Animal models for aberrations of gonadotropin action

During the last two decades a large number of genetically modified mouse lines with altered gonadotropin action have been generated. These mouse lines fall into three categories: the lack-of-function mice, gain-of-function mice, and the mice generated by breeding the abovementioned lines with other disease model lines. The mouse strains lacking gonadotropin action have elucidated the necessity of the pituitary hormones in pubertal development and function of gonads, and revealed the processes from the original genetic defect to the pathological phenotype such as hypo- or hypergonadotropic hypogonadism. Conversely, the strains of the second group depict consequences of chronic gonadotropin action. The lines vary from those expressing constitutively active receptors and those secreting follicle-stimulating hormone (FSH) with slowly increasing amounts to those producing human choriogonadotropin (hCG), amount of which corresponds to 2000-fold luteinizing hormone (LH)/hCG biological activity. Accordingly, the phenotypes diverge from mild anomalies and enhanced fertility to disrupted gametogenesis, but eventually chronic, enhanced and non-pulsatile action of both FSH and LH leads to female and male infertility and/or hyper- and neoplasias in most of the gonadotropin gain-of-function mice. Elevated gonadotropin levels also alter the function of several extra-gonadal tissues either directly or indirectly via increased sex steroid production. These effects include promotion of tumorigenesis in tissues such as the pituitary, mammary and adrenal glands. Finally, the crossbreedings of the current mouse strains with other disease models are likely to uncover the contribution of gonadotropins in novel biological systems, as exemplified by the recent crossbreed of LHCG receptor deficient mice with Alzheimer disease mice

A multilevel approach to understanding the determinants of maternal harsh parenting: the importance of maternal age and perceived partner support

Determinants of parenting are most often considered using one child per family within a cross-sectional design. In 182 families, the current study included two siblings and sought to predict maternal harsh parenting measured prospectively when each child was age 2 years from child gender, infant temperament, maternal age, maternal educational attainment, maternal depression and anxiety and maternal perceptions of partner support. Multilevel modeling was used to examine between- and within-family variance simultaneously. Mothers reported levels of harsh parenting that were similar towards both children (intraclass correlation = 0.69). Thus, the majority of variance in maternal perceptions of their harsh parenting resided between rather than within families and was accounted for in part by maternal age and maternal perceptions of partner support. Results are discussed in relation to family-wide determinants of harsh parenting, previous literature pertaining to parenting siblings and the potential avenues for future research and practice