Correlational Evidence between the Processing Speed Index, Coherent Motion Threshold, and Achievement Scores of Children With and Without Learning Disabilities

The purpose of this study was to determine the responses to three research questions. Is there an inverse relationship between PSI and CMT? Is a score on PSI associated with a child’s performance on math fluency and math calculation? Is CMT associated with PSI on math fluency and math calculation? Academic performance in math was measured by tests of math fluency and calculation. The study investigated the likelihood that a child with a slow PSI will have a high coherent motion threshold (CMT). The diagnostic status groups were comprised of 33 children from 2nd to 8th grades. The children were divided into three groups. One group of children with a learning disability in math only, one group of children with a learning disability in reading and in math, and one group of typically developing children. The group of typically developing subjects served as the control group, and the remaining two groups served as the experimental groups. A correlational research model was used to determine if a relationship exists between Coherent Motion and PSI. A linear regression analysis was conducted to test the correlation between CMT and PSI to gather data relative to the first research question. An Analysis of Variance (ANOVA) was conducted to further test Hypothesis One. Results indicated that there is a moderate negative relationship that exists between PSI and CMT. It was further hypothesized that PSI is associated with a child’s score on math fluency and math calculation, and that CMT is associated with PSI on math fluency and math calculation. A regression analysis was conducted to gather data relative to the second and third research question. Analysis of Variance (ANOVA) was conducted and the findings suggested a moderate negative relationship exist between CMT and PSI. A regression analysis of variance (ANOVA) was used to show the relationship between math fluency and PSI, math calculation and PSI, and math calculation along with math fluency and PSI. The results revealed that a strong direct relationship exists between math fluency, math calculation and processing speed. A regression model was created to determine if PSI and CMT, along with being identified as disabled, can be used as a predictor for math fluency and math calculation scores. When CMT is combined with PSI and students identified as having a disability, the findings revealed that it was not a strong predictor of math fluency and math calculation abilities

A microscopic model for d-wave charge carrier pairing and non-Fermi-liquid behavior in a purely repulsive 2D electron system

We investigate a microscopic model for strongly correlated electrons with both on-site and nearest neighbor Coulomb repulsion on a 2D square lattice. This exhibits a state in which electrons undergo a ``somersault'' in their internal spin-space (spin-flux) as they traverse a closed loop in external coordinate space. When this spin-1/2 antiferromagnetic (AFM) insulator is doped, the ground state is a liquid of charged, bosonic meron-vortices, which for topological reasons are created in vortex-antivortex pairs. The magnetic exchange energy of the distorted AFM background leads to a logarithmic vortex-antivortex attraction which overcomes the direct Coulomb repulsion between holes localized on the vortex cores. This leads to the appearance of pre-formed charged pairs. We use the Configuration Interaction (CI) Method to study the quantum translational and rotational motion of various charged magnetic solitons and soliton pairs. The CI method systematically describes fluctuation and quantum tunneling corrections to the Hartree-Fock Approximation (HFA). We find that the lowest energy charged meron-antimeron pairs exhibit d-wave rotational symmetry, consistent with the symmetry of the cuprate superconducting order parameter. For a single hole in the 2D AFM plane, we find a precursor to spin-charge separation in which a conventional charged spin-polaron dissociates into a singly charged meron-antimeron pair. This model provides a unified microscopic basis for (i) non-Fermi-liquid transport properties, (ii) d-wave preformed charged carrier pairs, (iii) mid-infrared optical absorption, (iv) destruction of AFM long range order with doping and other magnetic properties, and (v) certain aspects of angled resolved photo-emission spectroscopy (ARPES).Comment: 14 pages, 17 figure

Statins Enhance Clonal Growth of Late Outgrowth Endothelial Progenitors and Increase Myocardial Capillary Density in the Chronically Ischemic Heart

