Electrospinning is a promising method for the fabrication of fibers used for drug release system, due the ease of operation of the electrospinning process and the high surface to volume ratio, high loading capacity and high encapsulation efficiency of the obtained fibers. In this study release of tetracycline hydrochloride (TCH) from both monolithic and core-shell electrospun fibers of poly-lactic acid (PLA), poly-caprolactone (PCL) and their blend were studied. It was found that the drug release from the fibers depended on their composition. Core-shell fibers were designed with PCL and TCH in the core and with blends (PCL/PLA) of varying composition in the shell. A varying initial burst release was observed when the composition of the shell was varied. This illustrates that the burst release might be tunable which can be advantageous for many applications.

In humans, mutations in calmodulin cause cardiac arrhythmia. These mutations disrupt the ability of calmodulin to sense calcium concentrations and correctly regulate two central calcium channels, together obstructing heart rhythm. This correlation is well established, but also surprising since calmodulin is expressed in all tissues and interacts with hundreds of proteins. Until now, most studies have focused on cardiac cell function and regulation of specific cardiac targets, and thus potential other effects of these mutations have largely been unexplored. Here, we introduce the nematode Caenorhabditis elegans as an in vivo model to study effects of three human calmodulin mutations with different impairment on calcium binding. We find that arrhythmic effects of the calmodulin mutations N54I and D96V can be recapitulated in disruption of two rhythmic behaviors, pharynx pumping and defecation motor program. Interestingly, we also find that these mutations affect neuronal function, but in different ways. Whereas D96V sensitizes signaling at the neuromuscular junction, N54I has a protective effect. The mutation N98S did not affect rhythmic behavior, but impaired chemosensing. Therefore, pathogenic calmodulin mutations act through different mechanisms in rhythmic behavior and neuronal function in C. elegans, emphasizing the strength of using live multicellular models. Finally, our results support the hypothesis that human calmodulin mutations could also contribute to neurological diseases.