Biomass Straw Based Activated Porous Carbon Materials for High-Performance Supercapacitors

Biomass straws are often regarding as agricultural waste, usually burned off in rural areas, which results in severe resource waste and air pollution. In this work, biomass-based porous carbon material with a lamellar microstructure is obtained via simple hydrothermal and subsequent KOH activation, the optimum activate process is determined by the proportion of activator. Scanning electron microscopy (SEM) and nitrogen adsorption techniques are conducted to investigate the physical properties of the materials. Cyclic voltammetry and constant current discharge/charge in the three-electrode system and symmetrical double-layer capacitors results indicate the best electrochemical performance of SCA-1.5 electrode material, with a capacity of 250.0 F g-1 at 1.0 A g-1. And notably, high recycling stability at a high cycling rate of 1.0 A g-1 after 18,000 cycles

Knee loading protects against osteonecrosis of the femoral head by enhancing vessel remodeling and bone healing

Osteonecrosis of the femoral head is a serious orthopedic problem. Moderate loads with knee loading promote bone formation, but their effects on osteonecrosis have not been investigated. Using a rat model, we examined a hypothesis that knee loading enhances vessel remodeling and bone healing through the modulation of the fate of bone marrow-derived cells. In this study, osteonecrosis was induced by transecting the ligamentum teres followed by a tight ligature around the femoral neck. For knee loading, 5 N loads were laterally applied to the knee at 15 Hz for 5 min/day for 5 weeks. Changes in bone mineral density (BMD) and bone mineral content (BMC) of the femur were measured by pDEXA, and ink infusion was performed to evaluate vessel remodeling. Femoral heads were harvested for histomorphometry, and bone marrow-derived cells were isolated to examine osteoclast development and osteoblast differentiation. The results showed that osteonecrosis significantly induced bone loss, and knee loading stimulated both vessel remodeling and bone healing. The osteonecrosis group exhibited the lowest trabecular BV/TV (p b 0.001) in the femoral head, and lowest femoral BMD and BMC (both p b 0.01). However, knee loading increased trabecular BV/TV (p b 0.05) as well as BMD (pb 0.05) and BMC (p b 0.01). Osteonecrosis decreased the vessel volume (pb 0.001), vessel number (pb 0.001) and VEGF expression (p b 0.01), and knee loading increased them (pb 0.001, pb 0.001 and p b 0.01). Osteonecrosis activated osteoclast development, and knee loading reduced its formation, migration, adhesion and the level of “pit” formation (pb 0.001, pb 0.01, pb 0.001 and pb 0.001). Furthermore, knee loading significantly increased osteoblast differentiation and CFU-F (both p b 0.001). A significantly positive correlation was observed between vessel remodeling and bone healing (both p b 0.01). These results indicate that knee loading could be effective in repair osteonecrosis of the femoral head in a rat model. This effect might be attributed to promoting vessel remodeling, suppressing osteoclast development, and increasing osteoblast and fibroblast differentiation. In summary, the current study suggests that knee loading might potentially be employed as a non-invasive therapy for osteonecrosis of the femoral head

Effects of knee loading on obesity‐related nonalcoholic fatty liver disease in an ovariectomized mouse model with high fat diet

Aim Hormonal and nutritional disorders are the main causes of obesity and nonalcoholic fatty liver disease, especially in the elderly and postmenopausal women. Although physical activity may alleviate these disorders, the elderly may often have difficulty in conducting physical exercise. The purpose of this study was to investigate the therapeutic effect of knee loading, a new form of physical stimulation, on the symptom of obesity and fatty liver. Methods Using ovariectomized mice with high fat diet, we evaluated the effect of knee loading that applies gentle cyclic loads to the knee. Female C57BL/6 mice were divided into five groups: control (SCD), high fat diet (HF), HF with loading (HF+L), HF with ovariectomy (HF+OVX), and HF+OVX with loading (HF+OVX+L). Except for SCD, mice underwent sham operation or ovariectomy and maintained on high fat diet. After 6 weeks, the mice in HF+L and HF+OVX+L were treated with 6‐week knee loading. Results Compared to the obesity groups (HF and HF+OVX), knee loading significantly decreased a gain in body weight, liver weight, and white adipose tissue (all P<0.01). It also reduced the lipid level in the serum (P<0.01) and histological severity of hepatic steatosis (P<0.01). Furthermore, knee loading downregulated biomarkers related to the endoplasmic reticulum stress (GRP78, p‐eIF2α and ATF4) and altered biomarkers in autophagy (LC3 and p62). Conclusions Knee loading suppressed obesity‐associated metabolic alterations and hepatic steatosis, the effect with knee loading might be associated with suppression of the ER stress and promotion of autophagy

eIF2α signaling regulates ischemic osteonecrosis through endoplasmic reticulum stress

