Star Formation at z=2.481 in the Lensed Galaxy SDSS J1110+6459, I: Lens Modeling and Source Reconstruction

Using the combined resolving power of the Hubble Space Telescope and gravitational lensing, we resolve star-forming structures in a z~2.5 galaxy on scales much smaller than the usual kiloparsec diffraction limit of HST. SGAS J111020.0+645950.8 is a clumpy, star forming galaxy lensed by the galaxy cluster SDSS J1110+6459 at z = 0.659, with a total magnification ~30x across the entire arc. We use a hybrid parametric/non-parametric strong lensing mass model to compute the deflection and magnification of this giant arc, reconstruct the light distribution of the lensed galaxy in the source plane, and resolve the star formation into two dozen clumps. We develop a forward-modeling technique to model each clump in the source plane. We ray trace the model to the image plane, convolve with the instrumental point spread function (PSF), and compare with the GALFIT model of the clumps in the image plane, which decomposes clump structure from more extended emission. This technique has the advantage, over ray tracing, by accounting for the asymmetric lensing shear of the galaxy in the image plane and the instrument PSF. At this resolution, we can begin to study star formation on a clump-by-clump basis, toward the goal of understanding feedback mechanisms and the buildup of exponential disks at high redshift.Comment: 19 pages, 12 figures, accepted to Ap

Quality Assurance for KidsMatter Primary: a scoping paper

This Scoping Paper reviews and details options for the ongoing quality assurance of KidsMatter PrimaryThis scoping paper was commissioned and funded by beyondblue, the national depression initiative. The Flinders team wishes to thank and acknowledge beyondblue for their ongoing support throughout the development of this report

KidsMatter Early Childhood Evaluation in Services with High Proportions of Aboriginal and Torres Strait Islander Children

This is the report of an evaluation of the implementation of KidsMatter Early Childhood (KMEC) in early child care services with relatively higher proportions of Aboriginal or Torres Strait Islander children situated within the initial larger sample of 111 long day care services and preschools involved in the KMEC pilot phase during 2010 and 2011.KidsMatter: the Australian Early Childhood Service Mental Health Initiative, is developed in collaboration by the Australian Government Department of Health and Ageing, beyondblue, the Australian Psychological Society, and Early Childhood Australia

KidsMatter Early Childhood Evaluation Report

KidsMatter Early Childhood is the Australian national early childhood mental health promotion, prevention and early intervention initiative specifically developed for early childhood services. It was trialled in 111 long day care services and preschools during 2010 and 2011. KMEC involves the people who have a significant influence on young children’s lives – parents, carers, families and early childhood educators, along with a range of community and health professionals – in making a positive difference to young children’s mental health and wellbeing during this important developmental period. The KMEC initiative provides a framework to enable services to plan and implement evidencebased mental health promotion, prevention and early intervention strategies. These strategies aim to improve the mental health and wellbeing of children from birth to school age, reduce mental health difficulties among children, and achieve greater support for children experiencing mental health difficulties and their families.KidsMatter Australian Early Childhood Mental Health Initiative was developed through collaboration between beyondblue, the Australian Psychological Society and Early Childhood Australia, and with funding from the Australian Government Department of Health and Ageing and beyondblue

Star Formation at z = 2.481 in the Lensed Galaxy SDSS J1110+6459: Star Formation Down to 30 pc Scales

We present measurements of the surface density of star formation, the star-forming clump luminosity function, and the clump size distribution function, for the lensed galaxy SGAS J111020.0+645950.8 at a redshift of z =2.481. The physical size scales that we probe, radii r = 30-50 pc, are considerably smaller scales than have yet been studied at these redshifts. The star formation surface density we find within these small clumps is consistent with surface densities measured previously for other lensed galaxies at similar redshift. Twenty-two percent of the rest-frame ultraviolet light in this lensed galaxy arises from small clumps, with r is less than 100 pc. Within the range of overlap, the clump luminosity function measured for this lensed galaxy is remarkably similar to those of z is approximately 0 galaxies. In this galaxy, star-forming regions smaller than 100 pc-physical scales not usually resolved at these redshifts by current telescopes-are important locations of star formation in the distant universe. If this galaxy is representative, this may contradict the theoretical picture in which the critical size scale for star formation in the distant universe is of order 1 kiloparsec. Instead, our results suggest that current telescopes have not yet resolved the critical size scales of star-forming activity in galaxies over most of cosmic time

Increased resistance to biotrophic pathogens in the Arabidopsis constitutive induced resistance 1 mutant is EDS1 and PAD4-dependent and modulated by environmental temperature

