594 research outputs found
Bostonia. Volume 11
Founded in 1900, Bostonia magazine is Boston University's main alumni publication, which covers alumni and student life, as well as university activities, events, and programs
IKK/NF-κB signaling contributes to glioblastoma stem cell maintenance
// Amanda L. Rinkenbaugh 1,2 , Patricia C. Cogswell 2,3 , Barbara Calamini 4 , Denise E. Dunn 4 , Anders I. Persson 5,6 , William A. Weiss 5,6 , Donald C. Lo 4 and Albert S. Baldwin 2 1 Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, USA 2 Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA 3 Chordoma Foundation, Durham, NC, USA 4 Center for Drug Discovery and Department of Neurobiology, Duke University Medical Center, Durham, NC, USA 5 Helen Diller Family Comprehensive Cancer Center and Department of Neurology, University of California, San Francisco, CA, USA 6 Department of Neurological Surgery and Brain Tumor Research Center, University of California, San Francisco, CA, USA Correspondence to: Albert Baldwin, email: // Keywords : NF-κB, glioblastoma, cancer stem cells, tumor-initiating cells Received : March 14, 2016 Accepted : September 24, 2016 Published : October 06, 2016 Abstract Glioblastoma multiforme (GBM) carries a poor prognosis and continues to lack effective treatments. Glioblastoma stem cells (GSCs) drive tumor formation, invasion, and drug resistance and, as such, are the focus of studies to identify new therapies for disease control. Here, we identify the involvement of IKK and NF-κB signaling in the maintenance of GSCs. Inhibition of this pathway impairs self-renewal as analyzed in tumorsphere formation and GBM expansion as analyzed in brain slice culture. Interestingly, both the canonical and non-canonical branches of the NF-κB pathway are shown to contribute to this phenotype. One source of NF-κB activation in GBM involves the TGF-β/TAK1 signaling axis. Together, our results demonstrate a role for the NF-κB pathway in GSCs and provide a mechanistic basis for its potential as a therapeutic target in glioblastoma
The Vehicle, 1966, Vol. 8
Vol. 8
Table of Contents
CommentaryBill Moser & Avis Eaglestonpage 3
The Vengeance of the DeadStephen W. Gibbspage 5
Ode To A MeadowKathleen McCormackpage 12
Row OnDavid Helmpage 13
Sonnet 63R.L. Hudsonpage 14
UntitledKathleen McCormackpage 14
The Pure GoldDavid Helmpage 15
CommunionDavid Helmpage 15
PreludeMichael Baldwinpage 15
The AlbatrossKaren Cooleypage 16
The Albatross (photo)DeWittpage 17
Ruff and the VaseDavid Helmpage 18
LaBelleKathleen McCormackpage 19
Not Quite SoR.L. Hudsonpage 20
Feeling (no number)David Reifpage 21
Song at DuskDavid Helmpage 21
Arcadia RuminationsR.L. Hudsonpage 22
The BarWayne Johnsonpage 25
HelloWilliam Framepage 26
The ProcessJerry DeWittpage 27
The KillingAdrian Beardpage 30
The Amusement Park GameStephen W. Gibbspage 38
DamnMel Tylerpage 40
PainWilliam Framepage 40
UntitledSusan Champlinpage 41
Portrait of A Scholar As A Young ManStephen W. Gibbspage 42
The TimesW.D.Mpage 46
ParadoxW.D.M.page 46
MankindDavid Helmpage 47https://thekeep.eiu.edu/vehicle/1014/thumbnail.jp
The Vehicle, 1966, Vol. 8
Vol. 8
Table of Contents
CommentaryBill Moser & Avis Eaglestonpage 3
The Vengeance of the DeadStephen W. Gibbspage 5
Ode To A MeadowKathleen McCormackpage 12
Row OnDavid Helmpage 13
Sonnet 63R.L. Hudsonpage 14
UntitledKathleen McCormackpage 14
The Pure GoldDavid Helmpage 15
CommunionDavid Helmpage 15
PreludeMichael Baldwinpage 15
The AlbatrossKaren Cooleypage 16
The Albatross (photo)DeWittpage 17
Ruff and the VaseDavid Helmpage 18
LaBelleKathleen McCormackpage 19
Not Quite SoR.L. Hudsonpage 20
Feeling (no number)David Reifpage 21
Song at DuskDavid Helmpage 21
Arcadia RuminationsR.L. Hudsonpage 22
The BarWayne Johnsonpage 25
HelloWilliam Framepage 26
The ProcessJerry DeWittpage 27
The KillingAdrian Beardpage 30
The Amusement Park GameStephen W. Gibbspage 38
DamnMel Tylerpage 40
PainWilliam Framepage 40
UntitledSusan Champlinpage 41
Portrait of A Scholar As A Young ManStephen W. Gibbspage 42
The TimesW.D.Mpage 46
ParadoxW.D.M.page 46
MankindDavid Helmpage 47https://thekeep.eiu.edu/vehicle/1014/thumbnail.jp
Bronchus-associated lymphoid tissue–resident Foxp3+ T lymphocytes prevent antibody-mediated lung rejection
Scaffold Translation: Barriers Between Concept and Clinic
Translation of scaffold-based bone tissue engineering (BTE) therapies to clinical use remains, bluntly, a failure. This dearth of translated tissue engineering therapies (including scaffolds) remains despite 25 years of research, research funding totaling hundreds of millions of dollars, over 12,000 papers on BTE and over 2000 papers on BTE scaffolds alone in the past 10 years (PubMed search). Enabling scaffold translation requires first an understanding of the challenges, and second, addressing the complete range of these challenges. There are the obvious technical challenges of designing, manufacturing, and functionalizing scaffolds to fill the Form, Fixation, Function, and Formation needs of bone defect repair. However, these technical solutions should be targeted to