Osteonecrosis of the femoral head (ONFH) primarily results from ischemia/hypoxia to the femoral head, and one of the cellular manifestations is the endoplasmic reticulum (ER) stress. To understand possible linkage of ischemic osteonecrosis to the ER stress, a surgery-induced animal model was employed and salubrinal was administered to evaluate the role of ER stress. Salubrinal is a synthetic chemical that inhibits de-phosphorylation of eIF2α, and it can suppress cell death from the ER stress at a proper dose. The results indicated that the ER stress was associated with ONFH and salubrinal significantly improved ONFH-induced symptoms such as osteonecrosis, bone loss, reduction in vessel perfusion, and excessive osteoclastogenesis in the femoral head. Salubrinal also protected osteoblast development by upregulating the levels of ATF4, ALP and RUNX2, and it stimulated angiogenesis of endothelial cells through elevating ATF4 and VEGF. Collectively, the results support the notion that the ER stress is an important pathological outcome in the surgery-induced ONFH model, and salubrinal improves ONFH symptoms by enhancing angiogenesis and bone healing via suppressing the ER stress

Knee loading inhibits osteoclast lineage in a mouse model of osteoarthritis

Osteoarthritis (OA) is a whole joint disorder that involves cartilage degradation and periarticular bone response. Changes of cartilage and subchondral bone are associated with development and activity of osteoclasts from subchondral bone. Knee loading promotes bone formation, but its effects on OA have not been well investigated. Here, we hypothesized that knee loading regulates subchondral bone remodeling by suppressing osteoclast development, and prevents degradation of cartilage through crosstalk of bone-cartilage in osteoarthritic mice. Surgery-induced mouse model of OA was used. Two weeks application of daily dynamic knee loading significantly reduced OARSI scores and CC/TAC (calcified cartilage to total articular cartilage), but increased SBP (subchondral bone plate) and B.Ar/T.Ar (trabecular bone area to total tissue area). Bone resorption of osteoclasts from subchondral bone and the differentiation of osteoclasts from bone marrow-derived cells were completely suppressed by knee loading. The osteoclast activity was positively correlated with OARSI scores and negatively correlated with SBP and B.Ar/T.Ar. Furthermore, knee loading exerted protective effects by suppressing osteoclastogenesis through Wnt signaling. Overall, osteoclast lineage is the hyper responsiveness of knee loading in osteoarthritic mice. Mechanical stimulation prevents OA-induced cartilage degeneration through crosstalk with subchondral bone. Knee loading might be a new potential therapy for osteoarthritis patients

Maximizing the relationship of yield to site-specific management zones with object-oriented segmentation of hyperspectral images

Quick and low cost delineation of site-specific management zones (SSMZ) would improve applications of precision agriculture. In this study, a new method for delineating SSMZ using object-oriented segmentation of airborne imagery was demonstrated. Three remote sensing domains—spectral, spatial, and temporal- are exploited to improve the SSMZ relationship to yield. Common vegetation indices (VI), and first and second derivatives ([Formula: see text], [Formula: see text]) from twelve airborne hyperspectral images of a cotton field for one season [Formula: see text] were used as input layers for object-oriented segmentation. The optimal combination of VI, SSMZ size and crop phenological stage were used as input variables for SSMZ delineation, determined by maximizing the correlation to segmented yield monitor maps. Combining narrow band vegetation indices and object-oriented segmentation provided higher correlation between VI and yield at SSMZ scale than that at pixel scale by reducing multi-resource data noise. VI performance varied during the cotton growing season, providing better SSMZ delineation at the beginning and middle of the season (days after planting (DAP) 66–143).The optimal scale determined for SSMZ delineation was approximately 240 polygons for the study field, but the method also provided flexibility enabling the setting of practical scales for a given field. For a defined scale, the optimal single phenological stage for the study field was near July 11 (DAP 87) early in the growing season. SSMZs determined from multispectral VIs at a single stage were also satisfactory; compared to hyperspectral indices, temporal resolution of multi-spectral data seems more important for SSMZ delineation

eIF2α signaling regulates autophagy of osteoblasts and the development of osteoclasts in OVX mice

