144 research outputs found
Local starburst galaxies and their descendants
Despite strong interest in the starburst (hereafter SB) phenomenon, the
concept remains ill-defined. We use a strict definition of SB to examine the
statistical properties of local SB and post-starburst (hereafter PB) galaxies.
We also seek relationships to active galaxies. Potential SB galaxies are
selected from the SDSS DR7 and their stellar content is analysed. We apply an
age dependent dust attenuation correction and derive star formation rates
(SFR), ages and masses of the young and old populations. The photometric masses
nicely agree with dynamical masses derived from the H-alpha emission line
width. To select SB galaxies, we use the birthrate parameter b=SFR/,
requiring b>=3. The PB sample is selected from the citerion EW(Hdelta_abs)>=6
A. Only 1% of star-forming galaxies are found to be SB galaxies. They
contribute 3-6% to the stellar production and are therefore unimportant for the
local star formation activity. The median SB age is 70 Myr, roughly independent
of mass. The b-parameter strongly depends on burst age. Values close to b=60
are found at ages ~10 Myr, while almost no SBs are found at ages >1 Gyr. The
median baryonic burst mass fraction of sub-L* galaxies is 5%, decreasing slowly
with mass. The median mass fraction of the recent burst in the PB sample is
5-10%. The age-mass distribution of the progenitors of the PBs is bimodal with
a break at log(M)~10.6 above which the ages are doubled. The SB and PB
luminosity functions (hereafter LFs) follow each other closely until M_r~-21,
when AGNs begin to dominate. The PB LF continues to follow the AGN LF while SB
loose significance. This suggests that the number of luminous SBs is
underestimated by about one dex at high luminosities, due to large amounts of
dust and/or AGN blending. It also indicates that the SB phase preceded the AGN
phase. We also discuss the conditions for global gas outflow caused by stellar
feedback.Comment: Accepted for publication in Astronomy and Astrophysics. This is an
extended, substantially revised and corrected version with partly modified
conclusion
Size-Resolved Emission Factor for Particle generation Caused by Studded Tires - Experimental Results
Monitoring of northern climate exposure
Currently, facility managers are faced with many advanced decisions
regarding when and how to inspect, maintain, repair or renew existing facilities in a costeffective manner. The evolution of the deteriorations of road structures in reinforced
concrete depends on the exposure of the elements to water in liquid form or vapour and to
other aggressive agents such as chloride. Current models of ionic transport neglect the
effect of real ionic concentration in contact with concrete structures, it means boundary
conditions are considered with simple tendency as uniform concentration during the winter
period and model parameters are derived from the fitting method. Therefore, it implies in
ineffective prediction models of deterioration, i.e. steel rebar corrosion by chloride
presence or carbonation, alkali-granular reaction, acid attacks, etc. Structure are sensitive
to their environment and their interaction with it is directly related to the processes of
deterioration. The degradation of structures exposed to salt-laden mist is faster in the wetter
areas. On the contrary, the deterioration of the structures caused by salt spray in the drier
zone is slower. The structures, exposed to splashing (precipitation, wind, splash, etc.), have
a slower rate of degradation in the wetter regions. The amount of rain has an indirect effect
in the process of deterioration of the structure exposed to salt-laden mist because it changes
the contact time of chloride on the surface of the structures. For this purpose, a unique
exposure monitoring was developed. This mobile station, named MExStUL, contains an
atmospheric sensor and new possibilities of chloride detection contained in splashes, mist
and static water near the road improving the real exposure of structure and the boundary
conditions. First results highlight the real influence of environmental parameters on
structures durability on highways. Salt concentration is not uniform during winter period
and water thickness demonstrate important periods of drying
Genome-wide search for breast cancer linkage in large Icelandic non-BRCA1/2 families
Abstract
Introduction:
A significant proportion of high-risk breast cancer families are not explained by mutations in known genes. Recent genome-wide searches (GWS) have not revealed any single major locus reminiscent of BRCA1 and BRCA2, indicating that still unidentified genes may explain relatively few families each or interact in a way obscure to linkage analyses. This has drawn attention to possible benefits of studying populations where genetic heterogeneity might be reduced. We thus performed a GWS for linkage on nine Icelandic multiple-case non-BRCA1/2 families of desirable size for mapping highly penetrant loci. To follow up suggestive loci, an additional 13 families from other Nordic countries were genotyped for selected markers.
