Is relatively young age within a school year a risk factor for mental health problems and poor school performance? A population-based cross-sectional study of adolescents in Oslo, Norway

BACKGROUND: Several studies have shown that children who are relatively young within a school year are at greater risk for poorer school performance compared with their older peers. One study also reported that relative age within a school year is an independent risk factor for emotional and behavioral problems. The objective of this study was to test the hypothesis that relatively younger adolescents in the multiethnic population of Oslo have poorer school performance and more mental health problems than their relatively older classmates within the same school year. METHODS: This population-based cross-sectional study included all 10(th)-grade pupils enrolled in 2000 and 2001 in the city of Oslo. The participation rate was 88%. Of the 6,752 pupils in the study sample, 25% had a non-Norwegian background. Mental health problems were quantified using the abbreviated versions of Symptom Check List-25 (SCL-10) and the Strength and Difficulties Questionnaire (SDQ). Information on school performances and mental health problems were self-reported. We controlled for confounding factors including parental educational level, social support, gender, and ethnicity. RESULTS: The youngest one-third of pupils had significantly lower average school grades than the middle one-third and oldest one-third of their classmates (p < 0.001). Of the mental health problems identified in the questionnaires, the groups differed only on peer problems; the youngest one-third reported significantly more problems than the middle and oldest groups (p < 0.05). Age within a school year and gender showed significant interactions with total SDQ score, SDQ peer problems score, SDQ pro social score, and SCL-10 score. After stratifying for gender, the peer problem scores differed significantly between age groups only among boys. The SCL-10 score was significant, but only in girls and in the opposite direction to that expected, with the oldest pupils having significantly higher scores than the other two groups (p < 0.05). CONCLUSION: In adolescents from a multicultural city in Norway, relative age within a school year significantly influenced academic performance. In contrast to data from Great Britain, relative age within a school year was not an important risk factor for mental health problems in adolescents in Oslo

Lattice Boltzmann simulations of soft matter systems

This article concerns numerical simulations of the dynamics of particles immersed in a continuum solvent. As prototypical systems, we consider colloidal dispersions of spherical particles and solutions of uncharged polymers. After a brief explanation of the concept of hydrodynamic interactions, we give a general overview over the various simulation methods that have been developed to cope with the resulting computational problems. We then focus on the approach we have developed, which couples a system of particles to a lattice Boltzmann model representing the solvent degrees of freedom. The standard D3Q19 lattice Boltzmann model is derived and explained in depth, followed by a detailed discussion of complementary methods for the coupling of solvent and solute. Colloidal dispersions are best described in terms of extended particles with appropriate boundary conditions at the surfaces, while particles with internal degrees of freedom are easier to simulate as an arrangement of mass points with frictional coupling to the solvent. In both cases, particular care has been taken to simulate thermal fluctuations in a consistent way. The usefulness of this methodology is illustrated by studies from our own research, where the dynamics of colloidal and polymeric systems has been investigated in both equilibrium and nonequilibrium situations.Comment: Review article, submitted to Advances in Polymer Science. 16 figures, 76 page

Illiteracy, low educational status, and cardiovascular mortality in India

Background: Influence of education, a marker of SES, on cardiovascular disease (CVD) mortality has not been evaluated in low-income countries. To determine influence of education on CVD mortality a cohort study was performed in India. Methods: 148,173 individuals aged ≥ 35 years were recruited in Mumbai during 1991-1997 and followed to ascertain vital status during 1997-2003. Subjects were divided according to educational status into one of the five groups: illiterate, primary school ( ≦ 5 years of formal education), middle school (6-8 years), secondary school (9-10 years) and college (&gt; 10 years). Multivariate analyses using Cox proportional hazard model was performed an

Three-dimensional mapping of mechanical activation patterns, contractile dyssynchrony and dyscoordination by two-dimensional strain echocardiography: Rationale and design of a novel software toolbox

<p>Abstract</p> <p>Background</p> <p>Dyssynchrony of myocardial deformation is usually described in terms of variability only (e.g. standard deviations SD's). A description in terms of the spatio-temporal distribution pattern (vector-analysis) of dyssynchrony or by indices estimating its impact by expressing dyscoordination of shortening in relation to the global ventricular shortening may be preferential. Strain echocardiography by speckle tracking is a new non-invasive, albeit 2-D imaging modality to study myocardial deformation.</p> <p>Methods</p> <p>A post-processing toolbox was designed to incorporate local, speckle tracking-derived deformation data into a 36 segment 3-D model of the left ventricle. Global left ventricular shortening, standard deviations and vectors of timing of shortening were calculated. The impact of dyssynchrony was estimated by comparing the end-systolic values with either early peak values only (early shortening reserve ESR) or with all peak values (virtual shortening reserve VSR), and by the internal strain fraction (ISF) expressing dyscoordination as the fraction of deformation lost internally due to simultaneous shortening and stretching. These dyssynchrony parameters were compared in 8 volunteers (NL), 8 patients with Wolff-Parkinson-White syndrome (WPW), and 7 patients before (LBBB) and after cardiac resynchronization therapy (CRT).</p> <p>Results</p> <p>Dyssynchrony indices merely based on variability failed to detect differences between WPW and NL and failed to demonstrate the effect of CRT. Only the 3-D vector of onset of shortening could distinguish WPW from NL, while at peak shortening and by VSR, ESR and ISF no differences were found. All tested dyssynchrony parameters yielded higher values in LBBB compared to both NL and WPW. CRT reduced the spatial divergence of shortening (both vector magnitude and direction), and improved global ventricular shortening along with reductions in ESR and dyscoordination of shortening expressed by ISF.</p> <p>Conclusion</p> <p>Incorporation of local 2-D echocardiographic deformation data into a 3-D model by dedicated software allows a comprehensive analysis of spatio-temporal distribution patterns of myocardial dyssynchrony, of the global left ventricular deformation and of newer indices that may better reflect myocardial dyscoordination and/or impaired ventricular contractile efficiency. The potential value of such an analysis is highlighted in two dyssynchronous pathologies that impose particular challenges to deformation imaging.</p

