ABSTRACT
El retículo endoplásmico es un organelo abundante, dinámico y sensor de energía. Sus abundantes membranas, rugosa y lisa, se encuentran distribuidas en diferentes proporciones dependiendo del linaje y requerimiento celular. Su función es llevar a cabo la síntesis de proteínas y lípidos, y es el almacén principal de Ca2+ intracelular. La sobrecarga calórica y la glucolipotoxicidad generada por dietas hipercalóricas provoca la alteración del retículo endoplásmico, activando la respuesta a proteínas mal plegadas (UPR, Unfolded Protein Response, por sus siglas en inglés) como reacción al estrés celular relacionado con el retículo endoplásmico y cuyo objetivo es restablecer la homeostasis del organelo al disminuir el estrés oxidante, la síntesis de proteínas y la fuga de Ca2+. Sin embargo, durante un estrés crónico, la UPR induce formación de especies reactivas de oxígeno, inflamación y apoptosis, exacerbando el estado del retículo endoplásmico y propagando un efecto nocivo para los demás organelos. Es por ello que el estrés del retículo endoplásmico se ha considerado un inductor del inicio y desarrollo de enfermedades metabólicas, incluido el agravamiento de COVID-19. Hasta el momento, existen pocas estrategias para reestablecer la homeostasis del retículo endoplásmico, las cuales son dirigidas a los sensores que desencadenan la UPR. Por tanto, se justifica con urgencia la identificación de nuevos mecanismos y terapias novedosas relacionadas con mitigar el impacto del estrés del retículo endoplásmico y las complicaciones asociadas.
The endoplasmic reticulum is an abundant, dynamic and energy-sensing organelle. Its abundant membranes, rough and smooth, are distributed in different proportions depending on the cell lineage and requirement. Its function is to carry out protein and lipid synthesis, and it is the main intracellular Ca2+ store. Caloric overload and glycolipotoxicity generated by hypercaloric diets cause alteration of the endoplasmic reticulum, activating the Unfolded Protein Response (UPR) as a reaction to cellular stress related to the endoplasmic reticulum and whose objective is to restore the homeostasis of the organelle by decreasing oxidative stress, protein synthesis and Ca2+ leakage. However, during chronic stress, the UPR induces reactive oxygen species formation, inflammation and apoptosis, exacerbating the state of the endoplasmic reticulum and propagating a deleterious effect on the other organelles. This is why endoplasmic reticulum stress has been considered an inducer of the onset and development of metabolic diseases, including the aggravation of COVID-19. So far, few strategies exist to reestablish endoplasmic reticulum homeostasis, which are targeted to sensors that trigger UPR. Therefore, the identif ication of new mechanisms and novel therapies related to mitigating the impact of endoplasmic reticulum stress and associated complications is urgently warranted.
Subject(s)
Humans , Dietary Carbohydrates/adverse effects , Dietary Fats/adverse effects , Endoplasmic Reticulum/metabolism , Endoplasmic Reticulum Stress/physiology , COVID-19/complications , Metabolic Diseases/etiology , COVID-19/therapy , HomeostasisABSTRACT
Abstract Purpose: To assess long, intermediate and near uncorrected visual acuity after a tetrafocal diffractive intraocular lens implantation, presence of dystopic phenomenon and patient satisfaction after surgery. Methods: Retrospective, observational study performed in Puerta de Hierro Specialties Hospital, in Jalisco, México. That included 100 eyes after phacoemulsification surgery by femtosecond assistance, followed by tetrafocal diffractive intraocular lens implantation due to cataract. Long, intermediate and near visual acuity without correction was measured, and presence or absence of dystopic phenomenon, plus patient satisfaction after surgery. Results: A total of 100 eyes in 50 patients who underwent cataract surgery with phacoemulsification by femtosecond assistance were evaluated. 100% underwent bilateral phacoemulsification. Long, intermediate, and near visual acuity after three months was in the most patients 20/20 (46%), 20/15 (44%) and Jaeger 1 (48%) respectively. The percentage or patients who refers halos was 7%; and other associated symptoms in 18%, being astenopia the most prevalent. The removal of the lens was not required in any case. Conclusion: Tetrafocal diffractive intraocular lenses provides excellent intermediate vision (at 60 centimeters) and satisfactory near (30 centimeters) and long (6 meters) visual acuity.
