Screening for Cognitive Impairment in Primary Brain Tumor Patients: A Preliminary Investigation with the MMSE and RBANS

Introduction: The prevalence of mild cognition impairment (MCI) among older adults (≥65) is estimated to range between 10-20% (Langa & Levine, 2014). Integrated primary care allows opportunities for interdisciplinary consultation, screening, and intervention. The aim of this study is to explore the percentage of older adults reporting cognitive concerns during their first primary care psychology visits. It is hypothesized that these rates will mirror prevalence rates in other older adult community dwelling samples in primary care settings. Methods: A patient sample of older adults (≥60) was introduced to services following a referral from their primary care physician. Clinicians then identified problems that were discussed in session, including “cognitive concerns.” Descriptive statistics will be used to assess the percentage of older adults with “cognitive concerns” in this sample, compared to other community dwelling samples. Results: 267 older adults were identified within a larger sample of patients who received primary care psychology services. The percentage of older adults who were referred for “cognitive concerns” was 10.5% (n = 28), with 12.7% (n = 34) reporting “cognitive concerns” during their visit. Interestingly of the 28 older adults referred by their provider for “cognitive concerns,” less than 50% (n = 13) of those patients reported “cognitive concerns” as one of their problems in session. Discussion: This sample of older adults reported cognitive concerns in primary care psychology sessions at a rate that falls within the range identified in other community dwelling samples. Future research could further improve upon identification and screening of older adults with cognitive concerns by psychologists in primary care settings, as intervention for MCI can improve quality of life and may delay progression of dementia (Campbell et al., 2018; Eshkoor et al., 2015).https://scholarscompass.vcu.edu/gradposters/1088/thumbnail.jp

Dis-Integration from unitisation

This paper investigates the dis-integrative effects of unitisation/modularisation on the so called integrative and application orientated topics of Engineering Applications, and suggests possible solutions to the identified problems. Within the main aims of increasing student choice, providing flexibility and enhancing credit accumulation and transfer, many Universities have unitised their courses. In addition most University engineering departments are accredited by the relevant professional body which requires courses to provide a specified minimum of hours to 'core' units which has resulted in an overall reduction in hours given over to units which provide for the applications of those core units thus providing for a Total Engineering education. To resolve this problem requires departments to discover new ways of implementing the ideas of Total Engineering in a Total Teaching way. The paper looks at ways of increasing different modes of teaching within a traditional Electronic Engineering degree course. It is suggested that within an educational world of diminishing staff resources directed study and open-access facilities must be fully utilised

Predation scars may influence host susceptibility to pathogens: evaluating the role of corallivores as vectors of coral disease

Infectious diseases not regulated by host density, such as vector-borne diseases, have the potential to drive population declines and extinctions. Here we test the vector potential of the snail Drupella sp. and butterflyfish Chaetodon plebeius for two coral diseases, black band (BBD) and brown band (BrB) disease. Drupella transmitted BrB to healthy corals in 40% of cases immediately following feeding on infected corals, and even in 12% of cases 12 and 24 hours following feeding. However, Drupella was unable to transmit BBD in either transmission treatment. In a field experiment testing the vector potential of naturally-occurring fish assemblages, equivalent numbers of caged and uncaged coral fragments became infected with either BrB, BBD or skeletal eroding band, indicating that corallivorous fish were unlikely to have caused transmission. In aquaria, C. plebeius did not transmit either BBD or BrB, even following extended feeding on both infected and healthy nubbins. A literature review confirmed only four known coral disease vectors, all invertebrates, corroborating our conclusion that polyp-feeding fishes are unlikely to be vectors of coral diseases. This potentially because polyp-feeding fishes produce shallow lesions, not allowing pathogens to invade coral tissues. In contrast, corallivorous invertebrates that create deeper feeding scars increase pathogens transmission

The State of Self-Organized Criticality of the Sun During the Last Three Solar Cycles. II. Theoretical Model

