Exploring Teachers’ Implementation of Comparison in Algebra I

Discussions where teachers engage students in the comparison of multiple solution strategies to a single problem have been recommended in curriculum policy documents, yet integrating these discussions into teachers' normative routines is not widespread. In this paper, we begin to explore variations in teachers' implementation of Algebra I curriculum materials specifically focused on comparison. We explore (via case studies) implementation of the curriculum materials by two teachers with similar teaching backgrounds. The case studies suggest that these two teachers’ implementation of the comparison materials differed markedly, raising questions about possible factors which may have contributed to implementation differences

Learning from Comparison in Algebra

Mastery of algebra is an important yet difficult milestone for students, suggesting the need for more effective teaching strategies in the algebra classroom. Learning by comparing worked-out examples of algebra problems may be one such strategy. Comparison is a powerful learning tool from cognitive science that has shown promising results in prior small-scale studies in mathematics classrooms. This study reports on a yearlong randomized controlled trial testing the effect of an Algebra I supplemental comparison curriculum on students’ mathematical knowledge. 141 Algebra I teachers were randomly assigned to either implement the comparison curriculum as a supplement to their regular curriculum or to be a ‘business as usual’ control. Use of the supplemental curriculum was much less frequent than requested for many teachers, and there was no main effect of condition on student achievement. However, greater use of the supplemental curriculum was associated with greater procedural student knowledge. These findings suggest a role for comparison in the algebra classroom but also the challenges of supporting teacher integration of new materials into the curriculum

Broadband simulations for M_w 7.8 southern San Andreas earthquakes: Ground motion sensitivity to rupture speed

Using the high-performance computing resources of the Southern California Earthquake Center, we simulate broadband (0–10 Hz) ground motions for three M_w 7.8 rupture scenarios of the southern San Andreas fault. The scenarios incorporate a kinematic rupture description with the average rupture speed along the large slip portions of the fault set at 0.96, 0.89, and 0.84 times the local shear wave velocity. Consistent with previous simulations, a southern hypocenter efficiently channels energy into the Los Angeles region along the string of basins south of the San Gabriel Mountains. However, we find the basin ground motion levels are quite sensitive to the prescribed rupture speed, with peak ground velocities at some sites varying by over a factor of two for variations in average rupture speed of about 15%. These results have important implications for estimating seismic hazards in Southern California and emphasize the need for improved understanding of earthquake rupture processes

Improvements to the APBS biomolecular solvation software suite

The Adaptive Poisson-Boltzmann Solver (APBS) software was developed to solve the equations of continuum electrostatics for large biomolecular assemblages that has provided impact in the study of a broad range of chemical, biological, and biomedical applications. APBS addresses three key technology challenges for understanding solvation and electrostatics in biomedical applications: accurate and efficient models for biomolecular solvation and electrostatics, robust and scalable software for applying those theories to biomolecular systems, and mechanisms for sharing and analyzing biomolecular electrostatics data in the scientific community. To address new research applications and advancing computational capabilities, we have continually updated APBS and its suite of accompanying software since its release in 2001. In this manuscript, we discuss the models and capabilities that have recently been implemented within the APBS software package including: a Poisson-Boltzmann analytical and a semi-analytical solver, an optimized boundary element solver, a geometry-based geometric flow solvation model, a graph theory based algorithm for determining p$K_a$ values, and an improved web-based visualization tool for viewing electrostatics

Sepsis is associated with mitochondrial DNA damage and a reduced mitochondrial mass in the kidney of patients with sepsis-AKI

BACKGROUND: Sepsis is a life-threatening condition accompanied by organ dysfunction subsequent to a dysregulated host response to infection. Up to 60% of patients with sepsis develop acute kidney injury (AKI), which is associated with a poor clinical outcome. The pathophysiology of sepsis-associated AKI (sepsis-AKI) remains incompletely understood, but mitochondria have emerged as key players in the pathogenesis. Therefore, our aim was to identify mitochondrial damage in patients with sepsis-AKI. METHODS: We conducted a clinical laboratory study using "warm" postmortem biopsies from sepsis-associated AKI patients from a university teaching hospital. Biopsies were taken from adult patients (n = 14) who died of sepsis with AKI at the intensive care unit (ICU) and control patients (n = 12) undergoing tumor nephrectomy. To define the mechanisms of the mitochondrial contribution to the pathogenesis of sepsis-AKI, we explored mRNA and DNA expression of mitochondrial quality mechanism pathways, DNA oxidation and mitochondrial DNA (mtDNA) integrity in renal biopsies from sepsis-AKI patients and control subjects. Next, we induced human umbilical vein endothelial cells (HUVECs) with lipopolysaccharide (LPS) for 48 h to mimic sepsis and validate our results in vitro. RESULTS: Compared to control subjects, sepsis-AKI patients had upregulated mRNA expression of oxidative damage markers, excess mitochondrial DNA damage and lower mitochondrial mass. Sepsis-AKI patients had lower mRNA expression of mitochondrial quality markers TFAM, PINK1 and PARKIN, but not of MFN2 and DRP1. Oxidative DNA damage was present in the cytosol of tubular epithelial cells in the kidney of sepsis-AKI patients, whereas it was almost absent in biopsies from control subjects. Oxidative DNA damage co-localized with both the nuclei and mitochondria. Accordingly, HUVECs induced with LPS for 48 h showed an increased mnSOD expression, a decreased TFAM expression and higher mtDNA damage levels. CONCLUSION: Sepsis-AKI induces mitochondrial DNA damage in the human kidney, without upregulation of mitochondrial quality control mechanisms, which likely resulted in a reduction in mitochondrial mass

