High performance polyvinyl alcohol/lignin fibers with excellent mechanical and water resistance properties.

To address the shortcoming of Polyvinyl alcohol (PVA) fibers for food or medical packaging materials including low mechanical strength and poor water resistance, lignin (LN) was used as raw material, acetone/H2O as solvent to self-assemble into lignin nanoparticles (LNP) by adverse solvent precipitation approach, and then PVA/LNP composite fibers with different LNP contents were fabricated successfully by wet and dry spinning. Herein, vast hydrophilic hydroxyl groups in PVA decreased owing to the hydrogen bond between LN and PVA, Especially, with only 0.5 wt% loading of LNP into the PVA/LNP fibers, the diameter was 94.4 dtex, tensile strength was 10.1 cN/dtex (1279.8 MPa), initial modulus was 94.7 cN/dtex (12.0 GPa), the crystallinity was 56.7 %, the orientation was 97.1 %, and water contact angle was 103.1°. Compared with pure PVA fibers, the tensile strength of PVA/LNP-0.5 fibers was increased by 44.2 % and the contact angle was increased 37°. This work provides novel insights into obtaining lignin-reinforced PVA composite fibers with strong mechanical properties and excellent water resistance properties, indicating the potential of the PVA/LNP fibers for food or medical packaging application.

Waste Silicone Rubber in Three-Dimensional Conductive Networks as a Temperature and Movement Sensor.

Constructing a three-dimensional (3D) conductive network in a polymer matrix is a common method for preparing flexible sensors. However, the previously reported methods for constructing a 3D conductive network generally have shortcomings such as uncontrollable processes and insufficient network continuity, which limit the practical application of this method. In this work, we report a method for constructing a dual 3D conductive network. The carbon nanotube/graphene oxide co-continuous network (primary network) was introduced on the surface of the waste silicone rubber particles (WSRPs) through the adhesion of polydopamine (PDA), and then WSRPs were bonded into a porous skeleton using nanocellulose. The carbon fiber/carbon ball interconnection network (secondary network) was constructed in liquid silicone rubber (LSR) through the interaction of host-guest dendrimers and was filled into the WSRP skeleton. The dual 3D conductive network structure endowed the sensor with high electrical and thermal conductivity, outstanding stability, and excellent durability. In addition, the sensor showed high strain sensitivity and excellent stability when detecting human body temperature and motion behavior, and the pressure distribution can be spatially mapped through the sensor matrix. These demonstrations give our sensor high potential in the fields of smart devices, body monitoring, and human-machine interfaces.

Hydrophobic, breathable cellulose nonwoven fabrics for disposable hygiene applications.

Cellulose-based fabrics with suitably high hydrophobicity and good air-permeability are highly promising for disposable hygiene applications. Herein, a facile, one-step method is reported, which effectively converts the completely hydrophilic cellulose nonwoven substrate into highly hydrophobic fabrics (water contact angle of 130-135°) with preservation of a good air-permeability (variation ± 6% after modification compared to the original 1337 mm·s-1). Mono-isocyanates with bulky, hydrophobic moieties were adopted and 3-isocyanatopropyltrimethoxysilane (ISPTMOS) was found to be the most efficient one compared to tert-butyl isocyanate (TBIS) and m-toluene isocyanate (MTIS). The influence of the type and concentration of modifiers on the structure and key properties (hydrophobicity, air-permeability, breaking strength, flexibility) of the fabrics was systematically investigated. This approach has a great potential for industrial scale-up at the stage of post-finishing of nonwoven fabrics, which can be applied in medical, hygiene and personal care areas.

Preparation and characterization of PLLA/chitosan-graft-poly (ε-caprolactone) (CS-g-PCL) composite fibrous mats: The microstructure, performance and proliferation assessment.