Methods:
GWS was performed using 811 microsatellite markers providing about five centiMorgan (cM) resolution. Multipoint logarithm of odds (LOD) scores were calculated using parametric and nonparametric methods. For selected markers and cases, tumour tissue was compared to normal tissue to look for allelic loss indicative of a tumour suppressor gene.
Results:
The three highest signals were located at chromosomes 6q, 2p and 14q. One family contributed suggestive LOD scores (LOD 2.63 to 3.03, dominant model) at all these regions, without consistent evidence of a tumour suppressor gene. Haplotypes in nine affected family members mapped the loci to 2p23.2 to p21, 6q14.2 to q23.2 and 14q21.3 to q24.3. No evidence of a highly penetrant locus was found among the remaining families. The heterogeneity LOD (HLOD) at the 6q, 2p and 14q loci in all families was 3.27, 1.66 and 1.24, respectively. The subset of 13 Nordic families showed supportive HLODs at chromosome 6q (ranging from 0.34 to 1.37 by country subset). The 2p and 14q loci overlap with regions indicated by large families in previous GWS studies of breast cancer.
Conclusions:
Chromosomes 2p, 6q and 14q are candidate sites for genes contributing together to high breast cancer risk. A polygenic model is supported, suggesting the joint effect of genes in contributing to breast cancer risk to be rather common in non-BRCA1/2 families. For genetic counselling it would seem important to resolve the mode of genetic interaction
Genomic subtypes of breast cancer identified by array comparative genomic hybridization display distinct molecular and clinical characteristics
Abstract
Introduction
Breast cancer is a profoundly heterogeneous disease with respect to biologic and clinical behavior. Gene-expression profiling has been used to dissect this complexity and to stratify tumors into intrinsic gene-expression subtypes, associated with distinct biology, patient outcome, and genomic alterations. Additionally, breast tumors occurring in individuals with germline BRCA1 or BRCA2 mutations typically fall into distinct subtypes.
Methods
We applied global DNA copy number and gene-expression profiling in 359 breast tumors. All tumors were classified according to intrinsic gene-expression subtypes and included cases from genetically predisposed women. The Genomic Identification of Significant Targets in Cancer (GISTIC) algorithm was used to identify significant DNA copy-number aberrations and genomic subgroups of breast cancer.
Results
We identified 31 genomic regions that were highly amplified in > 1% of the 359 breast tumors. Several amplicons were found to co-occur, the 8p12 and 11q13.3 regions being the most frequent combination besides amplicons on the same chromosomal arm. Unsupervised hierarchical clustering with 133 significant GISTIC regions revealed six genomic subtypes, termed 17q12, basal-complex, luminal-simple, luminal-complex, amplifier, and mixed subtypes. Four of them had striking similarity to intrinsic gene-expression subtypes and showed associations to conventional tumor biomarkers and clinical outcome. However, luminal A-classified tumors were distributed in two main genomic subtypes, luminal-simple and luminal-complex, the former group having a better prognosis, whereas the latter group included also luminal B and the majority of BRCA2-mutated tumors. The basal-complex subtype displayed extensive genomic homogeneity and harbored the majority of BRCA1-mutated tumors. The 17q12 subtype comprised mostly HER2-amplified and HER2-enriched subtype tumors and had the worst prognosis. The amplifier and mixed subtypes contained tumors from all gene-expression subtypes, the former being enriched for 8p12-amplified cases, whereas the mixed subtype included many tumors with predominantly DNA copy-number losses and poor prognosis.
Conclusions
Global DNA copy-number analysis integrated with gene-expression data can be used to dissect the complexity of breast cancer. This revealed six genomic subtypes with different clinical behavior and a striking concordance to the intrinsic subtypes. These genomic subtypes may prove useful for understanding the mechanisms of tumor development and for prognostic and treatment prediction purposes
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