Virginia Principals\u27 Knowledge of Classroom Assessment and Support of Assessment for Learning Practices

The purpose of this study was to investigate the assessment literacy of Virginia principals and describe how principals with varying levels of assessment literacy integrate assessment leadership practices that support assessment for learning. This study investigated the differences in assessment literacy between elementary and secondary principals and across principals’ predominant method of training in assessment. Mertler and Campbell’s (2005) Assessment Literacy Inventory (ALI) was used to obtain measures of overall assessment literacy and determine relative strengths and weaknesses across the seven Standards for Teacher Competence in the Educational Assessment of Students. There were no significant differences in assessment literacy across levels or as a result of type of training in assessment. Participants scored highest in their ability to recognize unethical practices and their relative weakness was in developing assessment methods. Qualitative interviews were conducted with six principals with higher levels of assessment literacy and six principals with lower levels. Interviews were analyzed for assessment leadership practices related to: support of assessment for learning principals, alignment, professional development, balanced assessment, and ethical practices. Discrepancies between principals with higher and lower levels of assessment literacy were in the areas of professional development on learning targets and the alignment of instruction to learning targets. Principals with across levels of assessment literacy described using professional learning communities and instructional specialists to support grouping for instruction. Additionally, principals described balanced assessment systems with multiple measures of formative and summative assessments. There were commonalities in ethical practices and considerations across principals

Changes in Gait Characteristics Following a Concussion

Introduction: Recent literature has suggested that gait could potentially provide clinicians with a reliable way to determine if an athlete has sufficiently recovered from a concussion in order to return to participation. The Balance Error Scoring System has typically been used to determine if static and postural control have returned to baseline measurements. It has yet to be determined the level of gait recovery within 24 hours of sustaining a concussion (CD1), on the day the concussed athlete returns to BESS baseline (BBD), or the day they finally return to play (RTPD). Objective: The purpose of this study was to compare a concussed athlete\u27s gait to non-concussed athletes and normal controls, on specific days of their recovery process. Methods: In this study, 45 subjects were divided into groups; 15 concussed intercollegiate athletes (CONCs), 15 non-concussed teammates (NONCs), and 15 normal controls (NORMs) who did not participate in an intercollegiate sport. The NONCs were matched according to sport and gender, and the NORMs were matched to gender of the CONCs. The subjects walked on the GAITRite® walkway, where gait velocity, cadence, step length, step width, and double leg support times were calculated. The NONCs and CONCs walked the same number of days as their CONC match, until the CONC returned to participation. Results: Gait velocity showed significant group differences at CD1 (F= 3.670, p=.034), whereby CONCs had a mean gait velocity significantly less than the NORMs (1.21 + 0.16 m/s and 1.34 + 0.09 m/s respectively, p=.036). There were significant main effects for gait velocity, step length, step width, and double leg support times. Most of the subjects increased their gait velocity and step length (F=18.940 and p\u3c.001, F=16.542 and p\u3c.001), respectively) and decreased their double leg support times (F=14.395 and p\u3c.001) between CD1 and BBD. Subjects from CD1 to RTPD showed increases in gait velocity and step length (F= 11.901 and p=.001, F=10.553 and p=.002, respectively), and decreases in step width and double leg support times (F=11.976 and p=.001, and F=10.583, p=.002, respectively). However, there were no significant differences for gait velocity, cadence, step length, step width, or double leg support times between CONC and NONC, CONC and NORM, or NONC and NORM from CD1 to BBD, BBD to RTPD, or from CD1 to RTPD. Conclusion: These findings indicate that a concussed athlete shows slower gait velocity initially after a concussion at CD1, possibly indicating a conservative gait strategy that develops into normal gait patterns as BBD and RTPD occur. However, cadence, step length, step width, and double leg support times during single task walking may not be good indicators on whether an athlete has recovered their postural control. Therefore, it is recommended that a variety of concussion testing tools, including postural control measurements such as gait, be used to make a proper assessment of when the athlete may return to participation

Phosphorylation and calcium antagonistically tune myosin-binding protein C\u27s structure and function

During each heartbeat, cardiac contractility results from calcium-activated sliding of actin thin filaments toward the centers of myosin thick filaments to shorten cellular length. Cardiac myosin-binding protein C (cMyBP-C) is a component of the thick filament that appears to tune these mechanochemical interactions by its N-terminal domains transiently interacting with actin and/or the myosin S2 domain, sensitizing thin filaments to calcium and governing maximal sliding velocity. Both functional mechanisms are potentially further tunable by phosphorylation of an intrinsically disordered, extensible region of cMyBP-C\u27s N terminus, the M-domain. Using atomic force spectroscopy, electron microscopy, and mutant protein expression, we demonstrate that phosphorylation reduced the M-domain\u27s extensibility and shifted the conformation of the N-terminal domain from an extended structure to a compact configuration. In combination with motility assay data, these structural effects of M-domain phosphorylation suggest a mechanism for diminishing the functional potency of individual cMyBP-C molecules. Interestingly, we found that calcium levels necessary to maximally activate the thin filament mitigated the structural effects of phosphorylation by increasing M-domain extensibility and shifting the phosphorylated N-terminal fragments back to the extended state, as if unphosphorylated. Functionally, the addition of calcium to the motility assays ablated the impact of phosphorylation on maximal sliding velocities, fully restoring cMyBP-C\u27s inhibitory capacity. We conclude that M-domain phosphorylation may have its greatest effect on tuning cMyBP-C\u27s calcium-sensitization of thin filaments at the low calcium levels between contractions. Importantly, calcium levels at the peak of contraction would allow cMyBP-C to remain a potent contractile modulator, regardless of cMyBP-C\u27s phosphorylation state

