141 research outputs found
WALLABY Pilot Survey:The Diversity of Ram Pressure Stripping of the Galactic H I Gas in the Hydra Cluster
This study uses HI image data from the WALLABY pilot survey with the ASKAP
telescope, covering the Hydra cluster out to 2.5. We present the
projected phase-space distribution of HI-detected galaxies in Hydra, and
identify that nearly two thirds of the galaxies within may be in
the early stages of ram pressure stripping. More than half of these may be only
weakly stripped, with the ratio of strippable HI (i.e., where the galactic
restoring force is lower than the ram pressure in the disk) mass fraction (over
total HI mass) distributed uniformly below 90%. Consequently, the HI mass is
expected to decrease by only a few 0.1 dex after the currently strippable
portion of HI in these systems has been stripped. A more detailed look at the
subset of galaxies that are spatially resolved by WALLABY observations shows
that, while it typically takes less than 200 Myr for ram pressure stripping to
remove the currently strippable portion of HI, it may take more than 600 Myr to
significantly change the total HI mass. Our results provide new clues to
understanding the different rates of HI depletion and star formation quenching
in cluster galaxies.Comment: 25 pages, 10 figures, 1 table. Accepted for publication at Ap
FAST-ASKAP Synergy: Quantifying Coexistent Tidal and Ram-Pressure Strippings in the NGC 4636 Group
Combining new HI data from a synergetic survey of ASKAP WALLABY and FAST with
the ALFALFA data, we study the effect of ram-pressure and tidal interactions in
the NGC 4636 group. We develop two parameters to quantify and disentangle these
two effects on gas stripping in HI-bearing galaxies: the strength of external
forces at the optical-disk edge, and the outside-in extents of HI-disk
stripping. We find that gas stripping is widespread in this group, affecting
80% of HI-detected non-merging galaxies, and that 34% are experiencing both
types of stripping. Among the galaxies experiencing both effects, the strengths
(and extents) of ram-pressure and tidal stripping are independent of each
other. Both strengths are correlated with HI-disk shrinkage. The tidal strength
is related to a rather uniform reddening of low-mass galaxies
() when tidal stripping is the dominating effect. In
contrast, ram pressure is not clearly linked to the color-changing patterns of
galaxies in the group. Combining these two stripping extents, we estimate the
total stripping extent, and put forward an empirical model that can describe
the decrease of HI richness as galaxies fall toward the group center. The
stripping timescale we derived decreases with distance to the center, from
around to
near the center. Gas-depletion happens
since crossing for HI-rich galaxies,
but much quicker for HI-poor ones. Our results quantify in a physically
motivated way the details and processes of environmental-effects-driven galaxy
evolution, and might assist in analyzing hydrodynamic simulations in an
observational way.Comment: 44 pages, 22 figures, 5 tables, accepted for publication in ApJ.
Tables 4 and 5 are also available in machine-readable for
Role of Endoplasmic Reticulum Stress in α-TEA Mediated TRAIL/DR5 Death Receptor Dependent Apoptosis
Background -- α-TEA (RRR-α-tocopherol ether-linked acetic acid analog), a derivative of RRR-α-tocopherol (vitamin E) exhibits anticancer actions in vitro and in vivo in variety of cancer types. The objective of this study was to obtain additional insights into the mechanisms involved in α-TEA induced apoptosis in human breast cancer cells. Methodology/Principal Findings -- α-TEA induces endoplasmic reticulum (ER) stress as indicated by increased expression of CCAAT/enhancer binding protein homologous protein (CHOP) as well as by enhanced expression or activation of specific markers of ER stress such as glucose regulated protein (GRP78), phosphorylated alpha subunit of eukaryotic initiation factor 2 (peIF-2α), and spliced XBP-1 mRNA. Knockdown studies using siRNAs to TRAIL, DR5, JNK and CHOP as well as chemical inhibitors of ER stress and caspase-8 showed that: i) α-TEA activation of DR5/caspase-8 induces an ER stress mediated JNK/CHOP/DR5 positive amplification loop; ii) α-TEA downregulation of c-FLIP (L) protein levels is mediated by JNK/CHOP/DR5 loop via a JNK dependent Itch E3 ligase ubiquitination that further serves to enhance the JNK/CHOP/DR5 amplification loop by preventing c-FLIP's inhibition of caspase-8; and (iii) α-TEA downregulation of Bcl-2 is mediated by the ER stress dependent JNK/CHOP/DR5 signaling. Conclusion -- Taken together, ER stress plays an important role in α-TEA induced apoptosis by enhancing DR5/caspase-8 pro-apoptotic signaling and suppressing anti-apoptotic factors c-FLIP and Bcl-2 via ER stress mediated JNK/CHOP/DR5/caspase-8 signaling.The Clayton Foundation for Research, the National Institute of Environmental Health Sciences Center Grant ES007784, the Center for Molecular and Cellular Toxicology at the University of Texas at Austin and a NIEHS/NIH Toxicology Training Grant T32 ES07247. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Biological Sciences, School o
