On the Importance of Electroweak Corrections for Majorana Dark Matter Indirect Detection

Recent analyses have shown that the inclusion of electroweak corrections can alter significantly the energy spectra of Standard Model particles originated from dark matter annihilations. We investigate the important situation where the radiation of electroweak gauge bosons has a substantial influence: a Majorana dark matter particle annihilating into two light fermions. This process is in p-wave and hence suppressed by the small value of the relative velocity of the annihilating particles. The inclusion of electroweak radiation eludes this suppression and opens up a potentially sizeable s-wave contribution to the annihilation cross section. We study this effect in detail and explore its impact on the fluxes of stable particles resulting from the dark matter annihilations, which are relevant for dark matter indirect searches. We also discuss the effective field theory approach, pointing out that the opening of the s-wave is missed at the level of dimension-six operators and only encoded by higher orders.Comment: 25 pages, 6 figures. Minor corrections to match version published in JCA

Running into New Territory in SUSY Parameter Space

The LEP-II bound on the light Higgs mass rules out the vast majority of parameter space left to the Minimal Supersymmetric Standard Model (MSSM) with weak-scale soft-masses. This suggests the importance of exploring extensions of the MSSM with non-minimal Higgs physics. In this article, we explore a theory with an additional singlet superfield and an extended gauge sector. The theory has a number of novel features compared to both the MSSM and Next-to-MSSM, including easily realizing a light CP-even Higgs mass consistent with LEP-II limits, tan(beta) < 1, and a lightest Higgs which is charged. These features are achieved while remaining consistent with perturbative unification and without large stop-masses. Discovery modes at the Tevatron and LHC are discussed.Comment: 15 pages, 5 figures; Typo in equation (4.5) corrected; submitted to JHE

cAMP/CREB-regulated LINC00473 marks LKB1-inactivated lung cancer and mediates tumor growth

The LKB1 tumor suppressor gene is frequently mutated and inactivated in non–small cell lung cancer (NSCLC). Loss of LKB1 promotes cancer progression and influences therapeutic responses in preclinical studies; however, specific targeted therapies for lung cancer with LKB1 inactivation are currently unavailable. Here, we have identified a long noncoding RNA (lncRNA) signature that is associated with the loss of LKB1 function. We discovered that LINC00473 is consistently the most highly induced gene in LKB1-inactivated human primary NSCLC samples and derived cell lines. Elevated LINC00473 expression correlated with poor prognosis, and sustained LINC00473 expression was required for the growth and survival of LKB1-inactivated NSCLC cells. Mechanistically, LINC00473 was induced by LKB1 inactivation and subsequent cyclic AMP–responsive element–binding protein (CREB)/CREB-regulated transcription coactivator (CRTC) activation. We determined that LINC00473 is a nuclear lncRNA and interacts with NONO, a component of the cAMP signaling pathway, thereby facilitating CRTC/CREB-mediated transcription. Collectively, our study demonstrates that LINC00473 expression potentially serves as a robust biomarker for tumor LKB1 functional status that can be integrated into clinical trials for patient selection and treatment evaluation, and implicates LINC00473 as a therapeutic target for LKB1-inactivated NSCLC

Report on the 2013: Rapid assessment survey of marine species at New England Bays and Harbors

Introduced species (i.e., non-native species that have become established in\ud a new location) have increasingly been recognized as a concern as they have\ud become more prevalent in marine and terrestrial environments (Mooney and\ud Cleland 2001; Simberloff et al. 2005). The ability of introduced species to alter\ud population, community, and ecosystem structure and function, as well as\ud cause significant economic damage is well documented (Carlton 1989, 1996b,\ud 2000; Cohen and Carlton 1995; Cohen et al. 1995; Elton 1958; Meinesz et al.\ud 1993; Occhipinti-Ambrogi and Sheppard 2007; Pimentel et al. 2005; Thresher\ud 2000). The annual economic costs incurred from managing the approximately\ud 50,000 introduced species in the United States alone are estimated to be over\ud $120 billion (Pimentel et al. 2005).\ud Having a monitoring network in place to track new introductions and\ud distributional changes of introduced species is critical for effective\ud management, as these efforts may be more successful when species are\ud detected before they have the chance to become established. A rapid\ud assessment survey is one such method for early detection of introduced\ud species. With rapid assessment surveys, a team of taxonomic experts\ud record and monitor marine species–providing a baseline inventory of\ud native, introduced, and cryptogenic (i.e., unknown origin) species (as\ud defined by Carlton 1996a)–and document range expansions of previously\ud identified species.\ud Since 2000, five rapid assessment surveys have been conducted in New\ud England. These surveys focus on recording species at marinas, which often\ud are in close proximity to transportation vectors (i.e., recreational boats).\ud Species are collected from floating docks and piers because these structures\ud are accessible regardless of the tidal cycle. Another reason for sampling floating\ud docks and other floating structures is that marine introduced species are often\ud found to be more prevalent on artificial surfaces than natural surfaces (Glasby\ud and Connell 2001; Paulay et al. 2002). The primary objectives of these surveys\ud are to: (1) identify native, introduced, and cryptogenic marine species,\ud (2) expand on data collected in past surveys, (3) assess the introduction status\ud and range extensions of documented introduced species, and (4) detect new\ud introductions. This report presents the introduced, cryptogenic, and native\ud species recorded during the 2013 survey.CZM through NOAA NA13NOS4190040MIT Sea Grant through NOAA NA10OAR4170086

