208 research outputs found
Thermal Dileptons at LHC
We predict dilepton invariant-mass spectra for central 5.5 ATeV Pb-Pb
collisions at LHC. Hadronic emission in the low-mass region is calculated using
in-medium spectral functions of light vector mesons within hadronic many-body
theory. In the intermediate-mass region thermal radiation from the Quark-Gluon
Plasma, evaluated perturbatively with hard-thermal loop corrections, takes
over. An important source over the entire mass range are decays of correlated
open-charm hadrons, rendering the nuclear modification of charm and bottom
spectra a critical ingredient.Comment: 2 pages, 2 figures, contributed to Workshop on Heavy Ion Collisions
at the LHC: Last Call for Predictions, Geneva, Switzerland, 14 May - 8 Jun
2007 v2: acknowledgment include
Visualizing the Distribution of Synapses from Individual Neurons in the Mouse Brain
BACKGROUND:Proper function of the mammalian brain relies on the establishment of highly specific synaptic connections among billions of neurons. To understand how complex neural circuits function, it is crucial to precisely describe neuronal connectivity and the distributions of synapses to and from individual neurons. METHODS AND FINDINGS:In this study, we present a new genetic synaptic labeling method that relies on expression of a presynaptic marker, synaptophysin-GFP (Syp-GFP) in individual neurons in vivo. We assess the reliability of this method and use it to analyze the spatial patterning of synapses in developing and mature cerebellar granule cells (GCs). In immature GCs, Syp-GFP is distributed in both axonal and dendritic regions. Upon maturation, it becomes strongly enriched in axons. In mature GCs, we analyzed synapses along their ascending segments and parallel fibers. We observe no differences in presynaptic distribution between GCs born at different developmental time points and thus having varied depths of projections in the molecular layer. We found that the mean densities of synapses along the parallel fiber and the ascending segment above the Purkinje cell (PC) layer are statistically indistinguishable, and higher than previous estimates. Interestingly, presynaptic terminals were also found in the ascending segments of GCs below and within the PC layer, with the mean densities two-fold lower than that above the PC layer. The difference in the density of synapses in these parts of the ascending segment likely reflects the regional differences in postsynaptic target cells of GCs. CONCLUSIONS:The ability to visualize synapses of single neurons in vivo is valuable for studying synaptogenesis and synaptic plasticity within individual neurons as well as information flow in neural circuits
Imprinted CDKN1C Is a Tumor Suppressor in Rhabdoid Tumor and Activated by Restoration of SMARCB1 and Histone Deacetylase Inhibitors
SMARCB1 is deleted in rhabdoid tumor, an aggressive paediatric malignancy affecting the kidney and CNS. We hypothesized that the oncogenic pathway in rhabdoid tumors involved epigenetic silencing of key cell cycle regulators as a consequence of altered chromatin-remodelling, attributable to loss of SMARCB1, and that this hypothesis if proven could provide a biological rationale for testing epigenetic therapies in this disease. We used an inducible expression system to show that the imprinted cell cycle inhibitor CDKN1C is a downstream target for SMARCB1 and is transcriptionally activated by increased histone H3 and H4 acetylation at the promoter. We also show that CDKN1C expression induces cell cycle arrest, CDKN1C knockdown with siRNA is associated with increased proliferation, and is able to compete against the anti-proliferative effect of restored SMARCB1 expression. The histone deacetylase inhibitor (HDACi), Romidepsin, specifically restored CDKN1C expression in rhabdoid tumor cells through promoter histone H3 and H4 acetylation, recapitulating the effect of SMARCB1 on CDKNIC allelic expression, and induced cell cycle arrest in G401 and STM91-01 rhabdoid tumor cell lines. CDKN1C expression was also shown to be generally absent in clinical specimens of rhabdoid tumor, however CDKN1A and CDKN1B expression persisted. Our observations suggest that maintenance of CDKN1C expression plays a critical role in preventing rhabdoid tumor growth. Significantly, we report for the first time, parallels between the molecular pathways of SMARCB1 restoration and Romidepsin treatment, and demonstrate a biological basis for the further exploration of histone deacetylase inhibitors as relevant therapeutic reagents in the treatment of rhabdoid tumor
The James Webb Space Telescope Mission
Twenty-six years ago a small committee report, building on earlier studies,
expounded a compelling and poetic vision for the future of astronomy, calling
for an infrared-optimized space telescope with an aperture of at least .
With the support of their governments in the US, Europe, and Canada, 20,000
people realized that vision as the James Webb Space Telescope. A
generation of astronomers will celebrate their accomplishments for the life of
the mission, potentially as long as 20 years, and beyond. This report and the
scientific discoveries that follow are extended thank-you notes to the 20,000
team members. The telescope is working perfectly, with much better image
quality than expected. In this and accompanying papers, we give a brief
history, describe the observatory, outline its objectives and current observing
program, and discuss the inventions and people who made it possible. We cite
detailed reports on the design and the measured performance on orbit.Comment: Accepted by PASP for the special issue on The James Webb Space
Telescope Overview, 29 pages, 4 figure
Charged-particle nuclear modification factors in PbPb and pPb collisions at √sNN=5.02 TeV
The spectra of charged particles produced within the pseudorapidity window |η| 20 GeV, RpA exhibits weak momentum dependence and shows a moderate enhancement above unity.[Figure not available: see fulltext.]we acknowledge the enduring support for the construction and
operation of the LHC and the CMS detector provided by the following funding agencies:
BMWFW and FWF (Austria); FNRS and FWO (Belgium); CNPq, CAPES, FAPERJ,
and FAPESP (Brazil); MES (Bulgaria); CERN; CAS, MoST, and NSFC (China); COLCIENCIAS
(Colombia); MSES and CSF (Croatia); RPF (Cyprus); SENESCYT (Ecuador);
MoER, ERC IUT and ERDF (Estonia); Academy of Finland, MEC, and HIP (Finland);
CEA and CNRS/IN2P3 (France); BMBF, DFG, and HGF (Germany); GSRT (Greece);
OTKA and NIH (Hungary); DAE and DST (India); IPM (Iran); SFI (Ireland); INFN
(Italy); MSIP and NRF (Republic of Korea); LAS (Lithuania); MOE and UM (Malaysia);
BUAP, CINVESTAV, CONACYT, LNS, SEP, and UASLP-FAI (Mexico); MBIE (New
Zealand); PAEC (Pakistan); MSHE and NSC (Poland); FCT (Portugal); JINR (Dubna);
MON, RosAtom, RAS and RFBR (Russia); MESTD (Serbia); SEIDI and CPAN (Spain);
Swiss Funding Agencies (Switzerland); MST (Taipei); ThEPCenter, IPST, STAR and
NSTDA (Thailand); TUBITAK and TAEK (Turkey); NASU and SFFR (Ukraine); STFC
(United Kingdom); DOE and NSF (U.S.A.)
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