Sistema de Acreditación Universitaria en Chile: ¿Cuánto hemos avanzado?

Hasta mediados de los 80, el sistema universitario chileno puede ser considerado relativamente estático y pequeño, sin embargo, a partir de la reforma de 1981, empieza a transformarse en uno de gran dinamismo y alto crecimiento. Producto de esta expansión, en 1999 se sientan las bases del sistema de acreditación de educación superior en Chile, a partir de la creación de la Comisión Nacional de Acreditación de Pregrado (CNAP) y la Comisión Nacional de Acreditación de Postgrado (CONAP), instituciones que posteriormente se fusionan conformando la Comisión Nacional de Acreditación (CNA). Este trabajo analiza el estado actual de los procesos de acreditación universitaria en Chile -en el ámbito institucional, de programas de pregrado y postgrado- comparando un conjunto de indicadores según tipologías convencionales del sistema universitario nacional. El estudio es de tipo descriptivo sustentado en información de bases de datos oficiales de la CNA y el Consejo Nacional de Educación, sobre los resultados de los procesos de acreditación universitaria e indicadores institucionales. Los hallazgos dan cuenta de la diversidad institucional imperante y, especialmente, de la diversidad cualitativa en la oferta educacional universitaria chilena, tanto de pregrado como de posgrado

Los sistemas de informacion en la Municipalidad de Talca : diagnostico y propuesta

145 p.La presente investigación tiene como objetivo analizar los Sistemas de Información computacionales de la Ilustre Municipalidad de Talca, detectar posibles problemas en estos y darles una solución que permita la aplicación de Tecnologías de Información que se encuentren presentes en el mercado. En Ios casos que no sea posible aplicar dichas Tecnologías de Información se propondrán soluciones alternativas de carácter administrativo. Este trabajo intenta visualizar al funcionamiento municipal y a su grado de actualización y adaptación a Ios cambios que se producen en el medio ambiente y que afectan el servicio que esta organización le brinda a la ciudadanía. La gran cantidad de cambios que se producen en el ámbito informático y que se expresan a través de nuevas Tecnologías de Información hace necesario preguntarse como están absorbiendo estos cambios los Sistemas de Información que posee la Ilustre Municipalidad. Si existe un manejo eficiente de la información dentro de la Ilustre Municipalidad, el servicio que esta entrega será también mas eficiente y será percibido como de mayor calidad por parte de la ciudadanía. Con respecto a las soluciones que se plantean al final de esta investigación se hace necesario señalar que si son implementadas debe ser considerando que Ios cambios generalmente son resistidos por quienes se ven afectados y no hay por que pensar que esta será la excepción, por lo que es imprescindible preparar a los funcionarios para la introducción de nuevas tecnologías

Characterization of rat lung ICAM-1

Objective and Design: We expressed soluble rat ICAM-1, generated a polyclonal anti-ICAM-1 antibody, and studied ICAM-1 upregulation in lung inflammatory conditions. Bacterial and baculovirus expression systems were employed.¶ Material: 250 g adult, male Long Evans rats were used. For in vitro studies, rat pulmonary artery endothelial cells (RPAEC), rat alveolar macrophages and aortic rings were stimulated (as described below) and evaluated for ICAM-1 expression.¶ Treatment: RPAEC and macrophages were stimulated with lipopolysaccharide (LPS) and recombinant murine tumour necrosis factor α (TNFα). In vivo immunoglobulin G (IgG) immune complex-induced lung injury was employed.¶ Methods: Enzyme-linked immunoassay (ELISA) Western and Northern blot analyses and immunohistochemical evaluations were performed. All experiments were done at least in duplicate. Data were analyzed by two-tailed Student’s t-test.¶ Results: ICAM-1 expression of RPAEC was time- and dose-dependent, peaking at 6 h after LPS-stimulation. LPS and TNFα each enhanced ICAM-1 expression on alveolar macrophages (reaching a maximum at 2 h). In IgG immune complex-induced lung injury, ICAM-1 mRNA isolated from whole lung peaked at 4 h, while lung ICAM-1 protein peaked at 6 h.¶ Conclusions: Quantitation of ICAM-1 expression in vitro and in vivo suggests that ICAM-1 plays a central role in two lung inflammatory models. Furthermore, lung ICAM-1 upregulation involves at least two cell types: vascular endothelial cells and alveolar macrophages.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/41820/1/11-47-7-308_80470308.pd

