Effects of Fiber Density and Strain Rate on the Mechanical Properties of Electrospun Polycaprolactone Nanofiber Mats.

This study examines the effects of electrospun polycaprolactone (PCL) fiber density and strain rate on nanofiber mat mechanical properties. An automated track collection system was employed to control fiber number per mat and promote uniform individual fiber properties regardless of the duration of collection. Fiber density is correlated to the mechanical properties of the nanofiber mats.

Mechanical Considerations for Electrospun Nanofibers in Tendon and Ligament Repair.

Electrospun nanofibers possess unique qualities such as nanodiameter, high surface area to volume ratio, biomimetic architecture, and tunable chemical and electrical properties. Numerous studies have demonstrated the potential of nanofibrous architecture to direct cell morphology, migration, and more complex biological processes such as differentiation and extracellular matrix (ECM) deposition through topographical guidance cues. These advantages have created great interest in electrospun fibers for biomedical applications, including tendon and ligament repair.

Traumatic brain injury induced matrix metalloproteinase2 cleaves CXCL12α (stromal cell derived factor 1α) and causes neurodegeneration.

Traumatic brain injury (TBI), even at mild levels, can activate matrix metalloproteinases (MMPs) and the induction of neuroinflammation that can result in blood brain barrier breakdown and neurodegeneration. MMP2 has a significant role in neuroinflammation and neurodegeneration by modulating the chemokine CXCL12α (stromal cell derived factor SDF-1α) signaling pathway and the induction of apoptosis. SDF-1α is responsible for cell proliferation and differentiation throughout the nervous system and is also implicated in various neurodegenerative illnesses.

High Ca Influx During Traumatic Brain Injury Leads to Caspase-1-Dependent Neuroinflammation and Cell Death.

We investigated the hypothesis that high Ca influx during traumatic brain injury induces the activation of the caspase-1 enzyme, which triggers neuroinflammation and cell apoptosis in a cell culture model of neuronal stretch injury and an in vivo model of fluid percussion injury (FPI). We first established that stretch injury causes a rapid increase in the intracellular Ca level, which activates interleukin-converting enzyme caspase-1. The increase in the intracellular Ca level and subsequent caspase-1 activation culminates into neuroinflammation via the maturation of IL-1β.