Factores que inciden en la práctica de actividad física de la población en situación de discapacidad

El presente documento es el resumen de la propuesta técnica del proyecto de investigación denominado Determinantes de la práctica de actividad física en personas con discapacidad, sus familias, cuidadoras y cuidadores en Bogotá, fruto de la apuesta académica desarrollada por un equipo de investigadoras de los grupos de investigación en Actividad Física y Desarrollo Humano, y en Rehabilitación e Integración Social de la Persona con Discapacidad, de la Facultad de Rehabilitación y Desarrollo Humano, de la Universidad del Rosario. El proyecto de investigación obtuvo la financiación del Fondo de Investigaciones de la Universidad del Rosario (FIUR), para ser desarrollado durante el período de julio de 2008 a junio de 2009

The role of cardiac troponin T quantity and function in cardiac development and dilated cardiomyopathy

Background: Hypertrophic (HCM) and dilated (DCM) cardiomyopathies results from sarcomeric protein mutations, including cardiac troponin T (cTnT, TNNT2). We determined whether TNNT2 mutations cause cardiomyopathies by altering cTnT function or quantity; whether the severity of DCM is related to the ratio of mutant to wildtype cTnT; whether Ca2+ desensitization occurs in DCM; and whether absence of cTnT impairs early embryonic cardiogenesis. Methods and Findings: We ablated Tnnt2 to produce heterozygous Tnnt2+/ mice, and crossbreeding produced homozygous null Tnnt2-/-embryos. We also generated transgenic mice overexpressing wildtype (TGWT) or DCM mutant (TGK210Δ) Tnnt2. Crossbreeding produced mice lacking one allele of Tnnt2, but carrying wildtype (Tnnt2+/-/TGWT) or mutant (Tnnt2+/-/TGK210Δ) transgenes. Tnnt2+/-mice relative to wildtype had significantly reduced transcript (0.82 ± 0.06 [SD] vs. 1.00 ± 0.12 arbitrary units; p = 0.025), but not protein (1.01 ± 0.20 vs. 1.00 ± 0.13 arbitrary units; p = 0.44). Tnnt2+/-mice had normal hearts (histology, mass, left ventricular end diastolic diameter [LVEDD], fractional shortening [FS]). Moreover, whereas Tnnt2+/-/ TGK210Δ mice had severe DCM, TGK210Δ mice had only mild DCM (FS 18 ± 4 vs. 29 ± 7%; p < 0.01). The difference in severity of DCM may be attributable to a greater ratio of mutant to wildtype Tnnt2 transcript in Tnnt2+/-/TGK210Δ relative to TGK210Δ mice (2.42±0.08, p = 0.03). Tnnt2+/-/TGK210Δ muscle showed Ca2+ desensitization (pCa50 = 5.34 ± 0.08 vs. 5.58 ± 0.03 at sarcomere length 1.9 μm. p<0.01), but no difference in maximum force generation. Day 9.5 Tnnt2-/-embryos had normally looped hearts, but thin ventricular walls, large pericardial effusions, noncontractile hearts, and severely disorganized sarcomeres. Conclusions: Absence of one Tnnt2 allele leads to a mild deficit in transcript but not protein, leading to a normal cardiac phenotype. DCM results from abnormal function of a mutant protein, which is associated with myocyte Ca2+ desensitization. The severity of DCM depends on the ratio of mutant to wildtype Tnnt2 transcript. cTnT is essential for sarcomere formation, but normal embryonic heart looping occurs without contractile activity. © 2008 Ahmad et al

Transkingdom Networks: A Systems Biology Approach to Identify Causal Members of Host-Microbiota Interactions

Improvements in sequencing technologies and reduced experimental costs have resulted in a vast number of studies generating high-throughput data. Although the number of methods to analyze these "omics" data has also increased, computational complexity and lack of documentation hinder researchers from analyzing their high-throughput data to its true potential. In this chapter we detail our data-driven, transkingdom network (TransNet) analysis protocol to integrate and interrogate multi-omics data. This systems biology approach has allowed us to successfully identify important causal relationships between different taxonomic kingdoms (e.g. mammals and microbes) using diverse types of data

The Mitochondrial Ca(2+) Uniporter: Structure, Function, and Pharmacology.

Mitochondrial Ca(2+) uptake is crucial for an array of cellular functions while an imbalance can elicit cell death. In this chapter, we briefly reviewed the various modes of mitochondrial Ca(2+) uptake and our current understanding of mitochondrial Ca(2+) homeostasis in regards to cell physiology and pathophysiology. Further, this chapter focuses on the molecular identities, intracellular regulators as well as the pharmacology of mitochondrial Ca(2+) uniporter complex

