The Effects of Self-Regulated Learning Training on Teachers’ Self-Regulated Learning, Self-Efficacy for Teaching, and Perceived Instructional Effectiveness in Computer-Supported Collaborative Learning Environments

The effects of training on teachers’ self-regulated learning (SRL), self-efficacy for teaching, and perceived instructional effectiveness in computer-supported collaborative learning (CSCL) environments were investigated. Participants were 80 K-12 teachers who had recently transitioned to teaching in a CSCL environment when schools closed in response to the COVID- 19 pandemic. The researcher also explored how teachers use SRL skills in their learning and instruction. Training consisted of weekly collaborative meetings addressing pedagogy and technology connections. Participants in the treatment group received explicit training in SRL and practice applying concepts to their learning and instruction. Participants in both group conditions engaged in activities fostering reflection, goal setting, planning, monitoring, and motivation for learning and teaching in a CSCL environment. The quantitative results revealed no group differences between teachers’ SRL, self-efficacy for teaching, and perceived instructional effectiveness in CSCL. However, analyses of follow-up interviews and participants’ weekly reflections throughout the training intervention showed teachers in the treatment group more frequently and with greater specificity described their SRL skills by comparison to the teachers who did not receive explicit SRL training. These findings suggest training in SRL in CSCL environments likely contributes to teachers’ professional knowledge and skills as instructors in CSCL environments. Additionally, the granularity of measures likely impacts detection of SRL, self-efficacy for teaching, and perceived instructional effectiveness in CSCL environments

Teacher Support of Co- and Socially-Shared Regulation of Learning in Middle School Mathematics Classrooms

Social influences on classroom learning have a long research tradition and are critical components of self-regulated learning theories. More recently, researchers have explored the social influences of self-regulated learning in cooperative learning contexts. In these settings, co-regulation of learning and socially-shared regulation of learning strategies have been aligned with self-regulated learning theory. However, without specific training or structure, teachers are not likely to explicitly integrate SRL strategies into their teaching. We use case studies to better understand how Zimmerman\u27s theory of self-regulated learning (2008) and Hadwin\u27s conceptual framework of socially-shared regulation of learning (2018) emerge from teachers\u27 support of student-centered instruction. We purposely selected two proficient teachers for more extensive observations focused on student behaviors in teams. The observation instruments afford us a means of advancing research and practice with respect to how teamwork may elicit self- and socially-shared regulation of learning strategies. Consistent with previous findings, the teachers we observed seem to have made many pedagogical moves to explicitly prompt self- and team monitoring of learning during engagement with course content yet provided fewer opportunities for students to think through the planning and evaluation processes. These findings suggest the cooperative learning model implemented in these classrooms provides support for students\u27 co- and socially-shared regulation of learning

Gene Expression Signature of Normal Cell-of-Origin Predicts Ovarian Tumor Outcomes

The potential role of the cell-of-origin in determining the tumor phenotype has been raised, but not adequately examined. We hypothesized that distinct cells-of-origin may play a role in determining ovarian tumor phenotype and outcome. Here we describe a new cell culture medium for in vitro culture of paired normal human ovarian (OV) and fallopian tube (FT) epithelial cells from donors without cancer. While these cells have been cultured individually for short periods of time, to our knowledge this is the first long-term culture of both cell types from the same donors. Through analysis of the gene expression profiles of the cultured OV/FT cells we identified a normal cell-of-origin gene signature that classified primary ovarian cancers into OV-like and FT-like subgroups; this classification correlated with significant differences in clinical outcomes. The identification of a prognostically significant gene expression signature derived solely from normal untransformed cells is consistent with the hypothesis that the normal cell-of-origin may be a source of ovarian tumor heterogeneity and the associated differences in tumor outcome

Interpreting Cancer Genomes Using Systematic Host Perturbations by Tumour Virus Proteins

Genotypic differences greatly influence susceptibility and resistance to disease. Understanding genotype-phenotype relationships requires that phenotypes be viewed as manifestations of network properties, rather than simply as the result of individual genomic variations. Genome sequencing efforts have identified numerous germline mutations associated with cancer predisposition and large numbers of somatic genomic alterations. However, it remains challenging to distinguish between background, or “passenger” and causal, or “driver” cancer mutations in these datasets. Human viruses intrinsically depend on their host cell during the course of infection and can elicit pathological phenotypes similar to those arising from mutations. To test the hypothesis that genomic variations and tumour viruses may cause cancer via related mechanisms, we systematically examined host interactome and transcriptome network perturbations caused by DNA tumour virus proteins. The resulting integrated viral perturbation data reflects rewiring of the host cell networks, and highlights pathways that go awry in cancer, such as Notch signalling and apoptosis. We show that systematic analyses of host targets of viral proteins can identify cancer genes with a success rate on par with their identification through functional genomics and large-scale cataloguing of tumour mutations. Together, these complementary approaches result in increased specificity for cancer gene identification. Combining systems-level studies of pathogen-encoded gene products with genomic approaches will facilitate prioritization of cancer-causing driver genes so as to advance understanding of the genetic basis of human cancer