Defining the Functional Domain of Programmed Cell Death 10 through Its Interactions with Phosphatidylinositol-3,4,5-Trisphosphate

Cerebral cavernous malformations (CCM) are vascular abnormalities of the central nervous system predisposing blood vessels to leakage, leading to hemorrhagic stroke. Three genes, Krit1 (CCM1), OSM (CCM2), and PDCD10 (CCM3) are involved in CCM development. PDCD10 binds specifically to PtdIns(3,4,5)P3 and OSM. Using threading analysis and multi-template modeling, we constructed a three-dimensional model of PDCD10. PDCD10 appears to be a six-helical-bundle protein formed by two heptad-repeat-hairpin structures (α1–3 and α4–6) sharing the closest 3D homology with the bacterial phosphate transporter, PhoU. We identified a stretch of five lysines forming an amphipathic helix, a potential PtdIns(3,4,5)P3 binding site, in the α5 helix. We generated a recombinant wild-type (WT) and three PDCD10 mutants that have two (Δ2KA), three (Δ3KA), and five (Δ5KA) K to A mutations. Δ2KA and Δ3KA mutants hypothetically lack binding residues to PtdIns(3,4,5)P3 at the beginning and the end of predicted helix, while Δ5KA completely lacks all predicted binding residues. The WT, Δ2KA, and Δ3KA mutants maintain their binding to PtdIns(3,4,5)P3. Only the Δ5KA abolishes binding to PtdIns(3,4,5)P3. Both Δ5KA and WT show similar secondary and tertiary structures; however, Δ5KA does not bind to OSM. When WT and Δ5KA are co-expressed with membrane-bound constitutively-active PI3 kinase (p110-CAAX), the majority of the WT is co-localized with p110-CAAX at the plasma membrane where PtdIns(3,4,5)P3 is presumably abundant. In contrast, the Δ5KA remains in the cytoplasm and is not present in the plasma membrane. Combining computational modeling and biological data, we propose that the CCM protein complex functions in the PI3K signaling pathway through the interaction between PDCD10 and PtdIns(3,4,5)P3

Modeling mitochondrial dysfunctions in the brain: from mice to men

The biologist Lewis Thomas once wrote: “my mitochondria comprise a very large proportion of me. I cannot do the calculation, but I suppose there is almost as much of them in sheer dry bulk as there is the rest of me”. As humans, or indeed as any mammal, bird, or insect, we contain a specific molecular makeup that is driven by vast numbers of these miniscule powerhouses residing in most of our cells (mature red blood cells notwithstanding), quietly replicating, living independent lives and containing their own DNA. Everything we do, from running a marathon to breathing, is driven by these small batteries, and yet there is evidence that these molecular energy sources were originally bacteria, possibly parasitic, incorporated into our cells through symbiosis. Dysfunctions in these organelles can lead to debilitating, and sometimes fatal, diseases of almost all the bodies’ major organs. Mitochondrial dysfunction has been implicated in a wide variety of human disorders either as a primary cause or as a secondary consequence. To better understand the role of mitochondrial dysfunction in human disease, a multitude of pharmacologically induced and genetically manipulated animal models have been developed showing to a greater or lesser extent the clinical symptoms observed in patients with known and unknown causes of the disease. This review will focus on diseases of the brain and spinal cord in which mitochondrial dysfunction has been proven or is suspected and on animal models that are currently used to study the etiology, pathogenesis and treatment of these diseases

Identification of novel translational urinary biomarkers for acetaminophen-induced acute liver injury using proteomic profiling in mice

Contains fulltext : 108207.pdf (publisher's version ) (Open Access)Drug-induced liver injury (DILI) is the leading cause of acute liver failure. Currently, no adequate predictive biomarkers for DILI are available. This study describes a translational approach using proteomic profiling for the identification of urinary proteins related to acute liver injury induced by acetaminophen (APAP). Mice were given a single intraperitoneal dose of APAP (0-350 mg/kg bw) followed by 24 h urine collection. Doses of >/=275 mg/kg bw APAP resulted in hepatic centrilobular necrosis and significantly elevated plasma alanine aminotransferase (ALT) values (p<0.0001). Proteomic profiling resulted in the identification of 12 differentially excreted proteins in urine of mice with acute liver injury (p<0.001), including superoxide dismutase 1 (SOD1), carbonic anhydrase 3 (CA3) and calmodulin (CaM), as novel biomarkers for APAP-induced liver injury. Urinary levels of SOD1 and CA3 increased with rising plasma ALT levels, but urinary CaM was already present in mice treated with high dose of APAP without elevated plasma ALT levels. Importantly, we showed in human urine after APAP intoxication the presence of SOD1 and CA3, whereas both proteins were absent in control urine samples. Urinary concentrations of CaM were significantly increased and correlated well with plasma APAP concentrations (r = 0.97; p<0.0001) in human APAP intoxicants, who did not present with elevated plasma ALT levels. In conclusion, using this urinary proteomics approach we demonstrate CA3, SOD1 and, most importantly, CaM as potential human biomarkers for APAP-induced liver injury