Flexible Self-Powered Friction Piezoelectric Sensor Based on Structured PVDF-Based Composite Nanofiber Membranes.

With the rapid development of the economy and technology, intelligent wearable devices have gradually entered public life. Flexible sensors, as the main component of wearable devices, have been widely concerned. However, traditional flexible sensors need an external power supply, lacking flexibility and sustainable power supply. In this study, structured poly(vinylidene fluoride) (PVDF)-based composite nanofiber membranes doped with different mass fractions of MXene and zinc oxide (ZnO) were prepared by electrospinning and were then assembled to flexible self-powered friction piezoelectric sensors. The addition of MXene and ZnO endowed PVDF nanofiber membranes with better piezoelectric properties. The structured PVDF/MXene-PVDF/ZnO (PM/PZ) nanofiber membranes with a double-layer structure, interpenetrating structure, or core-shell structure could further enhance the piezoelectric properties of PVDF-based nanofiber membranes through the synergistic effects of filler doping and structural design. In particular, the output voltage of the self-powered friction piezoelectric sensor made of a core-shell PM/PZ nanofiber membrane showed a good linear relationship with the applied pressure and could produce a good piezoelectric response to the bending deformation caused by human motion.

SIRT1 promotes tumor-like invasion of fibroblast-like synoviocytes in rheumatoid arthritis via targeting TIMP1.

Suppression of tissue inhibitor of matrix metalloproteinase (TIMP) is associated with the tumor-like invasion of fibroblast-like synoviocytes (FLSs) that occurs during rheumatoid arthritis-related cartilage destruction. Silent information regulator 2 homolog1 (SIRT1), a histone deacetylase, is widely involved in transcriptional regulation, genomic stability, metabolism and DNA repair. Recent studies suggest that SIRT1 may also impact inflammatory response and the proliferation of FLSs in rheumatoid arthritis (RA). However, it is unknown whether SIRT1 has a role in the tumor-like invasion of FLSs in rheumatoid arthritis. Herein we report that SIRT1 contributes to FLS invasion and cartilage destruction via a TIMP1-dependent mechanism. Elevated SIRT1 in RA synovia suppresses TIMP1 expression via deacetylation of TIMP1-associated histones, thereby disrupting the binding of the transcription factor specificity protein 1 (Sp1) to the TIMP1 promoter. In rats with collagen-induced arthritis, depletion of SIRT1 remarkably promoted TIMP1 expression in synovial tissues and ameliorated cartilage destruction. These results describe a new role for SIRT1 and demonstrate its potential value as a therapeutic target for rheumatoid arthritis.

[Ecological compensation standard in Dongting Lake region of returning cropland to lake based on emergy analysis].

The annual emergy and currency value of the main ecological service value of returning cropland to lake in Dongting Lake region from 1999 to 2010 was calculated based on emergy analysis. The calculation method of ecological compensation standard was established by calculating annual total emergy of ecological service function increment since the starting year of returning cropland to lake, and the annual ecological compensation standard and compensation area were analyzed from 1999 to 2010. The results indicated that ecological compensation standard from 1999 to 2010 was 40.31-86.48 yuan x m(-2) with the mean of 57.33 yuan x m(-2). The ecological compensation standard presented an increase trend year by year due to the effect of eco-recovery of returning cropland to lake. The ecological compensation standard in the research area presented a swift and steady growth trend after 2005 mainly due to the intensive economy development of Hunan Province, suggesting the value of natural ecological resources would increase along with the development of society and economy. Appling the emergy analysis to research the ecological compensation standard could reveal the dynamics of annual ecological compensation standard, solve the abutment problem of matter flow, energy flow and economic flow, and overcome the subjective and arbitrary of environment economic methods. The empirical research of ecological compensation standard in Dongting Lake region showed that the emergy analysis was feasible and advanced.

Rescue of proinflammatory cytokine-inhibited chondrogenesis by the antiarthritic effect of melatonin in synovium mesenchymal stem cells via suppression of reactive oxygen species and matrix metalloproteinases.

Cartilage repair by mesenchymal stem cells (MSCs) often occurs in diseased joints in which the inflamed microenvironment impairs chondrogenic maturation and causes neocartilage degradation. In this environment, melatonin exerts an antioxidant effect by scavenging free radicals. This study aimed to investigate the anti-inflammatory and chondroprotective effects of melatonin on human MSCs in a proinflammatory cytokine-induced arthritic environment. MSCs were induced toward chondrogenesis in the presence of interleukin-1ß (IL-1ß) or tumor necrosis factor α (TNF-α) with or without melatonin. Levels of intracellular reactive oxygen species (ROS), hydrogen peroxide, antioxidant enzymes, and cell viability were then assessed. Deposition of glycosaminoglycans and collagens was also determined by histological analysis. Gene expression of chondrogenic markers and matrix metalloproteinases (MMPs) was assessed by real-time polymerase chain reaction. In addition, the involvement of the melatonin receptor and superoxide dismutase (SOD) in chondrogenesis was investigated using pharmacologic inhibitors. The results showed that melatonin significantly reduced ROS accumulation and increased SOD expression. Both IL-1ß and TNF-α had an inhibitory effect on the chondrogenesis of MSCs, but melatonin successfully restored the low expression of cartilage matrix and chondrogenic genes. Melatonin prevented cartilage degradation by downregulating MMPs. The addition of luzindole and SOD inhibitors abrogated the protective effect of melatonin associated with increased levels of ROS and MMPs. These results demonstrated that proinflammatory cytokines impair the chondrogenesis of MSCs, which was rescued by melatonin treatment. This chondroprotective effect was potentially correlated to decreased ROS, preserved SOD, and suppressed levels of MMPs. Thus, melatonin provides a new strategy for promoting cell-based cartilage regeneration in diseased or injured joints.