An Up-Close Look at Student-Centered Math Teaching: A Study of Highly Regarded High School Teachers and Their Students - Executive Summary

Today, far too many students see mathematics as a subject to be endured, rather than a subject of real-world importance and personal value. That doesn't have to be the case. When teachers use student-centered techniques to engage studentsin more active and authentic ways, they can transform math classrooms into lively learning environments in which studentstake charge of their own learning, collaborate with others, persist in solving complex problems, and make meaningfulconnections to the world around them. Through such experiences, students may come to appreciate mathematics as adiscipline that enriches their lives and their understanding of the world.While a growing body of research supports many of the principles of student-centered instruction, there is still a great dealto learn about how such approaches enhance student learning in mathematics. Recent calls for strengthening the STEMworkforce and for more rigorous K-12 standards via the Common Core State Standards have placed increased emphasison developing higher-order thinking and problem-solving skills in high school mathematics, heightening the need for moreinformation about how teachers can effectively engage students with math content.The American Institutes of Research (AIR), with support from the Nellie Mae Education Foundation, conducted a study ofhighly regarded high school math teachers to expand the research base in two important ways. First, rather than assumingstudent-centered instruction is a monolithic construct, the team used a case study approach to provide rich descriptions ofhow the approach plays out in several classrooms, taking into account how teachers' personal philosophy and the school'sinstructional context might influence their practice. The case study also provided insights into students' perspectives on different approaches to mathematics instruction. Second, the researchers look across a larger sample of classrooms to determine the effects of varying degrees of student-centeredness on students' engagement with learning and their problem-solving skills.This brief offers highlights from the study's design and findings. Readers are encouraged to access the full paper for more details

Growth, pork quality, and excretion characteristics of pigs fed Bt corn or non-transgenic corn

Two experiments (exp. 1 and exp. 2, respectively) were conducted to compare performance, pork quality, and excretion characteristics of pigs fed diets containing Bt 11 (Bt) or control corn (C: non-transgenic inbred lines for exp. 1, and a non-transgenic isoline for exp. 2). Experiment 1 involved barrows and gilts (total n = 64; initial BW = 64 kg and 60 kg), while in exp. 2, 120 barrows were used (initial BW = 17 kg). Pigs were allocated to pens, blocked by sex and BW. Isocaloric, isolysinic diets contained an indigestible marker in exp. 1. Feed disappearance and weight gain data, and excreta samples were collected weekly in exp. 1. Feed disappearance and weight gain data were collected weekly in exp. 2. No difference in ADG was observed, however, feed efficiency was greater for pigs fed the C diet. No corn effects were observed for hot carcass weight, loin eye area, or backfat depth. Hunter color ‘b’ values and values for chroma were significantly greater for pigs fed C diets (P = 0.02, \u3c 0.01, respectively) in exp. 1. In contrast, Hunter color ‘b’ values were significantly lower for pigs fed C diets (P = 0.05) in exp. 2. No corn effects were observed for proximate analyses of meat samples, N or P content of fecal and urine samples, nor N digestibility. Pigs fed C diets had greater apparent P digestibility (57.8% vs. 40.2%; P \u3c 0.0001)

Agenda for Translating Physical Activity, Nutrition, and Weight Management Interventions for Cancer Survivors into Clinical and Community Practice.

Evidence supporting physical activity, diet, and weight management for cancer survivors has grown, leading to the development of guidelines and interventions. The next step is to identify necessary practice and policy changes and to develop a research agenda to inform how interventions can be delivered to survivors most effectively and efficiently in health care settings and by community-based organizations. Here, an agenda is proposed for research, practice, and policy that incorporates recommendations for a range of programming options, a patient-centered, tailored screening and referral approach, and training needs for survivorship care providers and providers of exercise, nutrition, and weight management services. Research needs to focus on sustainability, dissemination, and implementation. Needed policy changes are presented, as well as opportunities to leverage current health care policies

Meta-analysis of genome-wide association studies from the CHARGE consortium identifies common variants associated with carotid intima media thickness and plaque

