Tapping into the Social Capital of African American Alumni of Urban High Schools

The purpose of this study was to identify and understand how African American alumni of urban high schools perceived that they could best contribute to their former schools. Despite numerous improvement efforts for several decades, the academic performance of urban high school students has failed to keep pace with that of their suburban counterparts. This research was framed around the premise that the rich legacies and diverse cultural experiences of African American alumni of urban high schools could mitigate the outside factors that negatively impact student performance at urban schools. These funds of knowledge, as Moll and Amanti (2005) described the cultural and cognitive resources that are derived from the lived experiences of marginalized people, are unique to African American alumni of urban high schools. The 45 participants of this study were African American alumni of two prominent urban high schools, Jean Ribault High School and William Raines High School, located in Jacksonville, Florida. Using Q methodology, participants sorted 38 statements reflecting how they perceived that African American alumni could best contribute to their former schools. The researcher then employed statistical software to correlate the 45 Q sorts, factor analyzed those correlations, and extracted five collectively held factors. However, since the fifth factor was bipolar, the researcher interpreted the five-factor solution as having six perspectives, one for each of the first four factors and two opposite perspectives for factor five. The six perspectives were named College Preparation, Relationship Building, Spirituality, Self-efficacy, Visibility (students), and Visibility (parents). Through the lens of social capital, these resulting perspectives were then systematically interpreted to provide a rich description of how African American alumni of urban high schools perceived that they could best contribute to their former schools

The Female Athlete Triad: An Assessment of Current Practices in Primary Care and Benefit of Educational Intervention

Background. The Female Athlete Triad (Triad) is characterized by negative energy balance, disordered menstrual cycles, and low bone mineral density. The understanding and practices of primary care physicians (PCPs) regarding the Triad and the benefit of an educational intervention were assessed. Methods. PCPs attending a regional conference were surveyed prior to, immediately after, and three months following the plenary lecture on the Triad. Surveys included knowledge about the components, diagnostics, treatment, clinician practice, and comfort level with regard to the Triad. Results. The pre-test survey was completed by 84 of 126 (67%) attendees. The lecture increased from 53% to 98% the proportion of PCPs who identified the three domains of the Triad. Knowledge scores improved over the course of the lecture (from 3.4 to 5.1, p < 0.05), particularly regarding Triad components (effect size = 1.2) and treatment (effect size = 1.6) with only small gains in diagnostic knowledge (effect size = 0.1 to 0.3). The three-month follow-up survey, completed by only seven clinicians (8%), suggested good retention of knowledge though little practice changes. Conclusions. A 50-minute educational session improved knowledge about the Triad. Particular improvement was noted in understanding the underlying etiology and treatment

Mitochondrial Ca2+ Uniporter and CaMKII in heart

The influx of cytosolic Ca2+ into mitochondria is mediated primarily by the mitochondrial calcium uniporter (MCU), a small-conductance, Ca2+-selective channel-. MCU modulates intracellular Ca2+ transients and regulates ATP production and cell death. Recently, Joiner et al. reported that MCU is regulated by mitochondrial CaMKII, and this regulation determines stress response in heart. They reported a very large current putatively mediated by MCU that was about two orders of magnitude greater than the MCU current (IMCU) that we previously measured in heart mitochondria. Also, the current traces presented by Joiner et al. showed unusually high fluctuations incompatible with the low single-channel conductance of MCU. Here we performed patch-clamp recordings from mouse heart mitochondria under the exact conditions used by Joiner et al. We confirmed that IMCU in cardiomyocytes is very small and showed that it is not directly regulated by CaMKII. Thus the currents presented by Joiner et al. do not correspond to MCU, and there is no direct electrophysiological evidence that CaMKII regulates MCU

Autoregulatory and structural control of CaMKII substrate specificity

Indiana University-Purdue University Indianapolis (IUPUI)Calcium/calmodulin (CaM)-dependent protein kinase II (CaMKII) is a multimeric holoenzyme composed of 8–14 subunits from four closely related isoforms (α, β, γ, δ). CaMKII plays a strategic, multifunctional role in coupling the universal second messenger calcium with diverse cellular processes including metabolism, cell cycle control, and synaptic plasticity. CaMKII exhibits broad substrate specificity, targeting numerous substrates with diverse phosphorylation motifs. Binding of the calcium sensor CaM to the autoregulatory domain (ARD) of CaMKII functions to couple kinase activation with calcium signaling. Important sites of autophosphorylation, namely T287 and T306/7 (δ isoform numbering), reside within the ARD and control either CaM dependence or ability to bind to CaMKII respectively, thus determining various activation states of the kinase. Because autophosphorylation is critical to the function of CaMKII in vivo, we sought to determine the relationship between the activation state of the kinase and substrate selectivity. We show that the ARD of activated CaMKII tunes substrate selectivity by competing for substrate binding to the catalytic domain, thus functioning as a selectivity filter. Specifically, in the absence of T287 autophosphorylation, substrate phosphorylation is limited to high-affinity, consensus substrates. T287 autophosphorylation restores maximal kinase activation and broad substrate selectivity by disengaging ARD filtering. The unique multimeric architecture of CaMKII is an ideal sensor which encodes calcium-spike frequency into graded levels of subunit activation/autophosphorylation within the holoenzyme. We find that differential activation states of the holoenzyme produce distinct substrate phosphorylation profiles. Maximal holoenzyme activation/autophosphorylation leads to further broadening of substrate specificity beyond the effect of autophosphorylation alone, which is consistent with multivalent avidity. Thus, the ability of calcium-spike frequency to regulate T287 autophosphorylation and holoenzyme activation permits cellular activity to dictate switch-like behavior in substrate selectivity that is required for diverse cellular responses by CaMKII

