Acanthamoeba castellanii trophozoites that survive multipurpose solutions are able to adhere to cosmetic contact lenses, increasing the risk of infection.

Amoebae of the genus Acanthamoeba are etiological agents of amoebic keratitis, for which up to now there is no treatment of choice and one of its main risk factors is the use of contact lenses, including cosmetic contact lenses. Recently there has been an increase in amoebic keratitis cases due to the use of cosmetic contact lenses. Therefore, having a solution for the care of lenses with an efficient disinfectant effect that prevents the adhesion of trophozoites to lenses becomes essential. This study was carried out to determine the effect of 8 multipurpose contact lenses care solutions on Acanthamoeba castellanii trophozoites viability, and the efficiency of two of them to prevent the trophozoites adherence onto two cosmetic contact lenses (Acuvue 2, approved by the US Food and Drug Administration, and Magic Eye CCL, not approved). After 3 h of interaction, only AO Sept Plus, OPTI FREE Replenish, Renu Plus, Bio True and Multiplus significantly reduced the number of viable trophozoites with respect to the control; at 6 h Renu Plus, and at 12 h Conta Soft Plus and Multiplus, maintained the inhibitory effect. Only Opti Free Pure Moist did not significantly reduce the number of viable trophozoites. Multiplus and Opti Free Pure Moist (selected for their greater and lesser antiamibic effect) significantly reduced trophozoite adherence to both lenses; however, Opti Free Pure Moist was more efficient, despite the fact that A. castellanii adhered similarly to both lenses. Our results show that in all the multipurpose solutions evaluated, hundreds of viable A. castellanii trophozoites remain after several hours of incubation. Therefore, storage of the lenses in their case with MPS maintains the potential risk of amoebic keratitis in, cosmetic contact lenses wearers. Moreover, the use of CCL, not approved by the FDA, can increase the risk factor for AK since its poor manufacture can favor the permanence of amoebae, in addition to being a risk for corneal integrity.

Mecanismos involucrados en la enfermedad renal relacionada con la obesidad / Mechanisms involved in renal illness related to obesity

RESUMEN Introducción: En las últimas tres décadas la prevalencia de adultos con sobrepeso y obesidad ha aumentado sustancialmente en todo el mundo. La acumulación de grasa abdominal y visceral está altamente correlacionada con efectos adversos renales, a través de la acumulación de tejido adiposo dentro y alrededor de los riñones y la acumulación intrarrenal de matriz extracelular. Esta glomerulopatía relacionada con la obesidad se caracteriza en etapas tempranas por hipertrofia glomerular con o sin glomeruloesclerosis segmentaria focal secundaria. Objetivo: Revisar los mecanismos involucrados en la enfermedad renal relacionada con la obesidad. Métodos: Se realizó una búsqueda bibliográfica en PubMed y Google Académico de 2013 a 2017 sobre este tema. Conclusiones: Los efectos nocivos de la obesidad en la vasculatura renal se deben al aumento de la presión arterial, inflamación, hiperglucemia, lipotoxicidad causada por un exceso de metabolismo no-β-oxidativo de los ácidos grasos, estrés oxidativo y activación de múltiples sistemas neurohumorales. El exceso de grasa visceral es una fuente de citocinas y otros factores que crean un medio de estrés oxidativo e inflamación que contribuyen a la disfunción endotelial, la rigidez vascular y al desarrollo de la aterosclerosis. La hiperfiltración e hipertrofia glomerular causan el daño renal asociado a la obesidad. La hiperfiltración compensatoria, que preserva el filtrado glomerular, se acompaña de expansión del volumen glomerular, incremento en los componentes de la matriz glomerular, células endoteliales y mesangiales. Tras la inflamación ocurre la neovascularización, mecanismo compensatorio para mantener la perfusión de los tejidos lesionados o isquémicos(AU)

ABSTRACT Introduction: The prevalence of overweight and obese adults has increased substantially worldwide, in the last three decades. The accumulation of abdominal and visceral fat is highly correlated with renal adverse effects, through the accumulation of adipose tissue in and around the kidneys and the intrarenal accumulation of extracellular matrix. This obesity-related glomerulopathy is characterized in early stages by glomerular hypertrophy with or without secondary focal segmental glomerulosclerosis. Objective: To review the mechanisms involved in the obesity related renal illness. Methods: A bibliographical search on this topic was carried out in PubMed and Academic Google databases from 2013 to 2017. Conclusions: The harmful effects of obesity on the renal vasculature are due to increased blood pressure, inflammation, hyperglycemia, lipotoxicity caused by an excess of non-β-oxidative metabolism of fatty acids, oxidative stress and activation of multiple neurohumoral systems. Excess visceral fat is a source of cytokines and other factors that create a means of oxidative stress and inflammation contributing to endothelial dysfunction, vascular stiffness and the development of atherosclerosis. Hyperfiltration and glomerular hypertrophy cause kidney damage associated with obesity. Compensatory hyperfiltration, which preserves the glomerular filtration rate, is accompanied by glomerular volume expansion, an increase in the components of the glomerular matrix, endothelial and mesangial cells. Following inflammation, neovascularization occurs, a compensatory mechanism to maintain perfusion of injured or ischemic tissues(AU)