Association between expression of the Bone morphogenetic proteins 2 and 7 in the repair of circumscribed cartilage lesions with clinical outcome

<p>Abstract</p> <p>Background</p> <p>Although there is much known about the role of BMPs in cartilage metabolism reliable data about the <it>in vivo </it>regulation in natural and surgically induced cartilage repair are still missing.</p> <p>Methods</p> <p>Lavage fluids of knee joints of 47 patients were collected during surgical therapy. 5 patients had no cartilage lesion and served as a control group, the other 42 patients with circumscribed cartilage defects were treated by microfracturing (19) or by an Autologous Chondrocyte Implantation (23). The concentrations of BMP-2 and BMP-7 were determined by ELISA. The clinical status was evaluated using the IKDC Score prior to and 1 year following the operation.</p> <p>Results</p> <p>High level expression in the control group was found for BMP-2, concentrations of BMP-7 remained below detection levels. No statistical differences could be detected in concentrations of BMP-2 or BMP-7 in the lavage fluids of knees with cartilage lesions compared to the control group. Levels of BMP-7 did not change after surgical cartilage repair, whereas concentrations of BMP-2 statistically significant increased after the intervention (p < 0.001). The clinical outcome following cartilage regenerating surgery increased after 1 year by 29% (p < 0.001). The difference of the IKDC score after 1 year and prior to the operation was used to quantify the degree of improvement following surgery. This difference statistically significant correlated with initial BMP-2 (R = 0.554, p < 0.001) but not BMP-7 (R = 0.031, n.s.) levels in the knee joints.</p> <p>Conclusions</p> <p>BMP-2 seems to play an important role in surgically induced cartilage repair; synovial expression correlates with the clinical outcome.</p

Inter- and intraobserver reliability of the MTM-classification for proximal humeral fractures: A prospective study

<p>Abstract</p> <p>Background</p> <p>A precise modular topographic-morphological (MTM) classification for proximal humeral fractures may address current classification problems. The classification was developed to evaluate whether a very detailed classification exceeding the analysis of fractured parts may be a valuable tool.</p> <p>Methods</p> <p>Three observers classified plain radiographs of 22 fractures using both a simple version (fracture displacement, number of parts) and an extensive version (individual topographic fracture type and morphology) of the MTM classification. Kappa-statistics were used to determine reliability.</p> <p>Results</p> <p>An acceptable reliability was found for the simple version classifying fracture displacement and fractured main parts. Fair interobserver agreement was found for the extensive version with individual topographic fracture type and morphology.</p> <p>Conclusion</p> <p>Although the MTM-classification covers a wide spectrum of fracture types, our results indicate that the precise topographic and morphological description is not delivering reproducible results. Therefore, simplicity in fracture classification may be more useful than extensive approaches, which are not adequately reliable to address current classification problems.</p

PPARα downregulates airway inflammation induced by lipopolysaccharide in the mouse

