Formulación de la estrategia de negocio para la microempresa ArteEnCasa aplicando la metodología EstraPyme

En el presente trabajo se realiza la formulación de la estrategia de negocio para la microempresa ArteEnCasa, a través de la aplicación del Modelo EstraPyme, diseñado por estudiantes de MBA de Eafit y avalado por la misma universidad para su aplicación en la formulación de estrategia de Pymes en Colombia. En el desarrollo de este trabajo se abordó el reto de la microempresa ArteEnCasa, respecto a cómo escalar el modelo de negocio para que sea autónomo y sostenible en el tiempo, para ello se realizaron un diagnóstico y un análisis a través de la recolección de datos y percepciones con el prestador del servicio, los clientes, usuarios y clientes futuros. Los resultados de este trabajo presentan la propuesta de valor y el modelo de negocio, tanto de los clientes actuales, como del segmento de clientes nuevos, en respuesta a la necesidad planteada.In this paper we formulate the business strategy for the microenterprise ArteEnCasa, through the application of the EstraPyme Model, designed by MBA students of Eafit and endorsed by the same university, for its application in the formulation of strategy of pymes in Colombia. In the development of this work, the challenge of the microenterprise ArteEnCasa was addressed, regarding how to scale the business model to be autonomous and sustainable over time, for which a diagnosis and analysis was made through data collection and perceptions with the service provider, customers, users and future customers. The results of this work present the value proposition and business model for both current customers and the new customer segment, in response to the need identified

Choroidal Vessel Wall: Hypercholesterolaemia-Induced Dysfunction and Potential Role of Statins

© 2012 Ramírez et al., licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Unidad Docente de Inmunología, Oftalmología y ORLFac. de Óptica y OptometríaTRUEMinisterio de Ciencia e Innovación de EspañaFundación Mutua MadrileñaUniversidad Complutense de Madridpu

Effects of Hypercholesterolaemia in the Retina

© 2012 Triviño et al., licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Unidad Docente de Inmunología, Oftalmología y ORLFac. de Óptica y OptometríaTRUEMinisterio de Ciencia e Innovación (MICINN)Fundación Mutua MadrileñaUniversidad Complutense de Madridpu

The Role of Autophagy in Eye Diseases

This research was funded by the Ophthalmological Network OFTARED (Enfermedades oculares: Prevención, detección precoz, tratamiento y rehabilitación de las patologías oculares) (RD16/0008/0005 and RD16/0008/0026) of the Institute of Health of Carlos III of the Spanish Ministry of Economy and by the European programme FEDER; and Network RETiBRAIN (La retina un modelo para investigar Neuroprotección en patologías del Sistema Nervioso Central) (RED2018-102499-T) of Spanish Ministry of Science and Innovation. And J.A.F.-A. is currently funded by a Predoctoral Fellowship (FPU17/01023) from the Spanish Ministry of Science, Innovation, and Universities; and I.L.-C. is currently funded by a Predoctoral Fellowship (CT42/18-CT43/18) from the Complutense University of Madrid.Autophagy is a catabolic process that ensures homeostasis in the cells of our organism. It plays a crucial role in protecting eye cells against oxidative damage and external stress factors. Ocular pathologies of high incidence, such as age-related macular degeneration, cataracts, glaucoma, and diabetic retinopathy are of multifactorial origin and are associated with genetic, environmental factors, age, and oxidative stress, among others; the latter factor is one of the most influential in ocular diseases, directly affecting the processes of autophagy activity. Alteration of the normal functioning of autophagy processes can interrupt organelle turnover, leading to the accumulation of cellular debris and causing physiological dysfunction of the eye. The aim of this study is to review research on the role of autophagy processes in the main ocular pathologies, which have a high incidence and result in high costs for the health system. Considering the role of autophagy processes in cell homeostasis and cell viability, the control and modulation of autophagy processes in ocular pathologies could constitute a new therapeutic approach.Depto. de Inmunología, Oftalmología y ORLFac. de MedicinaTRUEUnión EuropeaMinisterio de Ciencia e Innovación (España)Instituto de Salud Carlos IIIUniversidad Complutense de Madridpu

