Harrellpreston7198

Post-traumatic epilepsy (PTE) is one of the detrimental outcomes of traumatic brain injury (TBI), resulting in recurrent seizures that impact daily life. However, the pathological relationship between PTE and TBI remains unclear, and commonly prescribed antiepileptic drugs (AED) are ineffective against PTE. Fortunately, emerging research implicates neuroinflammation, particularly, tumor necrosis factor-α (TNF-α), as the key mediator for PTE development. Thus, this review aims to examine the available literature regarding the role of TNF-α in PTE pathology and, subsequently, evaluate TNF-α as a possible target for its treatment. A comprehensive literature search was conducted on four databases including PubMed, CINAHL, Embase, and Scopus. Articles with relevance in investigating TNF-α expression in PTE were considered in this review. Critical evaluation of four articles that met the inclusion criteria suggests a proportional relationship between TNF-α expression and seizure susceptibilit and that neutralization or suppression of TNF-α release results in reduced susceptibility to seizures. In conclusion, this review elucidates the importance of TNF-α expression in epileptogenesis postinjury and urges future research to focus more on clinical studies involving TNF-α, which may provide clearer insight into PTE prevention, therefore improving the lives of PTE patients.A simple methodology to controllably tune the pore size and Cr(VI) adsorption capacity was reported herein to synthesize a new series of conjugated microporous polyaniline (CMPA) networks. The well-ordered micropore was acquired through our very recent Bristol-Xi'an Jiaotong method, and the pore size was fine-tuned to increase with the increasing length of linkers, mimicking covalent organic frameworks and metal organic frameworks very much. selleck compound A selective ultrahigh adsorption capacity of 520.8 mg/g was achieved by CMPA-1 in a very fast manner, with a systematically gradual decrease to 173.9 mg/g of CMPA-3 by enlarging the pore size of the networks, featuring tunable adsorption capacity through molecular-size-recognition mechanism. Additionally, our robust CMPA networks, which were constructed by Buchwald-Hartwig chemistry, showed the complete function of polyaniline and were capable of providing, besides large storage capacity for Cr(III), at least 10 reductant/desorption-free cycles for effective Cr(VI) reduction and detoxication through their novel self-reducible redox states. Outcomes showed that our CMPAs could be applied as new self-healing scavengers in the next generation for Cr(VI) storage and detoxication.Transition-metal dichalcogenides (TMDs) hold great potential as an advanced electrocatalyst for oxygen evolution reaction (OER), but to date the activity of transition metal telluride catalysts are demonstrated to be poor for this reaction. In this study, we report the activation of CoTe2 for OER by doping secondary anions into Te vacancies to trigger a structural transition from the hexagonal to the orthorhombic phase. The achieved orthorhombic CoTe2 with partial vacancies occupied by P-doping exhibits an exceptional OER catalytic activity with an overpotential of only 241 mV at 10 mA cm-2 and a robust stability more than 24 h. The combined experimental and theoretical studies suggest that the defective phase transformation is controllable and allows the synergism of vacancy, doping as well as the reconstructed crystallographic structure, ensuring more exposure of catalytic active sites, rapid charge transfer, and energetically favorable intermediates. This vacancy occupation-driven strategy of structural transformation can also be manipulated by S- and Se-doping, which may offer useful guidance for developing tellurides-based electrocatalyst for OER.Cell migration on material surfaces is a fundament issue in the fields of biomaterials, cell biology, tissue engineering, regenerative medicine, etc. Herein, we aim to guide cell migration by flat microstripes with significant contrast of cell adhesion and varied geometric features of the adhesive stripes. To this end, we designed and fabricated cell-adhesive arginine-glycine-aspartate (RGD) microstripes on the nonfouling poly(ethylene glycol) (PEG) background and examined the microstripe-guided adhesion and migration of a few cell types. The migration of cell clusters adhering on the RGD regions was found to be significantly affected by the widths and arc radiuses of the guided microstripes. The cells migrated fastest on the straight microstripes with width of about 20 μm, which we defined as single file confined migration (SFCM). We also checked the possible left-right asymmetric bias of cell migration guided by combinatory microstripes with alternative wavy and quasi-straight stripes under a given width, and found that the velocity of CCW (counter clockwise) migration was higher than that of CW (clockwise) migration for primary rat mesenchymal stem cells (rMSCs), whereas no left-right asymmetric bias was observed for NIH3T3 (mouse embryonic fibroblast cell line) and Hela (human cervix epithelial carcinoma cell line) cells. Comparison of migration of cells on the nanotopological stripe and smooth surfaces further confirmed the importance of cell orientation coherence for guided cell migration and strengthened the superiority of SFCM.Aberrations in the Hedgehog (Hh) signaling pathway are responsible for a broad range of human cancers, yet only a subset rely on the activity of the clinical target, Smoothened (Smo). Emerging cases of cancers that are insensitive to Smo-targeting drugs demand new therapeutic targets and agents for inhibition. As such, we sought to pursue a recently discovered connection between the Hedgehog pathway transcription factors, the glioma-associated oncogene homologues (Glis), and protein kinase C (PKC) isozymes. Here, we report our assessment of a structurally diverse library of PKC effectors for their influence on Gli function. Using cell lines that employ distinct mechanisms of Gli activation up- and downstream of Smo, we identify a PKC effector that acts as a nanomolar Gli antagonist downstream of Smo through a mitogen-activated protein kinase kinase (MEK)-independent mechanism. This agent provides a unique tool to illuminate crosstalk between PKC isozymes and Hh signaling and new opportunities for therapeutic intervention in Hh pathway-dependent cancers.