BACKGROUND: Inflammation is a hallmark of acute lung injury and chronic airway diseases. In chronic airway diseases, it is associated with profound tissue remodeling. Peroxisome proliferator-activated receptor-α (PPARα) is a ligand-activated transcription factor, that belongs to the nuclear receptor family. Agonists for PPARα have been recently shown to reduce lipopolysaccharide (LPS)- and cytokine-induced secretion of matrix metalloproteinase-9 (MMP-9) in human monocytes and rat mesangial cells, suggesting that PPARα may play a beneficial role in inflammation and tissue remodeling. METHODS: We have investigated the role of PPARα in a mouse model of LPS-induced airway inflammation characterized by neutrophil and macrophage infiltration, by production of the chemoattractants, tumor necrosis factor-α (TNF-α), keratinocyte derived-chemokine (KC), macrophage inflammatory protein-2 (MIP-2) and monocyte chemoattractant protein-1 (MCP-1), and by increased MMP-2 and MMP-9 activity in bronchoalveolar lavage fluid (BALF). The role of PPARα in this model was studied using both PPARα-deficient mice and mice treated with the PPARα activator, fenofibrate. RESULTS: Upon intranasal exposure to LPS, PPARα(-/- )mice exhibited greater neutrophil and macrophage number in BALF, as well as increased levels of TNF-α, KC, MIP-2 and MCP-1, when compared to PPARα(+/+ )mice. PPARα(-/- )mice also displayed enhanced MMP-9 activity. Conversely, fenofibrate (0.15 to 15 mg/day) dose-dependently reduced the increase in neutrophil and macrophage number induced by LPS in wild-type mice. In animals treated with 15 mg/day fenofibrate, this effect was associated with a reduction in TNF-α, KC, MIP-2 and MCP-1 levels, as well as in MMP-2 and MMP-9 activity. PPARα(-/- )mice treated with 15 mg/day fenofibrate failed to exhibit decreased airway inflammatory cell infiltrate, demonstrating that PPARα mediates the anti-inflammatory effect of fenofibrate. CONCLUSION: Using both genetic and pharmacological approaches, our data clearly show that PPARα downregulates cell infiltration, chemoattractant production and enhanced MMP activity triggered by LPS in mouse lung. This suggests that PPARα activation may have a beneficial effect in acute or chronic inflammatory airway disorders involving neutrophils and macrophages

Mesenchymal Stem Cells Secrete Multiple Cytokines That Promote Angiogenesis and Have Contrasting Effects on Chemotaxis and Apoptosis

We have previously shown that mesenchymal stem cells (MSC) improve function upon integration in ischemic myocardium. We examined whether specific cytokines and growth factors produced by MSCs are able to affect angiogenesis, cellular migration and apoptosis. Conditioned media (CM) was prepared by culturing MSC for 48 hours. CM displayed significantly elevated levels of VEGF, Monocyte Chemoattractant Protein-1 (MCP-1), macrophage inflammatory protein-1α (MIP-1α), MIP-1β and monokine induced by IFN-γ (MIG) compared to control media. MSC contained RNA for these factors as detected by RT-PCR. CM was able to induce angiogenesis in canine vascular endothelial cells. MCP-1 and MIP-1α increased cell migration of MSC while VEGF reduced it. H9c2 cells treated with CM under hypoxic conditions for 24 hours displayed a 16% reduction in caspase-3 activity compared to controls. PI 3-kinase γ inhibitor had no effect on controls but reversed the effect of CM on caspase-3 activity. MCP-1 alone mimicked the protective effect of CM while the PI 3-Kγ inhibitor did not reverse the effect of MCP-1. CM reduced phospho-BAD (Ser112) and phospho-Akt (Ser473) while increasing phospho-Akt (Thr308). MCP-1 reduced the level of phospho-Akt (Ser473) while having no effect on the other two; the PI 3-Kγ inhibitor did not alter the MCP-1 effect. ERK 1/2 phosphorylation was reduced in CM treated H9c2 cells, and inhibition of ERK 1/2 reduced the phosphorylation of Akt (Ser473), Akt (Thr308) and Bad (Ser112). In conclusion, MSC synthesize and secrete multiple paracrine factors that are able to affect MSC migration, promote angiogenesis and reduce apoptosis. While both MCP-1 and PI3-kinase are involved in the protective effect, they are independent of each other. It is likely that multiple pro-survival factors in addition to MCP-1 are secreted by MSC which act on divergent intracellular signaling pathways