309 research outputs found

    Socio-ecological Predictors of Social Connection Among Older Adults

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    Decades of research has established an unequivocal link between states of social connection and health status. Lack of social connection, whether construed as social isolation or loneliness, negatively influences health and is highly associated with cardiovascular disease, high blood pressure, fall risk, and premature death. Despite extensive research on social isolation and loneliness, evidence relative to the broader construct of social connection suffers. Few studies inform practice standards for community-based organizations. This study aimed to develop a multidimensional, continuous composite variable of social connection and use the composite variable to examine predictors with a socio-ecological lens. A secondary data analysis was conducted with a sample of 12,116 older adults. The regression results showed that trauma, transition, and loss predicted lower social connection scores with greater strength than any of the other variables. Perceived barriers to access, housing type, and supportive services enrollment significantly predicted social connection, yet were overshadowed by the power of disruptive life events to negatively influence social connection. Additionally, the creation of a two-dimensional social connection measure underscored the criticality of subjective experiences of social connection. In this study, positive social connection scores were highest among the oldest. Missingness in the data rendered it impossible to validly include race or ethnicity, leaving important questions about health equity and racial equity unanswered. Findings can inform data collection, intake and screening processes, referral pathways, student and provider training, early identification, and strategic alliances between community-based service providers and adult protective services and victim assistance services

    Prostaglandin E2 Regulates AMPA Receptor Phosphorylation and Promotes Membrane Insertion in Preoptic Area Neurons and Glia during Sexual Differentiation

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    Sexual differentiation of the rodent brain is dependent upon the organizing actions of the steroid hormone, estradiol. In the preoptic area, a brain region critical for the expression of adult reproductive behavior, there are twice as many dendritic spine synapses per unit length on newborn male neurons compared to female neurons and this sex difference correlates with the expression of adult male copulatory behavior. The sex difference in the POA is achieved via estradiol's upregulation of the membrane-derived lipid signaling molecule prostaglandin E2 (PGE2); PGE2 is necessary and sufficient to masculinize both dendritic spine density and adult sexual behavior in rats. We have previously shown that PGE2 activates EP2 and EP4 receptors which increases protein kinase A (PKA) activity and that masculinized dendritic spine density and sex behavior are both dependent upon PKA as well as activation of AMPA type glutamate receptors. In the current experiments, we build upon this signaling cascade by determining that PGE2 induces phosphorylation of the AMPA receptor subunit, GluR1, which leads to increased AMPA receptor insertion at the membrane. Treating female pups on the day of birth with PGE2 induced the phosphorylation of GluR1 at the PKA-sensitive site within 2 hours of treatment, an effect that was blocked by co-administration of the PKA/AKAP inhibitor, HT31 with PGE2. Brief treatment of mixed neuronal/glial POA cultures with PGE2 or the cAMP/PKA stimulator, forskolin, increased membrane associated GluR1 in both neurons and glia. We speculate that PGE2 induced increases in AMPA receptor associated with the membrane underlies our previously observed increase in dendritic spine density and is a critical component in the masculinization of rodent sex behavior

    Sliding wear analysis of cobalt based alloys in nuclear reactor conditions

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    The study of the wear behaviour of cobalt based alloys in nuclear reactor environmental conditions is the focus of this work. The alloys are used in components within reactors due to their excellent wear and corrosion resistance and their high hardness in the high pressure and temperature water facing environment. In the nuclear reactor core, cobalt is irradiated producing a highly penetrative gamma emitting isotope, cobalt 60 from stable cobalt 59. Wear of the cobalt alloys, producing wear debris, exacerbates this problem as it may be transported and deposited at various locations throughout the primary loop increasing the potential of radiation exposure. Removing this problem will require the removal of cobalt from the system. In order for suitable replacement materials to be identified, a better understanding of the behaviour of these alloys in the prototypical working conditions must be obtained. This work focuses on two cobalt based alloys used in the ball and race components of rolling element bearings in the reactor core, Stellite 20 and Haynes 25, respectively. The sliding wear behaviour of the alloys in an environment designed to replicate reactor conditions is examined using a bespoke pin on disc tribometer. Wear measurement and microstructural and compositional analysis of the samples tested over a range of conditions are presented and discussed. Concurrent to the experimental work is the development of a wear prediction model using a semi analytical method. The model employs Archard’s wear law as the method of predicting wear using data obtained through experimentation. The accuracy of the semi analytical model is limited however it does give a good estimation for maximum wear depth of the test specimens

