and iron were between 80% and 90% of DRI range. However, the following nutrients did not meet the DRI requirements at all: vitamins A, B6 and C, folic acid, calcium, and zinc. Although growth was satisfactory in the vast majority of these children with autistic disorder, this study revealed serious deficiencies in the intakes of several vitamins and essential nutrients. [ABSTRACT FROM AUTHOR]

Abstract: To determine whether iptakalim inhibited endothelin-1(ET-1)-induced proliferation of human pulmonary arterial smooth muscle cells (PASMCs) through the activation of ATP-sensitive potassium (KATP) channel, the effect of iptakalim on the ET-1-induced proliferation of human PASMCs was examined by [3H]thymidine incorporation, staining with propidium iodide and flow cytometry analyses, measurement of cytosolic free Ca2+ concentration ([Ca2+]cyt) and Western blot for the phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in vitro. The results showed that iptakalim inhibited the ET-1-induced proliferation of human PASMCs, including [3H]thymidine incorporation and the transition of cell cycle phase, and blocked the ET-1-induced transient raise of [Ca2+]cyt, and the ET-1-induced phosphorylation of ERK1/2 in the human PASMCs. Iptakalim exerted a similar role as pinacidil did in human PASMCs and both inhibited the [3H] thymidine incorporation and the transition of cell cycle phase induced by ET-1 in the human PASMCs. Furthermore, we found that the inhibition of iptakalim and pinacidil on the ET-1-induced proliferation of human PASMCs was blocked by glyburide, a selective KATP channel antagonist. These findings provide a strong evidence to support that iptakalim acts as a specific KATP channel opener to antagonize the proliferating effect of ET-1 in the human PASMCs. This study provides further evidence that iptakalim may serve as another candidate drug to treat pulmonary hypertension. [Copyright &y& Elsevier]