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Enacting STEM education reform is a complex task and there are a variety of approaches that might be selected by change agents. When working on an institutional change project to impact multiple parts of the STEM education system, teams of change agents may select multiple strategies and tactics to enact at one time and over multiple years of a project. However, the literature lacks studies which document and analyze strategies and tactics used by change project teams in a way that can be useful for other change agents. The current study seeks to fill this gap by investigating National Science Foundation-funded change initiatives at three public research universities focused on encouraging the adoption of evidenced-based instructional practices by STEM faculty in order to understand the strategies used within and across projects. Qualitative framework analysis using the lens of the Henderson et al. (Journal of Research in Science Teaching 48(8): 952-984, 2011. https://doi.org/10.1002/tea.20439) Four Categories of Change Strategies Model showed that institutional projects enact a wide range of tactics that span the four strategies represented in the four categories of the model both across institutions and within each institution. The analysis documents a number of change tactics not previously described by the model and offers expanded definitions of the change processes that operate within each category in the context of institutional change projects. This descriptive work advances our understanding of the breadth and depth of actions taken by institutional change initiatives and provides insights into types of variations that might be observed based on different institutional contexts. The current analysis both affirms the value of the original model and identifies expanded ways to think about the four categories within the context of institutional change projects.

Background: Calls for science education reform have been made for decades in the USA. The recent call to produce one million new science, technology, engineering, and math (STEM) graduates over 10 years highlights the need to employ evidence-based instructional practices (EBIPs) in undergraduate STEM classes to create engaging and effective learning environments. EBIPs are teaching strategies that have been empirically demonstrated to positively impact student learning, attitudes, and achievement in STEM disciplines. However, the mechanisms and processes by which faculty learn about and choose to implement EBIPs remain unclear. To explore this problem area, we used social network analysis to examine how an instructor's knowledge and use of EBIPs may be influenced by their peers within a STEM department. We investigated teaching discussion networks in biology and chemistry departments at three public universities. Results: We report that tie strength and tie diversity vary between departments, but that mean indegree is not correlated with organizational rank or tenure status. We also describe that teaching discussion ties can often be characterized as strong ties based on two measures of tie strength. Further, we compare peer influence models and find consistent evidence that peer influence in these departments follows a network disturbances model. Conclusions: Our findings with respect to tie strength and tie diversity indicate that the social network structures in these departments vary in how conducive they might be to change. The correlation in teaching practice between discussion partner and peer influence models suggest that change agents should consider local social network characteristics when developing change strategies. In particular, change agents can expect that faculty may serve as opinion leaders regardless of their academic rank and that faculty can increase their use of EBIPs even if those they speak to about teaching use EBIPs comparatively less.

A brief refresher of the main aspects of the FRBR model, a review of various uses of FRBR, and a discussion of how the group 1 entity types apply in a serials context. We focus on levels (work/expression/ manifestation/item and whole/part), the number of entities in particular situations, and terminology. Examples of real-world serials are used to illustrate how the FRBR resource model applies to serials. [ABSTRACT FROM AUTHOR]

This article provides an overview of the Functional Requirements for Bibliographic Records (FRBR) with an emphasis on issues of interest to serialists. The basics of the Entity-Relationship (E-R) model are used to introduce the aspects of FRBR which can be used to model serial publications. Special attention is paid to the attributes and relationships of the article (the individual contribution in a periodical) and the article's relationship to its 'aggregated' work (the issue and the journal). This article includes a short discussion of the serial 'work' and of outstanding issues in the application of FRBR to serial works. [ABSTRACT FROM AUTHOR]

The author presents examples of electronic serial bibliographic records created following CONSER's aggregator-neutral record policy. Included is a comparison of bibliographic records created before and after the adoption of this policy and a discussion of OCLC's project to convert existing electronic serial bibliographic records to the new practice. [ABSTRACT FROM AUTHOR]