Mecanismos de inducción de la matriz extracelular en la nefropatía diabética / Mechanisms of induction of the extracellular matrix in diabetic nephropathy

La nefropatía diabética es una complicación grave en la diabetes mellitus. Sus principales cambios morfológicos típicos se deben al aumento de la cantidad de proteínas de la matriz extracelular. Los productos finales de glicación avanzada, resultado de la hiperglucemia, estimulan la producción de proteínas de la matriz extracelular en las células mesangiales, lo que resulta en la glomeruloesclerosis. Se revisan las alteraciones de las vías metabólicas que inducen la producción de factores que aumentan la síntesis de proteínas de la matriz extracelular y su acumulación durante el desarrollo de la nefropatía diabética. La glucosa intracelular elevada induce un aumento de angiotensina II y activación de proteína cinasa C, que a su vez, aumentan varios factores de crecimiento, como el transformante 1, el endotelial vascular, el de tejido conectivo, el epidérmico y el derivado de plaquetas, que llevan al incremento en la síntesis de proteínas de la matriz extracelular renal, como el colágeno, la fibronectina, la entactina y la laminina, lo que engrosará las membranas basales y expandirá progresivamente la matriz mesangial glomerular. Las metaloproteinasas de la matriz, que modulan la cantidad de proteínas de la matriz extracelular, son, a su vez, reguladas por los inhibidores tisulares de las metaloproteinasas(AU)

Diabetic nephropathy is a serious complication in diabetes mellitus. Its main and typical morphological changes are caused by the rise of the amount of the extracellulary matrix proteins. The final products of advanced glycation resulting from hyperglycemia stimulate the production of the extracellulary matrix proteins in the mesangial cells which leads to glomerulosclerosis. This article reviewed the alterations in the metabolic pathways that induce the production of factors capable of increasing the extracellulary matrix protein synthesis and their accumulation during the development of diabetic nephropathy. Elevated intracellular glucose leads to increased angiotensin II and C-kinase protein activation which, in turn, increase the number of several growth factors such as B1 transforming, vascular endothelial, connective tissue, epidermal and platelet-derived factors. All the above-mentioned causes more synthesis of renal extracellulary matrix proteins such as collagen, fibronectin, entactin and laminin which will thicken the basal membranes and will progresively extend the glomerular mesangial matrix. The matrix metalloproteins in charge of modulating the amount of proteins in the said matrix are then regulated by the tisular inhibitors of the metalloproteinases(AU)

Early co-expression of cyclooxygenase-2 and renin in the rat kidney cortex contributes to the development of N(G)-nitro-L-arginine methyl ester induced hypertension.

We investigated the involvement of cyclooxygenase-2 (COX-2) and the renin-angiotensin system in N(G)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension. Male Wistar rats were treated with L-NAME (75.0 mg·(kg body mass)(-1)·day(-1), in their drinking water) for different durations (1-33 days). COX-2 and renin mRNA were measured using real-time PCR in the renal cortex, and prostanoids were assessed in the renal perfusate, whereas angiotensin II (Ang II) and Ang (1-7) were quantified in plasma. In some rats, nitric oxide synthase inhibition was carried out in conjunction with oral administration of captopril (30.0 mg·kg(-1)·day(-1)) or celecoxib (1.0 mg·kg(-1)·day(-1)) for 2 or 19 days. We found a parallel increase in renocortical COX-2 and renin mRNA starting at day 2 of treatment with L-NAME, and both peaked at 19-25 days. In addition, L-NAME increased renal 6-Keto-PGF(1α) (prostacyclin (PGI2) metabolite) and plasma Ang II from day 2, but reduced plasma Ang (1-7) at day 19. Captopril prevented the increase in blood pressure, which was associated with lower plasma Ang II and increased COX-2-derived 6-Keto-PGF(1α) at day 2 and plasma Ang (1-7) at day 19. Celecoxib partially prevented the increase in blood pressure; this effect was associated with a reduction in plasma Ang II. These findings indicate that renal COX-2 expression increased in parallel with renin expression, renal PGI2 synthesis, and plasma Ang II in L-NAME-induced hypertension.