specific clinical indications (e.g., mandibular defects, spine fusion, long bone defects, etc.). Further, technical solutions should also address business challenges, including the need to obtain regulatory approval, meet specific market needs, and obtain private investment to develop products, again for specific clinical indications. Finally, these business and technical challenges present a much different model than the typical research paradigm, presenting the field with philosophical challenges in terms of publishing and funding priorities that should be addressed as well. In this article, we review in detail the technical, business, and philosophical barriers of translating scaffolds from Concept to Clinic. We argue that envisioning and engineering scaffolds as modular systems with a sliding scale of complexity offers the best path to addressing these translational challenges.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90495/1/ten-2Eteb-2E2011-2E0251.pd
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Patterns of sick-leave and health outcomes in injured workers with back pain
Little is known about the sick-leave experiences of workers who make a workers’ compensation claim for back pain. Our objective is to describe the 1-year patterns of sick-leave and the health outcomes of a cohort of workers who make a workers’ compensation claim for back pain. We studied a cohort of 1,831 workers from five large US firms who made incident workers’ compensation claims for back pain between January 1, 1999 and June 30, 2002. Injured workers were interviewed 1 month (n = 1,321), 6 months (n = 810) and 1 year (n = 462) following the onset of their pain. We described the course of back pain using four patterns of sick-leave: (1) no sick-leave, (2) returned to worked and stayed, (3) multiple episodes of sick-leave and (4) not yet returned to work. We described the health outcomes as back and/or leg pain intensity, functional limitations and health-related quality of life. We analyzed data from participants who completed all follow-up interviews (n = 457) to compute the probabilities of transition between patterns of sick-leave. A significant proportion of workers experienced multiple episodes of sick-leave (30.2%; 95% CI 25.0–35.1) during the 1-year follow-up. The proportion of workers who did not report sick-leave declined from 42.4% (95% CI 39.0–46.1) at 1 month to 33.6% (28.0–38.7) at 1 year. One year after the injury, 2.9% (1.6–4.9) of workers had not yet returned to work. Workers who did not report sick-leave and those who returned and stayed at work reported better health outcomes than workers who experienced multiple episodes of sick-leave or workers who had not returned to work. Almost a third of workers with an incident episode of back pain experience recurrent spells of work absenteeism during the following year. Our data suggest that stable patterns of sick-leave are associated with better health
Galaxy Zoo: dust and molecular gas in early-type galaxies with prominent dust lanes
We study dust and associated molecular gas in 352 nearby early-type galaxies
(ETGs) with prominent dust lanes. 65% of these `dusty ETGs' (D-ETGs) are
morphologically disturbed, suggesting a merger origin. This is consistent with
the D-ETGs residing in lower density environments compared to the controls
drawn from the general ETG population. 80% of D-ETGs inhabit the field
(compared to 60% of the controls) and <2% inhabit clusters (compared to 10% of
the controls). Compared to the controls, D-ETGs exhibit bluer UV-optical
colours (indicating enhanced star formation) and an AGN fraction that is more
than an order of magnitude greater (indicating higher incidence of nuclear
activity). The clumpy dust mass residing in large-scale features is estimated,
using the SDSS r-band images, to be 10^{4.5}-10^{6.5} MSun. A comparison to the
total (clumpy + diffuse) dust masses- calculated using the far-IR fluxes of 15%
of the D-ETGs that are detected by the IRAS- indicates that only ~20% of the
dust resides in these large-scale features. The dust masses are several times
larger than the maximum value expected from stellar mass loss, ruling out an
internal origin. The dust content shows no correlation with the blue
luminosity, indicating that it is not related to a galactic scale cooling flow.
No correlation is found with the age of the recent starburst, suggesting that
the dust is accreted directly in the merger rather than being produced in situ
by the triggered star formation. Using molecular gas-to-dust ratios of ETGs in
the literature we estimate that the median current and initial molecular gas
fraction are ~1.3% and ~4%, respectively. Recent work suggests that the merger
activity in nearby ETGs largely involves minor mergers (mass ratios between
1:10 and 1:4). If the IRAS-detected D-ETGs form via this channel, then the
original gas fractions of the accreted satellites are 20%-44%. [Abridged]Comment: 11 pages, 18 figures, 1 table, MNRAS (Accepted for publication- 2012
March 19
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