The Bacterial and Viral Complexity of Postinfectious Hydrocephalus in Uganda

Postinfectious hydrocephalus (PIH), often following neonatal sepsis, is the most common cause of pediatric hydrocephalus world-wide, yet the microbial pathogens remain uncharacterized. Characterization of the microbial agents causing PIH would lead to an emphasis shift from surgical palliation of cerebrospinal fluid (CSF) accumulation to prevention. We examined blood and CSF from 100 consecutive cases of PIH and control cases of non-postinfectious hydrocephalus (NPIH) in infants in Uganda. Genomic testing was undertaken for bacterial, fungal, and parasitic DNA, DNA and RNA sequencing for viral identification, and extensive bacterial culture recovery. We uncovered a major contribution to PIH from Paenibacillus , upon a background of frequent cytomegalovirus (CMV) infection. CMV was only found in CSF in PIH cases. A facultatively anaerobic isolate was recovered. Assembly of the genome revealed a strain of P. thiaminolyticus . In mice, this isolate designated strain Mbale , was lethal in contrast with the benign reference strain. These findings point to the value of an unbiased pan-microbial approach to characterize PIH in settings where the organisms remain unknown, and enables a pathway towards more optimal treatment and prevention of the proximate neonatal infections. One Sentence Summary We have discovered a novel strain of bacteria upon a frequent viral background underlying postinfectious hydrocephalus in Uganda

Paenibacillus infection with frequent viral coinfection contributes to postinfectious hydrocephalus in Ugandan infants

Postinfectious hydrocephalus (PIH), which often follows neonatal sepsis, is the most common cause of pediatric hydrocephalus worldwide, yet the microbial pathogens underlying this disease remain to be elucidated. Characterization of the microbial agents causing PIH would enable a shift from surgical palliation of cerebrospinal fluid (CSF) accumulation to prevention of the disease. Here, we examined blood and CSF samples collected from 100 consecutive infant cases of PIH and control cases comprising infants with non-postinfectious hydrocephalus in Uganda. Genomic sequencing of samples was undertaken to test for bacterial, fungal, and parasitic DNA; DNA and RNA sequencing was used to identify viruses; and bacterial culture recovery was used to identify potential causative organisms. We found that infection with the bacterium Paenibacillus, together with frequent cytomegalovirus (CMV) coinfection, was associated with PIH in our infant cohort. Assembly of the genome of a facultative anaerobic bacterial isolate recovered from cultures of CSF samples from PIH cases identified a strain of Paenibacillus thiaminolyticus. This strain, designated Mbale, was lethal when injected into mice in contrast to the benign reference Paenibacillus strain. These findings show that an unbiased pan-microbial approach enabled characterization of Paenibacillus in CSF samples from PIH cases, and point toward a pathway of more optimal treatment and prevention for PIH and other proximate neonatal infections

OCLER and FNLER tumor histopathology in immunodeficient nude (Nu/Nu) mice.

<p><b>A-B</b>, Hematoxylin and eosin (H&E) stains of representative formalin-fixed paraffin-embedded (FFPE) tumor sections from OCLER (A) and FNLER (B) xenografts revealed focal micropapillary structures. The predominant morphology was diffuse sheets of cells with a poorly differentiated tumor architecture (scale bar  =  20 µM). <b>C-D</b>, PAX8 immunoperoxidase stains of representative FFPE tumor sections from OCLER (C) and FNLER (D) xenografts confirmed that xenografts retained their PAX8 expression (scale bar  =  20 µM).</p

Tumor formation, tumor burden and ascites in the OCLER and FNLER xenograft model.

a<p>Values shown are means ± s.d. across all mice injected with each cell type that had any evaluable tumor mass (the sum of 1× intraperitoneal and 2× subcutaneous sites per mouse).</p>b<p>Formation of ascites was only evaluated among mice that developed tumors.</p>c<p><i>P</i>-values were calculated using the Mann-Whitney test.</p