Coronary artery disease and ischemic heart disease are leading causes of heart failure and death. Reduced blood flow to heart tissue leads to decreased heart function and symptoms of heart failure. Therapies to improve heart function in chronic coronary artery disease are important to identify. HMG-CoA reductase inhibitors (statins) are an important therapy for prevention of coronary artery disease, but also have non-cholesterol lowering effects. Our prior work showed that pravastatin improves contractile function in the chronically ischemic heart in pigs. Endothelial progenitor cells are a potential source of new blood vessels in ischemic tissues. While statins are known to increase the number of early outgrowth endothelial progenitor cells, their effects on late outgrowth endothelial progenitor cells (LOEPCs) and capillary density in ischemic heart tissue are not known. We hypothesized that statins exert positive effects on the mobilization and growth of late outgrowth EPCs, and capillary density in ischemic heart tissue.We determined the effects of statins on the mobilization and growth of late outgrowth endothelial progenitor cells from pigs. We also determined the density of capillaries in myocardial tissue in pigs with chronic myocardial ischemia with or without treatment with pravastatin. Pravastatin therapy resulted in greater than two-fold increase in CD31+ LOEPCs versus untreated animals. Addition of pravastatin or simvastatin to blood mononuclear cells increased the number of LOEPCs greater than three fold in culture. Finally, in animals with chronic myocardial ischemia, pravastatin increased capillary density 46%.Statins promote the derivation, mobilization, and clonal growth of LOEPCs. Pravastatin therapy in vivo increases myocardial capillary density in chronically ischemic myocardium, providing an in vivo correlate for the effects of statins on LOEPC growth in vitro. Our findings provide evidence that statin therapy can increase the density of capillaries in the chronically ischemic heart

Ruxolitinib for Glucocorticoid-Refractory Acute Graft-versus-Host Disease

BACKGROUND: Acute graft-versus-host disease (GVHD) remains a major limitation of allogeneic stem-cell transplantation; not all patients have a response to standard glucocorticoid treatment. In a phase 2 trial, ruxolitinib, a selective Janus kinase (JAK1 and JAK2) inhibitor, showed potential efficacy in patients with glucocorticoid-refractory acute GVHD. METHODS: We conducted a multicenter, randomized, open-label, phase 3 trial comparing the efficacy and safety of oral ruxolitinib (10 mg twice daily) with the investigator's choice of therapy from a list of nine commonly used options (control) in patients 12 years of age or older who had glucocorticoid-refractory acute GVHD after allogeneic stem-cell transplantation. The primary end point was overall response (complete response or partial response) at day 28. The key secondary end point was durable overall response at day 56. RESULTS: A total of 309 patients underwent randomization; 154 patients were assigned to the ruxolitinib group and 155 to the control group. Overall response at day 28 was higher in the ruxolitinib group than in the control group (62% [96 patients] vs. 39% [61]; odds ratio, 2.64; 95% confidence interval [CI], 1.65 to 4.22; P<0.001). Durable overall response at day 56 was higher in the ruxolitinib group than in the control group (40% [61 patients] vs. 22% [34]; odds ratio, 2.38; 95% CI, 1.43 to 3.94; P<0.001). The estimated cumulative incidence of loss of response at 6 months was 10% in the ruxolitinib group and 39% in the control group. The median failure-free survival was considerably longer with ruxolitinib than with control (5.0 months vs. 1.0 month; hazard ratio for relapse or progression of hematologic disease, non-relapse-related death, or addition of new systemic therapy for acute GVHD, 0.46; 95% CI, 0.35 to 0.60). The median overall survival was 11.1 months in the ruxolitinib group and 6.5 months in the control group (hazard ratio for death, 0.83; 95% CI, 0.60 to 1.15). The most common adverse events up to day 28 were thrombocytopenia (in 50 of 152 patients [33%] in the ruxolitinib group and 27 of 150 [18%] in the control group), anemia (in 46 [30%] and 42 [28%], respectively), and cytomegalovirus infection (in 39 [26%] and 31 [21%]). CONCLUSIONS: Ruxolitinib therapy led to significant improvements in efficacy outcomes, with a higher incidence of thrombocytopenia, the most frequent toxic effect, than that observed with control therapy

Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases

The production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular "reactive oxygen species" (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation. We review the considerable and wide-ranging evidence for the involvement of this combination of (su)peroxide and poorly liganded iron in a large number of physiological and indeed pathological processes and inflammatory disorders, especially those involving the progressive degradation of cellular and organismal performance. These diseases share a great many similarities and thus might be considered to have a common cause (i.e. iron-catalysed free radical and especially hydroxyl radical generation). The studies reviewed include those focused on a series of cardiovascular, metabolic and neurological diseases, where iron can be found at the sites of plaques and lesions, as well as studies showing the significance of iron to aging and longevity. The effective chelation of iron by natural or synthetic ligands is thus of major physiological (and potentially therapeutic) importance. As systems properties, we need to recognise that physiological observables have multiple molecular causes, and studying them in isolation leads to inconsistent patterns of apparent causality when it is the simultaneous combination of multiple factors that is responsible. This explains, for instance, the decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference

2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease

The recommendations listed in this document are, whenever possible, evidence based. An extensive evidence review was conducted as the document was compiled through December 2008. Repeated literature searches were performed by the guideline development staff and writing committee members as new issues were considered. New clinical trials published in peer-reviewed journals and articles through December 2011 were also reviewed and incorporated when relevant. Furthermore, because of the extended development time period for this guideline, peer review comments indicated that the sections focused on imaging technologies required additional updating, which occurred during 2011. Therefore, the evidence review for the imaging sections includes published literature through December 2011

