Dual refractive index and viscosity sensing using polymeric nanofibers optical structures

Porous materials have demonstrated to be ideal candidates for the creation of optical sensors with very high sensitivities. This is due both to the possibility of infiltrating the target substances into them and to their notable surface-to-volume ratio that provides a larger biosensing area. Among porous structures, polymeric nanofibers (NFs) layers fabricated by electrospinning have emerged as a very promising alternative for the creation of low-cost and easy-to-produce high performance optical sensors, for example, based on Fabry-Perot (FP) interferometers. However, the sensing performance of these polymeric NFs sensors is limited by the low refractive index contrast between the NFs porous structure and the target medium when performing in-liquid sensing experiments, which determines a very low amplitude of the FP interference fringes appearing in the spectrum. This problem has been solved with the deposition of a thin metal layer (∼ 3 nm) over the NFs sensing layer. We have successfully used these metal-coated FP NFs sensors to perform several real-time and in-flow refractive index sensing experiments. From these sensing experiments, we have also determined that the sponge-like structure of the NFs layer suffers an expansion/compression process that is dependent of the viscosity of the analyzed sample, what thus gives the possibility to perform a simultaneous dual sensing of refractive index and viscosity of a fluid

Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice

Mitochondrial morphology is shaped by fusion and division of their membranes. Here, we found that adult myocardial function depends on balanced mitochondrial fusion and fission, maintained by processing of the dynamin-like guanosine triphosphatase OPA1 by the mitochondrial peptidases YME1L and OMA1. Cardiac-specific ablation of Yme1l in mice activated OMA1 and accelerated OPA1 proteolysis, which triggered mitochondrial fragmentation and altered cardiac metabolism. This caused dilated cardiomyopathy and heart failure. Cardiac function and mitochondrial morphology were rescued by Oma1 deletion, which prevented OPA1 cleavage. Feeding mice a high-fat diet or ablating Yme1l in skeletal muscle restored cardiac metabolism and preserved heart function without suppressing mitochondrial fragmentation. Thus, unprocessed OPA1 is sufficient to maintain heart function, OMA1 is a critical regulator of cardiomyocyte survival, and mitochondrial morphology and cardiac metabolism are intimately linked