The legend of the large MCAS gains of 2000-2001.

Issues related to student, teacher, and school accountability have been at the forefront of current educational policy initiatives. Recently, the state of Massachusetts has become a focal point in debate regarding the efficacy of high-stakes accountability models based on an ostensibly large gain at 10th grade. This paper uses an IRT method for evaluating the validity of 10th grade performance gains from 2000 to 2001 on the Massachusetts Comprehensive Assessment System (MCAS) tests in English Language Arts (ELA) and mathematics. We conclude that a moderate gain was obtained in ELA and a small gain in mathematics

NEPC Review: High-Achieving Students in the Era of NCLB

A recent report from the Fordham Institute considers potential instructional policies for high-achieving students that should be considered in the forthcoming reauthorization of the No Child Left Behind Act. The report finds: 1) achievement growth among high-achieving students has been slower than that of low-achieving students; 2) this trend can be traced to state accountability practices; and 3) teachers would support new policies targeted to high achievers. This review examines several premises of the report&rsquo;s conclusions, both implicit and explicit. It concludes that evidence regarding the effects of accountability is inconsistent. It also concludes that teachers have a more nuanced view of allocating resources to high- and low-achievers than is recognized in the report.</p

NEPC Review: The Effect of Milwaukee's Parental Choice Program on Student Achievement in Milwaukee Public Schools

According to a new study of Milwaukee public schools, student achievement has benefited from voucher-based school competition. A novel method, using geocoding, was proposed for measuring the degree of competition within the city of Milwaukee and, in turn, for determining whether such competition has increased or decreased the achievement of public school students. Though a more traditional measurement of competition was eventually used in lieu of geocoding, the authors of the study determined that the overall effect of competition on student outcomes was positive over the seven-year span for which data were available. Specifically, it was argued that increased school choice improves the academic performance of students in traditional public schools who are voucher eligible by means of system-wide competitive pressures. Based on a review of several key issues&mdash;including statistical modeling and control, effect size interpretation, the role of explanation in causal inference, and the validity of reported conclusions&mdash;the practical effect of competition through vouchers appears to be small, if not negligible. It is also suggested that a number of methodological issues would benefit from greater clarity.</p

NEPC Review: KIPP Middle Schools: Impacts on Achievement and Other Outcomes

Using two different approaches, researchers from Mathematica Policy Research conclude that Knowledge Is Power Program (KIPP) students scored higher than comparison students not attending KIPP schools by an amount equivalent to 11 months of additional learning in math and about eight months in reading. The impact was unevenly distributed across KIPP schools, and a number of factors were identified that were weakly related to this variation in effectiveness. The evaluation study was carefully planned and executed, and the results are about the same magnitude as those from other experiments in education. The KIPP outcomes may be substantial if found to persist into later grades. The benefits, however, appear to be overstated in the evaluation study for two reasons. First, translating educational outcomes into “months” of additional learning is an inexact science and can lead to absurd results if taken literally. Second, reported measures of effectiveness that take attrition into account are smaller than the estimates used to draw conclusions about the effectiveness of KIPP. In addition, the effect of KIPP on higher-order reasoning is less certain than is portrayed in the report. The latter topic requires additional empirical work to provide greater clarity

An item response theory approach to longitudinal analysis with application to summer setback in preschool language/literacy

Background: As the popularity of classroom observations has increased, they have been implemented in many longitudinal studies with large probability samples. Given the complexity of longitudinal measurements, there is a need for tools to investigate both growth and the properties of the measurement scale. Methods: A practical IRT model with an embedded growth model is illustrated to examine the psychometric characteristics of classroom assessments for preschool children, and also to show how nonlinear learning over time can be investigated. This approach is applied to data collected for the Academic Rating Scale (ARS) in the literacy domain, which was administered on four occasions over two years. Results: The model enabled an effective illustration of overall and individual gains over two academic years. In particular, a significant de-acceleration in latent literacy skills during summer was observed. The results also provided psychometric support for the argument that ARS literacy can be used to assess developmental skill levels consistent with theories of early literacy acquisition. Conclusions: The proposed IRT approach provided growth parameters that are estimated directly, rather than obtaining these coefficients from estimated growth scores—which may result in biased and inconsistent estimates of growth parameters. The model is also capable of simultaneously representing parameters of items and persons