In order to achieve the electrospinning of chitosan in common organic solvents, amino-reserved CS-g-PCL was synthesized by one-step method. PLLA and dichloromethane/ethanol (CH2Cl2/EtOH) solvent were chosen to prepare a series of different compositions of PLLA/CS-g-PCL mats (8/2, 6/4, 4/6, 2/8 wt/wt%) by electrospinning. The SEM showed that the smooth defect-free and uniform nanofibers were collected except PLLA/CS-g-PCL 2/8 and pure CS-g-PCL, and the fiber diameter was decreased from 828 nm to 461 nm with the increasing content of CS-g-PCL. The mechanical properties of composite mats have decreased with increasing CS-g-PCL content, but much higher than neat PLLA. The water contact angle, water absorption rate, water-vapor transmission rate and in vitro degradation behavior were 129°-19°, 109%-482%, 1945-2517 g m-2 day-1 and 4-14%, respectively. The addition of CS-g-PCL imparted PLLA/CS-g-PCL electrospun mats on better properties, improving the nature defects of PLLA. The in vitro cell culture studies showed that PLLA/CS-g-PCL 6/4 exhibited a higher in vitro biocompatibility and a better ability for cell attachment, spreading, and proliferation, comparing with PLLA mats. Herein, PLLA/CS-g-PCL 6/4 electrospun mats with excellent performance, was considered the potential application as wound dressing in skin tissue engineering.

miR-301a Suppression within Fibroblasts Limits the Progression of Fibrosis through the TSC1/mTOR Pathway.

Pulmonary fibrosis has been characterized by abnormal proliferation of fibroblasts and massive deposition of the extracellular matrix, which results from a complex interplay of chronic injury and inflammatory responses. MicroRNA-301a (miR-301a) is activated by multiple inflammatory stimulators, contributing to multiple tumorigenesis and autoimmune diseases. This study showed that miR-301a was overexpressed in a bleomycin-induced murine model of pulmonary fibrosis and patients with idiopathic pulmonary fibrosis (IPF). In addition, miR-301a was activated by transforming growth factor ß (TGF-ß) and interleukin 6 (IL-6) in normal and IPF fibroblasts, which was markedly reversed by the signal transducer and activator of transcription 3 (STAT3) inhibitor. The genetic ablation of miR-301a in mice reduced bleomycin-induced lung fibrosis, and the downregulation of miR-301a restrained proliferation and activation of fibroblasts. Furthermore, this study demonstrated that TSC1 was a functional target of miR-301a in fibroblasts, and the negative regulation of TSC1 by miR-301a promoted the severity of pulmonary fibrosis through the mammalian target of rapamycin (mTOR) signaling pathway. The blocking of miR-301a by the intravenous injection of antagomiR-301a inhibited the proliferation of fibroblasts and the structural destruction of lung tissues in the bleomycin-induced lung fibrosis mouse model. The findings revealed the crucial role of the miR-301a/TSC1/mTOR axis in the pathogenesis of pulmonary fibrosis, suggesting that miR-301a might serve as a potential therapeutic target.

Gramicidin inhibits cholangiocarcinoma cell growth by suppressing EGR4.

Gramicidin is a well-known antibiotic and recently was reported to induced tumour cell death, however, little is understood about the molecular mechanism of gramicidin as a therapeutic agent for solid tumours. Here, we investigated the role of gramicidin in cholangiocarcinoma cells. We found that gramicidin A inhibits cholangiocarcinoma cell growth and induced the necrotic cell death. We used next generation sequencing to analyse gene expression profiles of cholangiocarcinoma cells treated with gramicidin. We identified 265 differentially expressed genes in cholangiocarcinoma cells between PBS treatment and gramicidin treatment. EGR4 was confirmed to be a target of gramicidin-induced cell growth inhibition. Furthermore, we demonstrated that downregulation of EGR4 in cholangiocarcinoma cells leads to restraining tumour cell growth. Of note, EGR4 was expressed at highest levels in cholangiocarcinoma tissues among 17 types of human cancers, and EGR4 expression positively correlated with several growth factors associated with cholangiocarcinoma. Our findings ascertain that EGR4 is a potential target in cholangiocarcinoma and suppressing EGR4 by gramicidin establish an essential mechanism for bile duct carcinoma progression.

