Is learning really just believing? A meta-analysis of self-efficacy and achievement in SLA

The positive psychology movement (Seligman, 1998) has contributed to the proclamation of a positive turn in second language acquisition (SLA) (MacIntyre et al., 2016). Within the context of individual differences, self-efficacy (Bandura, 1997), an individual’s judgment of their capability to achieve goals, has gained particular interest in language learning (e.g., Lake, 2013). The present study meta-analyzes a body of research that has investigated the relationship between second language (L2) self-efficacy and L2 achievement by exploring 1) reporting practices in this domain, 2) the strength and direction of the relationship, and 3) the effects of moderator variables on the self-efficacy-achievement link. A comprehensive literature search uncovered 37 studies, which contributed to a total of 40 independent samples (N = 23,050). The average observed effect in the sample was r = .46. A moderator analysis showed systematic variations in the effect size for learners’ first language, target language, proficiency level, and both self-efficacy and achievement type. We discuss our findings with respect to theoretical constructs and methodological practices and suggest implications for L2 pedagogy and future research into self-efficacy in SLA.The positive psychology movement (Seligman, 1998) has contributed to the proclamation of a positive turn in second language acquisition (SLA) (MacIntyre et al., 2016). Within the context of individual differences, self-efficacy (Bandura, 1997), an individual’s judgment of their capability to achieve goals, has gained particular interest in language learning (e.g., Lake, 2013). The present study meta-analyzes a body of research that has investigated the relationship between second language (L2) self-efficacy and L2 achievement by exploring 1) reporting practices in this domain, 2) the strength and direction of the relationship, and 3) the effects of moderator variables on the self-efficacy-achievement link. A comprehensive literature search uncovered 37 studies, which contributed to a total of 40 independent samples (N = 23,050). The average observed effect in the sample was r = .46. A moderator analysis showed systematic variations in the effect size for learners’ first language, target language, proficiency level, and both self-efficacy and achievement type. We discuss our findings with respect to theoretical constructs and methodological practices and suggest implications for L2 pedagogy and future research into self-efficacy in SLA

(Co)constructing critical pedagogies: Expanding on our department’s approach to language teaching

In this report, we—the members of a curriculum working group (CWG) in Penn State’s German department—describe our efforts to decenter our German language sequence by integrating critical pedagogies into our department’s existing communicative language teaching (CLT) approach. We trace our process towards this goal, beginning with an exploration into and analysis of two critical pedagogies, namely Antiracist Pedagogy (ARP) and Social Justice Pedagogy (SJP). We ultimately adopt SJP because we find it to be a better fit for our purposes in German language instruction. We offer a framework to evaluate and didacticize existing as well as newly created course materials, guided by social justice (SJ) learning objectives. To illustrate our work, we describe the creation and implementation of an instructional unit in an intermediate German language course. Reflections from this course’s instructor and student reactions concerning this unit’s instruction—as well as SJP in the language classroom in general—make evident the importance of critical perspectives regarding curricular development in fostering equitable classrooms

Cytosolic 5'-nucleotidase 1A is overexpressed in pancreatic cancer and mediates gemcitabine resistance by reducing intracellular gemcitabine metabolites.

BACKGROUND: Cytosolic 5'-nucleotidase 1A (NT5C1A) dephosphorylates non-cyclic nucleoside monophosphates to produce nucleosides and inorganic phosphates. Here, we investigate NT5C1A expression in pancreatic ductal adenocarcinoma (PDAC) and its impact on gemcitabine metabolism and therapeutic efficacy. METHODS: NT5C1A expression was determined by semiquantitative immunohistochemistry using tissue microarrays. Gemcitabine metabolites and response were assessed in several human and murine PDAC cell lines using crystal violet assays, Western blot, viability assays, and liquid chromatography tandem mass-spectrometry (LC-MS/MS). FINDINGS: NT5C1A was strongly expressed in tumor cells of a large subgroup of resected PDAC patients in two independent patient cohorts (44-56% score 2 and 8-26% score 3, n = 414). In contrast, NT5C1A was expressed at very low levels in the tumor stroma, and neither stromal nor tumoral expression was a prognostic marker for postoperative survival. In vitro, NT5C1A overexpression increased gemcitabine resistance by reducing apoptosis levels and significantly decreased intracellular amounts of cytotoxic dFdCTP in +NT5C1A tumor cells. Co-culture experiments with conditioned media from +NT5C1A PSCs improved gemcitabine efficacy in tumor cells. In vivo, therapeutic efficacy of gemcitabine was significantly decreased and serum levels of the inactive gemcitabine metabolite dFdU significantly increased in mice bearing NT5C1A overexpressing tumors. INTERPRETATION: NT5C1A is robustly expressed in tumor cells of resected PDAC patients. Moreover, NT5C1A mediates gemcitabine resistance by decreasing the amount of intracellular dFdCTP, leading to reduced tumor cell apoptosis and larger pancreatic tumors in mice. Further studies should clarify the role of NT5C1A as novel predictor for gemcitabine treatment response in patients with PDAC

