A Comprehensive Library of X-ray Pulsars in the Small Magellanic Cloud: Time Evolution of their Luminosities and Spin Periods

We have collected and analyzed the complete archive of {\itshape XMM-Newton\} (116), {\itshape Chandra\} (151), and {\itshape RXTE\} (952) observations of the Small Magellanic Cloud (SMC), spanning 1997-2014. The resulting observational library provides a comprehensive view of the physical, temporal and statistical properties of the SMC pulsar population across the luminosity range of $L_X= 10^{31.2}$--$10^{38}$~erg~s$^{-1}$. From a sample of 67 pulsars we report $\sim$1654 individual pulsar detections, yielding $\sim$1260 pulse period measurements. Our pipeline generates a suite of products for each pulsar detection: spin period, flux, event list, high time-resolution light-curve, pulse-profile, periodogram, and spectrum. Combining all three satellites, we generated complete histories of the spin periods, pulse amplitudes, pulsed fractions and X-ray luminosities. Some pulsars show variations in pulse period due to the combination of orbital motion and accretion torques. Long-term spin-up/down trends are seen in 12/11 pulsars respectively, pointing to sustained transfer of mass and angular momentum to the neutron star on decadal timescales. Of the sample 30 pulsars have relatively very small spin period derivative and may be close to equilibrium spin. The distributions of pulse-detection and flux as functions of spin-period provide interesting findings: mapping boundaries of accretion-driven X-ray luminosity, and showing that fast pulsars ($P<$10 s) are rarely detected, which yet are more prone to giant outbursts. Accompanying this paper is an initial public release of the library so that it can be used by other researchers. We intend the library to be useful in driving improved models of neutron star magnetospheres and accretion physics.Comment: 17 pages, 11 + 58 (appendix) figures. To appear in the Astrophysical Journal Supplemen

Background matching in the brown shrimp Crangon crangon : adaptive camouflage and behavioural-plasticity

A combination of burrowing behaviour and very efficient background matching makes the brown shrimp Crangon crangon almost invisible to potential predators and preys. This raises questions on how shrimp succeed in concealing themselves in the heterogeneous and dynamic estuarine habitats they inhabit and what type of environmental variables and behavioural factors affect their colour change abilities. Using a series of behavioural experiments, we show that the brown shrimp is capable of repeated fast colour adaptations (20% change in dark pigment cover within one hour) and that its background matching ability is mainly influenced by illumination and sediment colour. Novel insights are provided on the occurrence of non-adaptive (possibly stress) responses to background changes after long-time exposure to a constant background colour or during unfavourable conditions for burying. Shrimp showed high levels of intra- and inter-individual variation, demonstrating a complex balance between behavioural-plasticity and environmental adaptation. As such, the study of crustacean colour changes represents a valuable opportunity to investigate colour adaptations in dynamic habitats and can help us to identify the mayor environmental and behavioural factors influencing the evolution of animal background matching

Charge-based interaction conserved within histone H3 lysine 4 (H3K4) methyltransferase complexes is needed for protein stability, histone methylation, and gene expression

Histone H3 lysine 4 (H3K4) methyltransferases are conserved from yeast to humans, assemble in multisubunit complexes, and are needed to regulate gene expression. The yeast H3K4 methyltransferase complex, Set1 complex or complex of proteins associated with Set1 (COMPASS), consists of Set1 and conserved Set1-associated proteins: Swd1, Swd2, Swd3, Spp1, Bre2, Sdc1, and Shg1. The removal of the WD40 domain-containing subunits Swd1 and Swd3 leads to a loss of Set1 protein and consequently a complete loss ofH3K4methylation. However, until now, how these WD40 domain-containing proteins interact with Set1 and contribute to the stability of Set1 and H3K4 methylation has not been determined. In this study, we identified small basic and acidic patches that mediate protein interactions between theC terminus of Swd1 and the nSET domain of Set1. Absence of either the basic or acidic patches of Set1 and Swd1, respectively, disrupts the interaction between Set1 and Swd1, diminishes Set1 protein levels, and abolishesH3K4methylation. Moreover, these basic and acidic patches are also important for cell growth, telomere silencing, and gene expression. We also show that the basic and acidic patches of Set1 and Swd1 are conserved in their human counter-parts SET1A/B and RBBP5, respectively, and are needed for the protein interaction between SET1A and RBBP5. Therefore, this charge-based interaction is likely important for maintaining the protein stability of the human SET1A/B methyltransferase complexes so that proper H3K4 methylation, cell growth, and gene expression can also occur in mammals. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc

“I'll Give You the World”: Socioeconomic Differences in Parental Support of Adult Children