[Identification of differentially expressed genes between lung adenocarcinoma and squamous cell carcinoma using transcriber signature analysis].

OBJECTIVE: To analyze the differentially expressed genes (DEGs) between lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) with bioinformatics analysis and search for potential biomarkers for clinical diagnosis of nonsmall cell lung cancer (NSCLC). METHODS: The gene expression profiling datasets of LUAD and LUSC were acquired. The transcriptome differences between LUAD and LUSC were identified using R language processing and t-test analysis. The differential expressions of the genes were shown by Venn diagram. The DEGs identified by GEO2R were analyzed with DAVID and Ingenuity Pathway Analysis (IPA) to identify the signaling pathways and biomarkers that could be used for differential diagnosis of LUAD and LUSC. The TCGA data and the biomarker expression data from clinical lung cancer samples were used to verify the differential expressions of the Osteoarthritis pathway and LXR/RXR between LUAD and LUSC. We further examined the differential expressions of miR-181 and its two target genes, WNT5A and MBD2, in 23 clinical specimens of lung squamous cell carcinoma and the paired adjacent tissues. RESULTS: GEO data analysis identified 851 DEGs (including 276 up-regulated and 575 down-regulated genes) in LUAD and 885 DEGs (including 406 up-regulated and 479 down-regulated genes) in LUSC. DAVID and IPA analysis revealed that leukocyte migration and inflammatory responses were more abundant in LUAD than in LUSC. Osteoarthritis pathway was inhibited in LUAD and activated in LUSC. IPA analysis showed that transcription factors (GATA4, RELA, YBX1, TP63 and MBD2), cytokines (WNT5A and IL1A) and microRNAs (miR-34a, miR-181b and miR-15a) differed significantly between LUAD and LUSC. miR-34a with IL-1A, miR-15a with YBX1, and miR-181b with WNT5A and MBD2 could serve as the paired microRNA and mRNA targets for differential diagnosis of NSCLC subtypes. Analysis of the clinical samples showed an increased expression of miR-181b-5p and the down-regulation of WNT5A, which could be used as molecular markers for the diagnosis of LUSC. CONCLUSIONS: Through transcriptome analysis, we identified candidate genes, paired microRNAs and pathways for differentiating LUAD and LUSC, and they can provide novel differential diagnosis and therapeutic strategies for LUAD and LUSC.

[Effects of organophosphorus insecticides on G protein-coupled receptor kinase-2 mediated phosphorylation of M2 muscarinic receptors].

OBJECTIVE: To explore the effect of organophosphorus insecticides (OPs) on G protein-coupled receptor kinase 2 mediated phosphorylation of M2 muscarinic receptors in vitro and to understand an alternative target of the OPs for human and other animals. METHODS: The acetylcholine M2 muscarinic receptors (mAChR2) were purified from rat brain by single step affinity chromatography. In vitro experiments, the purified mAChR2, G-protein coupled receptor kinase 2 (GRK2) and the (gamma-p32) labeled ATP were incubated with paraoxon (PO), chlorpyrifos oxon (CPO) or chlorpyrifos (CPF) of varying concentrations. The proteins were separated by the polyacrylamide gel electrophoresis. The gels were dried and the phosphorylation of mAChR2 was detected with autoradiograms. Bands containing M2 receptor were excised and counted by liquid scintillation. RESULTS: CPO inhibited phosphorylation of M2 muscarinic receptors by GRK2 with a median inhibition concentration (IC(50)) at 70 micromol/L. CPF also inhibited M2 receptors phosphorylation, but was less potent and less efficacious than that of CPO. PO and parathion (PT) had little effect on the receptor phosphorylation under the same conditions. CPO and CPF didn't inhibit the beta2 Adrenalin (beta2-AR) receptor phosphorylation also mediated by GRK2. CONCLUSION: CPO and CPF can selectively inhibit the GRK2 mediated mAChR2 phosphorylation while PO and PT have no this effect.