An analysis and evaluation of the WeFold collaborative for protein structure prediction and its pipelines in CASP11 and CASP12

Every two years groups worldwide participate in the Critical Assessment of Protein Structure Prediction (CASP) experiment to blindly test the strengths and weaknesses of their computational methods. CASP has significantly advanced the field but many hurdles still remain, which may require new ideas and collaborations. In 2012 a web-based effort called WeFold, was initiated to promote collaboration within the CASP community and attract researchers from other fields to contribute new ideas to CASP. Members of the WeFold coopetition (cooperation and competition) participated in CASP as individual teams, but also shared components of their methods to create hybrid pipelines and actively contributed to this effort. We assert that the scale and diversity of integrative prediction pipelines could not have been achieved by any individual lab or even by any collaboration among a few partners. The models contributed by the participating groups and generated by the pipelines are publicly available at the WeFold website providing a wealth of data that remains to be tapped. Here, we analyze the results of the 2014 and 2016 pipelines showing improvements according to the CASP assessment as well as areas that require further adjustments and research

Search for residual prostate cancer on pT0 radical prostatectomy after positive biopsy

Reported incidence of no residual prostate cancer (i.e. pathological stage pT0) on radical prostatectomy ranges from 0.07 to 4.2%. The incidence is higher after neoadjuvant endocrine treatment. The aim of this study was to search for residual cancer on radical prostatectomy (RP) specimens when an initial sampling failed to find the cancer in patients with positive biopsy. Our database of 1,328 consecutive patients whose biopsies and RP specimen were both examined at the Polytechnic University-United Hospitals of the Marche Region between March 1995 and June 2006 was reviewed. The radical prostatectomies were grossly completely sampled and examined with the whole mount technique. We identified eight patients (i.e. 0.6%; three untreated and five hormonally treated preoperatively, i.e. 0.3 and 0.8%, respectively, of the total number of RPs included in the study) with positive biopsy and with no residual cancer in the initial routine histological examination of the RP. The RP of this group of eight was subjected to additional sectioning and evaluation of the paraffin blocks of the prostatectomy, also after block-flipping, immunostaining with an antibody against CAM 5.2, p63, PSA, and alpha-methylacyl-CoA racemase, and DNA specimen identity analysis. There were no cases with a false positive biopsy diagnosis, and cancer was not overlooked or missed in the initial routine histological examination of any of the 8 pT0 RPs. A minute focus of cancer (the diameter was always below 2.0 mm) was found on the additional sections in five. In particular, cancer was found after block-flipping in one of them. In an additional case, cancer was eventually discovered after immunostaining tissue sections for cytokeratin CAM 5.2, for p63 and PSA. In the remaining two cases (one untreated and the other hormonally treated), cancer was not found (0.15% of the 1,328 RPs included in the study); the review of the description of the macroscopic appearance of the RP and of its slides revealed that part of the peripheral zone corresponding to the site of the positive biopsy was missing, i.e. not removed from the patient at the time of the operation at least in one of the two. DNA specimen analysis confirmed the identity of the biopsy and prostatectomy in both. An extensive search for residual cancer reduces the number of pT0 RPs after a positive biopsy from 0.6 to 0.15%. It is recommended to have the needle biopsy reviewed, carefully look again at the radical prostatectomy, do deeper sections and then flip certain paraffin blocks. In addition, atypical foci should be stained for basal cell markers and often AMACR, especially in hormone-treated cases. If a block is missing part of the peripheral zone (capsular incision), this should be commented on. DNA analysis for tissue identity should be performed when the other steps have been taken without finding cancer