25th annual computational neuroscience meeting: CNS-2016

The same neuron may play different functional roles in the neural circuits to which it belongs. For example, neurons in the Tritonia pedal ganglia may participate in variable phases of the swim motor rhythms [1]. While such neuronal functional variability is likely to play a major role the delivery of the functionality of neural systems, it is difficult to study it in most nervous systems. We work on the pyloric rhythm network of the crustacean stomatogastric ganglion (STG) [2]. Typically network models of the STG treat neurons of the same functional type as a single model neuron (e.g. PD neurons), assuming the same conductance parameters for these neurons and implying their synchronous firing [3, 4]. However, simultaneous recording of PD neurons shows differences between the timings of spikes of these neurons. This may indicate functional variability of these neurons. Here we modelled separately the two PD neurons of the STG in a multi-neuron model of the pyloric network. Our neuron models comply with known correlations between conductance parameters of ionic currents. Our results reproduce the experimental finding of increasing spike time distance between spikes originating from the two model PD neurons during their synchronised burst phase. The PD neuron with the larger calcium conductance generates its spikes before the other PD neuron. Larger potassium conductance values in the follower neuron imply longer delays between spikes, see Fig. 17.Neuromodulators change the conductance parameters of neurons and maintain the ratios of these parameters [5]. Our results show that such changes may shift the individual contribution of two PD neurons to the PD-phase of the pyloric rhythm altering their functionality within this rhythm. Our work paves the way towards an accessible experimental and computational framework for the analysis of the mechanisms and impact of functional variability of neurons within the neural circuits to which they belong

Cytosolic 5′-nucleotidase 1A is overexpressed in pancreatic cancer and mediates gemcitabine resistance by reducing intracellular gemcitabine metabolitesResearch in context

Background: Cytosolic 5′-nucleotidase 1A (NT5C1A) dephosphorylates non-cyclic nucleoside monophosphates to produce nucleosides and inorganic phosphates. Here, we investigate NT5C1A expression in pancreatic ductal adenocarcinoma (PDAC) and its impact on gemcitabine metabolism and therapeutic efficacy. Methods: NT5C1A expression was determined by semiquantitative immunohistochemistry using tissue microarrays. Gemcitabine metabolites and response were assessed in several human and murine PDAC cell lines using crystal violet assays, Western blot, viability assays, and liquid chromatography tandem mass-spectrometry (LC-MS/MS). Findings: NT5C1A was strongly expressed in tumor cells of a large subgroup of resected PDAC patients in two independent patient cohorts (44–56% score 2 and 8–26% score 3, n = 414). In contrast, NT5C1A was expressed at very low levels in the tumor stroma, and neither stromal nor tumoral expression was a prognostic marker for postoperative survival. In vitro, NT5C1A overexpression increased gemcitabine resistance by reducing apoptosis levels and significantly decreased intracellular amounts of cytotoxic dFdCTP in +NT5C1A tumor cells. Co-culture experiments with conditioned media from +NT5C1A PSCs improved gemcitabine efficacy in tumor cells. In vivo, therapeutic efficacy of gemcitabine was significantly decreased and serum levels of the inactive gemcitabine metabolite dFdU significantly increased in mice bearing NT5C1A overexpressing tumors. Interpretation: NT5C1A is robustly expressed in tumor cells of resected PDAC patients. Moreover, NT5C1A mediates gemcitabine resistance by decreasing the amount of intracellular dFdCTP, leading to reduced tumor cell apoptosis and larger pancreatic tumors in mice. Further studies should clarify the role of NT5C1A as novel predictor for gemcitabine treatment response in patients with PDAC. Keywords: Cytosolic 5′-nucleotidase 1A, Chemotherapeutic resistance, Gemcitabine, Pancreatic cance

Landscape of Biomarkers and Actionable Gene Alterations in Adenocarcinoma of GEJ and Stomach—A Real World Data Analysis

After several years of negative phase III trials in gastric and esophageal cancer, a significant breakthrough in the treatment of metastatic adenocarcinomas of the gastroesophageal junction (GEJ) and stomach (GC) is now becoming evident with the emerging of precision oncology and implementation of molecular targets in tumor treatment. In addition, new generation studies such as umbrella and basket trials are focused on these molecular targets, which makes an early molecular diagnosis based on IHC/ISH and NGS necessary. The required companion diagnostics of Her2neu overamplification or PD-L1 expression is based on immunohistochemistry (IHC) or additionally in situ hybridization (ISH) in case of an IHC Her2neu score of 2+. However, there are investigator-dependent differences in the assessment of Her2neu amplification and different PD-L1 scoring systems obtained by IHC/ISH. The use of high-throughput technologies such as next-generation sequencing (NGS) holds the potential to standardize the analysis and thus make them more comparable. In the presented study, real-world multigene sequencing data of 72 Caucasian patients diagnosed with metastatic adenocarcinomas of GEJ and stomach were analyzed. In the clinical companion diagnostics, we found ESCAT level I molecular targets in one-third of our patients, which directly determined the therapy. In addition, we found potential targets in 14/72 patients (19.4%) who potentially qualify for precision therapies in corresponding molecular studies. The study highlights the importance of comprehensive molecular profiling for precision treatment of GEJ/GC and indicates that a biomarker evaluation should be performed for all patients with metastatic adenocarcinomas before the initiation of first-line treatment and during second-line or subsequent treatment