The impact of a parent-child pre-kindergarten program on the parent involvement perceptions, attitudes and practices of primary teachers in the Omaha public schools.

THE IMPACT OF A PARENT-CHILD PRE-KINDERGARTEN PROGRAM ON THE PARENT INVOLVEMENT PERCEPTIONS, AITITUDES AND PRACTICES OF PRIMARY TEACHERS IN THE OMAHA PUBLIC SCHOOLS This study is a causal-comparative examination of the impact of a pre-kindergarten program with a mandatory parent involvement component on primary teachers\u27 perceptions, practices and attitudes toward parent involvement in a public school district located in a metropolitan area. A 56 question survey, based upon one from the publication Hopkins Survey of Schools and Family Connections, Questionnaires for Teachers, Parents and Students, was sent to 285 primary teachers of kindergarten, first, second and third grades. The survey was self-reporting with guaranteed anonymity. Independent variables included the presence of a pre-kindergarten program and the grade level taught. Dependent variables included perceptions, practices and attitudes towards parent involvement. Both one-way and two-way analyses of variance were run to examine the variables. The results of the survey indicated that the presence of a Parent-Child Pre-Kindergarten currently has no impact on primary teachers\u27 perceptions, attitudes and practices of parent involvement in the Omaha Public School District. Differences were found by grade level taught in the practices teachers use to involve parents. Kindergarten teachers showed a higher use of parent involvement practices than first, second or third grade teachers. No difference was seen in the grade level taught in either perceptions or attitudes. Over­ all, the survey indicated that primary teachers perceived parent involvement as an important part of the school curriculum. However, teachers showed more unity than diversity in their perceptions, attitudes and practices of parent involvement regardless of the presence of a Parent-Child Pre-Kindergarten program within a school building

Near-identical star formation rate densities from Hα and FUV at redshift zero

For the first time both Hα and far-ultraviolet (FUV) observations from an Hɪ-selected sample are used to determine the dust-corrected star formation rate density (SFRD: ṗ) in the local Universe. Applying the two star formation rate indicators on 294 local galaxies, we determine log(ṗ Hα) = -1.168 +0.13 -0.05 [M⊙yr^-1 Mpc^-3] and log(ṗ FUV) = -1.171 +0.12 -0.13 [M⊙yr^-1 Mpc^-3]. These values are derived from scaling Hα and FUV observations to the Hɪ mass function. Galaxies were selected to uniformly sample the full Hɪ mass (MHɪ) range of the Hɪ Parkes All-Sky Survey (MHɪ ~ 10^7 to ~10^10.7 M⊙). The approach leads to relatively larger sampling of dwarf galaxies compared to optically selected surveys. The low Hɪ mass, low luminosity, and low surface brightness galaxy populations have, on average, lower Hα/FUV flux ratios than the remaining galaxy populations, consistent with the earlier results of Meurer. The near-identical Hα- and FUV-derived SFRD values arise with the low Hα/FUV flux ratios of some galaxies being offset by enhanced Hα from the brightest and high mass galaxy populations. Our findings confirm the necessity to fully sample the Hɪ mass range for a complete census of local star formation to include lower stellar mass galaxies which dominate the local Universe.Partial funding for the SINGG and SUNGG surveys came from NASA grants NAG5-13083 (LTSA program), GALEX GI04-0105-0009 (NASA GALEX Guest Investigator grant), and NNX09AF85G (GALEX archival grant) to GR Meurer

Acetylation-dependent regulation of endothelial Notch signalling by the SIRT1 deacetylase.

Notch signalling is a key intercellular communication mechanism that is essential for cell specification and tissue patterning, and which coordinates critical steps of blood vessel growth. Although subtle alterations in Notch activity suffice to elicit profound differences in endothelial behaviour and blood vessel formation, little is known about the regulation and adaptation of endothelial Notch responses. Here we report that the NAD(+)-dependent deacetylase SIRT1 acts as an intrinsic negative modulator of Notch signalling in endothelial cells. We show that acetylation of the Notch1 intracellular domain (NICD) on conserved lysines controls the amplitude and duration of Notch responses by altering NICD protein turnover. SIRT1 associates with NICD and functions as a NICD deacetylase, which opposes the acetylation-induced NICD stabilization. Consequently, endothelial cells lacking SIRT1 activity are sensitized to Notch signalling, resulting in impaired growth, sprout elongation and enhanced Notch target gene expression in response to DLL4 stimulation, thereby promoting a non-sprouting, stalk-cell-like phenotype. In vivo, inactivation of Sirt1 in zebrafish and mice causes reduced vascular branching and density as a consequence of enhanced Notch signalling. Our findings identify reversible acetylation of the NICD as a molecular mechanism to adapt the dynamics of Notch signalling, and indicate that SIRT1 acts as rheostat to fine-tune endothelial Notch responses

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field