This study evaluated The Transporters, an animated series designed to enhance emotion comprehension in children with autism spectrum conditions (ASC). n = 20 children with ASC (aged 4-7) watched The Transporters everyday for 4 weeks. Participants were tested before and after intervention on emotional vocabulary and emotion recognition at three levels of generalization. Two matched control groups of children (ASC group, n = 18 and typically developing group, n = 18) were also assessed twice without any intervention. The intervention group improved significantly more than the clinical control group on all task levels, performing comparably to typical controls at Time 2. We conclude that using The Transporters significantly improves emotion recognition in children with ASC. Future research should evaluate the series' effectiveness with lower-functioning individuals.

The G protein-coupled receptor GPR54 (AXOR12, OT7T175) is central to acquisition of reproductive competency in mammals. Peptide ligands (kisspeptins) for this receptor are encoded by the Kiss1 gene, and administration of exogenous kisspeptins stimulates hypothalamic gonadotropin-releasing hormone (GnRH) release in several species, including humans. To establish that kisspeptins are the authentic agonists of GPR54 in vivo and to determine whether these ligands have additional physiological functions we have generated mice with a targeted disruption of the Kiss1 gene. Kiss1-null mice are viable and healthy with no apparent abnormalities but fail to undergo sexual maturation. Mutant female mice do not progress through the estrous cycle, have thread-like uteri and small ovaries, and do not produce mature Graffian follicles. Mutant males have small testes, and spermatogenesis arrests mainly at the early haploid spermatid stage. Both sexes have low circulating gonadotropin (luteinizing hormone and follicle-stimulating hormone) and sex steroid (␤-estradiol or testosterone) hormone levels. Migration of GnRH neurons into the hypothalamus appears normal with appropriate axonal connections to the median eminence and total GnRH content. The hypothalamicpituitary axis is functional in these mice as shown by robust luteinizing hormone secretion after peripheral administration of kisspeptin. The virtually identical phenotype of Gpr54-and Kiss1-null mice provides direct proof that kisspeptins are the true physiological ligand for the GPR54 receptor in vivo. Kiss1 also does not seem to play a vital role in any other physiological processes other than activation of the hypothalamic-pituitary-gonadal axis, and loss of Kiss1 cannot be overcome by compensatory mechanisms.Gpr54 ͉ kisspeptin ͉ mouse ͉ puberty N euroendocrine events within the hypothalamus control sexual maturation and seasonal breeding in mammals (1). The gonadotropin-releasing hormone (GnRH)-induced secretion of the gonadotropic hormones luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary is essential to invoke puberty and maintain reproductive function. The G protein-coupled receptor GPR54 (2) is a key protein involved in the pubertal activation of the hypothalamic pituitary gonadal axis because mice and humans with mutations in this receptor are sterile with hypogonadotropic hypogonadism (3-7).A series of overlapping peptide ligands (kisspeptins) for the GPR54 receptor are produced by the Kiss1 gene (8-10). Kiss1 mRNA is expressed in hypothalamic regions that regulate gonadotropin secretion including the anteroventral periventricular nucleus (AVPV), the periventricular nucleus, and the arcuate nucleus (ARC) (11). Kiss1 expression increases at puberty in rodents (12-14) and primates (15) and fluctuates during the rat estrous cycle (12,16). Kiss1 expression is also subject to differential regulation by sex steroids, providing a plausible mechanism for the feedback control of gonadotropin secretion by these hormones (17, 18). Ad...

Vascular endothelial growth factor (VEGF) is a potent secreted factor that promotes angiogenesis and maintains the integrity of the endothelium. Levels of VEGF are increased in many tumors and are elevated in women with pre-eclampsia, a serious disease of pregnancy. Here we show by in situ hybridization that the trophoblast contains the mRNA encoding a soluble version of the VEGF receptor known as Flt-1 (sFlt-1: initially described by Kendall and Thomas, PNAS 90:10705-10709). Binding assays and Western blotting of villus-conditioned media confirmed the production of sFlt-1. Serum from pregnant women was found to contain a VEGF-binding protein that was not present in serum from men or nonpregnant women. As determined by heparin affinity, column fractionation, and cross-linking, this protein was identical to sFlt-1. Taken together, these results show that the placenta secretes sFlt-1, which would be expected to be a VEGF antagonist. This is the first report of production of the sFlt-1 receptor in vivo, and it reveals a new mechanism for naturally regulating this potent angiogenic agent. The presence of such an antagonist suggests that regulation of VEGF action is essential to successful pregnancy. This has important implications for the activity of VEGF locally and systemically in other conditions.