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/112275/1/jomf12204.pd

Renal Pelviceal Keratinizing Squamous Metaplasia with Sparing of Pyramidal Zones

Metaplastic changes in the urothelium of the upper urinary tract are relatively infrequent. Metaplasia may present as either squamous or less often glandular differentiation. The process may be associated with chronic inflammation or associated chronic infections. There may be malignant transformation to either squamous cell carcinoma or adenocarcinoma. The demarcation of the metaplastic process in the minor calyces has not been well documented to date. We report the case of a 74-year-old female patient who presented with a history of chronic renal disease and acute pyohydronephrosis. The patient underwent a nephroureterectomy which revealed keratinizing desquamative squamous metaplasia throughout the renal pelvis and upper urinary tract with abrupt termination of metaplasia at the junction of the renal pelvis and the minor calyx (pyramidal zone). Immunohistochemical evaluation documents metaplastic urothelium stained positive for CK5, before converting sharply to simple cuboidal epithelium in the minor calyx (pyramidal zones) which stained positive CK7. At the junction of the metaplastic components and low cuboidal lined minor calyceal surfaces, the underlying stroma showed loss of ureteral muscularis mucosa with transition to renal parenchymal type stroma. We believe that this observation is unique and potentially relevant to the etiology and pathophysiology of pelviceal metaplasia

Relationship tensions and mood: Adult children’s daily experience of aging parents’ stubbornness

This study examined middle‐aged individuals’ reports of parents’ behaviors commonly attributed to stubbornness. Middle‐aged adults (N = 192) completed a 7‐day diary reporting their mood and how often they felt their parents (N = 254) engaged in behaviors often described as “stubbornness” (insistent or risky). Thirty‐one percent of middle‐aged children reported insistent behaviors, and 17% reported risky behaviors by their parent(s). Daily reports of parent behaviors attributed to stubbornness were positively associated with parent–child relationship quality, parent functional limitations, and child neuroticism. Reports of perceived parent insistent behaviors were also associated with greater daily negative mood among adult children. Findings highlight the impact of adult children’s daily perceptions of parent behaviors commonly attributed to stubbornness on the individual and relationship.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142899/1/pere12229_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/142899/2/pere12229.pd

NCBI Epigenomics: a new public resource for exploring epigenomic data sets

The Epigenomics database at the National Center for Biotechnology Information (NCBI) is a new resource that has been created to serve as a comprehensive public resource for whole-genome epigenetic data sets (www.ncbi.nlm.nih.gov/epigenomics). Epigenetics is the study of stable and heritable changes in gene expression that occur independently of the primary DNA sequence. Epigenetic mechanisms include post-translational modifications of histones, DNA methylation, chromatin conformation and non-coding RNAs. It has been observed that misregulation of epigenetic processes has been associated with human disease. We have constructed the new resource by selecting the subset of epigenetics-specific data from general-purpose archives, such as the Gene Expression Omnibus, and Sequence Read Archives, and then subjecting them to further review, annotation and reorganization. Raw data is processed and mapped to genomic coordinates to generate ‘tracks’ that are a visual representation of the data. These data tracks can be viewed using popular genome browsers or downloaded for local analysis. The Epigenomics resource also provides the user with a unique interface that allows for intuitive browsing and searching of data sets based on biological attributes. Currently, there are 69 studies, 337 samples and over 1100 data tracks from five well-studied species that are viewable and downloadable in Epigenomics

The SMC5/6 complex prevents genotoxicity upon APOBEC3A-mediated replication stress

Mutational patterns caused by APOBEC3 cytidine deaminase activity are evident throughout human cancer genomes. In particular, the APOBEC3A family member is a potent genotoxin that causes substantial DNA damage in experimental systems and human tumors. However, the mechanisms that ensure genome stability in cells with active APOBEC3A are unknown. Through an unbiased genome-wide screen, we define the Structural Maintenance of Chromosomes 5/6 (SMC5/6) complex as essential for cell viability when APOBEC3A is active. We observe an absence of APOBEC3A mutagenesis in human tumors with SMC5/6 dysfunction, consistent with synthetic lethality. Cancer cells depleted of SMC5/6 incur substantial genome damage from APOBEC3A activity during DNA replication. Further, APOBEC3A activity results in replication tract lengthening which is dependent on PrimPol, consistent with re-initiation of DNA synthesis downstream of APOBEC3A-induced lesions. Loss of SMC5/6 abrogates elongated replication tracts and increases DNA breaks upon APOBEC3A activity. Our findings indicate that replication fork lengthening reflects a DNA damage response to APOBEC3A activity that promotes genome stability in an SMC5/6-dependent manner. Therefore, SMC5/6 presents a potential therapeutic vulnerability in tumors with active APOBEC3A