Trajectories of Change in Parent-Child Interaction Therapy Outcomes in Latinx Families: Implications for Cultural Adaptation.

Objective: Parent-Child Interaction Therapy (PCIT) is a parenting program in which caregivers must achieve "skill criteria" in using and avoiding to complete treatment. Despite PCIT's emphasis on these skills, little is known about how Latinx caregivers acquire these Western-based parenting practices and whether cultural mismatches lead to inequities in outcomes. This study compared the trajectories of change in PCIT skills and treatment outcomes of Latinx and non-Latinx White families.

Exploration of the MCMC Wald test with linear regression.

Recently, Asparouhov and Muthén Structural Equation Modeling: A Multidisciplinary Journal, 28, 1-14, (2021a, 2021b) proposed a variant of the Wald test that uses Markov chain Monte Carlo machinery to generate a chi-square test statistic for frequentist inference. Because the test's composition does not rely on analytic expressions for sampling variation and covariation, it potentially provides a way to get honest significance tests in cases where the likelihood-based test statistic's assumptions break down (e.g.

A simple Monte Carlo method for estimating power in multilevel designs.

Estimating power for multilevel models is complex because there are many moving parts, several sources of variation to consider, and unique sample sizes at Level 1 and Level 2. Monte Carlo computer simulation is a flexible tool that has received considerable attention in the literature. However, much of the work to date has focused on very simple models with one predictor at each level and one cross-level interaction effect, and approaches that do not share this limitation require users to specify a large set of population parameters.

Autoshortloop feedback regulation of pulsatile gonadotropin-releasing hormone (GnRH) secretion by its metabolite, GnRH-(1-5).

Given the central role of the decapeptide gonadotropin-releasing hormone (GnRH) in reproductive function, our long-term objective is to delineate the underlying mechanism regulating these reproductive processes. The outcome of GnRH secretion is in part dependent on the proteolytic metabolism of this decapeptide. In contrast to the belief that the metabolism of GnRH serves only as a degradative process that removes excess GnRH, we have shown that a metabolite of the decapeptide, GnRH-(1-5), can directly regulate GnRH gene expression and reproductive behavior.

Hypothalamic molecular changes underlying natural reproductive senescence in the female rat.

The role of the hypothalamus in female reproductive senescence is unclear. Here we identified novel molecular neuroendocrine changes during the natural progression from regular reproductive cycles to acyclicity in middle-aged female rats, comparable with the perimenopausal progression in women. Expression of 48 neuroendocrine genes was quantified within three hypothalamic regions: the anteroventral periventricular nucleus, the site of steroid positive feedback onto GnRH neurons; the arcuate nucleus (ARC), the site of negative feedback and pulsatile GnRH release; and the median eminence (ME), the site of GnRH secretion.

Disruption of reproductive aging in female and male rats by gestational exposure to estrogenic endocrine disruptors.

Polychlorinated biphenyls (PCBs) are industrial contaminants and known endocrine-disrupting chemicals. Previous work has shown that gestational exposure to PCBs cause changes in reproductive neuroendocrine processes. Here we extended work farther down the life spectrum and tested the hypothesis that early life exposure to Aroclor 1221 (A1221), a mixture of primarily estrogenic PCBs, results in sexually dimorphic aging-associated alterations to reproductive parameters in rats, and gene expression changes in hypothalamic nuclei that regulate reproductive function.

Endocrine disruption of brain sexual differentiation by developmental PCB exposure.

In mammals, sexual differentiation of the hypothalamus occurs during prenatal and early postnatal development due in large part to sex differences in hormones. These early organizational processes are critically important for the attainment and maintenance of adult reproductive functions. We tested the hypothesis that perinatal exposure to polychlorinated biphenyls (PCBs) that disrupt hormonal pathways would perturb reproductive maturation and the sexually dimorphic development of neuroendocrine systems in the preoptic area (POA).

Pulsatile gonadotropin-releasing hormone release from hypothalamic explants of male marmoset monkeys compared with male rats.

