Live Tissue Imaging Shows Reef Corals Elevate pH under Their Calcifying Tissue Relative to Seawater

The threat posed to coral reefs by changes in seawater pH and carbonate chemistry (ocean acidification) raises the need for a better mechanistic understanding of physiological processes linked to coral calcification. Current models of coral calcification argue that corals elevate extracellular pH under their calcifying tissue relative to seawater to promote skeleton formation, but pH measurements taken from the calcifying tissue of living, intact corals have not been achieved to date. We performed live tissue imaging of the reef coral Stylophora pistillata to determine extracellular pH under the calcifying tissue and intracellular pH in calicoblastic cells. We worked with actively calcifying corals under flowing seawater and show that extracellular pH (pHe) under the calicoblastic epithelium is elevated by ∼0.5 and ∼0.2 pH units relative to the surrounding seawater in light and dark conditions respectively. By contrast, the intracellular pH (pHi) of the calicoblastic epithelium remains stable in the light and dark. Estimates of aragonite saturation states derived from our data indicate the elevation in subcalicoblastic pHe favour calcification and may thus be a critical step in the calcification process. However, the observed close association of the calicoblastic epithelium with the underlying crystals suggests that the calicoblastic cells influence the growth of the coral skeleton by other processes in addition to pHe modification. The procedure used in the current study provides a novel, tangible approach for future investigations into these processes and the impact of environmental change on the cellular mechanisms underpinning coral calcification

Effect of Testosterone on Insulin Stimulated IRS1 Ser Phosphorylation in Primary Rat Myotubes—A Potential Model for PCOS-Related Insulin Resistance

Polycystic ovary syndrome (PCOS) is characterized by a hyperandrogenic state and frequently develops skeletal muscle insulin resistance. We determined whether testosterone adversely affects insulin action by increasing serine phosphorylation of IRS-1(636/639) in differentiated rat skeletal muscle myotubes. The phosphorylation of Akt, mTOR, and S6K, downstream targets of the PI3-kinase-IRS-1 complex were also studied.Primary differentiated rat skeletal muscle myotubes were subjected to insulin for 30 min after 16-hour pre-exposure to either low (20 ng/ml) or high (200 ng/ml) doses of testosterone. Protein phosphorylation of IRS-1 Ser(636/639), Akt Ser(473), mTOR-Ser(2448), and S6K-Thr(389) were measured by Western blot with signal intensity measured by immunofluorescence.Cells exposed to 100 nM of insulin had increased IRS-1 Ser(636/639) and Akt Ser(473) phosphorylation. Cells pre-exposed to low-dose testosterone had significantly increased insulin-induced mTOR-Ser(2448) and S6K-Thr(389) phosphorylation (p<0.05), and further increased insulin-induced IRS-1 Ser(636/639) phosphorylation (p = 0.042) compared to control cells. High-dose testosterone pre-exposure attenuated the insulin-induced mTOR-Ser(2448) and S6K-Thr(389) phosphorylation.The data demonstrated an interaction between testosterone and insulin on phosphorylation of intracellular signaling proteins, and suggests a link between a hyperandrogenic, hyperinsulinemic environment and the development of insulin resistance involving serine phosphorylation of IRS-1 Ser(636/639). These results may guide further investigations of potential mechanisms of PCOS-related insulin resistance

Regulation of MicroRNA Biogenesis: A miRiad of mechanisms

microRNAs are small, non-coding RNAs that influence diverse biological functions through the repression of target genes during normal development and pathological responses. Widespread use of microRNA arrays to profile microRNA expression has indicated that the levels of many microRNAs are altered during development and disease. These findings have prompted a great deal of investigation into the mechanism and function of microRNA-mediated repression. However, the mechanisms which govern the regulation of microRNA biogenesis and activity are just beginning to be uncovered. Following transcription, mature microRNA are generated through a series of coordinated processing events mediated by large protein complexes. It is increasingly clear that microRNA biogenesis does not proceed in a 'one-size-fits-all' manner. Rather, individual classes of microRNAs are differentially regulated through the association of regulatory factors with the core microRNA biogenesis machinery. Here, we review the regulation of microRNA biogenesis and activity, with particular focus on mechanisms of post-transcriptional control. Further understanding of the regulation of microRNA biogenesis and activity will undoubtedly provide important insights into normal development as well as pathological conditions such as cardiovascular disease and cancer

Do stimulation and support in the early childhood home environment and best friendship quality in adolescence predict adult personality?

BACKGROUND: The aim of this study was to determine whether stimulation and support in early childhood and best friendship quality in adolescence predict adult personality. PARTICIPANTS AND PROCEDURE: We used data from 123 individuals from an ongoing longitudinal study, with multiple assessment phases and modalities (observation, parental rating, self-report) to investigate prospective associations between stimulation and support in the home in early childhood (age 1-2), best friendship quality in adolescence (age 15), and the Big Five personality traits in adulthood (age 29) controlling for temperament, socioeconomic status (SES), and gender. RESULTS: After controlling for temperament, SES, and gender, we found that early childhood stimulation and support was related to adult openness to experiences, but not the other four traits, and that best friendship quality in adolescence was related to adult extraversion and agreeableness, but not conscientiousness, neuroticism, or openness to experiences. CONCLUSIONS: The study contributes to research indicating that while personalities are relatively stable, they are not fixed at an early age and may be related to experiences and salient relationships throughout development. There is a dearth of research investigating such associations and the available findings are inconsistent. Conclusions about the relations between experiences such as stimulation and support in the home in early childhood or best friendship quality in adolescence and adult personality should thus be viewed skeptically until replicated

Do stimulation and support in the early childhood home environment and best friendship quality in adolescence predict adult personality?

