55 research outputs found

    The lunar wake at 6.8 R(L): WIND magnetic field observations

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    We report on WIND magnetic field observations at ∼6.8 RL downstream of the moon on 27th December 1994. The moon was in the solar wind during the encounter. IMP‐8 observations are used to determine baseline IMF conditions, and therefore determine those features in the WIND data which are related to its proximity to the moon. Previous Explorer 35 observations suggest that the lunar wake is not detectable beyond a downstream distance of ∼4 RL. However, despite the distance of WIND from the moon, we observe a slight decrease in field intensity just prior to the spacecraft entering the optical shadow, a slight field strength enhancement whilst in shadow, and perhaps a weak depression once the spacecraft reemerges into sunlight. These signatures closely resemble, but are weaker than, the previous observations. We conclude that a lunar wake did extend to these distances at the time of this encounter. We also note a rotation in field direction some distance outside of the wake signature which may be attributed to the crossing of the lunar mach cone boundary. We discuss the observations in terms of simple models of the solar wind interaction with an insulating body

    Upstream ULF waves and energetic electrons associated with the lunar wake: Detection of precursor activity

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    We present observations of precursor ULF wave activity and energetic electron flows detected by the WIND spacecraft just prior to entry of the lunar wake on 27 December 1994. This activity occurs upstream of the wake on field lines directly connected to the wake penumbra region. The activity ceases near the penumbra entrance. The observations of upstream ULF wave activity and solar wind counterstreaming electron flows is similar to observations made upstream of collisionless bow shocks. Analogously, the wake precursor region is characterized by thermalization and information propagation ahead of the wake structure

    Rehabilitation goals of people with spinal cord injuries can be classified against the International Classification of Functioning, Disability and Health Core Set for spinal cord injuries

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    Objectives: To establish whether inter-professional rehabilitation goals from people with non-traumatic spinal cord injury (SCI) can be classified against the International Classification of Functioning, Disability and Health (ICF) SCI Comprehensive and Brief Core Sets early postacute situation. Setting: Neurological rehabilitation unit. Methods: Rehabilitation goals of 119 patients with mainly incomplete and non-traumatic SCIs were classified against the ICF SCI Core Sets following established linking rules. Results: A total of 119 patients generated 1509 goals with a mean (and s.d.) of 10.5 (9.1) goals per patient during the course of their inpatient rehabilitation stay. Classifying the 1509 rehabilitation goals against the Comprehensive ICF Core Set generated 2909 ICF codes. Only 69 goals (4.6%) were classified as ‘not definable (ND)’. Classifying the 1509 goals against the Brief ICF Core Set generated 2076 ICF codes. However, 751(49.8%) of these goals were classified as ‘ND’. In the majority of goals (95.7%), the ICF code description was not comprehensive enough to fully express the goals set in rehabilitation. In particular, the notion of quality of movement or specificity and measurability aspects of a goal (usually described with the criteria and acronyms SMART) could not be expressed through the ICF codes. Conclusion: Inter-professional rehabilitation goals can be broadly described by the ICF Comprehensive Core Set for SCI but not the Brief Core Set

    The places parents go: understanding the breadth, scope, and experiences of activity spaces for parents

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    The final publication is available at Springer via https://doi.org/10.1007/s10708-015-9690-yNeighborhood environments are related to parenting behaviors, which in turn have a life-long effect on children’s health and well-being. Activity spaces, which measure individual routine patterns of movement, may be helpful in assessing how physical and social environments shape parenting. In this study we use qualitative data and GIS mapping from four California cities to examine parental activity spaces. Parents described a number of factors that shape their activity spaces including caregiving status, the age of their children, and income. Parental activity spaces also varied between times (weekends vs. weekdays) and places (adult-only vs. child-specific places). Knowing how to best capture and study parental activity spaces could identify mechanisms by which environmental factors influence parenting behaviors and child health

    Association between substance use and psychosocial characteristics among adolescents of the Seychelles

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    BACKGROUND: We examined the associations between substance use (cigarette smoking, alcohol drinking, and cannabis use) and psychosocial characteristics at the individual and family levels among adolescents of the Seychelles, a rapidly developing small island state in the African region. METHODS: A school survey was conducted in a representative sample of 1432 students aged 11-17 years from all secondary schools. Data came from a self-administered anonymous questionnaire conducted along a standard methodology (Global School-based Health Survey, GSHS). Risk behaviors and psychosocial characteristics were dichotomized. Association analyses were adjusted for a possible classroom effect. RESULTS: The prevalence of cigarette smoking, alcohol drinking and cannabis use was higher in boys than in girls and increased with age. Age-adjusted and multivariate analyses showed that several individual level characteristics (e.g. suicidal ideation and truancy) and family level characteristics (e.g. poor parental monitoring) were associated with substance use among students. CONCLUSIONS: Our results suggest that health promotion programs should simultaneously address multiple risk behaviors and take into account a wide range of psychosocial characteristics of the students at the individual and family levels

    Selective mGluR1 Antagonist EMQMCM Inhibits the Kainate-Induced Excitotoxicity in Primary Neuronal Cultures and in the Rat Hippocampus