Star Formation Rate Indicators in Wide-Field Infrared Survey Preliminary Release

With the goal of investigating the degree to which theMIR luminosity in theWidefield Infrared Survey Explorer (WISE) traces the SFR, we analyze 3.4, 4.6, 12 and 22 {\mu}m data in a sample of {\guillemotright} 140,000 star-forming galaxies or star-forming regions covering a wide range in metallicity 7.66 < 12 + log(O/H) < 9.46, with redshift z < 0.4. These star-forming galaxies or star-forming regions are selected by matching the WISE Preliminary Release Catalog with the star-forming galaxy Catalog in SDSS DR8 provided by JHU/MPA 1.We study the relationship between the luminosity at 3.4, 4.6, 12 and 22 {\mu}m from WISE and H\alpha luminosity in SDSS DR8. From these comparisons, we derive reference SFR indicators for use in our analysis. Linear correlations between SFR and the 3.4, 4.6, 12 and 22 {\mu}m luminosity are found, and calibrations of SFRs based on L(3.4), L(4.6), L(12) and L(22) are proposed. The calibrations hold for galaxies with verified spectral observations. The dispersion in the relation between 3.4, 4.6, 12 and 22 {\mu}m luminosity and SFR relates to the galaxy's properties, such as 4000 {\deg}A break and galaxy color.Comment: 10 pages, 3 figure

Secondary Traumatic Stress:Prevalence and Symptomology Amongst Detective Officers Investigating Child Protection Cases

It has been increasingly recognised that individuals exposed to the trauma of others within their professional roles can be affected by secondary traumatic stress (STS). Despite this recognition, there is a dearth of literature examining the prevalence of secondary traumatic stress amongst police officers in the UK. This study aims to meet this gap. Sixty-three Detective Officers from Family Protection Units (FPU(s)), primarily engaged in child protection/abuse investigations, self-reported their experiences and symptoms associated with STS through a questionnaire. Findings indicate that over half of the respondents experienced STS symptoms with 11% reporting levels of symptoms that were in the high or severe range. This study is significant in that it provides empirical evidence of issues that have so far been little documented in the UK and considers the implications for policing policy and practice in terms of the health and well-being of serving police officers

Neutrino Mass and μ→e+γ\mu \rightarrow e + \gamma from a Mini-Seesaw

The recently proposed "mini-seesaw mechanism" combines naturally suppressed Dirac and Majorana masses to achieve light Standard Model neutrinos via a low-scale seesaw. A key feature of this approach is the presence of multiple light (order GeV) sterile-neutrinos that mix with the Standard Model. In this work we study the bounds on these light sterile-neutrinos from processes like \mu ---> e + \gamma, invisible Z-decays, and neutrinoless double beta-decay. We show that viable parameter space exists and that, interestingly, key observables can lie just below current experimental sensitivities. In particular, a motivated region of parameter space predicts a value of BR(\mu ---> e + \gamma) within the range to be probed by MEG.Comment: 1+26 pages, 7 figures. v2 JHEP version (typo's fixed, minor change to presentation, results unchanged

Beyond the standard seesaw: neutrino masses from Kahler operators and broken supersymmetry

We investigate supersymmetric scenarios in which neutrino masses are generated by effective d=6 operators in the Kahler potential, rather than by the standard d=5 superpotential operator. First, we discuss some general features of such effective operators, also including SUSY-breaking insertions, and compute the relevant renormalization group equations. Contributions to neutrino masses arise at low energy both at the tree level and through finite threshold corrections. In the second part we present simple explicit realizations in which those Kahler operators arise by integrating out heavy SU(2)_W triplets, as in the type II seesaw. Distinct scenarios emerge, depending on the mechanism and the scale of SUSY-breaking mediation. In particular, we propose an appealing and economical picture in which the heavy seesaw mediators are also messengers of SUSY breaking. In this case, strong correlations exist among neutrino parameters, sparticle and Higgs masses, as well as lepton flavour violating processes. Hence, this scenario can be tested at high-energy colliders, such as the LHC, and at lower energy experiments that measure neutrino parameters or search for rare lepton decays.Comment: LaTeX, 34 pages; some corrections in Section

Non-homologous end-joining pathway associated with occurrence of myocardial infarction: gene set analysis of genome-wide association study data

&lt;p&gt;Purpose: DNA repair deficiencies have been postulated to play a role in the development and progression of cardiovascular disease (CVD). The hypothesis is that DNA damage accumulating with age may induce cell death, which promotes formation of unstable plaques. Defects in DNA repair mechanisms may therefore increase the risk of CVD events. We examined whether the joints effect of common genetic variants in 5 DNA repair pathways may influence the risk of CVD events.&lt;/p&gt; &lt;p&gt;Methods: The PLINK set-based test was used to examine the association to myocardial infarction (MI) of the DNA repair pathway in GWAS data of 866 subjects of the GENetic DEterminants of Restenosis (GENDER) study and 5,244 subjects of the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER) study. We included the main DNA repair pathways (base excision repair, nucleotide excision repair, mismatch repair, homologous recombination and non-homologous end-joining (NHEJ)) in the analysis.&lt;/p&gt; &lt;p&gt;Results: The NHEJ pathway was associated with the occurrence of MI in both GENDER (P = 0.0083) and PROSPER (P = 0.014). This association was mainly driven by genetic variation in the MRE11A gene (PGENDER = 0.0001 and PPROSPER = 0.002). The homologous recombination pathway was associated with MI in GENDER only (P = 0.011), for the other pathways no associations were observed.&lt;/p&gt; &lt;p&gt;Conclusion: This is the first study analyzing the joint effect of common genetic variation in DNA repair pathways and the risk of CVD events, demonstrating an association between the NHEJ pathway and MI in 2 different cohorts.&lt;/p&gt