The observed powerlaw distributions of solar flare parameters can be interpreted in terms of a nonlinear dissipative system in the state of self-organized criticality (SOC). We present a universal analytical model of a SOC process that is governed by three conditions: (i) a multiplicative or exponential growth phase, (ii) a randomly interrupted termination of the growth phase, and (iii) a linear decay phase. This basic concept approximately reproduces the observed frequency distributions. We generalize it to a randomized exponential-growth model, which includes also a (log-normal) distribution of threshold energies before the instability starts, as well as randomized decay times, which can reproduce both the observed occurrence frequency distributions and the scatter of correlated parametyers more realistically. With this analytical model we can efficiently perform Monte-Carlo simulations of frequency distributions and parameter correlations of SOC processes, which are simpler and faster than the iterative simulations of cellular automaton models. Solar cycle modulations of the powerlaw slopes of flare frequency distributions can be used to diagnose the thresholds and growth rates of magnetic instabilities responsible for solar flares.Comment: Part II of Paper I: The State of Self-Organized Criticality of the Sun During the Last Three Solar Cycles. I. Observation

Modeling the transition from decompensated to pathological hypertrophy

Background--Long-chain acyl-CoA synthetases (ACSL) catalyze the conversion of long-chain fatty acids to fatty acyl-CoAs. Cardiac-specific ACSL1 temporal knockout at 2 months results in a shift from FA oxidation toward glycolysis that promotes mTORC1-mediated ventricular hypertrophy. We used unbiased metabolomics and gene expression analyses to examine the early effects of genetic inactivation of fatty acid oxidation on cardiac metabolism, hypertrophy development, and function. Methods and Results--Global cardiac transcriptional analysis revealed differential expression of genes involved in cardiac metabolism, fibrosis, and hypertrophy development in Acsl1 H-/- hearts 2 weeks after Acsl1 ablation. Comparison of the 2- and 10-week transcriptional responses uncovered 137 genes whose expression was uniquely changed upon knockdown of cardiac ACSL1, including the distinct upregulation of fibrosis genes, a phenomenon not observed after complete ACSL1 knockout. Metabolomic analysis identified metabolites altered in hearts displaying partially reduced ACSL activity, and rapamycin treatment normalized the cardiac metabolomic fingerprint. Conclusions--Short-term cardiac-specific ACSL1 inactivation resulted in metabolic and transcriptional derangements distinct from those observed upon complete ACSL1 knockout, suggesting heart-specific mTOR (mechanistic target of rapamycin) signaling that occurs during the early stages of substrate switching. The hypertrophy observed with partial Acsl1 ablation occurs in the context of normal cardiac function and is reminiscent of a physiological process, making this a useful model to study the transition from physiological to pathological hypertrophy

BRG1 and BRM function antagonistically with c-MYC in adult cardiomyocytes to regulate conduction and contractility

Rationale The contractile dysfunction that underlies heart failure involves perturbations in multiple biological processes ranging from metabolism to electrophysiology. Yet the epigenetic mechanisms that are altered in this disease state have not been elucidated. SWI/SNF chromatin-remodeling complexes are plausible candidates based on mouse knockout studies demonstrating a combined requirement for the BRG1 and BRM catalytic subunits in adult cardiomyocytes. Brg1/Brm double mutants exhibit metabolic and mitochondrial defects and are not viable although their cause of death has not been ascertained. Objective To determine the cause of death of Brg1/Brm double-mutant mice, to test the hypothesis that BRG1 and BRM are required for cardiac contractility, and to identify relevant downstream target genes. Methods and results A tamoxifen-inducible gene-targeting strategy utilizing αMHC-Cre-ERT was implemented to delete both SWI/SNF catalytic subunits in adult cardiomyocytes. Brg1/Brm double-mutant mice were monitored by echocardiography and electrocardiography, and they underwent rapidly progressive ventricular dysfunction including conduction defects and arrhythmias that culminated in heart failure and death within 3 weeks. Mechanistically, BRG1/BRM repressed c-Myc expression, and enforced expression of a DOX-inducible c-MYC trangene in mouse cardiomyocytes phenocopied the ventricular conduction defects observed in Brg1/Brm double mutants. BRG1/BRM and c-MYC had opposite effects on the expression of cardiac conduction genes, and the directionality was consistent with their respective loss- and gain-of-function phenotypes. To support the clinical relevance of this mechanism, BRG1/BRM occupancy was diminished at the same target genes in human heart failure cases compared to controls, and this correlated with increased c-MYC expression and decreased CX43 and SCN5A expression. Conclusion BRG1/BRM and c-MYC have an antagonistic relationship regulating the expression of cardiac conduction genes that maintain contractility, which is reminiscent of their antagonistic roles as a tumor suppressor and oncogene in cancer

