Complete larval development of the hermit crabs Clibanarius aequabilis and Clibanarius erythropus (Decapoda : Anomura : Diogenidae), under laboratory conditions, with a revision of the larval features of genus Clibanarius

The complete larval development (four zoeae and one megalopa) of Clibanarius aequabilis and C. erythropus, reared under laboratory conditions, is described and illustrated. The larval stages of the two northeastern Atlantic Clibanarius species cannot be easily differentiated. Their morphological characters are compared with those of other known Clibanarius larvae. The genus Clibanarius is very homogeneous with respect to larval characters. All Clibanarius zoeae display a broad and blunt rostrum, smooth abdominal segments and an antennal scale without a terminal spine. Beyond the second zoeal stage, the fourth telson process is present as a fused spine, and the uropods are biramous. In the fourth larval stage all species display a mandibular palp. The Clibanarius megalopa presents weakly developed or no ocular scales, symmetrical chelipeds, apically curved corneous dactylus in the second and third pereiopods, and 5-11 setae on the posterior margin of the telson. Apart from the number of zoeal stages, Clibanarius species may be separated, beyond the second zoeal stage, by the telson formula and the morphology of the fourth telson process.info:eu-repo/semantics/publishedVersio

Reaching the top but not feeling on top of the world: Examining women’s internalized power threats

This is the final version. Available on open access from Frontiers Media via the DOI in this recordData availability statement: The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.More and more women are breaking the glass ceiling to obtain positions of power. Yet with this rise, some women experience threats to their power. Here we focus on women’s perceived threats to the stability of their power and the degree to which women feel they do not deserve their power positions, as reflected in their impostor feelings. The present research identifies key workplace characteristics that are associated with these internalized power threats with survey data collected among 185 women in high-power positions. We find that negative workplace experiences (i.e., gender discrimination, denigrating treatment, lack of cultural fit, and lack of mentoring) are associated with a greater sense of power threat, which in turn relates to adverse workplace outcomes (i.e., reduced job satisfaction and increased emotional exhaustion and opting-out intentions). With this unique sample of high-powered women, our findings help illustrate the forces that make women experience power as precarious, thereby shedding light on the disadvantages these women face. We provide suggestions on how to reduce women’s internalized power threats

Contextualizing the Impostor “Syndrome”

This is the final version. Available on open access from Frontiers Media via the DOI in this recordData Availability Statement: The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the corresponding author.The impostor “syndrome” refers to the notion that some individuals feel as if they ended up in esteemed roles and positions not because of their competencies, but because of some oversight or stroke of luck. Such individuals therefore feel like frauds or “impostors.” Despite the fact that impostor feelings are often linked to marginalized groups in society, to date, research predominantly approaches this phenomenon as an issue of the individual: pointing toward individuals for the roots and solutions of the “syndrome.” Drawing from a rich body of social and organizational psychology research, in this perspectives piece, we propose a shift in how scholars conceptualize and empirically examine this phenomenon. Instead of framing the insecurities of individuals belonging to marginalized groups solely as a problem that arises within these individuals, we argue that it is critical for future research to consider the important role of the environment in eliciting their impostor feelings as well. By doing so, we can address the contextual roots of individuals’ impostor feelings, and offer more structural and effective solutions.European Research Council (ERC

Small inhibitor of Bcl-2, HA14-1, selectively enhanced the apoptotic effect of cisplatin by modulating Bcl-2 family members in MDA-MB-231 breast cancer cells

Inhibition or downregulation of Bcl-2 represents a new therapeutic approach to by-pass chemoresistance in cancer cells. Therefore, we explored the potential of this approach in breast cancer cells. Cisplatin and paclitaxel induced apoptosis in a dose-dependent manner in MCF-7 (drug-sensitive) and MDA-MB-231 (drug-insensitive) cells. Furthermore, when we transiently silenced Bcl-2, both cisplatin and paclitaxel induced apoptosis more than parental cells. Dose dependent induction of apoptosis by drugs was enhanced by the pre-treatment of these cells with HA14-1, a Bcl-2 inhibitor. Although the effect of cisplatin was significant on both cell lines, the effect of paclitaxel was much less potent only in MDA-MB-231 cells. To further understand the distinct role of drugs in MDA-MB-231 cells pretreated with HA14-1, caspases and Bcl-2 family proteins were studied. The apoptotic effect of cisplatin with or without HA14-1 pre-treatment is shown to be caspase-dependent. Among pro-apoptotic Bcl-2 proteins, Bax and Puma were found to be up-regulated whereas Bcl-2 and Bcl-x(L) were down-regulated when cells were pretreated with HA14-1 followed by paclitaxel or cisplatin. Enforced Bcl-2 expression in MDA-MB-231 cells abrogated the sensitizing effect of HA14-1 in cisplatin induced apoptosis. These results suggest that the potentiating effect of HA14-1 is drug and cell type specific and may not only depend on the inhibition of Bcl-2. Importantly, alteration of other pro-apoptotic or anti-apoptotic Bcl-2 family members may dictate the apoptotic response when HA14-1 is combined with chemotherapeutic drugs