Isoform-Specific Inactivation and Aggregation of CaMKII under Ischemic-Like Conditions

poster abstractCalcium-Calmodulin Dependent Protein Kinase II (CaMKII), an enzyme critical for learning and memory, inactivates and self-associates into sedimentable aggregates following ischemic insults such as stroke or traumatic brain injury; the extent of inactivation correlates increased neuronal dysfunction and death. CaMKII α and β—isoforms found primarily in neurons—are well documented in their response to ischemic stress; α aggregates and undergoes catalytic inactivation quickly while β does not. However, γ and δ—primarily found in glial cells—are not well studied under these conditions. Previous research by our lab suggests that loss of CaMKII signaling in astrocytes may contribute to reduced glutamate uptake and neurotoxic ATP release. Therefore, there is a need to elucidate the role of the astrocytic CaMKII isoforms in ischemic stress. This study aims to investigate CaMKII δ and γ’s response to artificial ischemic conditions compared to CaMKII α. Activity assay of cell lysates expressing the four different human genes of CaMKII (α, β, γ, and δ) reveal that, under artificial ischemic conditions, δ undergoes very minimal loss of activity over time while γ experiences robust inactivation. We then used light scattering to compare α, δ, and γ sedimentation in real time and found that δ had an aggregation profile similar to α yet γ’s was radically different. A follow-up time-course sedimentation assay suggests that δ becomes sedimentable and undergoes an upwards molecular weight shift akin to α over time, indicative of autophosphorylation, but that γ begins partially sedimentable before becoming completely soluble upon activation, contrary to our hypothesis. This suggests that each isoform responds differentially to activation under ischemic-like conditions and that aggregation is not necessarily correlative with inactivation. We are currently characterizing endogenous astrocytic CaMKII expression and activity to later determine if these findings persist in a cellular environment under ischemic-like conditions. Mentor: Andy Hudmon, Stark Neurosciences Research Institute, IU School of Medicine, IUPUI, Indianapolis, I

Examining Culturally Responsive Understandings within an Undergraduate Teacher Education Program

This article examines how a group of elementary and secondary preservice teachers engaged in understanding “culture” and culturally responsive teaching while enrolled in an early program course. We analyze how culturally-related experiences, emotions, and perspectives contribute to the overall understanding of cultural competency training in teacher education. Preservice teachers varied in their use of individual- and structural-orientations, in isolation and in combination, as they developed and progressed as socially just teachers. These findings reveal that despite attempts to develop and shift toward asset-based perspectives, far more culturally embedded coursework and practicum experiences are necessary. This paper includes a reflection on the effectiveness of posing meaningful, reflective questions for preservice teachers as they experienced the concept of “culture” based on their own funds of knowledge

Using the Predicted Structure of the Amot Coiled Coil Homology Domain to Understand Lipid Binding

Angiomotins (Amots) are a family of adapter proteins that modulate cellular polarity, differentiation, proliferation, and migration. Amot family members have a characteristic lipid-binding domain, the coiled coil homology (ACCH) domain that selectively targets the protein to membranes, which has been directly linked to its regulatory role in the cell. Several spot blot assays were used to validate the regions of the domain that participate in its membrane association, deformation, and vesicle fusion activity, which indicated the need for a structure to define the mechanism. Therefore, we sought to understand the structure-function relationship of this domain in order to find ways to modulate these signaling pathways. After many failed attempts to crystallize the ACCH domain of each Amot family member for structural analysis, we decided to pursue homologous models that could be refined using small angle x-ray scattering data. Theoretical models were produced using the homology software SWISS-MODEL and threading software I-TASSER and LOMETS, followed by comparison to SAXS data for model selection and refinement. We present a theoretical model of the domain that is driven by alpha helices and short random coil regions. These alpha helical regions form a classic dimer interface followed by two wide spread legs that we predict to be the lipid binding interface