CI and CO in Nearby Spiral Galaxies -- I. Line Ratio and Abundance Variations at ~ 200 pc Scales

We present new neutral atomic carbon [CI](3P1-3P0) mapping observations within the inner ~7 kpc and ~4 kpc of the disks of NGC3627 and NGC4321 at a spatial resolution of 190 pc and 270 pc, respectively, using the ALMA Atacama Compact Array (ACA). We combine these with the CO(2-1) data from PHANGS-ALMA, and literature [CI] and CO data for two other starburst and/or active galactic nucleus (AGN) galaxies (NGC1808, NGC7469), to study: a) the spatial distributions of CI and CO emission; b) the observed line ratio RCICO = I_[CI](1-0)/I_CO(2-1) as a function of various galactic properties; and c) the abundance ratio of [CI/CO]. We find excellent spatial correspondence between CI and CO emission and nearly uniform RCICO ~0.1 across the majority of the star-forming disks of NGC3627 and NGC4321. However, RCICO strongly varies from ~0.05 at the centre of NGC4321 to >0.2-0.5 in NGC1808's starburst centre and NGC7469's centre with an X-ray AGN. Meanwhile, RCICO does not obviously vary with $U$, similar to the prediction of PDR models. We also find a mildly decreasing RCICO with an increasing metallicity over 0.7-0.85 solar metallicity, consistent with the literature. Assuming various typical ISM conditions representing GMCs, active star-forming regions and strong starbursting environments, we calculate the LTE radiative transfer and estimate the [CI/CO] abundance ratio to be ~0.1 across the disks of NGC3627 and NGC4321, similar to previous large-scale findings in Galactic studies. However, this abundance ratio likely has a substantial increase to ~1 and >1-5 in NGC1808's starburst and NGC7469's strong AGN environments, respectively, in line with the expectations for cosmic-ray dominated region (CRDR) and X-ray dominated region (XDR) chemistry. Finally, we do not find a robust evidence for a generally CO-dark, CI-bright gas in the disk areas we probed. (abbreviated)Comment: 23 pages, 13 figures and one table in total (17 pages and 9 figures in main text). Accepted for publication in A&A. For associated data cubes and moment maps, see https://www.canfar.net/storage/vault/list/phangs/RELEASES/DZLIU_etal_202

3-Deazaneplanocin A (DZNep), an Inhibitor of the Histone Methyltransferase EZH2, Induces Apoptosis and Reduces Cell Migration in Chondrosarcoma Cells

ObjectiveGrowing evidences indicate that the histone methyltransferase EZH2 (enhancer of zeste homolog 2) may be an appropriate therapeutic target in some tumors. Indeed, a high expression of EZH2 is correlated with poor prognosis and metastasis in many cancers. In addition, 3-Deazaneplanocin A (DZNep), an S-adenosyl-L homocysteine hydrolase inhibitor which induces EZH2 protein depletion, leads to cell death in several cancers and tumors. The aim of this study was to determine whether an epigenetic therapy targeting EZH2 with DZNep may be also efficient to treat chondrosarcomas.MethodsEZH2 expression was determined by immunohistochemistry and western-blot. Chondrosarcoma cell line CH2879 was cultured in the presence of DZNep, and its growth and survival were evaluated by counting adherent cells periodically. Apoptosis was assayed by cell cycle analysis, Apo2.7 expression using flow cytometry, and by PARP cleavage using western-blot. Cell migration was assessed by wound healing assay.ResultsChondrosarcomas (at least with high grade) highly express EZH2, at contrary to enchondromas or chondrocytes. In vitro, DZNep inhibits EZH2 protein expression, and subsequently reduces the trimethylation of lysine 27 on histone H3 (H3K27me3). Interestingly, DZNep induces cell death of chondrosarcoma cell lines by apoptosis, while it slightly reduces growth of normal chondrocytes. In addition, DZNep reduces cell migration.ConclusionThese results indicate that an epigenetic therapy that pharmacologically targets EZH2 via DZNep may constitute a novel approach to treat chondrosarcomas