Effects of the Spin-Orbit and Tensor Interactions on the M1M1 and E2E2 Excitations in Light Nuclei

The effects of varying the spin-orbit and tensor components of a realistic interaction on $M1$ excitation rates and $B(E2)'s$ are studied on nuclei in the $0p$ and $1s-0d$ shells. Not only the total $M1$ but also the spin and orbital parts separately are studied. The single-particle energies are first calculated with the same interaction that is used between the valence nucleons. Later this stringent condition is relaxed somewhat and the $1s$ level is raised relative to $0d$. For nuclei up to $^{28}Si$, much better results i.e stronger $B(M1)$ rates are obtained by increasing the strength of the spin-orbit interaction relative to the free value. This is probably also true for $^{32}S$, but $^{36}Ar$ presents some difficulties. The effects of weakening the tensor interaction are also studied. On a more subtle level, the optimum spin-orbit interaction in the lower half of the $s-d$ shell, as far as $M1$ excitations are concerned, is substantially larger than the difference $E(J=3/2^+)_1-E(J=5/2^+)_1=5.2~MeV$ in $^{17}O$. A larger spin-orbit splitting is also needed to destroy the triaxiality in $^{22}Ne$. Also studied are how much $M1$ orbital and spin strength lies in an observable region and how much is buried in the grass at higher energies. It is noted that for many nuclei the sum $B(M1)_{orbital}+B(M1)_{spin}$ is very close to $B(M1)_{total}$, indicating that the summed cross terms are very small.Comment: 39 pages, revtex 3.

Galileo dust data from the jovian system: 2000 to 2003

The Galileo spacecraft was orbiting Jupiter between Dec 1995 and Sep 2003. The Galileo dust detector monitored the jovian dust environment between about 2 and 370 R_J (jovian radius R_J = 71492 km). We present data from the Galileo dust instrument for the period January 2000 to September 2003. We report on the data of 5389 particles measured between 2000 and the end of the mission in 2003. The majority of the 21250 particles for which the full set of measured impact parameters (impact time, impact direction, charge rise times, charge amplitudes, etc.) was transmitted to Earth were tiny grains (about 10 nm in radius), most of them originating from Jupiter's innermost Galilean moon Io. Their impact rates frequently exceeded 10 min^-1. Surprisingly large impact rates up to 100 min^-1 occurred in Aug/Sep 2000 when Galileo was at about 280 R_J from Jupiter. This peak in dust emission appears to coincide with strong changes in the release of neutral gas from the Io torus. Strong variability in the Io dust flux was measured on timescales of days to weeks, indicating large variations in the dust release from Io or the Io torus or both on such short timescales. Galileo has detected a large number of bigger micron-sized particles mostly in the region between the Galilean moons. A surprisingly large number of such bigger grains was measured in March 2003 within a 4-day interval when Galileo was outside Jupiter's magnetosphere at approximately 350 R_J jovicentric distance. Two passages of Jupiter's gossamer rings in 2002 and 2003 provided the first actual comparison of in-situ dust data from a planetary ring with the results inferred from inverting optical images.Comment: 59 pages, 13 figures, 6 tables, submitted to Planetary and Space Scienc