    Prostaglandins, masculinization and its disorders:effects of fetal exposure of the rat to the cyclooxygenase inhibitor- indomethacin

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    Recent studies have established that masculinization of the male reproductive tract is programmed by androgens in a critical fetal β€˜masculinization programming window’ (MPW). What is peculiar to androgen action during this period is, however, unknown. Studies from 20 years ago in mice implicated prostaglandin (PG)-mediation of androgen-induced masculinization, but this has never been followed up. We therefore investigated if PGs might mediate androgen effects in the MPW by exposing pregnant rats to indomethacin (which blocks PG production by inhibiting cyclooxygenase activity) during this period and then examining if androgen production or action (masculinization) was affected. Pregnant rats were treated with indomethacin (0.8 mg/kg/day; e15.5–e18.5) to encompass the MPW. Indomethacin exposure decreased fetal bodyweight (e21.5), testis weight (e21.5) and testicular PGE2 (e17.5, e21.5), but had no effect on intratesticular testosterone (ITT; e17.5) or anogenital index (AGI; e21.5). Postnatally, AGI, testis weight and blood testosterone were unaffected by indomethacin exposure and no cryptorchidism or hypospadias occurred. Penis length was normal in indomethacin-exposed animals at Pnd25 but was reduced by 26% (p<0.001) in adulthood, an effect that is unexplained. Our results demonstrate that indomethacin can effectively decrease intra-testicular PGE2 level. However, the resulting male phenotype does not support a role for PGs in mediating androgen-induced masculinization during the MPW in rats. The contrast with previous mouse studies is unexplained but may reflect a species difference

    Male-like sexual behavior of female mouse lacking fucose mutarotase

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    <p>Abstract</p> <p>Background</p> <p>Mutarotases are recently characterized family of enzymes that are involved in the anomeric conversions of monosaccharides. The mammalian fucose mutarotase (FucM) was reported in cultured cells to facilitate fucose utilization and incorporation into protein by glycosylation. However, the role of this enzyme in animal has not been elucidated.</p> <p>Results</p> <p>We generated a mutant mouse specifically lacking the fucose mutarotase (FucM) gene. The <it>FucM </it>knockout mice displayed an abnormal sexual receptivity with a drastic reduction in lordosis score, although the animals were fertile due to a rare and forced intromission by a typical male. We examined the anteroventral periventricular nucleus (AVPv) of the preoptic region in brain and found that the mutant females showed a reduction in tyrosine hydoxylase positive neurons compared to that of a normal female. Furthermore, the mutant females exhibited a masculine behavior, such as mounting to a normal female partner as well as showing a preference to female urine. We found a reduction of fucosylated serum alpha-fetoprotein (AFP) in a mutant embryo relative to that of a wild-type embryo.</p> <p>Conclusions</p> <p>The observation that <it>FucM</it><sup>-/- </sup>female mouse exhibits a phenotypic similarity to a wild-type male in terms of its sexual behavior appears to be due to the neurodevelopmental changes in preoptic area of mutant brain resembling a wild-type male. Since the previous studies indicate that AFP plays a role in titrating estradiol that are required to consolidate sexual preference of female mice, we speculate that the reduced level of AFP in <it>FucM</it><sup>-/- </sup>mouse, presumably resulting from the reduced fucosylation, is responsible for the male-like sexual behavior observed in the FucM knock-out mouse.</p

    Dopaminergic Activation of Estrogen Receptors Induces Fos Expression within Restricted Regions of the Neonatal Female Rat Brain

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    Steroid receptor activation in the developing brain influences a variety of cellular processes that endure into adulthood, altering both behavior and physiology. Recent data suggests that dopamine can regulate expression of progestin receptors within restricted regions of the developing rat brain by activating estrogen receptors in a ligand-independent manner. It is unclear whether changes in neuronal activity induced by dopaminergic activation of estrogen receptors are also region specific. To investigate this question, we examined where the dopamine D1-like receptor agonist, SKF 38393, altered Fos expression via estrogen receptor activation. We report that dopamine D1-like receptor agonist treatment increased Fos protein expression within many regions of the developing female rat brain. More importantly, prior treatment with an estrogen receptor antagonist partially reduced D1-like receptor agonist-induced Fos expression only within the bed nucleus of the stria terminalis and the central amygdala. These data suggest that dopaminergic activation of estrogen receptors alters neuronal activity within restricted regions of the developing rat brain. This implies that ligand-independent activation of estrogen receptors by dopamine might organize a unique set of behaviors during brain development in contrast to the more wide spread ligand activation of estrogen receptors by estrogen
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