Background/aims: Anthracyclines, such as doxorubicin and daunorubicin, can cause chronic, cumulative dose-related cardiotoxicity. This can be prevented by dexrazoxane, a putative iron chelator. Disorders of iron metabolism, including altered IRP1-IRE binding may be an important mechanism of anthracycline cardiotoxicity. This study was designed to examine the role of IRP1-IRE binding in a chronic model of daunorubicin cardiotoxicity and whether dexrazoxane could prevent such changes in IRP1-IRE binding due to daunorubicin.Methods: Young adult, Fischer 344 rats received daunorubicin 2.5 mg/kg iv once per week for 6 weeks with (N, 9) and without(N, 11) pretreatment with ip dexrazoxane 50 mg/kg. Other groups received saline (controls; N, 8) or dexrazoxane alone (N, 9). Rats were sacrificed either 4h (for IRP1/IRE binding) or 2 weeks (for IRP1/IRE binding and atrial functional studies) after the last dose of daunorubicin.Results: Contractility (dF/dt) in atrial tissue was significantly reduced in daunorubicin-treated compared to control rats (dF/dt 10.1 +/− 1.0 vs. 32.9 +/− 3.1 g/sec; P < 0.001). dF/dt was unchanged in rats given daunorubicin with dexrazoxane pretreatment (dF/dt 26.9 +/− 2.9 g/sec). Left ventricular IRP1/IRE binding was not significantly affected by daunorubicin treatment either 4h or 2 weeks after treatment.Conclusions: IRP1/IRE binding may not be altered in chronic anthracycline cardiotoxicity. Dexrazoxane protects against chronic anthracycline cardiotoxicity in the rat.Clinical Pharmacology & Therapeutics (2005) 79, P61–P61; doi: 10.1016/j.clpt.2005.12.220 [ABSTRACT FROM AUTHOR]

Facioscapulohumeral muscular dystrophy is caused by incomplete epigenetic repression of the transcription factor DUX4 in skeletal muscle. A copy of DUX4 is located within each unit of the D4Z4 macrosatellite repeat array and its derepression in somatic cells is caused by either repeat array contraction (FSHD1) or by mutations in the chromatin repressor SMCHD1 (FSHD2). While DUX4 expression has thus far only been detected in FSHD muscle and muscle cell cultures, and increases with in vitro myogenic differentiation, the D4Z4 chromatin structure has only been studied in proliferating myoblasts or non-myogenic cells. We here show that SMCHD1 protein levels at D4Z4 decline during muscle cell differentiation and correlate with DUX4 derepression. In FSHD2, but not FSHD1, the loss of SMCHD1 repressor activity is partially compensated by increased Polycomb Repressive Complex 2 (PRC2)-mediated H3K27 trimethylation at D4Z4, a situation that can be mimicked by SMCHD1 knockdown in control myotubes. In contrast, moderate overexpression of SMCHD1 results in DUX4 silencing in FSHD1 and FSHD2 myotubes demonstrating that DUX4 derepression in FSHD is reversible. Together, we show that in FSHD1 and FSHD2 the decline in SMCHD1 protein levels during muscle cell differentiation renders skeletal muscle sensitive to DUX4.

Although regulation of histone methylation is believed to contribute to embryonic stem cell (ESC) self-renewal, the mechanisms remain obscure. We show here that the histone H3 trimethyl lysine 4 (H3K4me3) demethylase, KDM5B, is a downstream Nanog target and critical for ESC self-renewal. Although KDM5B is believed to function as a promoter-bound repressor, we find that it paradoxically functions as an activator of a gene network associated with self-renewal. ChIP-Seq reveals that KDM5B is predominantly targeted to intragenic regions and that it is recruited to H3K36me3 via an interaction with the chromodomain protein MRG15. Depletion of KDM5B or MRG15 increases intragenic H3K4me3, increases cryptic intragenic transcription, and inhibits transcriptional elongation of KDM5B target genes. We propose that KDM5B activates self-renewal-associated gene expression by repressing cryptic initiation and maintaining an H3K4me3 gradient important for productive transcriptional elongation.