Carotid intima media thickness (cIMT) and plaque determined by ultrasonography are established measures of subclinical atherosclerosis that each predicts future cardiovascular disease events. We conducted a meta-analysis of genome-wide association data in 31,211 participants of European ancestry from nine large studies in the setting of the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. We then sought additional evidence to support our findings among 11,273 individuals using data from seven additional studies. In the combined meta-analysis, we identified three genomic regions associated with common carotid intima media thickness and two different regions associated with the presence of carotid plaque (P < 5 × 10 -8). The associated SNPs mapped in or near genes related to cellular signaling, lipid metabolism and blood pressure homeostasis, and two of the regions were associated with coronary artery disease (P < 0.006) in the Coronary Artery Disease Genome-Wide Replication and Meta-Analysis (CARDIoGRAM) consortium. Our findings may provide new insight into pathways leading to subclinical atherosclerosis and subsequent cardiovascular events

SARS-CoV-2 spike protein induces endothelial inflammation via ACE2 independently of viral replication

COVID-19, caused by SARS-CoV-2, is a respiratory disease associated with inflammation and endotheliitis. Mechanisms underling inflammatory processes are unclear, but angiotensin converting enzyme 2 (ACE2), the receptor which binds the spike protein of SARS-CoV-2 may be important. Here we investigated whether spike protein binding to ACE2 induces inflammation in endothelial cells and determined the role of ACE2 in this process. Human endothelial cells were exposed to SARS-CoV-2 spike protein, S1 subunit (rS1p) and pro-inflammatory signaling and inflammatory mediators assessed. ACE2 was modulated pharmacologically and by siRNA. Endothelial cells were also exposed to SARS-CoV-2. rSP1 increased production of IL-6, MCP-1, ICAM-1 and PAI-1, and induced NFkB activation via ACE2 in endothelial cells. rS1p increased microparticle formation, a functional marker of endothelial injury. ACE2 interacting proteins involved in inflammation and RNA biology were identified in rS1p-treated cells. Neither ACE2 expression nor ACE2 enzymatic function were affected by rSP1. Endothelial cells exposed to SARS-CoV-2 virus did not exhibit viral replication. We demonstrate that rSP1 induces endothelial inflammation via ACE2 through processes that are independent of ACE2 enzymatic activity and viral replication. We define a novel role for ACE2 in COVID-19- associated endotheliitis

Performance of Risk-Based Criteria for Targeting Acute HIV Screening in San Francisco

Federal guidelines now recommend supplemental HIV RNA testing for persons at high risk for acute HIV infection. However, many rapid HIV testing sites do not include HIV RNA or p24 antigen testing due to concerns about cost, the need for results follow-up, and the impact of expanded venipuncture on clinic flow. We developed criteria to identify patients in a municipal STD clinic in San Francisco who are asymptomatic but may still be likely to have acute infection.Data were from patients tested with serial HIV antibody and HIV RNA tests to identify acute HIV infection. BED-CEIA results were used to classify non-acute cases as recent or longstanding. Demographics and self-reported risk behaviors were collected at time of testing. Multivariate models were developed and preliminarily evaluated using predictors associated with recent infection in bivariate analyses as a proxy for acute HIV infection. Multivariate models demonstrating ≥70% sensitivity for recent infection while testing ≤60% of patients in this development dataset were then validated by determining their performance in identifying acute infections.From 2004-2007, 137 of 12,622 testers had recent and 36 had acute infections. A model limiting acute HIV screening to MSM plus any one of a series of other predictors resulted in a sensitivity of 83.3% and only 47.6% of patients requiring testing. A single-factor model testing only patients reporting any receptive anal intercourse resulted in 88.9% sensitivity with only 55.2% of patients requiring testing.In similar high risk HIV testing sites, acute screening using "supplemental" HIV p24 antigen or RNA tests can be rationally targeted to testers who report particular HIV risk behaviors. By improving the efficiency of acute HIV testing, such criteria could facilitate expanded acute case identification

Tumor Necrosis Factor α Inhibits Expression of the Iron Regulating Hormone Hepcidin in Murine Models of Innate Colitis

