This study intends to develop novel two antimicrobial phenolic chitosan Schiff bases (I) and (II) via coupling of chitosan with Indole-3-carboxaldehyde and 4-dimethylaminobenzaldehyde, respectively, for boosting the antimicrobial activity of native chitosan. The alterations in the chemical structure and morphology of the Schiff bases were verified using FT-IR, electronic spectrum analysis, and SEM, whereas the thermal properties were investigated by TGA and DSC instruments. The results obtained from the potentiometric analysis referred that the degrees of substitution were 1.15 and 12.05% for Schiff bases (I) and (II), respectively. The antimicrobial activities of Schiff base (I) were significantly augmented more than Schiff base (II) and chitosan. Minimum inhibitory concentration (MIC) of Schiff base (I) was perceived at 50 µg/ml against tested microorganisms except for B. cereus and C. albicans. The highest concentration of Schiff base (I) could inhibit the growth of Gram-positive up to 99%. However, Schiff base (II) recorded the maximum inhibition rate versus Gram-positive approximately 82%. The cytotoxicity of the developed materials was estimated by MTT assay that substantiated their safety to fibroblast cells. The findings emphasized that the developed Schiff bases might be implemented as antimicrobial contenders to pure chitosan for treatments of wound infections.

Hemorrhage is the major hindrance over the wound healing, which triggers microbial infections and might provoke traumatic death. Herein, new hemostatic and antibacterial PVA/Kaolin composite sponges were crosslinked using a freeze-thawing approach and boosted by penicillin–streptomycin (Pen-Strep). Physicochemical characteristics of developed membranes were analyzed adopting Fourier transformed infrared spectroscopy (FT-IR), scanning electron microscopy (SEM), a thermal gravimetric analyzer (TGA), and differential scanning calorimetry (DSC). Furthermore, the impacts of kaolin concentrations on porosity, swelling behavior, gel fraction, and degradation of the membranes were investigated. SEM analyses revealed a spongy-like structure of hydrogels associated with high dispersion of kaolin inside PVA matrix. The thermal characteristics of PVA/Kaolin were significantly ameliorated compared to the prime PVA. Moreover, the results exhibited significant variations of swelling performance, surface roughness and pore capacity due to the alterations of kaolin contents. Besides, the adhesive strength ability was manifestly enhanced for PVA-K0.1 sponge. Biomedical evaluations including antibacterial activity, blood clotting index and thrombogenicity of the membranes were studied. The contact of PVA/Kaolin to blood revealed notable augmentation in blood clotting. Furthermore, the incorporation of kaolin into PVA presented mild diminution in antibacterial activities. Moreover, PVA/Kaolin composites illustrated no cellular toxicity towards fibroblast cells. These remarkable features substantiate that the PVA-K0.1 sponge could be applied as a multifunctional wound dressing.

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Increase in the size of human neocortex-acquired in evolution-accounts for the unique cognitive capacity of humans. This expansion reflects the evolutionarily enhanced proliferative ability of basal progenitors (BPs), including the basal radial glia and basal intermediate progenitors (bIPs) in mammalian cortex, which may have been acquired through epigenetic alterations in BPs. However, how the epigenome in BPs differs across species is not known. Here, we report that histone H3 acetylation is a key epigenetic regulation in bIP amplification and cortical expansion. Through epigenetic profiling of sorted bIPs, we show that histone H3 lysine 9 acetylation (H3K9ac) is low in murine bIPs and high in human bIPs. Elevated H3K9ac preferentially increases bIP proliferation, increasing the size and folding of the normally smooth mouse neocortex. H3K9ac drives bIP amplification by increasing expression of the evolutionarily regulated gene, Trnp1, in developing cortex. Our findings demonstrate a previously unknown mechanism that controls cortical architecture.