Endocrine-disrupting alkylphenols are widespread in the blood of lobsters from southern New England and adjacent offshore areas

Author Posting. © National Shellfisheries Association , 2012. This article is posted here by permission of National Shellfisheries Association for personal use, not for redistribution. The definitive version was published in Journal of Shellfish Research 31 (2012): 563-571, doi:10.2983/035.031.0216.Endocrine-disrupting pollutants in rivers and oceans represent a poorly understood but potentially serious threat to the integrity of aquatic and coastal ecosystems. We surveyed the hemolymph of lobsters from across southern New England and adjacent offshore areas for 3 endocrine-disrupting alkylphenols. We found all 3 compounds in hemolymph from every year and almost every region sampled. Prevalence of contamination varied significantly between regions, ranging from 45% of lobsters from southern Massachusetts to 17% of lobsters from central Long Island Sound. Mean contamination levels varied significantly as a function of region, year sampled, and collection trip, and were highest overall in lobsters from western Long Island Sound and lowest in lobsters from central Long Island Sound. Surprisingly, lobsters from offshore areas were not less contaminated than lobsters from inshore areas. Contamination levels also did not vary as a function of lobster size or shell disease signs. Contaminated lobsters held in the laboratory did not retain alkylphenols, suggesting that hemolymph contamination levels represent recent, rather than long-term, exposure. Our data set is the first, to our knowledge, to survey endocrine-disrupting contaminants in a population across such a broad temporal and spatial scale. We show that alkylphenol contamination is a persistent, widespread, but environmentally heterogeneous problem in lobster populations in southern New England and adjacent offshore areas. Our work raises serious questions about the prevalence and accumulation of these endocrine-disrupting pollutants in an important fishery species.This work was supported by the National Marine Fisheries Service as the New England Lobster Research Initiative: Lobster Shell Disease under NOAA grant NA06NMF4720100 to the University of Rhode Island Fisheries Center

Shedding light on the elusive role of endothelial cells in cytomegalovirus dissemination.

Cytomegalovirus (CMV) is frequently transmitted by solid organ transplantation and is associated with graft failure. By forming the boundary between circulation and organ parenchyma, endothelial cells (EC) are suited for bidirectional virus spread from and to the transplant. We applied Cre/loxP-mediated green-fluorescence-tagging of EC-derived murine CMV (MCMV) to quantify the role of infected EC in transplantation-associated CMV dissemination in the mouse model. Both EC- and non-EC-derived virus originating from infected Tie2-cre(+) heart and kidney transplants were readily transmitted to MCMV-naïve recipients by primary viremia. In contrast, when a Tie2-cre(+) transplant was infected by primary viremia in an infected recipient, the recombined EC-derived virus poorly spread to recipient tissues. Similarly, in reverse direction, EC-derived virus from infected Tie2-cre(+) recipient tissues poorly spread to the transplant. These data contradict any privileged role of EC in CMV dissemination and challenge an indiscriminate applicability of the primary and secondary viremia concept of virus dissemination

Association of estradiol and visceral fat with structural brain networks and memory performance in adults

Importance Changes in estradiol during aging are associated with increased dementia risk. It remains unclear how estradiol supports cognitive health and whether risk factors, such as midlife obesity, are exacerbated by estrogen loss. Objectives To assess whether visceral adipose tissue (VAT) moderates the association between age and brain network structure and to investigate whether estradiol moderates the association between VAT and brain network structure. Design, Setting, and Participants Cross-sectional study of data from 974 cognitively healthy adults in Germany who participated in the Health Study of the Leipzig Research Centre for Civilization Diseases, a previously described population-based cohort study. Two moderation analyses were performed, including VAT as the moderator variable between age and brain network structure and estradiol as the moderator variable between VAT and brain network structure. The study was conducted from August 1, 2011, to November 23, 2014. Analyses were conducted from August 2017 to September 201

