Flexible Three-Dimensional Force Tactile Sensor Based on Velostat Piezoresistive Films.

The development of a high-performance, low-cost, and simply fabricated flexible three-dimensional (3D) force sensor is essential for the future development of electronic skins suitable for the detection of normal and shear forces for several human motions. In this study, a sandwich-structured flexible 3D force tactile sensor based on a polyethylene-carbon composite material (velostat) is presented. The sensor has a large measuring range, namely, 0-12 N in the direction of the normal force and 0-2.6 N in the direction of the shear force. For normal forces, the sensitivity is 0.775 N-1 at 0-1 N, 0.107 N-1 between 1 and 3 N, and 0.003 N-1 at 3 N and above. For shear forces, the measured sensitivity is 0.122 and 0.12 N-1 in x- and y-directions, respectively. Additionally, the sensor exhibits good repeatability and stability after 2500 cycles of loading and releasing. The response and recovery times of the sensor are as fast as 40 and 80 ms, respectively. Furthermore, we prepared a glove-like sensor array. When grasping the object using the tactile glove, the information about the force applied to the sensing unit can be transmitted through a wireless system in real-time and displayed on a personal computer (PC). The prepared flexible 3D force sensor shows broad application prospects in the field of smart wearable devices.

Engineering crystal water in potassium ammonium vanadate for fast Zn-ion storage.

The effect of different annealing temperatures on the electrochemical performance of potassium ammonium vanadate (KNVO) was investigated, and the annealed KNVO regained H2O from the aqueous electrolyte to achieve an optimal structural water content during activation. In addition, the accompanying oxygen vacancies further promoted Zn2+ diffusion kinetics of the KNVO cathode in AZIBs and achieved excellent rate performance (344 mA h g-1 at 10 A g-1).

The Mutation of the DNA-Binding Domain of Fur Protein Enhances the Pathogenicity of Edwardsiella piscicida via Inducing Overpowering Pyroptosis.

Edwardsiella piscicida is an important fish pathogen with a broad host that causes substantial economic losses in the aquaculture industry. Ferric uptake regulator (Fur) is a global transcriptional regulator and contains two typical domains, the DNA-binding domain and dimerization domain. In a previous study, we obtained a mutant strain of full-length fur of E. piscicida, TX01Δfur, which displayed increased siderophore production and stress resistance factors and decreased pathogenicity. To further reveal the regulatory mechanism of Fur, the DNA-binding domain (N-terminal) of Fur was knocked out in this study and the mutant was named TX01Δfur2. We found that TX01Δfur2 displayed increased siderophore production and enhanced adversity tolerance, including a low pH, manganese, and high temperature stress, which was consistent with the phenotype of TX01Δfur. Contrary to TX01Δfur, whose virulence was weakened, TX01Δfur2 displayed an ascended invasion of nonphagocytic cells and enhanced destruction of phagocytes via inducing overpowering or uncontrollable pyroptosis, which was confirmed by the fact that TX01Δfur2 induced higher levels of cytotoxicity, IL-1ß, and p10 in macrophages than TX01. More importantly, TX01Δfur2 displayed an increased global virulence to the host, which was confirmed by the result that TX01Δfur2 caused higher lethality outcomes for healthy tilapias than TX01. These results demonstrate that the mutation of the Fur N-terminal domain augments the resistance level against the stress and pathogenicity of E. piscicida, which is not dependent on the bacterial number in host cells or host tissues, although the capabilities of biofilm formation and the motility of TX01Δfur2 decline. These interesting findings provide a new insight into the functional analysis of Fur concerning the regulation of virulence in E. piscicida and prompt us to explore the subtle regulation mechanism of Fur in the future.

Correlation of changes in serum S100ß, NSE and inflammatory factor levels with MMSE and MoCA in intracranial tumor patients with cognitive impairment.

Changes in serum neuron-specific enolase (NSE) level, S100ß protein concentration and inflammatory factor levels and their correlations with cognitive impairment Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scores in intracranial tumor patients with cognitive impairment were explored. Seventy patients diagnosed with intracranial tumor based on clinical symptoms and computed tomography (CT) images were selected and divided into non-cognitive impairment group (MoCA score ≥26 points, n=44) and cognitive impairment group (MoCA score <26 points, n=26) in accordance with the comprehensive cognitive function evaluation scores. Next, the serum NSE level, S100ß protein concentration and inflammatory factor levels were detected, and their relationships with MMSE and MoCA scores were analyzed via Pearsons correlation analysis. The MoCA and MMSE scores in non-cognitive impairment group were higher than those in cognitive impairment group (P<0.05). NSE and S100ß levels were higher in non-cognitive impairment group compared with cognitive impairment group (P<0.05). In addition, the levels of interleukin-6 (IL-6), IL-8 and tumor necrosis factor-α (TNF-α) were higher in cognitive impairment group than those in non-cognitive impairment group (P<0.05). The levels of patient's serum NSE, S100ß protein and inflammatory factors were negatively related to MMSE and MoCA scores (P<0.05). The changes in serum NSE, S100ß protein and inflammatory factor levels in patients with cognitive impairment can reflect the severity of the disease to a certain extent and are directly related to cognitive impairment. Accurate and comprehensive assessment of cognitive function of patients and early development of effective and targeted cognitive interventions are of certain clinical practical value for the improvement of prognosis.

AMD3100 Accelerates Reendothelialization of Neointima in Rabbit Saccular Aneurysm After Flow Diverter Treatment.

OBJECTIVE: We sought to inspect the role of AMD3100, which acts as an antagonist of stromal cell-derived factor-1/CXC chemokine receptor 4 on the formation of neointima in rabbit saccular aneurysm after flow diverter (FD) treatment. METHODS: Twenty saccular aneurysm models were established by using porcine pancreatic elastase. Three weeks later, a Tubridge FD was implanted into the saccular aneurysm. All treated models were immediately divided into 2 groups: the AMD3100 group was subcutaneously injected with AMD3100 (5 mg/kg per day), while the control group received saline. Morphology and thickness of the neointima were investigated 2 and 4 weeks after FD treatment, using hard tissue section and masson trichrome staining. Scanning electron microscope was used to observe endothelial-like cells, and fluorescence quantitative polymerase chain reaction was used to determine mRNA expression of neointima biomarkers, such as kinase insert domain receptor, VE-cadherin, CD34, and Tie2. RESULTS: Two and 4 weeks after FD treatment, the AMD3100 group had more endothelial-like cells than the control group in the neointima. Masson trichrome staining showed that the neointima in the AMD3100 group was more intact and thicker than that in the control group. Furthermore, increased mRNA levels of kinase insert domain receptor, VE-cadherin, and Tie2 in the neointima were found in the AMD3100 group compared with the control group. CONCLUSIONS: Interval use of AMD3100 promotes the formation of neointima in rabbit saccular aneurysm and facilitates the endothelialization of the neointima after FD treatment.