Widespread forest vertebrate extinctions induced by a mega hydroelectric dam in lowland Amazonia

Mega hydropower projects in tropical forests pose a major emergent threat to terrestrial and freshwater biodiversity worldwide. Despite the unprecedented number of existing, underconstruction and planned hydroelectric dams in lowland tropical forests, long-term effects on biodiversity have yet to be evaluated. We examine how medium and large-bodied assemblages of terrestrial and arboreal vertebrates (including 35 mammal, bird and tortoise species) responded to the drastic 26-year post-isolation history of archipelagic alteration in landscape structure and habitat quality in a major hydroelectric reservoir of Central Amazonia. The Balbina Hydroelectric Dam inundated 3,129 km2 of primary forests, simultaneously isolating 3,546 land-bridge islands. We conducted intensive biodiversity surveys at 37 of those islands and three adjacent continuous forests using a combination of four survey techniques, and detected strong forest habitat area effects in explaining patterns of vertebrate extinction. Beyond clear area effects, edge-mediated surface fire disturbance was the most important additional driver of species loss, particularly in islands smaller than 10 ha. Based on species-area models, we predict that only 0.7% of all islands now harbor a species-rich vertebrate assemblage consisting of ≥80% of all species. We highlight the colossal erosion in vertebrate diversity driven by a man-made dam and show that the biodiversity impacts of mega dams in lowland tropical forest regions have been severely overlooked. The geopolitical strategy to deploy many more large hydropower infrastructure projects in regions like lowland Amazonia should be urgently reassessed, and we strongly advise that long-term biodiversity impacts should be explicitly included in pre-approval environmental impact assessments

Measurement of the Branching Fraction of J/psi --> pi+ pi- pi0

Using 58 million J/psi and 14 million psi' decays obtained by the BESII experiment, the branching fraction of J/psi --> pi+ pi- pi0 is determined. The result is (2.10+/-0.12)X10^{-2}, which is significantly higher than previous measurements.Comment: 9 pages, 8 figures, RevTex

First observation of psi(2S)-->K_S K_L

The decay psi(2S)-->K_S K_L is observed for the first time using psi(2S) data collected with the Beijing Spectrometer (BESII) at the Beijing Electron Positron Collider (BEPC); the branching ratio is determined to be B(psi(2S)-->K_S K_L) = (5.24\pm 0.47 \pm 0.48)\times 10^{-5}. Compared with J/psi-->K_S K_L, the psi(2S) branching ratio is enhanced relative to the prediction of the perturbative QCD ``12%'' rule. The result, together with the branching ratios of psi(2S) decays to other pseudoscalar meson pairs (\pi^+\pi^- and K^+K^-), is used to investigate the relative phase between the three-gluon and the one-photon annihilation amplitudes of psi(2S) decays.Comment: 5 pages, 4 figures, 2 tables, submitted to Phys. Rev. Let

From normal cell types to malignant phenotypes

The phenotypic diversity of breast cancer has been proposed to result from different target cell types undergoing oncogenic transformation and giving rise to cancer stem cells. Global gene expression profiling revealed distinct molecular phenotypes and some of these signatures were held to reflect the cell of origin, with the basal carcinomas arising from basal/progenitor cells. Recent work challenges this view by providing evidence that luminal precursor cells are involved in the pathogenesis of basal breast cancers and has made new links between normal cell populations and molecular tumor phenotypes

Dietary magnesium, not calcium, prevents vascular calcification in a mouse model for pseudoxanthoma elasticum

Pseudoxanthoma elasticum (PXE) is a heritable disorder characterized by ectopic calcification of connective tissue in skin, Bruch’s membrane of the eye, and walls of blood vessels. PXE is caused by mutations in the ABCC6 gene, but the exact etiology is still unknown. While observations on patients suggest that high calcium intake worsens the clinical symptoms, the patient organization PXE International has published the dietary advice to increase calcium intake in combination with increased magnesium intake. To obtain more data on this controversial issue, we examined the effect of dietary calcium and magnesium in the Abcc6−/− mouse, a PXE mouse model which mimics the clinical features of PXE. Abcc6−/− mice were placed on specific diets for 3, 7, and 12 months. Disease severity was measured by quantifying calcification of blood vessels in the kidney. Raising the calcium content in the diet from 0.5% to 2% did not change disease severity. In contrast, simultaneous increase of both calcium (from 0.5% to 2.0%) and magnesium (from 0.05% to 0.2%) slowed down the calcification significantly. Our present findings that increase in dietary magnesium reduces vascular calcification in a mouse model for PXE should stimulate further studies to establish a dietary intervention for PXE