28 research outputs found
Barred Galaxies in the Abell 901/2 Supercluster with STAGES
We present a study of bar and host disk evolution in a dense cluster
environment, based on a sample of ~800 bright (MV <= -18) galaxies in the Abell
901/2 supercluster at z~0.165. We use HST ACS F606W imaging from the STAGES
survey, and data from Spitzer, XMM-Newton, and COMBO-17. We identify and
characterize bars through ellipse-fitting, and other morphological features
through visual classification. (1) We explore three commonly used methods for
selecting disk galaxies. We find 625, 485, and 353 disk galaxies, respectively,
via visual classification, a single component S'ersic cut (n <= 2.5), and a
blue-cloud cut. In cluster environments, the latter two methods miss 31% and
51%, respectively, of visually-identified disks. (2) For moderately inclined
disks, the three methods of disk selection yield a similar global optical bar
fraction (f_bar-opt) of 34% +10%/-3%, 31% +10%/-3%, and 30% +10%/-3%,
respectively. (3) f_bar-opt rises in brighter galaxies and those which appear
to have no significant bulge component. Within a given absolute magnitude bin,
f_bar-opt is higher in visually-selected disk galaxies that have no bulge as
opposed to those with bulges. For a given morphological class, f_bar-opt rises
at higher luminosities. (4) For bright early-types, as well as faint late-type
systems with no evident bulge, the optical bar fraction in the Abell 901/2
clusters is comparable within a factor of 1.1 to 1.4 to that of field galaxies
at lower redshifts (5) Between the core and the virial radius of the cluster at
intermediate environmental densities, the optical bar fraction does not appear
to depend strongly on the local environment density and varies at most by a
factor of ~1.3. We discuss the implications of our results for the evolution of
bars and disks in dense environments.Comment: accepted for publication in ApJ, abstract abridged, for high
resolution figures see
http://www.as.utexas.edu/~marinova/STAGES/STAGES_bars.pd
Lipid Interacting Regions in Phosphate Stress Glycosyltransferase atDGD2 from Arabidopsis thaliana
Biological Earth observation with animal sensors
Space-based tracking technology using low-cost miniature tags is now delivering data on fine-scale animal movement at near-global scale. Linked with remotely sensed environmental data, this offers a biological lens on habitat integrity and connectivity for conservation and human health; a global network of animal sentinels of environmen-tal change
Evidenzbasierte Psychotherapie bei Abhängigkeitserkrankungen
Hintergrund
Abhängigkeitserkrankungen bilden die Gruppe der häufigsten psychischen Störungen. Trotz eines breiten Behandlungsangebots an psychotherapeutischen Interventionen ist der Anteil der Patienten, die eine evidenzbasierte Behandlung bzw. im Rahmen der ambulanten Versorgung eine psychotherapeutische Behandlung erhalten, sehr gering.
Ziel der Arbeit
Vor diesem Hintergrund soll eine Neubewertung der empirischen Evidenz für die Wirksamkeit verschiedener psychotherapeutischer Behandlungsansätze vorgenommen werden und Handlungsempfehlungen für die Praxis abgeleitet werden.
Material und Methoden
Es wurde eine umfassende Literaturrecherche in einem mehrstufigen Vorgehen in den relevanten nationalen und internationalen Datenbanken durchgeführt. Anschließend erfolgte eine Analyse der aktuellen Leitlinien, Übersichtsarbeiten und Primärstudien zum Thema Therapie bei Abhängigkeitserkrankungen.
Ergebnisse
Es konnten insgesamt 3 aktuelle nationale Leitlinien, 2 Reviews sowie 16 Primärstudien identifiziert werden. Insbesondere können kognitive Verhaltenstherapie, verhaltenstherapeutische Interventionen und die motivationalen Interventionen als evidenzbasierte Behandlungsansätze bei verschiedenen Abhängigkeitserkrankungen betrachtet werden. Bei Tabakabhängigkeit können alternativ auch hypnotherapeutische Maßnahmen empfohlen werden. Interessant für die Praxis sind auch die neuen Behandlungsmethoden wie das neurokognitive Training und die achtsamkeitsbasierten Interventionen.