X-ray absorption spectroscopy (XAS) at the sulfur ( approximately 2470 eV) and chlorine ( approximately 2822 eV) K-edges has been applied to a series of 4Fe-4S model complexes. These are compared to 2Fe-2S model complexes to obtain insight into the localized ground state in the mixed-valence dimer versus the delocalized ground state in the mixed-valence tetramer. The preedges of hypothetical delocalized mixed-valence dimers [Fe(2)S(2)](+) are estimated using trends from experimental data and density functional calculations, for comparison to the delocalized mixed-valence tetramer [Fe(4)S(4)](2+). The differences between these two mixed-valence sites are due to the change of the sulfide-bridging mode from micro(2) to micro(3). The terminal chloride and thiolate ligands are used as spectator ligands for the electron density of the iron center. From the intensity of the preedge, the covalency of the terminal ligands is found to increase in the tetramer as compared to the dimer. This is associated with a higher effective nuclear charge on the iron in the tetramer (derived from the energies of the preedge). The micro(3)-bridging sulfide in the tetramer has a reduced covalency per bond (39%) as compared to the micro(2)-bridging sulfide in the dimer (51%). A simple perturbation model is used to derive a quadratic dependence of the superexchange coupling constant J on the covalency of the metal ions with the bridging ligands. This relationship is used to estimate the superexchange contribution in the tetramer (J = -156 cm(-)(1)) as compared to the mixed-valence dimer (J = -360 cm(-)(1)). These results, combined with estimates for the double exchange and the vibronic coupling contributions of the dimer sub-site of the tetramer, lead to a delocalized S(t) = (9)/(2) spin ground state for the mixed-valence dimer in the tetramer. Thus, the decrease in the covalency, hence the superexchange pathway associated with changing the bridging mode of the sulfides from micro(2) to micro(3) on going from the dimer to the tetramer, significantly contributes to the delocalization of the excess electron over the dimer sub-site in the tetramer.

Cardiac effects of anthracyclines or their metabolites may include both the stimulation and inhibition of Ca(2+) release from sarcoplasmic reticulum. In this study, the ability of daunorubicin and its primary metabolite, daunorubicinol, to stimulate and inhibit Ca(2+) release from canine sarcoplasmic reticulum (SR) vesicles was investigated. It was observed that both daunorubicin and daunorubicinol were several fold more potent at inhibiting than they were at stimulating SR Ca(2+) release. Respective IC50 inhibition of daunorubicin and daunorubicinol for caffeine-induced calcium release was 1.2 and 0.6 microM, and for spontaneous Ca(2+) release was 3 and 1 microM. EC50's for daunorubicin- and daunorubicinol-induced calcium release were 30 and 15 microM, respectively. Inhibition of either spontaneous or caffeine-induced SR Ca(2+) release was inversely related to the amount of Ca(2+) loaded into the SR before exposure to daunorubicin or daunorubicinol. The free-radical scavenger dithiothreitol did not attenuate the ability of anthracyclines to inhibit SR Ca(2+) release. A nonquinone daunorubicin derivative, 5-iminodaunorubicin, was less potent than daunorubicin at inhibiting caffeine-induced Ca(2+) release. These data suggest anthracyclines and their metabolites may produce cardiotoxicity through free-radical independent, concentration-dependent effects on SR Ca(2+) release. These effects involve either inhibition or stimulation of SR Ca(2+) release and are partly dependent upon the presence of the quinone moiety., (Copyright 2000 Academic Press.)

Anthracyclines, such as daunorubicin (Daun), and other quinone-containing compounds can stimulate the formation of toxic free radicals. The present study tests the hypothesis that the quinone moiety of Daun, by increasing free-radical production, disrupts sarcoplasmic reticulum (SR) function and thereby inhibits myocardial contractility in vitro. We compared Daun with its quinone-deficient analogue, 5-iminodaunorubicin (5-ID), using experimental interventions to produce various contractile states that depend on SR function. At concentrations of Daun or 5-ID that did not alter contractility (dF/dt) of steady-state contractions (1 Hz) in electrically paced atria isolated from adult rabbits, only Daun significantly attenuated the positive inotropic effects on dF/dt of increased rest intervals (PRP; post-rest potentiation) or increased stimulation frequencies. Attenuation was to 98+/-6% at 1 Hz, and 73+/-8 and 67+/-8% for 30 and 60 sec PRP, respectively, and 73+/-3 and 63 +/-3% at 2 and 3 Hz, respectively, for 88 microM Daun (P<0.05, vs pre-drug baseline values, mean +/- SEM). These effects of Daun were similar to those of caffeine (2 mM), an agent well known to deplete cardiac SR calcium. We also examined the effect of Daun in isolated neonatal rabbit atria, which lack mature, functional SR; Daun did not alter the force-frequency relationship or PRP contractions. Additional studies in Ca(2+)-loaded SR microsomes indicated that both Daun and 5-ID opened Ca(2+) release channels, with Daun being 20-fold more potent than 5-ID in this respect. Neither anthracycline, however, induced free-radical formation in SR preparations (assayed via nicking of supercoiled DNA) prior to stimulating Ca(2+) release. Thus, our results indicate that Daun impairs myocardial contractility in vitro by selectively interfering with SR function; the quinone moiety of Daun appears to mediate this cardiotoxic effect, acting through a mechanism that does not involve free radicals.