Background The aim of this study was to determine whether stimulation and support in early childhood and best friendship quality in adolescence predict adult personality. Participants and procedure We used data from 123 individuals from an ongoing longitudinal study, with multiple assessment phases and modalities (observation, parental rating, self-report) to investigate prospective associations between stimulation and support in the home in early childhood (age 1-2), best friendship quality in adolescence (age 15), and the Big Five personality traits in adulthood (age 29) controlling for temperament, socioeconomic status (SES), and gender. Results After controlling for temperament, SES, and gender, we found that early childhood stimulation and support was related to adult openness to experiences, but not the other four traits, and that best friendship quality in adolescence was related to adult extraversion and agreeableness, but not conscientiousness, neuroticism, or openness to experiences. Conclusions The study contributes to research indicating that while personalities are relatively stable, they are not fixed at an early age and may be related to experiences and salient relationships throughout development. There is a dearth of research investi-gating such associations and the available findings are inconsistent. Conclusions about the relations between experiences such as stimulation and support in the home in early childhood or best friendship quality in adolescence and adult personal-ity should thus be viewed skeptically until replicated

Designing a blueprint for coral reef survival

Maintaining coral reef ecosystems is a social imperative, because so many people depend on coral reefs for food production, shoreline protection, and livelihoods. The survival of reefs this century, however, is threatened by the mounting effects of climate change. Climate mitigation is the foremost and essential action to prevent coral reef ecosystem collapse. Without it, reefs will become extremely diminished within the next 20–30 years. Even with strong climate mitigation, however, existing conservation measures such as marine protected areas and fisheries management are no longer sufficient to sustain the ecosystem and many additional and innovative actions to increase reef resilience must also be taken. In this paper we assess the suite of protections and actions in terms of their potential to be effective according to a set of criteria that include effectiveness, readiness, co-benefits and disbenefits. Even with the best scientific innovation, saving coral reefs will require a well-funded, well-designed, and rapidly executed strategy with political and social commitments at the level of other grand challenges.publishe

There was no contamination of non-myoblast cells in our primary culture of rat skeletal muscle cells.

<p>Cells were positively stained with MHCI-antibody (Green Florescence).</p

The effect of insulin in Akt Ser⁴⁷³ phosphorylation with or without pre-exposure of low and high dose testosterone.

<p>(A). The effect of insulin alone on Akt phosphorylation after insulin treatment for 10, 20, 30, 60, and 120 minutes; Insulin significantly increased Akt Ser⁴⁷³ phosphorylation at all time points except 20 minutes; (B). Cells were pre-exposed to low-dose (20ng/ml) or high-dose (200ng/ml) of testosterone for 16 hours before insulin treatment. No change in Akt Ser⁴⁷³ phosphorylation was observed between T treated and non-T treated cells. Representative western blots are shown above the bar graphs. The four experimental groups are: control cells without insulin (C−I), control cells plus insulin (C+I), testosterone exposed cells without insulin (T−I), and testosterone exposed cells plus insulin (T+I). The phosphorylated signal of Akt Ser⁴⁷³ is normalized to total Akt in the sample.</p

The effect of insulin in S6K Thr³⁸⁹ phosphorylation with or without pre-exposure of low and high dose testosterone.

<p>(A). The effect of insulin alone on S6K Thr³⁸⁹ phosphorylation after insulin treatment for 10, 20, 30, 60, and 120 minutes; Insulin significantly increased S6K Thr³⁸⁹ phosphorylation after 60 minutes; (B). Cells were pre-exposed to low-dose (20ng/ml) or high-dose (200ng/ml) of testosterone for 16 hours before insulin treatment. Compared to non-testosterone treated cells, S6K Thr³⁸⁹ phosphorylation was significantly increased with low-dose testosterone treatment. Representative western blots are shown above the bar graphs. The four experimental groups are: control cells without insulin (C−I), control cells plus insulin (C+I), testosterone exposed cells without insulin (T−I), and testosterone exposed cells plus insulin (T+I). The phosphorylated signal of S6K Thr³⁸⁹ is normalized to total S6K in the sample.</p

The effect of insulin in IRS-1 phosphorylation with or without pre-exposure of low and high dose testosterone.

<p>(A). The effect of insulin alone on IRS-1 phosphorylation after insulin treatment for 10, 20, 30, 60, and 120 minutes; Insulin significantly increased IRS-1 Ser^636/639 phosphorylation after 120 minutes; (B). Cells were pre-exposed to low-dose (20ng/ml) or high-dose (200ng/ml) of testosterone for 16 hours before insulin treatment. Compared to non-testosterone treated (control) cells, IRS-1 Ser^636/639 phosphorylation was significantly increased with both low and high-dose testosterone exposure. Representative western blots are shown above the bar graphs. The four experimental groups are: control cells without insulin (C−I), control cells plus insulin (C+I), testosterone exposed cells without insulin (T−I), and testosterone exposed cells plus insulin (T+I). The phosphorylated signal of IRS-1 Ser^636/639 is normalized to total IRS-1 in the sample.</p