Toddlers' impulsivity, inhibitory control, and maternal eating-related supervision in relation to toddler body mass index: Direct and interactive effects.

Previous studies have noted that child temperament characteristics, such as aspects of self-regulation, as well as parental feeding practices contribute to children's body mass index (BMI), and have implications for identifying children who may be at risk of being overweight or obese. While studies have considered children's temperament or maternal feeding practices separately, few have considered these correlates of children's BMI jointly or in interaction in relation to children's BMI. The current study included 179 mother-child dyads participating in a longitudinal study.

Maternal executive functioning as a mechanism in the intergenerational transmission of parenting: Preliminary evidence.

Multiple lines of inquiry, including experimental animal models, have recently converged to suggest that executive functioning (EF) may be one mechanism by which parenting behavior is transmitted across generations. In the current investigation, we empirically test this notion by examining relations between maternal EF and parenting behaviors during mother-infant interactions, and by examining the role of maternal EF in the intergenerational transmission of parenting behavior. Mother-infant dyads (N = 150) in a longitudinal study participated.

Clinical and genetic findings in Hungarian patients with X-linked juvenile retinoschisis.

Purpose: To determine clinical phenotypes, examine the age dependency of X-linked juvenile retinoschisis (XLRS), and identify mutations in the retinoschisis1 gene (RS1) in 13 Hungarian (Caucasian) families with this disease.

Methods: This study included 72 members in 13 families. Complete ophthalmological examinations, including optical coherence tomography (OCT) and full-field and multifocal electroretinography (ERG), were performed on 20 affected males, 13 female carriers, and 27 healthy controls.

Truncation of retinoschisin protein associated with a novel splice site mutation in the RS1 gene.

Purpose: To present the ocular findings of a Hungarian family with X-linked juvenile retinoschisis (XLRS) and to reveal a novel putative splice mutation leading to serious truncation of retinoschisin (RS1) protein. Our genetic results were compared to a mouse model of XLRS.

Methods: Complete ophthalmic examinations were performed on five members (two male patients, two female carriers, and one healthy fraternal male twin) of the family.

Epidermal growth factor receptor (EGFR) high gene copy number and activating mutations in lung adenocarcinomas are not consistently accompanied by positivity for EGFR protein by standard immunohistochemistry.

The purpose of this study was to investigate whether detectable protein biomarker overexpression is a prerequisite for the presence of increased gene copy number or activating mutations and responsiveness to the epidermal growth factor receptor (EGFR) inhibitors gefitinib and erlotinib in patients with lung adenocarcinomas. EGFR status was prospectively analyzed in tumor biopsy samples by three methods: protein expression (n = 117) by standardized immunohistochemistry (IHC), gene copy number (n = 97) by fluorescent in situ hybridization (FISH), and mutation analysis by sequencing (n = 126). Fifty-nine percent of the samples were positive by IHC, 40% were positive by FISH, and 13.

[Epidermal growth factor receptor (EGFR): therapeutic target in the treatment of lung adenocarcinoma].

Revolution in biotechnology made possible to identify those gene errors, which via their encoded proteins (mostly kinase enzymes) are key players in tumor development, growth and progression, and could be considered as molecular targets in tumor diagnosis and therapy. Activity of EGFR (epidermal growth factor receptor), an outstanding representative of the regulatory cell surface receptors, can be inhibited by drugs proved for clinical use. In the past year many groups observed that those lung adenocarcinoma cells, which contain activating mutation in the tyrosine kinase domain of EGFR show remarkable sensitivity to anti-EGFR compounds.