RESUMO
Diabetes produces several changes in the body triggered by high glycemia. Some of these changes include altered metabolism, structural changes in blood vessels and chronic inflammation. The eye and particularly the retinal ganglion cells (RGCs) are not spared, and the changes eventually lead to cell loss and visual function impairment. Understanding the mechanisms resulting in RGC damage and loss from diabetic retinopathy is essential to find an effective treatment. This review focuses mainly on the signaling pathways and molecules involved in RGC loss and the potential therapeutic approaches for the prevention of this cell death. Throughout the manuscript it became evident that multiple factors of different kind are responsible for RGC damage. This shows that new therapeutic agents targeting several factors at the same time are needed. Alpha-1 antitrypsin as an anti-inflammatory agent may become a suitable option for the treatment of RGC loss because of its beneficial interaction with several signaling pathways involved in RGC injury and inflammation. In conclusion, alpha-1 antitrypsin may become a potential therapeutic agent for the treatment of RGC loss and processes behind diabetic retinopathy.
Assuntos
Diabetes Mellitus/patologia , Retinopatia Diabética/patologia , Células Ganglionares da Retina/patologia , Animais , Morte Celular , Diabetes Mellitus/tratamento farmacológico , Diabetes Mellitus/metabolismo , Retinopatia Diabética/tratamento farmacológico , Retinopatia Diabética/metabolismo , Humanos , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Inflamação/patologia , Terapia de Alvo Molecular , Células Ganglionares da Retina/efeitos dos fármacos , Células Ganglionares da Retina/metabolismo , Transdução de Sinais/efeitos dos fármacosRESUMO
The objective of this article is to examine end of life decisions made by neonatologists of Córdoba, Argentina. An anonymous questionnaire was designed to investigate neonatologists' decisions on when to initiate or withdraw treatment in critical neonates. All neonatologists who take care of critically ill neonates in Córdoba participated in the survey. More than 75% of them would initiate treatment in preterm infants with uncertain prognosis based on the viability of the newborn. Because it is common to find that critically ill neonates lack sufficient diagnostic information at birth, this attitude seems to manifest a certain therapeutic activism. However, more than 80% of physicians withdraw futile treatments that do not produce benefits. Cordoban neonatologists initiate medical treatment based on the current clinical conditions of neonates, applying a certain degree of therapeutic activism. Doctors withdraw neonatal treatment when it is considered futile.
Assuntos
Estado Terminal/mortalidade , Tomada de Decisões/ética , Recém-Nascido Prematuro , Médicos/ética , Assistência Terminal , Argentina , Atitude do Pessoal de Saúde , Humanos , Recém-Nascido , Inquéritos e QuestionáriosRESUMO
PURPOSE: Platelet-rich plasma (PRP) is an autologous substance with adhesive properties. We aimed at developing and testing the efficacy of a method for PRP preparation in rabbits. MATERIALS AND METHODS: An in vitro study was carried out to obtain PRP from forty rabbits and to analyze the number of platelets and type of substance needed to trigger platelet activation. To induce platelet activation, 5%, 10%, 25% and 50% CaCl solutions were used. Then, an in vivo study was performed in twelve rabbits to test PRP adhesiveness in lamellar corneal graft. A control group made up of six rabbits underwent corneal transplantation without using PRP. RESULTS: 5% CaCl was the most effective concentration in activating PRP, with a mean time of 19 minutes. An attached corneal flap was seen 3 months after surgery. A detached corneal button was seen in all controls. CONCLUSION: Our method was able to produce rabbit-derived PRP with suitable properties for soft tissue adhesion. These results could be useful for researchers of the growing fields of tissue repair and experimental transplantation.