Diskussion
Die Studienlage ist zum Teil inkonsistent oder numerisch unzureichend trotz hoher Qualität. Weitere Forschungsarbeiten werden benötigt, die sich mit verschiedenen Substanzabhängigkeiten und Patientengruppen beschäftigen
Recommended from our members
Visualizing locus-specific sister chromatid exchange reveals differential patterns of replication stress-induced fragile site breakage.
Chromosomal fragile sites are genomic loci sensitive to replication stress which accumulate high levels of DNA damage, and are frequently mutated in cancers. Fragile site damage is thought to arise from the aberrant repair of spontaneous replication stress, however successful fragile site repair cannot be calculated using existing techniques. Here, we report a new assay measuring recombination-mediated repair at endogenous genomic loci by combining a sister chromatid exchange (SCE) assay with fluorescent in situ hybridization (SCE-FISH). Using SCE-FISH, we find that endogenous and exogenous replication stress generated unrepaired breaks and SCEs at fragile sites. We also find that distinct sources of replication stress induce distinct patterns of breakage: ATR inhibition induces more breaks at early replicating fragile sites (ERFS), while ERFS and late-replicating common fragile sites (CFS) are equally fragile in response to aphidicolin. Furthermore, SCEs were suppressed at fragile sites near centromeres in response to replication stress, suggesting that genomic location influences DNA repair pathway choice. SCE-FISH also measured successful recombination in human primary lymphocytes, and identificed the proto-oncogene BCL2 as a replication stress-induced fragile site. These findings demonstrate that SCE-FISH frequency at fragile sites is a sensitive indicator of replication stress, and that large-scale genome organization influences DNA repair pathway choice
Neighborhoods and Obesity in Later Life
Objectives. We examined the influence of neighborhood
environment on the weight status of adults 55 years and older
Protective effect of Growth Hormone-Releasing Hormone agonist in bacterial toxin-induced pulmonary barrier dysfunction
Rationale: Antibiotic treatment of patients infected with G(−) or G(+) bacteria promotes release of the toxins lipopolysaccharide (LPS) and pneumolysin (PLY) in their lungs. Growth Hormone-releasing Hormone (GHRH) agonist JI-34 protects human lung microvascular endothelial cells (HL-MVEC), expressing splice variant 1 (SV-1) of the receptor, from PLY-induced barrier dysfunction. We investigated whether JI-34 also blunts LPS-induced hyperpermeability. Since GHRH receptor (GHRH-R) signaling can potentially stimulate both cAMP-dependent barrier-protective pathways as well as barrier-disruptive protein kinase C pathways, we studied their interaction in GHRH agonist-treated HL-MVEC, in the presence of PLY, by means of siRNA-mediated protein kinase A (PKA) depletion. Methods: Barrier function measurements were done in HL-MVEC monolayers using Electrical Cell substrate Impedance Sensing (ECIS) and VE-cadherin expression by Western blotting. Capillary leak was assessed by Evans Blue dye (EBD) incorporation. Cytokine generation in broncho-alveolar lavage fluid (BALF) was measured by multiplex analysis. PKA and PKC-α activity were assessed by Western blotting. Results: GHRH agonist JI-34 significantly blunts LPS-induced barrier dysfunction, at least in part by preserving VE-cadherin expression, while not affecting inflammation. In addition to activating PKA, GHRH agonist also increases PKC-α activity in PLY-treated HL-MVEC. Treatment with PLY significantly decreases resistance in control siRNA-treated HL-MVEC, but does so even more in PKA-depleted monolayers. Pretreatment with GHRH agonist blunts PLY-induced permeability in control siRNA-treated HL-MVEC, but fails to improve barrier function in PKA-depleted PLY-treated monolayers. Conclusions: GHRH signaling in HL-MVEC protects from both LPS and PLY-mediated endothelial barrier dysfunction and concurrently induces a barrier-protective PKA-mediated and a barrier-disruptive PKC-α-induced pathway in the presence of PLY, the former of which dominates the latter