Properties of the Galactic population of cataclysmic variables in hard X-rays

We measure the spatial distribution and hard X-ray luminosity function of cataclysmic variables (CVs) using the INTEGRAL all-sky survey in the 17-60 keV energy band. The vast majority of the INTEGRAL detected CVs are intermediate polars with luminosities in the range 10^{32}-10^{34} erg/sec. The scale height of the Galactic disk population of CVs is found to be 130{+90}{-50} pc. The CV luminosity function measured with INTEGRAL in hard X-rays is compatible with that previously determined at lower energies (3--20 keV) using a largely independent sample of sources detected by RXTE (located at |b|>10deg as opposed to the INTEGRAL sample, strongly concentrated to the Galactic plane). The cumulative 17-60 keV luminosity density of CVs per unit stellar mass is found to be (1.3+/-0.3)x10^{27} erg/sec/Msun and is thus comparable to that of low-mass X-ray binaries in this energy band. Therefore, faint but numerous CVs are expected to provide an important contribution to the cumulative hard X-ray emission of galaxies.Comment: 8 pages, 8 figures. Submitted to A&

Type-III intermittency in a four-level coherently pumped laser

We study a homogeneously broadened four-level model for a coherently pumped laser with pump and laser fields having crossed linear polarizations. For a parameter range of the type explored in the experiments by Tang et al. [Phys. Rev. A 44, R35 (1991)] the system exhibits a family of type-III-intermittency transitions to chaos in which the onset of intermittency is preceded by period-2, period-3, or period-4 states. We find similarities but also differences between the results of our theory and their experimental results

From trial to population: A study of a family-based community intervention for childhood overweight implemented at scale

To assess how outcomes associated with participation in a family-based weight management intervention (MEND 7–13, Mind, Exercise, Nutrition..Do it!) for childhood overweight or obesity implemented at scale in the community vary by child, family, neighbourhood and MEND programme characteristics

The Adaptor Function of TRAPPC2 in Mammalian TRAPPs Explains TRAPPC2-Associated SEDT and TRAPPC9-Associated Congenital Intellectual Disability

Background: The TRAPP (Transport protein particle) complex is a conserved protein complex functioning at various steps in vesicle transport. Although yeast has three functionally and structurally distinct forms, TRAPPI, II and III, emerging evidence suggests that mammalian TRAPP complex may be different. Mutations in the TRAPP complex subunit 2 (TRAPPC2) cause X-linked spondyloepiphyseal dysplasia tarda, while mutations in the TRAPP complex subunit 9 (TRAPPC9) cause postnatal mental retardation with microcephaly. The structural interplay between these subunits found in mammalian equivalent of TRAPPI and those specific to TRAPPII and TRAPPIII remains largely unknown and we undertook the present study to examine the interaction between these subunits. Here, we reveal that the mammalian equivalent of the TRAPPII complex is structurally distinct from the yeast counterpart thus leading to insight into mechanism of disease. Principal Findings: We analyzed how TRAPPII- or TRAPPIII- specific subunits interact with the six-subunit core complex of TRAPP by co-immunoprecipitation in mammalian cells. TRAPPC2 binds to TRAPPII-specific subunit TRAPPC9, which in turn binds to TRAPPC10. Unexpectedly, TRAPPC2 can also bind to the putative TRAPPIII-specific subunit, TRAPPC8. Endogenous TRAPPC9-positive TRAPPII complex does not contain TRAPPC8, suggesting that TRAPPC2 binds to either TRAPPC9 or TRAPPC8 during the formation of the mammalian equivalents of TRAPPII or TRAPPIII, respectively. Therefore, TRAPPC2 serves as an adaptor for the formation of these complexes. A disease-causing mutation of TRAPPC2, D47Y, failed to interact with either TRAPPC9 or TRAPPC8, suggesting that aspartate 47 in TRAPPC2 is at or near the site of interaction with TRAPPC9 or TRAPPC8, mediating the formation of TRAPPII and/or TRAPPIII. Furthermore, disease-causing deletional mutants of TRAPPC9 all failed to interact with TRAPPC2 and TRAPPC10. Conclusions: TRAPPC2 serves as an adaptor for the formation of TRAPPII or TRAPPIII in mammalian cells. The mammalian equivalent of TRAPPII is likely different from the yeast TRAPPII structurally. © 2011 Zong et al.published_or_final_versio