Simulation Modelling Study of Self-Assembled Nanoparticle Coatings for Retinal Implants

The electrode resolution of current retinal prostheses is still far from matching the densities of retinal neurons. Decreasing electrode diameter increases impedance levels thus deterring effective stimulation of neurons. One solution is to increase the surface roughness of electrodes, which can be done via nanoparticle coatings. This paper explores a Lattice Gas Model of the drying-mediated self-assembly of nanoparticle mixtures. The model includes representations for different types of nanoparticles, solvent, vapour, substrate and the energetic relationships between these elements. The dynamical aspect of the model is determined by energy minimization, stochastic fluctuations and physical constraints. The model attempts to unravel the relationships between different experimental conditions (e.g. evaporation rate, substrate characteristics and solvent viscosity) and the surface roughness of resulting assemblies. Some of the main results include the facts that the assemblies formed by nanoparticles of different sizes can boost roughness in specific circumstances and that the optimized assemblies can exhibit walled or stalagmite structures. This study provides a set of simulation modelling experiments that if confirmed in the laboratory may result in new and useful materials.     

Aging hair follicles rejuvenated by transplantation to a young subcutaneous environment

We demonstrate in the present study that young host mice rejuvenate aged hair follicles after transplantation. Young mice promote the hair shaft growth of transplanted old hair follicles, as well as young follicles, in contrast to old host mice, which did not support hair-shaft growth from transplanted old or young follicles. Nestin-expressing hair follicle-associated pluripotent (HAP) stem cells of transplanted old and young hair follicles remained active in young host nude mice. In contrast, the nestin-expressing HAP stem cells in young and old hair follicles transplanted to old nude mice were not as active as in young nude host mice. The present study shows that transplanted old hair follicles were rejuvenated by young host mice, suggesting that aging may be reversible.     

Effect of P-glycoprotein Inhibition on the Penetration of Ceftriaxone Across the Blood–Brain Barrier

Neurochemical Research - Recent studies indicate that inhibition of the efflux transporter P-glycoprotein (P-gp) at the blood–brain barrier (BBB) may represent a putative strategy to increase...     

Drug-resistant cancer cell-derived exosomal EphA2 promotes breast cancer metastasis via the EphA2-Ephrin A1 reverse signaling

Tumor metastasis induced by drug resistance is a major challenge in successful cancer treatment. Nevertheless, the mechanisms underlying the pro-invasive and metastatic ability of drug resistance remain elusive. Exosome-mediated intercellular communications between cancer cells and stromal cells in tumor microenvironment are required for cancer initiation and progression. Recent reports have shown that communications between cancer cells also promote tumor aggression. However, little attention has been regarded on this aspect. Herein, we demonstrated that drug-resistant cell-derived exosomes promoted the invasion of sensitive breast cancer cells. Quantitative proteomic analysis showed that EphA2 was rich in exosomes from drug-resistant cells. Exosomal EphA2 conferred the invasive/metastatic phenotype transfer from drug-resistant cells to sensitive cells. Moreover, exosomal EphA2 activated ERK1/2 signaling through the ligand Ephrin A1-dependent reverse pathway rather than the forward pathway, thereby promoting breast cancer progression. Our findings indicate the key functional role of exosomal EphA2 in the transmission of aggressive phenotype between cancer cells that do not rely on direct cell–cell contact. Our study also suggests that the increase of EphA2 in drug-resistant cell-derived exosomes may be an important mechanism of chemotherapy/drug resistance-induced breast cancer progression.Subject terms: Breast cancer, Metastasis     

Synergistic effects of focus ultrasound with different frequency and hematoprphyrin on human tumor cells

Human hematopoietic cell K₅₆₂, human melenonla cell LiBr and human stomach cancer cells were exposed to ultrasound (US, 1.75 W/cm², 1.4, 2.16 and 2.4 MHz)in vitro in the presence or absence of hematoporphyrin (Hp, 100 μg/mL). The cell damaging effects of treatments were determined by means of the Trypan Blue dye exclusion test, MTT test and FDA test. The experimental results showed that the same cell line had different sensibilities to the US of different frequencies, and different cell line had different damage at the same acoustical radiation. The cornbined treatment with US and Hp enhanced greatly the cell damage, and no sensibility of insonation cells to US with Hp was observed. The cell damage tests showed that the results of MTT test corresponded well with that of Trypan Blue dye test.     

LPS induces fibroblast-like synoviocytes RSC-364 cells to pyroptosis through NF-κB mediated dual signalling pathway

Journal of Molecular Histology - Rheumatoid arthritis (RA) is a chronic, progressive, and systemic inflammatory joint disease characterized by synovial inflammation and joint damage. Abnormal...     

Modulation of GluK2a Subunit-containing Kainate Receptors by 14-3-3 Proteins

Kainate receptors (KARs) are one of the ionotropic glutamate receptors that mediate excitatory postsynaptic currents (EPSCs) with characteristically slow kinetics. Although mechanisms for the slow kinetics of KAR-EPSCs are not totally understood, recent evidence has implicated a regulatory role of KAR-associated proteins. Here, we report that decay kinetics of GluK2a-containing receptors is modulated by closely associated 14-3-3 proteins. 14-3-3 binding requires PKC-dependent phosphorylation of serine residues localized in the carboxyl tail of the GluK2a subunit. In transfected cells, 14-3-3 binding to GluK2a slows desensitization kinetics of both homomeric GluK2a and heteromeric GluK2a/GluK5 receptors. Moreover, KAR-EPSCs at mossy fiber-CA3 synapses decay significantly faster in the 14-3-3 functional knock-out mice. Collectively, these results demonstrate that 14-3-3 proteins are an important regulator of GluK2a-containing KARs and may contribute to the slow decay kinetics of native KAR-EPSCs.