Análisis teórico-práctico de los requisitos y presupuestos de la Ley 100 de 1993 y Ley 797 de 2003

Artículo de investigaciónEste trabajo hace un análisis detallado del Sistema Pensional Colombiano, partiendo de la multiplicidad de regímenes de transición que se han presentado derivadas de las reformas a través del tiempo y la problemática que ello a generado, para luego detallar los requisitos necesarios para obtener las diferentes modalidades de pensión, tanto en el Régimen de Ahorro Individual con Solidaridad RAIS, como en el Régimen de Prima Media con Prestación Definida RPM. Finalmente, contiene un breve análisis del Acto Legislativo 01 de 2005.48 p.INTRODUCCIÓN 1. PLANTEAMIENTO DEL PROBLEMA 2. OBJETO DE LA INVESTIGACION 3. REGIMEN DE TRANSICION 4. LEY 100 DE 1993 5. LEY 797 DE 2003 6. ACTO LEGISLATIVO 01 DE 2005 CONCLUSIONESPregradoAbogad

Trim28 regulates histone modifications of E-cadherin and N-cadherin promoters.

<p><i>A</i>, ChIP assays were conducted in control and Trim28 knockdown A549 cells. Quantitative PCR was performed to examine the occupancy of IgG, acetylated histone 3 K9, dimethylated histone 3 K9, and trimethylated histone 3 K9 on E-cadherin and N-cadherin promoters. B, ChIP assays were conducted in control and Trim28 stably expressed A549 cells. Quantitative PCR was performed to examine the occupancy of IgG, acetylated histone 3 K9, dimethylated histone 3 K9, and trimethylated histone 3 K9 on E-cadherin and N-cadherin promoters.</p

Hypothetical model to explain the role of Trim28 in the stages of lung adenocarcinoma.

<p>This model explains this work and our previous work demonstrating a tumor suppressor role for Trim28 <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0101040#pone.0101040-Chen1" target="_blank">[9]</a>.</p

Trim28 expression is induced by TGF-β.

<p><i>A</i> and <i>B</i>, A549 and H358 stably expressing non-silencing shRNA and Trim28 shRNA were treated with TGF-β (2 ng/ml) for 3 to 10 days. Whole cell lysates and RNA extracts were subjected to western blotting using the indicated antibodies (A) and real-time PCR (B). <i>Asterisks</i> represent significant <i>p</i> values, *: <i>p</i><0.05.</p

Trim28 knockdown attenuates cell migration.

<p><i>A</i>, control and Trim28 knockdown H358 cells were subjected to wound-healing assay. Cells were photographed right after scratch, and 24 hrs and 48 hrs after scratch. <i>B</i>, control and Trim28 knockdown A549 cells were subjected to wound healing assay in the absence or presence of serum. Cells were photographed right after scratch and 24 hrs later. <i>C</i>, control and Trim28 knockdown cells were plated in triplicate on the top wells of Matrigel-coated or non-coated chambers. After 18 hours, cells that had invaded through the Matrigel layer were fixed and stained. The percentage of invasive cells is shown in the bar graph. <i>Asterisks</i> represent significant <i>p</i> values, *: <i>p</i><0.05. <i>D</i>, control and Trim28 knockdown A549 cells were cultured in a three-dimensional model and treated with TGF-β (5 ng/ml) for 72 hrs. RNA was extracted from the cells and subjected to real-time PCR. The expression of target genes was determined.</p

Trim28 is required for TGF-β-induced EMT.

<p><i>A</i>, control and Trim28 knockdown cells were treated with TGF-β or left untreated. Cells were photographed at 40× magnification. <i>B</i>, RNA was extracted from control and Trim28 knockdown A549 cells treated with TGF-β as above or left untreated. Real-time PCR was performed and the expression of target genes was determined. <i>C</i>, control and Trim28 knockdown A549 and H358 cells were treated with TGF-β (2 ng/ml) until morphology changes were observed or left untreated. Whole cell lysates were subjected to western blotting using antibodies as indicated.</p

Induction of apoptosis after treatment with TGFβ-1 and dasatinib.

<p>(A) A549 cells were treated with 100 nM of dasatinib, 1000 nM of AZD0530, or erlotinib with or without 5 ng/mL TGFβ-1 for 48 hours. (B) A549 cells were pre-treated with 10 µg/mL cycloheximide (CHX) for 1 hour, followed by TGFβ-1 plus or minus dasatinib. After incubation, cells were harvested, lysed, and PARP cleavage detected by Western Blot analysis. (C) A549 cells were seeded in 96-well plates at 5×10³ per well. <i>C</i>ells were treated, and Cell Player 96-Well Kinetic Caspase 3/7 Reagent was added simultaneously. Treatments were done in triplicate. Values are shown as the average number of caspase 3/7 positive cells from 3 independent experiments.</p

Combination TGFβ-1 and dasatinib treatment effect on phosphorylation of canonical and non-canonical TGFβ pathway intermediaries.

<p>A549 NSCLC cells were treated with DMSO, 5 ng/mL TGFβ-1, 100 nM dasatinib, or a combination of 5 ng/mL TGFβ-1 and 100 nM dasatinib for different amounts of time (1 hour for detection of pSmad2 and pSmad3, and 48 hours for detection of pSrc). After incubation, whole cell lysates were collected and subjected to Western blotting with the indicated antibodies.</p

Inhibition of cell growth of A549 cells treated with TGFβ-1 and dasatinib.

<p>(A) A549 cells were treated with DMSO, different concentrations of TGFβ-1 (0–10 ng/mL; white bars), different concentrations of dasatinib (0–400 nM; black bars), or a combination of TGFβ-1 and dasatinib (dashed bars) for 48 hours. Treatment of cells with both agents resulted in increase inhibition (**), as compared to when cells were treated with either agent alone (*). (B) A549 cells were treated with DMSO, 5 ng/mL TGFβ-1, 100 nM dasatinib, or a combination of 5 ng/mL TGFβ-1 and 100 nM dasatinib for 48 hours. After 48 hours, propidium iodide stained cells were analyzed to determine cell cycle distribution and analyzed as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0114131#s2" target="_blank">Materials and Methods</a>.</p

3D Docked Pose and Interactions of dasatinib and bosutinib with TβR-I 3D rendering of the binding pose of (A) dasatinib and (B) bosutinib docked into TβR-1.

<p>Protein is represented by purple carbon cartoon representation with residues surrounding a ligand are in line representation. Bosutinib is colored with magenta carbons and dasatinib with green carbons. Hydrogen bonds represented by dashed yellow lines with distances (gray) and interacting residue (black) labeled. A π-π stacking interaction between the phenyl of TYR-219 and the pyrimidine of dasatinib is circled in red.</p