Communication as power : the relationship to marital satisfaction

This study focused on communication as a form of power and its impact on marital satisfaction. Specifically, females may appear to have more power because they speak more often in conversations. However, when dissected, the amount women speak may be a result of lower power status, requiring them to work harder to achieve their desired level of power in the relationship. Successful talkovers, unsuccessful talkovers, support statements, and nonsupport statements were examined to determine their impact on couples\u27 marital satisfaction. Secondary data was utilized for the current study; the original study pertained to the investigation of the relationship between physiological arousal and demand/withdraw patterns. Seventy-three married couples (73 men and 73 women) were recruited for the original study via newspaper advertisements, advertisements posted on bulletin boards, and word-of-mouth in the local schools and community. Paired t-tests and simple linear regression analyses revealed that males\u27 and females\u27 unsuccessful talkover ratios and nonsupport statement ratios were significantly different. In addition, successful talkovers, unsuccessful talkovers, support statements, and nonsupport statements were not found to significantly influence males\u27 or females\u27 marital satisfaction. Relevance to family therapy and clinical implications are discussed

Gestational and Chronic Low-Dose PFOA Exposures and Mammary Gland Growth and Differentiation in Three Generations of CD-1 Mice

Background: Prenatal exposure to perfluorooctanoic acid (PFOA), a ubiquitous industrial surfactant, has been reported to delay mammary gland development in female mouse offspring (F1) and the treated lactating dam (P0) after gestational treatments at 3 and 5 mg PFOA/kg/day

White adipose remodeling during browning in mice involves YBX1 to drive thermogenic commitment

Objective: Increasing adaptive thermogenesis by stimulating browning in white adipose tissue is a promising method of improving metabolic health. However, the molecular mechanisms underlying this transition remain elusive. Our study examined the molecular determinants driving the differentiation of precursor cells into thermogenic adipocytes. Methods: In this study, we conducted temporal high-resolution proteomic analysis of subcutaneous white adipose tissue (scWAT) after cold exposure in mice. This was followed by loss- and gain-of-function experiments using siRNA-mediated knockdown and CRISPRa-mediated induction of gene expression, respectively, to evaluate the function of the transcriptional regulator Y box-binding protein 1 (YBX1) during adipogenesis of brown pre-adipocytes and mesenchymal stem cells. Transcriptomic analysis of mesenchymal stem cells following induction of endogenous Ybx1 expression was conducted to elucidate transcriptomic events controlled by YBX1 during adipogenesis. Results: Our proteomics analysis uncovered 509 proteins differentially regulated by cold in a time-dependent manner. Overall, 44 transcriptional regulators were acutely upregulated following cold exposure, among which included the cold-shock domain containing protein YBX1, peaking after 24 h. Cold-induced upregulation of YBX1 also occurred in brown adipose tissue, but not in visceral white adipose tissue, suggesting a role of YBX1 in thermogenesis. This role was confirmed by Ybx1 knockdown in brown and brite preadipocytes, which significantly impaired their thermogenic potential. Conversely, inducing Ybx1 expression in mesenchymal stem cells during adipogenesis promoted browning concurrent with an increased expression of thermogenic markers and enhanced mitochondrial respiration. At a molecular level, our transcriptomic analysis showed that YBX1 regulates a subset of genes, including the histone H3K9 demethylase Jmjd1c, to promote thermogenic adipocyte differentiation. Conclusion: Our study mapped the dynamic proteomic changes of murine scWAT during browning and identified YBX1 as a novel factor coordinating the genomic mechanisms by which preadipocytes commit to brite/beige lineage