Very low levels of atherogenic lipoproteins and the risk for cardiovascular events:a meta-analysis of statin trials

BACKGROUND Levels of atherogenic lipoproteins achieved with statin therapy are highly variable, but the consequence of this variability for cardiovascular disease risk is not well-documented

Lipid-Modifying Therapies and Risk of Pancreatitis:a Meta-analysis

CONTEXT: Statin therapy has been associated with pancreatitis in observational studies. Although lipid guidelines recommend fibrate therapy to reduce pancreatitis risk in persons with hypertriglyceridemia, fibrates may lead to the development of gallstones, a risk factor for pancreatitis. OBJECTIVE: To investigate associations between statin or fibrate therapy and incident pancreatitis in large randomized trials. DATA SOURCES: Relevant trials were identified in literature searches of MEDLINE, EMBASE, and Web of Science (January 1, 1994, for statin trials and January 1, 1972, for fibrate trials, through June 9, 2012). Published pancreatitis data were tabulated where available (6 trials). Unpublished data were obtained from investigators (22 trials). STUDY SELECTION: We included randomized controlled cardiovascular end-point trials investigating effects of statin therapy or fibrate therapy. Studies with more than 1000 participants followed up for more than 1 year were included. DATA EXTRACTION: Trial-specific data described numbers of participants developing pancreatitis and change in triglyceride levels at 1 year. Trial-specific risk ratios (RRs) were calculated and combined using random-effects model meta-analysis. Between-study heterogeneity was assessed using the I2 statistic. RESULTS: In 16 placebo- and standard care-controlled statin trials with 113,800 participants conducted over a weighted mean follow-up of 4.1 (SD, 1.5) years, 309 participants developed pancreatitis (134 assigned to statin, 175 assigned to control) (RR, 0.77 [95% CI, 0.62-0.97; P = .03; I2 = 0%]). In 5 dose-comparison statin trials with 39,614 participants conducted over 4.8 (SD, 1.7) years, 156 participants developed pancreatitis (70 assigned to intensive dose, 86 assigned to moderate dose) (RR, 0.82 [95% CI, 0.59-1.12; P = .21; I2 = 0%]). Combined results for all 21 statin trials provided RR 0.79 (95% CI, 0.65-0.95; P = .01; I2 = 0%). In 7 fibrate trials with 40,162 participants conducted over 5.3 (SD, 0.5) years, 144 participants developed pancreatitis (84 assigned to fibrate therapy, 60 assigned to placebo) (RR, 1.39 [95% CI, 1.00-1.95; P = .053; I2 = 0%]). CONCLUSION: In a pooled analysis of randomized trial data, use of statin therapy was associated with a lower risk of pancreatitis in patients with normal or mildly elevated triglyceride levels

Primary prevention of coronary heart disease: guidance from Framingham: a statement for healthcare professionals from the AHA Task Force on Risk Reduction. American Heart Association

This statement discusses the new Framingham Heart Study charts for estimating (CHD) coronary heart disease risk, their essential features, and their appropriate use. In addition, several issues related to CHD prevention raised by these charts are examined. Other issues of risk management not considered in these charts are also addressed

Guide to primary prevention of cardiovascular diseases. A statement for healthcare professionals from the Task Force on Risk Reduction. American Heart Association Science Advisory and Coordinating Committee

The clinical and public health approaches to primary prevention are complementary. Primary prevention refers to guidance given to persons with no known cardiovascular disease. Physicians can contribute to the public health approach through patient education. The first goal of prevention is to prevent the development of risk factors. Physicians should instruct all patients about adopting healthy life habits that will prevent intensification of risk factors. Patient education should be family oriented. Ideally, risk factor prevention begins in childhood. Preventing cigarette smoking by children and adolescents is a prime goal. Another major goal is prevention of overweight and obesity in children and weight gain in adults; overweight lies at the heart of several risk factors. Encouraging life habits that incorporate regular physical activity, especially walking, and active recreational sports likewise will decrease intensity of risk factors. Patients and their families should be encouraged to reduce their intake of cholesterol and saturated fats by using unsaturated vegetable oils instead of animal-based saturated fats and adopting the habit of eating smaller portions. Evaluation of the family history may reveal that other family members need intervention to avoid developing cardiovascular disease. Adoption of healthy life habits and early intervention will mitigate the severity of risk factors that are the result of aging and genetic factors