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    Abundant evidence suggests that indirect inhibitory modulation of glutamatergic transmission, via metabotropic glutamatergic receptors (mGluR), may induce neuroprotection. The present study was designed to determine whether the selective antagonist of mGluR1 (3-ethyl-2-methyl-quinolin-6-yl)-(4-methoxy-cyclohexyl)-methanone methanesulfonate (EMQMCM), showed neuroprotection against the kainate (KA)-induced excitotoxicity in vitro and in vivo. In in vitro studies on mouse primary cortical and hippocampal neuronal cultures, incubation with KA (150 μM) induced strong degeneration [measured as lactate dehydrogenase (LDH) efflux] and apoptosis (measured as caspase-3 activity). EMQMCM (0.1–100 μM) added 30 min to 6 h after KA, significantly attenuated the KA-induced LDH release and prevented the increase in caspase-3 activity in the cultures. Those effects were dose- and time-dependent. In in vivo studies KA (2.5 nmol/1 μl) was unilaterally injected into the rat dorsal CA1 hippocampal region. Degeneration was calculated by counting surviving neurons in the CA pyramidal layer using stereological methods. It was found that EMQMCM (5–10 nmol/1 μl) injected into the dorsal hippocampus 30 min, 1 h, or 3 h (the higher dose only) after KA significantly prevented the KA-induced neuronal degeneration. In vivo microdialysis studies in rat hippocampus showed that EMQMCM (100 μM) significantly increased γ-aminobutyric acid (GABA) and decreased glutamate release. When perfused simultaneously with KA, EMQMCM substantially increased GABA release and prevented the KA-induced glutamate release. The obtained results indicate that the mGluR1 antagonist, EMQMCM, may exert neuroprotection against excitotoxicity after delayed treatment (30 min to 6 h). The role of enhanced GABAergic transmission in the neuroprotection is postulated

    Transcriptome Profiling of Whole Blood Cells Identifies PLEK2 and C1QB in Human Melanoma

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    Developing analytical methodologies to identify biomarkers in easily accessible body fluids is highly valuable for the early diagnosis and management of cancer patients. Peripheral whole blood is a "nucleic acid-rich" and "inflammatory cell-rich" information reservoir and represents systemic processes altered by the presence of cancer cells.We conducted transcriptome profiling of whole blood cells from melanoma patients. To overcome challenges associated with blood-based transcriptome analysis, we used a PAXgene™ tube and NuGEN Ovation™ globin reduction system. The combined use of these systems in microarray resulted in the identification of 78 unique genes differentially expressed in the blood of melanoma patients. Of these, 68 genes were further analyzed by quantitative reverse transcriptase PCR using blood samples from 45 newly diagnosed melanoma patients (stage I to IV) and 50 healthy control individuals. Thirty-nine genes were verified to be differentially expressed in blood samples from melanoma patients. A stepwise logit analysis selected eighteen 2-gene signatures that distinguish melanoma from healthy controls. Of these, a 2-gene signature consisting of PLEK2 and C1QB led to the best result that correctly classified 93.3% melanoma patients and 90% healthy controls. Both genes were upregulated in blood samples of melanoma patients from all stages. Further analysis using blood fractionation showed that CD45(-) and CD45(+) populations were responsible for the altered expression levels of PLEK2 and C1QB, respectively.The current study provides the first analysis of whole blood-based transcriptome biomarkers for malignant melanoma. The expression of PLEK2, the strongest gene to classify melanoma patients, in CD45(-) subsets illustrates the importance of analyzing whole blood cells for biomarker studies. The study suggests that transcriptome profiling of blood cells could be used for both early detection of melanoma and monitoring of patients for residual disease

    Identification of Tumor Suppressors and Oncogenes from Genomic and Epigenetic Features in Ovarian Cancer

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    The identification of genetic and epigenetic alterations from primary tumor cells has become a common method to identify genes critical to the development and progression of cancer. We seek to identify those genetic and epigenetic aberrations that have the most impact on gene function within the tumor. First, we perform a bioinformatic analysis of copy number variation (CNV) and DNA methylation covering the genetic landscape of ovarian cancer tumor cells. We separately examined CNV and DNA methylation for 42 primary serous ovarian cancer samples using MOMA-ROMA assays and 379 tumor samples analyzed by The Cancer Genome Atlas. We have identified 346 genes with significant deletions or amplifications among the tumor samples. Utilizing associated gene expression data we predict 156 genes with altered copy number and correlated changes in expression. Among these genes CCNE1, POP4, UQCRB, PHF20L1 and C19orf2 were identified within both data sets. We were specifically interested in copy number variation as our base genomic property in the prediction of tumor suppressors and oncogenes in the altered ovarian tumor. We therefore identify changes in DNA methylation and expression for all amplified and deleted genes. We statistically define tumor suppressor and oncogenic features for these modalities and perform a correlation analysis with expression. We predicted 611 potential oncogenes and tumor suppressors candidates by integrating these data types. Genes with a strong correlation for methylation dependent expression changes exhibited at varying copy number aberrations include CDCA8, ATAD2, CDKN2A, RAB25, AURKA, BOP1 and EIF2C3. We provide copy number variation and DNA methylation analysis for over 11,500 individual genes covering the genetic landscape of ovarian cancer tumors. We show the extent of genomic and epigenetic alterations for known tumor suppressors and oncogenes and also use these defined features to identify potential ovarian cancer gene candidates

    School Effects on the Wellbeing of Children and Adolescents

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    Well-being is a multidimensional construct, with psychological, physical and social components. As theoretical basis to help understand this concept and how it relates to school, we propose the Self-Determination Theory, which contends that self-determined motivation and personality integration, growth and well-being are dependent on a healthy balance of three innate psychological needs of autonomy, relatedness and competence. Thus, current indicators involve school effects on children’s well-being, in many diverse modalities which have been explored. Some are described in this chapter, mainly: the importance of peer relationships; the benefits of friendship; the effects of schools in conjunction with some forms of family influence; the school climate in terms of safety and physical ecology; the relevance of the teacher input; the school goal structure and the implementation of cooperative learning. All these parameters have an influence in promoting optimal functioning among children and increasing their well-being by meeting the above mentioned needs. The empirical support for the importance of schools indicates significant small effects, which often translate into important real-life effects as it is admitted at present. The conclusion is that schools do make a difference in children’s peer relationships and well-being
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