Blends of synthetic plastic-derived polypeptide with Hydroxypropylmethylcellulose and polyvinyl alcohol: unraveling the specific interaction parameters, morphology and thermal stability of the polymers couple

The medleys of the plastic-derived polypeptide with commercially available polymers believably the suitable candidate for pharmaceutical and biomedical importance. The current research is focussed on the synthesis of a novel plastic-mimetic polypeptide (PLP), poly(IPAVG) by the solution phase method (where I, P, A, V, and G represent Isoleucine, Proline, Alanine, Valine, and Glycine, respectively). The miscibility attributes of PLP/polyvinyl alcohol (PVA) and PLP/hydroxypropylmethylcellulose (HPMC) blends were examined by viscometry and by other advanced analytical tools for different weight proportions. It is shown by the viscometry that the PLP/HPMC and PLP/PVA form an immiscible blend system at 10(omicron)C and further, the FTIR spectra of poly (IPAVG) /HPMC and poly (IPAVG) /PVA blend membranes manifest the lack of intermolecular interactions. DSC results proved the dual Tg for one blend proportion and lower Tg values for all other blend systems. The thermal property of the blends with different compositions was evaluated by thermogravimetric analysis (TGA). The TGA results showed that the blends possess inferior thermal stability to the native ones. The surface morphology was analyzed by SEM indicated the heterogeneity and X-ray diffraction (XRD) revealed the absence of any change in crystallinity advocated the immiscibility of the blends. Further, we ventured to prepare the non-woven fabrics from the solutions of 1-10 wt% concentrations at the voltages within 20-30 kV by electrospinning. The droplet formed at the spinneret failed to reach the collector plate, and consequently, no films developed for the collector device

Ca²⁺-signaling in airway smooth muscle cells is altered in T-bet knock-out mice

<p>Abstract</p> <p>Background</p> <p>Airway smooth muscle cells (ASMC) play a key role in bronchial hyperresponsiveness (BHR). A major component of the signaling cascade leading to ASMC contraction is calcium. So far, agonist-induced Ca²⁺-signaling in asthma has been studied by comparing innate properties of inbred rat or mouse strains, or by using selected mediators known to be involved in asthma. T-bet knock-out (KO) mice show key features of allergic asthma such as a shift towards T_H2-lymphocytes and display a broad spectrum of asthma-like histological and functional characteristics. In this study, we aimed at investigating whether Ca²⁺-homeostasis of ASMC is altered in T-bet KO-mice as an experimental model of asthma.</p> <p>Methods</p> <p>Lung slices of 100 to 200 μm thickness were obtained from T-bet KO- and wild-type mice. Airway contraction in response to acetylcholine (ACH) was measured by video-microscopy and Ca²⁺-signaling in single ASMC of lung slices was assessed using two-photon-microscopy.</p> <p>Results</p> <p>Airways from T-bet KO-mice showed increased baseline airway tone (BAT) and BHR compared to wild-type mice. This could be mimicked by incubation of lung slices from wild-type mice with IL-13. The increased BAT was correlated with an increased incidence of spontaneous changes in intracellular Ca²⁺-concentrations, whereas BHR correlated with higher ACH-induced Ca²⁺-transients and an increased proportion of ASMC showing Ca²⁺-oscillations. Emptying intracellular Ca²⁺-stores using caffeine or cyclopiazonic acid induced higher Ca²⁺-elevations in ASMC from T-bet KO- compared to wild-type mice.</p> <p>Conclusion</p> <p>Altered Ca²⁺-homeostasis of ASMC contributes to increased BAT and BHR in lung slices from T-bet KO-mice as a murine asthma model. We propose that a higher Ca²⁺-content of the intracellular Ca²⁺-stores is involved in the pathophysiology of these changes.</p