Integrating Evidence-Based Practices into Public Relations Education

Public relations continue to play an essential and changing role in society, requiring the regular reassessment of the education of future public relations practitioners. Academics and practitioners often differ in how they view the public relations field, how they define the discipline, and how they view the major pedagogical approaches. This paper explores the impact of integrating three different perspectives in public relations education, including practitioner perspective, client perspective, and the evidence-based perspective. Results from students’ reaction papers and an online questionnaire suggest that integrating an evidence-based approach improves the competence and clarity of communications counsel provided by aspiring practitioners

The application of 2H2O to measure skeletal muscle protein synthesis

Skeletal muscle protein synthesis has generally been determined by the precursor:product labeling approach using labeled amino acids (e.g., [13C]leucine or [13C]-, [15N]-, or [2H]phenylalanine) as the tracers. Although reliable for determining rates of protein synthesis, this methodological approach requires experiments to be conducted in a controlled environment, and as a result, has limited our understanding of muscle protein renewal under free-living conditions over extended periods of time (i.e., integrative/cumulative assessments). An alternative tracer, 2H2O, has been successfully used to measure rates of muscle protein synthesis in mice, rats, fish and humans. Moreover, perturbations such as feeding and exercise have been included in these measurements without exclusion of common environmental and biological factors. In this review, we discuss the principle behind using 2H2O to measure muscle protein synthesis and highlight recent investigations that have examined the effects of feeding and exercise. The framework provided in this review should assist muscle biologists in designing experiments that advance our understanding of conditions in which anabolism is altered (e.g., exercise, feeding, growth, debilitating and metabolic pathologies)

Healthcare access dimensions and uterine cancer survival: a national cancer database study

ObjectiveDisparities exist throughout diagnosis, treatment, and survival for Black patients with uterine cancer. There is limited data on how several healthcare access (HCA) dimensions contribute to these disparities in patients with advanced stage uterine cancer.MethodsUsing the National Cancer Database (NCDB), we identified patients aged 40-89 years with Stage III-IV uterine cancer between 2004-2015 who received chemotherapy and/or radiotherapy. Race/ethnicity were classified as non-Hispanic (NH)-Black, Hispanic, and NH-White. Variables defined in the NCDB were used to assess HCA affordability, availability, and accessibility. Kaplan-Meier estimates, log-rank test, and multivariable Cox proportional hazards models were used to analyze overall survival.ResultsOf 43,134 patients, 78.8% of the cohort identified as NH-White, 15.3% NH-Black, and 5.9% Hispanic. NH-Black patients were the most likely to have type II (75.6% vs. 53.9% and 55.4%) and stage IV (40.8% vs. 30.7% and 32.3%) disease compared to NH-White and Hispanic patients. NH-Black patients were more likely than NH-White and Hispanic patients to have government funded insurance (58.6% vs. 50.3% and 50.4%), live in low-income areas (46.4% vs. 14.2% and 29.9%), and receive only chemotherapy (53.5% vs. 43.1% and 46.2%). Having private insurance and receiving treatment at an academic facility were positive predictors of survival. NH-Black patients had worse survival than NH-White patients after adjusting for clinical characteristics and healthcare access dimensions (HR 1.29; 95% CI 1.24, 1.34).ConclusionWhile HCA affordability and availability predicted survival in patients with advanced stage uterine cancer, additional factors contribute to racial disparities. Compared to NH-White patients, NH-Black patients had more aggressive disease, received only chemotherapy rather than combined therapy, and had worse survival regardless of cancer subtype. Additional dimensions of healthcare access must be explored to remedy uterine cancer disparities

Myosin-binding protein C displaces tropomyosin to activate cardiac thin filaments and governs their speed by an independent mechanism