An electrostatic switch displaces phosphatidylinositol phosphate kinases from the membrane during phagocytosis

PIP5K is held at the membrane of forming phagosomes by a conserved, positively charged patch. During particle engulfment, the surface charge of the phagosome decreases, releasing PIP5K and enabling phagocytosis to proceed

Defective Membrane Remodeling in Neuromuscular Diseases: Insights from Animal Models

Proteins involved in membrane remodeling play an essential role in a plethora of cell functions including endocytosis and intracellular transport. Defects in several of them lead to human diseases. Myotubularins, amphiphysins, and dynamins are all proteins implicated in membrane trafficking and/or remodeling. Mutations in myotubularin, amphiphysin 2 (BIN1), and dynamin 2 lead to different forms of centronuclear myopathy, while mutations in myotubularin-related proteins cause Charcot-Marie-Tooth neuropathies. In addition to centronuclear myopathy, dynamin 2 is also mutated in a dominant form of Charcot-Marie-Tooth neuropathy. While several proteins from these different families are implicated in similar diseases, mutations in close homologues or in the same protein in the case of dynamin 2 lead to diseases affecting different tissues. This suggests (1) a common molecular pathway underlying these different neuromuscular diseases, and (2) tissue-specific regulation of these proteins. This review discusses the pathophysiology of the related neuromuscular diseases on the basis of animal models developed for proteins of the myotubularin, amphiphysin, and dynamin families. A better understanding of the common mechanisms between these neuromuscular disorders will lead to more specific health care and therapeutic approaches

Listeria pathogenesis and molecular virulence determinants

The gram-positive bacterium Listeria monocytogenes is the causative agent of listeriosis, a highly fatal opportunistic foodborne infection. Pregnant women, neonates, the elderly, and debilitated or immunocompromised patients in general are predominantly affected, although the disease can also develop in normal individuals. Clinical manifestations of invasive listeriosis are usually severe and include abortion, sepsis, and meningoencephalitis. Listeriosis can also manifest as a febrile gastroenteritis syndrome. In addition to humans, L. monocytogenes affects many vertebrate species, including birds. Listeria ivanovii, a second pathogenic species of the genus, is specific for ruminants. Our current view of the pathophysiology of listeriosis derives largely from studies with the mouse infection model. Pathogenic listeriae enter the host primarily through the intestine. The liver is thought to be their first target organ after intestinal translocation. In the liver, listeriae actively multiply until the infection is controlled by a cell-mediated immune response. This initial, subclinical step of listeriosis is thought to be common due to the frequent presence of pathogenic L. monocytogenes in food. In normal indivuals, the continual exposure to listerial antigens probably contributes to the maintenance of anti-Listeria memory T cells. However, in debilitated and immunocompromised patients, the unrestricted proliferation of listeriae in the liver may result in prolonged low-level bacteremia, leading to invasion of the preferred secondary target organs (the brain and the gravid uterus) and to overt clinical disease. L. monocytogenes and L. ivanovii are facultative intracellular parasites able to survive in macrophages and to invade a variety of normally nonphagocytic cells, such as epithelial cells, hepatocytes, and endothelial cells. In all these cell types, pathogenic listeriae go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. In this way, listeriae disseminate in host tissues sheltered from the humoral arm of the immune system. Over the last 15 years, a number of virulence factors involved in key steps of this intracellular life cycle have been identified. This review describes in detail the molecular determinants of Listeria virulence and their mechanism of action and summarizes the current knowledge on the pathophysiology of listeriosis and the cell biology and host cell responses to Listeria infection. This article provides an updated perspective of the development of our understanding of Listeria pathogenesis from the first molecular genetic analyses of virulence mechanisms reported in 1985 until the start of the genomic era of Listeria research