GYY4137-Derived Hydrogen Sulfide Donates Electrons to the Mitochondrial Electron Transport Chain via Sulfide:Quinone Oxidoreductase in Endothelial Cells

The protective effects of hydrogen sulphide (H2S) to limit oxidative injury and preserve mitochondrial function during sepsis, ischemia/reperfusion, and neurodegenerative diseases have prompted the development of soluble H2S-releasing compounds such as GYY4137. Yet, the effects of GYY4137 on the mitochondrial function of endothelial cells remain unclear, while this cell type comprises the first target cell after parenteral administration. Here, we specifically assessed whether human endothelial cells possess a functional sulfide:quinone oxidoreductase (SQOR), to oxidise GYY4137-released H2S within the mitochondria for electron donation to the electron transport chain. We demonstrate that H2S administration increases oxygen consumption by human umbilical vein endothelial cells (HUVECs), which does not occur in the SQOR-deficient cell line SH-SY5Y. GYY4137 releases H2S in HUVECs in a dose- and time-dependent fashion as quantified by oxygen consumption and confirmed by lead acetate assay, as well as AzMC fluorescence. Scavenging of intracellular H2S using zinc confirmed intracellular and intramitochondrial sulfur, which resulted in mitotoxic zinc sulfide (ZnS) precipitates. Together, GYY4137 increases intramitochondrial H2S and boosts oxygen consumption of endothelial cells, which is likely governed via the oxidation of H2S by SQOR. This mechanism in endothelial cells may be instrumental in regulating H2S levels in blood and organs but can also be exploited to quantify H2S release by soluble donors such as GYY4137 in living systems.</p

Accountability Work: Examining the Values, Technologies and Work Practices that Facilitate Transparency in Charities

Charities are subject to stringent transparency and accountability requirements from government and funders to ensure that they are conducting work and spending money appropriately. Charities are increasingly important to civic life and have unique characteristics as organisations. This provides a rich space in which HCI researchers may learn from and affect both held notions of transparency and accountability, and the relationships between these organisations and their stakeholders. We conducted ethnographic fieldwork and workshops over a seven month period at a charity. We aimed to understand how the transparency obligations of a charity manifest through work and how the workers of a charity reason about transparency and accountability as an everyday practice. Our findings highlight how organisations engage in presenting different accounts of their work; how workers view their legal transparency obligations in contrast with their accountability to their everyday community; and how their labour does not translate well to outcome measures or metrics. We discuss implications for the design of future systems that support organisations to produce accounts of their work as part of everyday practice

Chloroquine and inhibition of Toll-like receptor 9 protect from sepsis-induced acute kidney injury

Mortality from sepsis has remained high despite recent advances in supportive and targeted therapies. Toll-like receptors (TLRs) sense bacterial products and stimulate pathogenic innate immune responses. Mice deficient in the common adapter protein MyD88, downstream from most TLRs, have reduced mortality and acute kidney injury (AKI) from polymicrobial sepsis. However, the identity of the TLR(s) responsible for the host response to polymicrobial sepsis is unknown. Here, we show that chloroquine, an inhibitor of endocytic TLRs (TLR3, 7, 8, 9), improves sepsis-induced mortality and acute kidney injury in a clinically relevant polymicrobial sepsis mouse model, even when administered 6h after the septic insult. Chloroquine administration attenuated the decline in renal function, splenic apoptosis, serum markers of damage to other organs, and prototypical serum pro- and anti-inflammatory cytokines TNF-alpha and IL-10. An oligodeoxynucleotide inhibitor (H154) of TLR9 and TLR9-deficient mice mirror the actions of chloroquine in all functional parameters that we tested. In addition, chloroquine decreased TLR9 protein abundance in spleen, further suggesting that TLR9 signaling may be a major target for the protective actions of chloroquine. Our findings indicate that chloroquine improves survival by inhibiting multiple pathways leading to polymicrobial sepsis, and that chloroquine and TLR9 inhibitors represent viable broad-spectrum and targeted therapeutic strategies, respectively, that are promising candidates for further clinical development

The effects of frequent nocturnal home hemodialysis: the Frequent Hemodialysis Network Nocturnal Trial

Prior small studies have shown multiple benefits of frequent nocturnal hemodialysis compared to conventional three times per week treatments. To study this further, we randomized 87 patients to three times per week conventional hemodialysis or to nocturnal hemodialysis six times per week, all with single-use high-flux dialyzers. The 45 patients in the frequent nocturnal arm had a 1.82-fold higher mean weekly stdKt/Vurea, a 1.74-fold higher average number of treatments per week, and a 2.45-fold higher average weekly treatment time than the 42 patients in the conventional arm. We did not find a significant effect of nocturnal hemodialysis for either of the two coprimary outcomes (death or left ventricular mass (measured by MRI) with a hazard ratio of 0.68, or of death or RAND Physical Health Composite with a hazard ratio of 0.91). Possible explanations for the left ventricular mass result include limited sample size and patient characteristics. Secondary outcomes included cognitive performance, self-reported depression, laboratory markers of nutrition, mineral metabolism and anemia, blood pressure and rates of hospitalization, and vascular access interventions. Patients in the nocturnal arm had improved control of hyperphosphatemia and hypertension, but no significant benefit among the other main secondary outcomes. There was a trend for increased vascular access events in the nocturnal arm. Thus, we were unable to demonstrate a definitive benefit of more frequent nocturnal hemodialysis for either coprimary outcome