Global mismatches in aboveground and belowground biodiversity

Human activities are accelerating global biodiversity change and have resulted in severely threatened ecosystem services. A large proportion of terrestrial biodiversity is harbored by soil, but soil biodiversity has been omitted from many global biodiversity assessments and conservation actions, and understanding of global patterns of soil biodiversity remains limited. In particular, the extent to which hotspots and coldspots of aboveground and soil biodiversity overlap is not clear. We examined global patterns of these overlaps by mapping indices of aboveground (mammals, birds, amphibians, vascular plants) and soil (bacteria, fungi, macrofauna) biodiversity that we created using previously published data on species richness. Areas of mismatch between aboveground and soil biodiversity covered 27% of Earth's terrestrial surface. The temperate broadleaf and mixed forests biome had the highest proportion of grid cells with high aboveground biodiversity but low soil biodiversity, whereas the boreal and tundra biomes had intermediate soil biodiversity but low aboveground biodiversity. While more data on soil biodiversity are needed, both to cover geographic gaps and to include additional taxa, our results suggest that protecting aboveground biodiversity may not sufficiently reduce threats to soil biodiversity. Given the functional importance of soil biodiversity and the role of soils in human well-being, soil biodiversity should be considered further in policy agendas and conservation actions by adapting management practices to sustain soil biodiversity and considering soil biodiversity when designing protected areas.Peer reviewe

Effects of perfluorooctanoic acid on mouse mammary gland development and differentiation resulting from cross-foster and restricted gestational exposures

The adverse consequences of developmental exposures to perfluorooctanoic acid (PFOA) are established in mice, and include impaired development of the mammary gland (MG). However, the relationships between timing or route of exposure, and consequences in the MG have not been characterized. To address the effects of these variables on the onset and persistence of MG effects in female offspring, timed pregnant CD-1 dams received PFOA by oral gavage over various gestational durations. Cross-fostering studies identified the 5 mg/kg dose, under either lactational- or intrauterine-only exposures, to delay MG development as early as postnatal day (PND) 1, persisting beyond PND 63. Intrauterine exposure during the final days of pregnancy caused adverse MG developmental effects similar to that of extended gestational exposures. These studies confirm a window of MG sensitivity in late fetal and early neonatal life, and demonstrate developmental PFOA exposure results in early and persistent MG effects, suggesting permanent consequences

Histopathologic changes in the uterus, cervix and vagina of immature CD-1 mice exposed to low doses of perfluorooctanoic acid (PFOA) in a uterotrophic assay

The estrogenic and antiestrogenic potential of perfluorooctanoic acid (PFOA) was assessed using an immature mouse uterotrophic assay and by histologic evaluation of the uterus, cervix and vagina following treatment. Female offspring of CD-1 dams were weaned at 18 days old and assigned to groups of equal weight, and received 0, 0.01, 0.1, or 1 mg PFOA/kg BW/d by gavage with or without 17-β estradiol (E2, 500 μg/kg/d) from PND18-20 (n=8/treatment/block). At 24 hr after the third dose (PND 21), uteri were removed and weighed. Absolute and relative uterine weights were significantly increased in the 0.01 mg/kg PFOA only group. Characteristic estrogenic changes were present in all E2-treated mice; however, they were minimally visible in the 0.01 PFOA only mice. These data suggest that at a low dose PFOA produces minimal histopathologic changes in the reproductive tract of immature female mice, and does not antagonize the cellular effects of E2

Analysis of PFOA in dosed CD-1 mice. Part 2: Disposition of PFOA in tissues and fluids from pregnant and lactating mice and their pups

Previous studies in mice with multiple gestational exposures to perfluorooctanoic acid (PFOA) demonstrate numerous dose dependent growth and developmental effects which appeared to worsen if offspring exposed in utero nursed from PFOA-exposed dams. To evaluate the disposition of PFOA in the pregnant and lactating dam and her offspring, time-pregnant CD-1 mice received a single 0, 0.1, 1, or 5 mg PFOA/kg BW dose (n = 25/dose group) by gavage on gestation day 17. Maternal and pup fluids and tissues were collected over time. Pups exhibited significantly higher serum PFOA concentrations than their respective dams, and their body burden increased after birth until at least postnatal day 8, regardless of dose. The distribution of milk:serum PFOA varied by dose and time, but was typically in excess of 0.20. These data suggest that milk is a substantial PFOA exposure route in mice and should be considered in risk assessment modeling designs for this compound