The Arabidopsis constitutive induced resistance 1 ( cir1 ) mutant displays salicylic acid (SA)-dependent constitutive expression of defence genes and enhanced resistance to biotrophic pathogens. To further characterise the role of CIR1 in plant immunity we conducted epistasis analyses with two key components of the SA-signalling branch of the defence network, ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and PHYTOALEXIN DEFICIENT4 (PAD4). We demonstrate that the constitutive defence phenotypes of cir1 require both EDS1 and PAD4, indicating that CIR1 lies upstream of the EDS1-PAD4 regulatory node in the immune signalling network. In light of this finding we examined EDS1 expression in cir1 and observed increased protein, but not mRNA levels in this mutant, suggesting that CIR1 might act as a negative regulator of EDS1 via a post-transcriptional mechanism. Finally, as environmental temperature is known to influence the outcome of plant-pathogen interactions, we analysed cir1 plants grown at 18, 22 or 25°C. We found that susceptibility to Pseudomonas syringae pv. tomato ( Pst ) DC3000 is modulated by temperature in cir1 . Greatest resistance to this pathogen (relative to PR-1:LUC control plants) was observed at 18°C, while at 25°C no difference in susceptibility between cir1 and control plants was apparent. The increase in resistance to Pst DC3000 at 18°C correlated with a stunted growth phenotype, suggesting that activation of defence responses may be enhanced at lower temperatures in the cir1 mutant

Cardiomyocyte-Specific Human Bcl2-Associated Anthanogene 3 P209L Expression Induces Mitochondrial Fragmentation, Bcl2-Associated Anthanogene 3 Haploinsufficiency, and Activates p38 Signaling

Supplemental Data Supplemental Table S1 Download Supplemental Table S2 Download Supplemental Table S3 Download Supplemental Table S4 Download Supplemental Data Supplemental material for this article can be found at . The Bcl2-associated anthanogene (BAG) 3 protein is a member of the BAG family of cochaperones, which supports multiple critical cellular processes, including critical structural roles supporting desmin and interactions with heat shock proteins and ubiquitin ligases intimately involved in protein quality control. The missense mutation P209L in exon 3 results in a primarily cardiac phenotype leading to skeletal muscle and cardiac complications. At least 10 other Bag3 mutations have been reported, nine resulting in a dilated cardiomyopathy for which no specific therapy is available. We generated αMHC-human Bag3 P209L transgenic mice and characterized the progressive cardiac phenotype in vivo to investigate its utility in modeling human disease, understand the underlying molecular mechanisms, and identify potential therapeutic targets. We identified a progressive heart failure by echocardiography and Doppler analysis and the presence of pre-amyloid oligomers at 1 year. Paralleling the pathogenesis of neurodegenerative diseases (eg, Parkinson disease), pre-amyloid oligomers–associated alterations in cardiac mitochondrial dynamics, haploinsufficiency of wild-type BAG3, and activation of p38 signaling were identified. Unexpectedly, increased numbers of activated cardiac fibroblasts were identified in Bag3 P209L Tg+ hearts without increased fibrosis. Together, these findings point to a previously undescribed therapeutic target that may have application to mutation-induced myofibrillar myopathies as well as other common causes of heart failure that commonly harbor misfolded proteins

BRG1 and BRM SWI/SNF ATPases redundantly maintain cardiomyocyte homeostasis by regulating cardiomyocyte mitophagy and mitochondrial dynamics in vivo

There has been an increasing recognition that mitochondrial perturbations play a central role in human heart failure. Discovery of mitochondrial networks, whose function is to maintain the regulation of mitochondrial biogenesis, autophagy (‘mitophagy’) and mitochondrial fusion/fission, are new potential therapeutic targets. Yet our understanding of how the molecular underpinning of these processes is just emerging. We recently identified a role of the SWI/SNF ATP-dependent chromatin remodeling complexes in the metabolic homeostasis of the adult cardiomyocyte using cardiomyocyte-specific and inducible deletion of the SWI/SNF ATPases BRG1 and BRM in adult mice (Brg1/Brm double mutant mice). To build upon these observations in early alterated metabolism, the present study looks at the subsequent alterations in mitochondrial quality control mechanisms in the impaired adult cardiomyocyte. We identified that Brg1/Brm double-mutant mice exhibited an increased mitochondrial biogenesis, increases in ‘mitophagy’, and alterations in mitochondrial fission and fusion that led to small, fragmented mitochondria. Mechanistically, increases in the autophagy and mitophagy-regulated proteins Beclin1 and Bnip3 were identified, paralleling changes seen in human heart failure. Cardiac mitochondrial dynamics were perturbed including decreased mitochondria size, reduced number, and altered expression of genes regulating fusion (Mfn1, Opa1) and fission (Drp1). We also identified cardiac protein amyloid accumulation (aggregated fibrils) during disease progression along with an increase in pre-amyloid oligomers and an upregulated unfolded protein response including increased GRP78, CHOP, and IRE-1 signaling. Together, these findings described a role for BRG1 and BRM in mitochondrial quality control, by regulating mitochondrial number, mitophagy, and mitochondrial dynamics not previously recognized in the adult cardiomyocyte. As epigenetic mechanisms are critical to the pathogenesis of heart failure, these novel pathways identified indicate that SWI/SNF chromatin remodeling functions are closely linked to mitochondrial quality control mechanisms