The present study was conducted to quantify in vitro gonadotropin-releasing hormone (GnRH) release parameters in the male marmoset. We established primary cultures of marmoset hypothalamic tissues for approximately 2 days (marmosets) to assess GnRH release profiles in vitro in hypothalamic explants from testis-intact and gonadectomized males. Pulsatile GnRH release profiles were readily demonstrated from in vitro hypothalamic explants isolated from adult male marmoset monkeys.

Cell death mechanisms in GT1-7 GnRH cells exposed to polychlorinated biphenyls PCB74, PCB118, and PCB153.

Exposure to endocrine disrupting chemicals (EDCs) such as polychlorinated biphenyls (PCBs) causes functional deficits in neuroendocrine systems. We used an immortalized hypothalamic GT1-7 cell line, which synthesizes the neuroendocrine peptide gonadotropin-releasing hormone (GnRH), to examine the neurotoxic and endocrine disrupting effects of PCBs and their mechanisms of action. Cells were treated for 1, 4, 8, or 24 h with a range of doses of a representative PCB from each of three classes: coplanar (2,4,4',5-tetrachlorobiphenyl: PCB74), dioxin-like coplanar (2',3,4,4',5' pentachlorobiphenyl: PCB118), non-coplanar (2,2',4,4',5,5'-hexachlorobiphenyl: PCB153), or their combination.

Effects of perinatal polychlorinated biphenyls on adult female rat reproduction: development, reproductive physiology, and second generational effects.

Perinatal exposures to endocrine-disrupting chemicals, such as polychlorinated biphenyls (PCBs), can cause latent effects on reproductive function. Here, we tested whether PCBs administered during late pregnancy would compromise reproductive physiology in both the fetally exposed female offspring (F1 generation), as well as in their female offspring (F2 generation). Pregnant Sprague-Dawley rats were treated with the PCB mixture, Aroclor 1221 (A1221; 0, 0.

NMDA receptor subunit NR2b: effects on LH release and GnRH gene expression in young and middle-aged female rats, with modulation by estradiol.

Background/aims: The loss of reproductive capacity during aging involves changes in the neural regulation of the hypothalamic gonadotropin-releasing hormone (GnRH) neurons controlling reproduction. This neuronal circuitry includes glutamate receptors on GnRH neurons. Previously, we reported an increase in the expression of the NR2b subunit protein of the NMDA receptor on GnRH neurons in middle-aged compared to young female rats.

LHRH-(1-5): a bioactive peptide regulating reproduction.

Luteinizing hormone-releasing hormone-I (LHRH-I) was isolated from the mammalian hypothalamus and shown to be the primary regulator of reproduction through its initiation of pituitary gonadotropin release. Subsequently, it has also been shown to have non-pituitary actions. Although the regulation of LHRH-I synthesis and release has been extensively studied, there is additional evidence to suggest that processing of the peptide represents another layer of regulation.

Short-term hormone release from adult female rat hypothalamic and pituitary explants is not altered by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

2, 3, 7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has adverse effects on reproduction, in part due to direct actions at the ovary. It is unclear whether effects are further mediated by glands that regulate ovarian function. We investigated whether effects of TCDD are mediated via the hypothalamic-pituitary axis.

Dissecting autocrine effects on pulsatile release of gonadotropin-releasing hormone in cultured rat hypothalamic tissue.

The control of reproductive function is manifested centrally through the control of hypothalamic release of gonadotropin-releasing hormone (GnRH) in episodic events or pulses. For GnRH release to occur in pulses, GnRH neurons must coordinate release events periodically to elicit a bolus of GnRH. We used a perifusion culture system to examine the release of GnRH from both intact hypothalami and enzymatically dispersed hypothalamic cells after challenge with GnRH analogs to evaluate the role of anatomical neuronal connections on autocrine/paracrine signals by GnRH on GnRH neurons.

Aging-related changes in release of growth hormone and luteinizing hormone in female rhesus monkeys.

A decline in somatic function with aging in women is associated with a decrease in GH release and a loss of estrogen after menopause. As an initial step to establish a monkey model for the neuroendocrine mechanisms underlying somatopause and menopause, we have conducted three experiments in unrestrained aged (approximately 25.7-yr-old) and young (approximately 5.