Retinal glial changes in Alzheimer's disease – A review

Alzheimer's disease (AD) is a neurodegenerative dementia characterized by the deposition of extracellular β-amyloid (Aβ) plaques and the presence of neurofibrillary tangles. Until now, the techniques used to analyze these deposits have been difficult to access, invasive, and expensive. This leads us to consider new access routes to the central nervous system (CNS), allowing us to diagnose the disease before the first symptoms appear. Recent studies have shown that microglial and macroglial cell activation could play a role in the development of this disease. Glial cells in the CNS can respond to various damages, such as neurodegenerative pathologies, with morphological and functional changes. These changes are a common feature in neurodegenerative diseases, including AD. The retina is considered an extension of the CNS and has a population of glial cells similar to that of the CNS. When glial cells are activated, various molecules are released and changes in glial cell expression occur, which can be indicators of neuronal damage. The objective of this review is to compile the most relevant findings in the last 10 years relating to alterations in the eye in AD, and the role that glial cells play in the degenerative process in the retina in the context of neurodegeneration

Macular Thickness Decrease in Asymptomatic Subjects at High Genetic Risk of Developing Alzheimer’s Disease: An OCT Study

In this case control study, we examined the retinal thickness of the different layers in the macular region and peripapillary retinal nerve fiber layer (RNFL) with optical coherence tomography (OCT) in healthy cognitive subjects (from 51 to 74 years old) at high genetic risk for developing Alzheimer’s disease (AD). Thirty-five subjects with a family history of Alzheimer disease (AD) (FH+) and ApoE ɛ4 carriers and 29 age-matched control subjects without a family history of AD (FH−) and ApoE ɛ4 non-carriers were included. Compared to FH− ApoE ɛ4 non-carriers, in FH+ ApoE ɛ4 carriers, there were statistically significant decreases (p < 0.05) in (i) the foveal area of mRNFL; (ii) the inferior and nasal sectors in the outer and inner macular ring in the inner plexiform layer (IPL); (iii) the foveal area and the inferior sector in the outer macular ring in the inner nuclear layer (INL); and (iv) the inferior sector of the outer macular ring in the outer plexiform layer (OPL). However, no statistically significant differences were found in the peripapillary thickness of RNFL between both study groups. In subjects with cognitive health and high genetic risk for the development of AD, initial changes appeared in the macular area. OCT could be a promising, cost-effective and non-invasive test useful in early AD, before the onset of clinical symptoms

Microglial Activation in the Retina of a Triple-Transgenic Alzheimer’s Disease Mouse Model (3xTg-AD)

Alzheimer’s disease (AD) is the most common type of dementia in the world. The main biomarkers associated with AD are protein amyloid-β (Aβ) plaques and protein tau neurofibrillary tangles, which are responsible for brain neuroinflammation mediated by microglial cells. Increasing evidence has shown that the retina can also be affected in AD, presenting some molecular and cellular changes in the brain, such as microglia activation. However, there are only a few studies assessing such changes in the retinal microglia in animal models of AD. These studies use retinal sections, which have some limitations. In this study, we performed, for the first time in a triple-transgenic AD mouse model (3xTg-AD), a quantitative morphometric analysis of microglia activation (using the anti-Iba-1 antibody) in retinal whole-mounts, allowing visualization of the entire microglial cell, as well as its localization along the extension of the retina in different layers. Compared to age-matched animals, the retina of 3xTg-AD mice presents a higher number of microglial cells and a thicker microglial cell body area. Moreover, the microglia migrate, reorient, and retract their processes, changing their localization from a parallel to a perpendicular position relative to the retinal surface. These findings demonstrate clear microglia remodeling in the retina of 3xTg-AD mice