Myosin-binding protein C (MyBP-C) is an accessory protein of striated muscle thick filaments and a modulator of cardiac muscle contraction. Defects in the cardiac isoform, cMyBP-C, cause heart disease. cMyBP-C includes 11 Ig- and fibronectin-like domains and a cMyBP-C-specific motif. In vitro studies show that in addition to binding to the thick filament via its C-terminal region, cMyBP-C can also interact with actin via its N-terminal domains, modulating thin filament motility. Structural observations of F-actin decorated with N-terminal fragments of cMyBP-C suggest that cMyBP-C binds to actin close to the low Ca(2+) binding site of tropomyosin. This suggests that cMyBP-C might modulate thin filament activity by interfering with tropomyosin regulatory movements on actin. To determine directly whether cMyBP-C binding affects tropomyosin position, we have used electron microscopy and in vitro motility assays to study the structural and functional effects of N-terminal fragments binding to thin filaments. 3D reconstructions suggest that under low Ca(2+) conditions, cMyBP-C displaces tropomyosin toward its high Ca(2+) position, and that this movement corresponds to thin filament activation in the motility assay. At high Ca(2+), cMyBP-C had little effect on tropomyosin position and caused slowing of thin filament sliding. Unexpectedly, a shorter N-terminal fragment did not displace tropomyosin or activate the thin filament at low Ca(2+) but slowed thin filament sliding as much as the larger fragments. These results suggest that cMyBP-C may both modulate thin filament activity, by physically displacing tropomyosin from its low Ca(2+) position on actin, and govern contractile speed by an independent molecular mechanism

YAP1 expression predicts sensitivity to dual AKT/P70S6K inhibition in ovarian and uterine malignancies

Purpose: The PI3K/AKT/P70S6K pathway is an attractive therapeutic target in ovarian and uterine malignancies due to its high rate of dysregulation and key roles in tumor growth. Here, we examined the biological effects of MSC2363318A, which is a novel inhibitor of AKT1, AKT3, and P70S6K. Experimental Design: Orthotopic murine models of ovarian and uterine cancer were utilized to study the effect of MSC2363318A on survival and regression. Moreover, in vitro experiments (MTT, Western blot analysis, plasmid transfection, and reverse phase protein array [RPPA]) were carried out to characterize underlying mechanisms and potential biomarkers of response. Results: MSC2363318A decreased tumor growth and metastases in multiple murine orthotopic models of ovarian (SKOV3ip1, HeyA8, and Igrov1) and uterine (Hec1a) cancer and reduced proliferation (Ki67) and angiogenesis (CD31) indices and increased cell death (cleaved caspase-3) markers. Synergy between MSC2363318A and paclitaxel was observed in vitro in protected (IC50 ≥ 5 µM) cell lines. RPPA identified YAP1 as a candidate marker to predict cell lines that were most sensitive to MSC2363318A (R=0.675, p=0.0015). After establishment of a bevacizumab resistant endothelial cell line, RF-24, we demonstrate that resensitization to bevacizumab occurs with the addition of MSC2363318A. Conclusions: MSC2363318A has therapeutic efficacy in multiple pre-clinical models of ovarian and uterine cancer. These findings support clinical development of dual AKT/P70S6K inhibition

Proteome Dynamics with Heavy Water — Instrumentations, Data Analysis, and Biological Applications

The quantitative assessment of the synthesis of individual proteins has been greatly hindered by the lack of a high-throughput nonradioactive method. We recently developed a method that we call “proteome dynamics” and software that enables high-throughput kinetic analyses of peptides on a proteome-wide scale. Previous studies established that oral administration of heavy water (2H2O or deuterium oxide, D2O) is safe and well tolerated in humans. Briefly, a loading dose of 2H2O, a nonradioactive isotope, is administered in drinking water. 2H2O rapidly labels body water and transfers 2H from 2H2O to 2H-labeled amino acids, which incorporates into proteins dependent upon the rate of synthesis of the specific protein. Proteins are analyzed by high-resolution mass spectrometry and protein synthesis is calculated using specialized software. We have established the effectiveness of this method for plasma and mitochondrial proteins. We demonstrated that fasting has a differential effect on the synthesis rates of proteins. We also applied this method to assess the effect of heart failure on the stability of mitochondrial proteins. In this review, we describe the study design, instrumentation, data analysis, and biological application of heavy water-based proteome turnover studies. We summarize this chapter with the challenges in the field and future directions

Myosin-binding protein C corrects an intrinsic inhomogeneity in cardiac excitation-contraction coupling

The beating heart exhibits remarkable contractile fidelity over a lifetime, which reflects the tight coupling of electrical, chemical, and mechanical elements within the sarcomere, the elementary contractile unit. On a beat-to-beat basis, calcium is released from the ends of the sarcomere and must diffuse toward the sarcomere center to fully activate the myosin- and actin-based contractile proteins. The resultant spatial and temporal gradient in free calcium across the sarcomere should lead to nonuniform and inefficient activation of contraction. We show that myosin-binding protein C (MyBP-C), through its positioning on the myosin thick filaments, corrects this nonuniformity in calcium activation by exquisitely sensitizing the contractile apparatus to calcium in a manner that precisely counterbalances the calcium gradient. Thus, the presence and correct localization of MyBP-C within the sarcomere is critically important for normal cardiac function, and any disturbance of MyBP-C localization or function will contribute to the consequent cardiac pathologies