The emergence of PK–12 blended capital partnerships: a framework for understanding how urban school leaders and outside partners work together

Increasingly, school-based partnerships have been tied to education reform and the entrance of new private capital into the PK-12 sector. As a result, what may have been an at-will school-business partnership in the 1980s may today resemble an embedded multi-partner arrangement around professional development, teacher evaluation, or turnaround support. From curriculum to practice, and from human resources to operations, the notion of a simple YMCA after school partnership is being replaced by a new wave of collaborations focused on school improvement, integration, and scalability. The purpose of this investigation is to consider the historical context of public-private PK-12 partnerships and elucidate how recent policies emphasizing—sometimes mandating—collaboration between schools and outside agencies can lead to benefits and challenges for PK-12 leaders at the site level. A major challenge to school leaders is that they are relatively unfamiliar with managing partnerships in general, which leaves them even more unprepared to deal with new arrangements that are complex and reform-driven (Bennett & Thompson, 2011). This investigation introduces a new conceptual framework for understanding the environment in which school partnerships exist today. By coupling sources from a multitude of cross-disciplinary fields, such as urban studies, business, nonprofit management, and organizational theory, an effort is made to explain the emergence of this new system from both a historical and theoretical perspective. Further we introduce a proposed PK-12 Blended Capital Typology and methodology for analyzing how decision-making and accountability is shared between partners in these arrangements. Through a single sample case, our goal is to emerge with themes that will support additional research using this framework

Beyond the Public-Private Nexus: A Framework for Examining School Partnership Governance in a Blended Capital Reality

Increasingly, school-based partnerships have been tied to education reform and the entrance of private capital into the PK-12 space, most prominently from a philanthropy sector that contributes nearly $60 billion annually to education causes.  As a result, what may have been an at-will school-business partnership in the 1980s may today resemble an embedded multi-partner arrangement around professional development, teacher evaluation, or turnaround support. In this paper, a new framework is introduced to situate school-based collaborations in a contemporary context, notably acknowledging that schools today live in a new “blended capital” reality involving diverse sector influences, multiple sources of private and public funding, and therefore multiple measures of efficacy and accountability

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Symbolic execution is an intuitive strategy to verify sequential programs, which can be automated to a large extent. We have successfully carried over this method of proof to the interactive verification of concurrent systems. The resulting strategy can be applied to the verification of complex parallel programs and arbitrary (linear) temporal formulas. Our underlying logic is defined such that operators for parallel programs and temporal logic can be arbitrarily nested. We support interleaving with explicit blocking, nondeterministic choice, and others. Most important, the semantics of all of the operators are compositional. Thus, systems can be abstracted and proofs can be decomposed. This ensures that our strategy of proof can be applied to the verification of large, concurrent systems. iii iv Preface The idea of concurrency is becoming more and more important in computer science, a

Functional Interactions between Distinct Sodium Channel Cytoplasmic Domains through the Action of Calmodulin*

Sodium channels are fundamental signaling molecules in excitable cells, and are molecular targets for local anesthetic agents and intracellular free Ca2+ ([Ca2+]i). Two regions of NaV1.5 have been identified previously as [Ca2+]i-sensitive modulators of channel inactivation. These include a C-terminal IQ motif that binds calmodulin (CaM) in different modes depending on Ca2+ levels, and an immediately adjacent C-terminal EF-hand domain that directly binds Ca2+. Here we show that a mutation of the IQ domain (A1924T; Brugada Syndrome) that reduces CaM binding stabilizes NaV1.5 inactivation, similarly and more extensively than even reducing [Ca2+]i. Because the DIII-DIV linker is an essential structure in NaV1.5 inactivation, we evaluated this domain for a potential CaM binding interaction. We identified a novel CaM binding site within the linker, validated its interaction with CaM by NMR spectroscopy, and revealed its micromolar affinity by isothermal titration calorimetry. Mutation of three consecutive hydrophobic residues (Phe1520-Ile1521-Phe1522) to alanines in this CaM-binding domain recapitulated the electrophysiology phenotype observed with mutation of the C-terminal IQ domain: NaV1.5 inactivation was stabilized; moreover, mutations of either CaM-binding domain abolish the well described stabilization of inactivation by lidocaine. The direct physical interaction of CaM with the C-terminal IQ domain and the DIII-DIV linker, combined with the similarity in phenotypes when CaM-binding sites in either domain are mutated, suggests these cytoplasmic structures could be functionally coupled through the action of CaM. These findings have bearing upon Na+ channel function in genetically altered channels and under pathophysiologic conditions where [Ca2+]i impacts cardiac conduction

Speeding the Recovery from Ultraslow Inactivation of Voltage-Gated Na+ Channels by Metal Ion Binding to the Selectivity Filter: A Foot-on-the-Door?

Slow inactivated states in voltage-gated ion channels can be modulated by binding molecules both to the outside and to the inside of the pore. Thus, external K+ inhibits C-type inactivation in Shaker K+ channels by a “foot-in-the-door” mechanism. Here, we explore the modulation of a very long-lived inactivated state, ultraslow inactivation (IUS), by ligand binding to the outer vestibule in voltage-gated Na+ channels. Blocking the outer vestibule by a mutant μ-conotoxin GIIIA substantially accelerated recovery from IUS. A similar effect was observed if Cd2+ was bound to a cysteine engineered to the selectivity filter (K1237C). In K1237C channels, exposed to 30 μM Cd2+, the time constant of recovery from IUS was decreased from 145.0 ± 10.2 s to 32.5 ± 3.3 s (P < 0.001). Recovery from IUS was only accelerated if Cd2+ was added to the bath solution during recovery (V = −120 mV) from IUS, but not when the channels were selectively exposed to Cd2+ during the development of IUS (−20 mV). These data could be explained by a kinetic model in which Cd2+ binds with high affinity to a slow inactivated state (IS), which is transiently occupied during recovery from IUS. A total of 50 μM Cd2+ produced an ∼8 mV hyperpolarizing shift of the steady-state inactivation curve of IS, supporting this kinetic model. Binding of lidocaine to the internal vestibule significantly reduced the number of channels entering IUS, suggesting that IUS is associated with a conformational change of the internal vestibule of the channel. We propose a molecular model in which slow inactivation (IS) occurs by a closure of the outer vestibule, whereas IUS arises from a constriction of the internal vestibule produced by a widening of the selectivity filter region. Binding of Cd2+ to C1237 promotes the closure of the selectivity filter region, thereby hastening recovery from IUS. Thus, Cd2+ ions may act like a foot-on-the-door, kicking the IS gate to close

Permafrost collapse alters soil carbon stocks, respiration, CH4, and N2O in upland tundra

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