Bone loss in postmenopausal osteoporosis is induced chiefly by an imbalance of bone-forming osteoblasts and bone-resorbing osteoclasts. Salubrinal is a synthetic compound that inhibits de-phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2α). Phosphorylation of eIF2α alleviates endoplasmic reticulum (ER) stress, which may activate autophagy. We hypothesized that eIF2α signaling regulates bone homeostasis by promoting autophagy in osteoblasts and inhibiting osteoclast development. To test the hypothesis, we employed salubrinal to elevate the phosphorylation of eIF2α in an ovariectomized (OVX) mouse model and cell cultures. In the OVX model, salubrinal prevented abnormal expansion of rough ER and decreased the number of acidic vesiculars. It regulated ER stress-associated signaling molecules such as Bip, p-eIF2α, ATF4 and CHOP, and promoted autophagy of osteoblasts via regulation of eIF2α, Atg7, LC3, and p62. Salubrinal markedly alleviated OVX-induced symptoms such as reduction of bone mineral density and bone volume fraction. In primary bone-marrow-derived cells, salubrinal increased the differentiation of osteoblasts, and decreased the formation of osteoclasts by inhibiting nuclear factor of activated T-cells cytoplasmic 1 (NFATc1). Live cell imaging and RNA interference demonstrated that suppression of osteoclastogenesis is in part mediated by Rac1 GTPase. Collectively, this study demonstrates that ER stress-autophagy axis plays an important role in OVX mice. Bone-forming osteoblasts are restored by maintaining phosphorylation of eIF2α, and bone-resorbing osteoclasts are regulated by inhibiting NFATc1 and Rac1 GTPase

Reversible Interlayer Sliding and Conductivity Changes in Adaptive Tetrathiafulvalene-Based Covalent Organic Frameworks.

Ordered interlayer stacking is intrinsic in two-dimensional covalent organic frameworks (2D COFs) and has strong implications on COF's optoelectronic properties. Reversible interlayer sliding, corresponding to shearing of 2D layers along their basal plane, is an appealing dynamic control of both structures and properties, yet it remains unexplored in the 2D COF field. Herein, we demonstrate that the reversible interlayer sliding can be realized in an imine-linked tetrathiafulvalene (TTF)-based COF TTF-DMTA. The solvent treatment induces crystalline phase changes between the proposed staircase-like sql net structure and a slightly slipped eclipsed sql net structure. The solvation-induced crystallinity changes correlate well with reversible spectroscopic and electrical conductivity changes as demonstrated in oriented COF thin films. In contrast, no reversible switching is observed in a related TTF-TA COF, which differs from TTF-DMTA in terms of the absence of methoxy groups on the phenylene linkers. This work represents the first 2D COF example of which eclipsed and staircase-like aggregated states are interchangeably accessed via interlayer sliding, an uncharted structural feature that may enable applications such as chemiresistive sensors

Role of endoplasmic reticulum stress in disuse osteoporosis

Osteoporosis is a major skeletal disease with low bone mineral density, which leads to an increased risk of bone fracture. Salubrinal is a synthetic chemical that inhibits dephosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2α) in response to endoplasmic reticulum (ER) stress. To understand possible linkage of osteoporosis to ER stress, we employed an unloading mouse model and examined the effects of salubrinal in the pathogenesis of disuse osteoporosis. The results presented several lines of evidence that osteoclastogenesis in the development of osteoporosis was associated with ER stress, and salubrinal suppressed unloading-induced bone loss. Compared to the age-matched control, unloaded mice reduced the trabecular bone area/total area (B.Ar/T.Ar) as well as the number of osteoblasts, and they increased the osteoclasts number on the trabecular bone surface in a time-dependent way. Unloading-induced disuse osteoporosis significantly increased the expression of Bip, p-eIF2α and ATF4 in short-term within 6 h of tail suspension, but time-dependent decreased in HU2d to HU14d. Furthermore, a significant correlation of ER stress with the differentiation of osteoblasts and osteoclasts was observed. Administration of salubrinal suppressed the unloading-induced decrease in bone mineral density, B.Ar/T.Ar and mature osteoclast formation. Salubrinal also increased the colony-forming unit-fibroblasts and colony-forming unit-osteoblasts. It reduced the formation of mature osteoclasts, suppressed their migration and adhesion, and increased the expression of Bip, p-eIF2α and ATF4. Electron microscopy showed that rough endoplasmic reticulum expansion and a decreased number of ribosomes on ER membrane were observed in osteoblast of unloading mice, and the abnormal ER expansion was significantly improved by salubrinal treatment. A TUNEL assay together with CCAAT/enhancer binding protein homologous protein (CHOP) expression indicated that ER stress-induced osteoblast apoptosis was rescued by salubrinal. Collectively, the results support the notion that ER stress plays a key role in the pathogenesis of disuse osteoporosis, and salubrinal attenuates unloading-induced bone loss by altering proliferation and differentiation of osteoblasts and osteoclasts via eIF2α signaling