Resumo Objetivo: Avaliar a acuidade visual de longe, intermediária e de perto após o implante de lente intra-ocular difrativa tetrafocal, presença de fenômenos distópicos e satisfação do paciente após a cirurgia. Métodos: Estudo retrospectivo, observacional, realizado em Puerta de Hierro Hospital de Especialidades, em Jalisco, México. Isso incluiu 100 olhos após a cirurgia de facoemulsificação pela presença de laser de femtosegundo, seguida por implante de lente intra-ocular difrativa tetrafocal devido à catarata ou cirurgia facorrefractiva. Foi medida a acuidade visual de longe, intermediária e de perto, e a presença ou ausência de fenômenos distópicos, além da satisfação do paciente após a cirurgia. Resultados: Um total de 100 olhos em 50 pacientes submetidos à cirurgia de catarata com facoemulsificação por femtosegundo foram avaliados. 100% foram submetidos a facoemulsificação bilateral. A acuidade visual para longe, intermediária e de perto após três meses foi na maioria dos pacientes 20/20 (46%), 20/15 (44%) e Jaeger 1 (48%) respectivamente. A porcentagem ou pacientes que se referem a halos foi de 7%; e outros sintomas associados em 18%, sendo a astenopia a mais prevalente. A remoção da lente não foi necessária em nenhum caso. Conclusão: A lente intra-ocular difrativa tetrafocal fornece excelente visão intermediária (a 60 centímetros) e acuidade visual satisfatória de perto a (30 centímetros) e de longe (6 metros).
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Aged , Phacoemulsification/methods , Lens Implantation, Intraocular/methods , Lenses, Intraocular , Presbyopia/surgery , Presbyopia/diagnosis , Refraction, Ocular/physiology , Cataract/diagnosis , Visual Acuity/physiology , Retrospective Studies , Treatment Outcome , Patient Satisfaction , Observational StudyABSTRACT
El propósito de este trabajo es dar a conocer las bases moleculares de la fisiopatología de la diabetes mellitus, con el fin de prevenir la enfermedad o mejorar el tratamiento. La diabetes mellitus es una enfermedad compleja, donde la hiperglucemia crónica provoca complicaciones en distintos órganos. En esta condición aumentan las especies reactivas de oxígeno como resultado de su autooxidacción, por lo que su metabolismo propicia la acumulación de metabolitos como la fructosa, el sorbitol y las triosas fosfato. Éstos últimos generan α-oxoaldehídos reactivos con alta capacidad de unirse a proteínas y generar estrés oxidativo. Además, hay aumento de la síntesis de diacilgliceroles a partir de las triosas fosfato, las cuales activan a la pro teína cinasa C. Por otra parte, la alteración de la proporción normal entre los nucleótidos de niacinamida reducidos con respecto a los oxidados conduce a una baja eficiencia de los sistemas antioxidantes. Finalmente, estas desregulaciones metabólicas causan alteración en la transducción de la señal, en la expresión anormal de genes, además de daño tisular, lo que propicia complicaciones en los pacientes con diabetes.
The knowledge of the molecular basis of diabetes mellitus physiopathology will allow improvements in treatment or prevention of the disease. Diabetes mellitus is a complex disease in which hyperglycemia leads to complications in several organs. In this condition, there is increase in reactive oxygen species (ROS) as a result of glucose autooxidation; its metabolism produces accumulation of metabolites such as fructose, sorbitol, and triose phosphate. The latter generates α oxoaldehydes with high capacity to produce protein glycation and oxidative stress. Moreover, there is an increase in synthesis of diacylglycerol from triose phosphate, which activates protein kinase C. On the other hand, alteration of normal ratio between reduced and oxidized niacinamide nucleotides leads to low efficiency of antioxidative systems. Finally, this metabolic dysregulation causes altered signal transduction, abnormal gene expression, and tissue damage, resulting in development of diabetic complications.