G protein-coupled receptor kinase 5 mediates Tazarotene-induced gene 1-induced growth suppression of human colon cancer cells
<p>Abstract</p> <p>Background</p> <p>Tazarotene-induced gene 1 (TIG1) is a retinoid-inducible type II tumour suppressor gene. The B isoform of TIG1 (TIG1B) inhibits growth and invasion of cancer cells. Expression of TIG1B is frequently downregulated in various cancer tissues; however, the expression and activities of the TIG1A isoform are yet to be reported. Therefore, this study investigated the effects of the TIG1A and TIG1B isoforms on cell growth and gene expression profiles using colon cancer cells.</p> <p>Methods</p> <p>TIG1A and TIG1B stable clones derived from HCT116 and SW620 colon cancer cells were established using the GeneSwitch system; TIG1 isoform expression was induced by mifepristone treatment. Cell growth was assessed using the WST-1 cell proliferation and colony formation assays. RNA interference was used to examine the TIG1 mediating changes in cell growth. Gene expression profiles were determined using microarray and validated using real-time polymerase chain reaction, and Western blot analyses.</p> <p>Results</p> <p>Both TIG1 isoforms were expressed at high levels in normal prostate and colon tissues and were downregulated in colon cancer cell lines. Both TIG1 isoforms significantly inhibited the growth of transiently transfected HCT116 cells and stably expressing TIG1A and TIG1B HCT116 and SW620 cells. Expression of 129 and 55 genes was altered upon induction of TIG1A and TIG1B expression, respectively, in stably expressing HCT116 cells. Of the genes analysed, 23 and 6 genes were upregulated and downregulated, respectively, in both TIG1A and TIG1B expressing cells. Upregulation of the G-protein-coupled receptor kinase 5 (GRK5) was confirmed using real-time polymerase chain reaction and Western blot analyses in both TIG1 stable cell lines. Silencing of TIG1A or GRK5 expression significantly decreased TIG1A-mediated cell growth suppression.</p> <p>Conclusions</p> <p>Expression of both TIG1 isoforms was observed in normal prostate and colon tissues and was downregulated in colon cancer cell lines. Both TIG1 isoforms suppressed cell growth and stimulated GRK5 expression in HCT116 and SW620 cells. Knockdown of GRK5 expression alleviated TIG1A-induced growth suppression of HCT116 cells, suggesting that GRK5 mediates cell growth suppression by TIG1A. Thus, TIG1 may participate in the downregulation of G-protein coupled signaling by upregulating GRK5 expression.</p
Large expert-curated database for benchmarking document similarity detection in biomedical literature search
Document recommendation systems for locating relevant literature have mostly relied on methods developed a decade ago. This is largely due to the lack of a large offline gold-standard benchmark of relevant documents that cover a variety of research fields such that newly developed literature search techniques can be compared, improved and translated into practice. To overcome this bottleneck, we have established the RElevant LIterature SearcH consortium consisting of more than 1500 scientists from 84 countries, who have collectively annotated the relevance of over 180 000 PubMed-listed articles with regard to their respective seed (input) article/s. The majority of annotations were contributed by highly experienced, original authors of the seed articles. The collected data cover 76% of all unique PubMed Medical Subject Headings descriptors. No systematic biases were observed across different experience levels, research fields or time spent on annotations. More importantly, annotations of the same document pairs contributed by different scientists were highly concordant. We further show that the three representative baseline methods used to generate recommended articles for evaluation (Okapi Best Matching 25, Term Frequency-Inverse Document Frequency and PubMed Related Articles) had similar overall performances. Additionally, we found that these methods each tend to produce distinct collections of recommended articles, suggesting that a hybrid method may be required to completely capture all relevant articles. The established database server located at https://relishdb.ict.griffith.edu.au is freely available for the downloading of annotation data and the blind testing of new methods. We expect that this benchmark will be useful for stimulating the development of new powerful techniques for title and title/abstract-based search engines for relevant articles in biomedical research.Peer reviewe
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