Background: Abnormal expression of the liver peptide hormone hepcidin, a key regulator of iron homeostasis, contributes to the pathogenesis of anemia in conditions such as inflammatory bowel disease (IBD). Since little is known about the mechanisms that control hepcidin expression during states of intestinal inflammation, we sought to shed light on this issue using mouse models. Methodology/Principal Findings: Hepcidin expression was evaluated in two types of intestinal inflammation caused by innate immune activation—dextran sulfate sodium (DSS)-induced colitis in wild-type mice and the spontaneous colitis occurring in T-bet/Rag2-deficient (TRUC) mice. The role of tumor necrosis factor (TNF) $\alpha$ was investigated by in vivo neutralization, and by treatment of a hepatocyte cell line, as well as mice, with the recombinant cytokine. Expression and activation of Smad1, a positive regulator of hepcidin transcription, were assessed during colitis and following administration or neutralization of TNF$\alpha$. Hepcidin expression progressively decreased with time during DSS colitis, correlating with changes in systemic iron distribution. TNF$\alpha$ inhibited hepcidin expression in cultured hepatocytes and non-colitic mice, while TNF$\alpha$ neutralization during DSS colitis increased it. Similar results were obtained in TRUC mice. These effects involved a TNF$\alpha$-dependent decrease in Smad1 protein but not mRNA. Conclusions/Significance: TNF$\alpha$ inhibits hepcidin expression in two distinct types of innate colitis, with down-regulation of Smad1 protein playing an important role in this process. This inhibitory effect of TNF$\alpha$ may be superseded by other factors in the context of T cell-mediated colitis given that in the latter form of intestinal inflammation hepcidin is usually up-regulated

Dynamic Replacement of Histone H3 Variants Reprograms Epigenetic Marks in Early Mouse Embryos

Upon fertilization, reprogramming of gene expression is required for embryo development. This step is marked by DNA demethylation and changes in histone variant composition. However, little is known about the molecular mechanisms causing these changes and their impact on histone modifications. We examined the global deposition of the DNA replication-dependent histone H3.1 and H3.2 variants and the DNA replication-independent H3.3 variant after fertilization in mice. We showed that H3.3, a euchromatic marker of gene activity, transiently disappears from the maternal genome, suggesting erasure of the oocyte-specific modifications carried by H3.3. After fertilization, H3.2 is incorporated into the transcriptionally silent heterochromatin, whereas H3.1 and H3.3 occupy unusual heterochromatic and euchromatin locations, respectively. After the two-cell stage, H3.1 and H3.3 variants resume their usual respective locations on heterochromatin and euchromatin. Preventing the incorporation of H3.1 and H3.2 by knockdown of the histone chaperone CAF-1 induces a reciprocal increase in H3.3 deposition and impairs heterochromatin formation. We propose that the deposition of different H3 variants influences the functional organization of chromatin. Taken together, these findings suggest that dynamic changes in the deposition of H3 variants are critical for chromatin reorganization during epigenetic reprogramming

Epstein-Barr Virus Evades CD4+ T Cell Responses in Lytic Cycle through BZLF1-mediated Downregulation of CD74 and the Cooperation of vBcl-2

Evasion of immune T cell responses is crucial for viruses to establish persistence in the infected host. Immune evasion mechanisms of Epstein-Barr virus (EBV) in the context of MHC-I antigen presentation have been well studied. In contrast, viral interference with MHC-II antigen presentation is less well understood, not only for EBV but also for other persistent viruses. Here we show that the EBV encoded BZLF1 can interfere with recognition by immune CD4+ effector T cells. This impaired T cell recognition occurred in the absence of a reduction in the expression of surface MHC-II, but correlated with a marked downregulation of surface CD74 on the target cells. Furthermore, impaired CD4+ T cell recognition was also observed with target cells where CD74 expression was downregulated by shRNA-mediated inhibition. BZLF1 downregulated surface CD74 via a post-transcriptional mechanism distinct from its previously reported effect on the CIITA promoter. In addition to being a chaperone for MHC-II αβ dimers, CD74 also functions as a surface receptor for macrophage Migration Inhibitory Factor and enhances cell survival through transcriptional upregulation of Bcl-2 family members. The immune-evasion function of BZLF1 therefore comes at a cost of induced toxicity. However, during EBV lytic cycle induced by BZLF1 expression, this toxicity can be overcome by expression of the vBcl-2, BHRF1, at an early stage of lytic infection. We conclude that by inhibiting apoptosis, the vBcl-2 not only maintains cell viability to allow sufficient time for synthesis and accumulation of infectious virus progeny, but also enables BZLF1 to effect its immune evasion function