The research on urban flood resilience will contribute to building a more resilient city and provide valuable reference for municipal decision-makers. There are many frameworks and approaches for ...empirical studies on what constitutes urban flood resilience and how to evaluate it. In this study, a typical region suffering from flood disaster in China-Jiangsu Province was selected as the study area, including 13 prefecture-level cities. The pressure-state-response (PSR) framework, the projection pursuit based on real-coded accelerated genetic algorithm (RAGA-PP) and the technique for order preference by similarity to an ideal solution based on the Kullback-Leibler distance (KL-TOPSIS) were combined to develop a hybrid multi-criteria approach for assessing urban flood resilience. Then the grey relational analysis obtained the important factors. The results illustrate that (1) the development of each subsystem in the city is uncoordinated, that is, the pressure-subsystem has little influence on urban flood resilience, while the state-subsystem and the response-subsystem have great influence. (2) The urban flood resilience in Jiangsu Province presents obvious polarization trend, that is, Southern Jiangsu is more resilient than Northern Jiangsu. The underlying factors are closely related to the level of economic development. Furthermore, the proposed method provides a practical evaluation approach for other fields.
The rechargeable zinc‐ion battery is regarded as a promising candidate for the next‐generation energy storage system, however, zinc dendrite growth and hydrogen evolution reaction (HER) have greatly ...hindered the practical application of the battery. Herein, a functionalized, nano‐engineering Zn2+ coordinated carboxylate cellulose solid‐state electrolyte (denoted as Zn‐CCNF@XG) for zinc‐ion battery is constructed through a straightforward approach. According to the experimental and density functional theory (DFT) results of dissociation energy, the notably decreased dissociation energy by −COOH is favorable to Zn2+ de‐coordinating and rapid ion‐hopping in Zn‐CCNF@XG to achieve high ionic conductivity and transference number. More importantly, the engineered molecular channels are beneficial to enlarging the distance between the nanofibril chains, providing a larger space for the movement of Zn2+. Benefiting from the coordination of Zn2+ with −OH in carboxylate cellulose nanofibrils, Zn‐CCNF@XG as a good ionic conductor displays a high ionic conductivity of 1.17 × 10−4 S cm−1 and transference number of 0.78. The Zn||NaV3O8·1.5H2O full cell with Zn‐CCNF@XG maintains a capacity retention of 83.46% with a coulombic efficiency of 99.99% after 3000 cycles (1 A g−1). The proposed strategy by introducing a functional group to cellulose nanofibrils effectively avoids the dendrite and HER, providing valuable guidelines for the practical application of zinc‐ion batteries.
Functionalizing and nano‐engineering strategies are utilized to explore cellulose as a novel solid‐state Zn2+ conductor (Zn‐CCNF@XG). The introduction of −COOH is favorable to Zn2+ rapid ion‐hopping with low energy barrier and high ionic conductivity (1.17 × 10−4 S cm−1), showing an efficient and instructive strategy for high ionic conductivity, ionic transference number, and stability of SSEs.
The TrkB receptor is critical for the control of energy balance, as mutations in its gene (NTRK2) lead to hyperphagia and severe obesity. The main neural substrate mediating the appetite-suppressing ...activity of TrkB, however, remains unknown. Here, we demonstrate that selective Ntrk2 deletion within paraventricular hypothalamus (PVH) leads to severe hyperphagic obesity. Furthermore, chemogenetic activation or inhibition of TrkB-expressing PVH (PVH
) neurons suppresses or increases food intake, respectively. PVH
neurons project to multiple brain regions, including ventromedial hypothalamus (VMH) and lateral parabrachial nucleus (LPBN). We find that PVH
neurons projecting to LPBN are distinct from those to VMH, yet Ntrk2 deletion in PVH neurons projecting to either VMH or LPBN results in hyperphagia and obesity. Additionally, TrkB activation with BDNF increases firing of these PVH neurons. Therefore, TrkB signaling is a key regulator of a previously uncharacterized neuronal population within the PVH that impinges upon multiple circuits to govern appetite.
A variable universe fuzzy proportional‐integral‐differential (PID) algorithm was designed and first application for a laser power stabilization system. To validate the algorithm's effectiveness, it ...is applied to the simulation model of Simulink and the experimental system based on an acousto‐optic modulator. The results demonstrate that the variable universe fuzzy PID presents higher control precision, better robustness, and can suppress long‐term drift phenomena compared with the traditional feedback control algorithm. The algorithm design method in this paper has significant reference and guidance value for laser power stabilization system.
MicroRNAs (miRNAs) are reported as vital participators in the pathophysiological course of neuropathic pain. However, the underlying mechanisms of the functional roles of miRNAs in neuropathic pain ...are largely unknown. This study was designed to explore the potential role of miR‐150 in regulating the process of neuropathic pain in a rat model established by chronic sciatic nerve injury (CCI). Overexpression of miR‐150 greatly alleviated neuropathic pain development and reduced inflammatory cytokine expression, including COX‐2, interleukin IL‐6, and tumor necrosis factor (TNF)‐α in CCI rats. By bioinformatic analysis, 3′‐untranslated region (UTR) of Toll‐like receptor (TLR5) was predicted to be a target of miR‐150. TLR5 commonly serves as an important regulator of inflammation. Overexpression of miR‐150 significantly suppressed the expression of TLR5 in vitro and in vivo. Furthermore, upregulation of TLR5 decreased the miR‐150 expression and downregulation of TLR5 increased miR‐150, respectively. Overexpression of TLR5 significantly reversed the miR‐150‐induced suppressive effects on neuropathic pain. In conclusion, our current study indicates that miR‐150 may inhibit neuropathic pain development of CCI rats through inhibiting TLR5‐mediated neuroinflammation. Our findings suggest that miR‐150 may provide a novel therapeutic target for neuropathic pain treatment.
Our study uncovered a critical role of miR‐150 in neuropathic pain. The mechanisms of miR‐150 in regulating neuropathic pain development may involve the TLR5‐mediated neuroinflammation both in vitro and in vivo. MiR‐150 may be identified as a novel therapeutic target for neuropathic pain treatment.
•The crude polysaccharides (EPS) from L. helveticus MB2-1 have high viscosity.•Isolation and characterization of three EPS fractions from L. helveticus MB2-1.•Three purified EPS fractions had similar ...average molecular weight (about 2×105Da).•The EPS exhibited high antioxidant and metal ion chelating activities in vitro.•The acidic EPS from L. helveticus MB2-1 had potentials as natural antioxidant.
In the present study, the crude polysaccharides (EPS) from Lactobacillus helveticus MB2-1 were fermented with reconstituted whey medium and further fractionated on DEAE-52 cellulose and Sephadex G-100 chromatography to afford three purified fractions of EPS-1, EPS-2 and EPS-3. Then, their preliminary structures and antioxidant activities in vitro were investigated. Three purified EPS fractions (EPS-1, EPS-2 and EPS-3) had similar molecular weight distributions (about 2×105Da), and it was composed of galactose, glucose and mannose with a molar ratio of 1.33:2.75:1.00, 1.00:1.43:9.34 and 1.17:1.00:2.96, respectively. In addition, the antioxidant activity of EPS-1, EPS-2 and EPS-3 was evaluated with the in vitro scavenging abilities. The results indicated that both crude and purified EPS showed strong scavenging activities on three kinds of radical and chelating activities on ferrous ion, and their antioxidant activities decreased in the order of crude EPS>EPS-3>EPS-2>EPS-1.
Multiple organ damage in severe acute respiratory syndrome (SARS) patients is common; however, the pathogenesis remains controversial. This study was to determine whether the damage was correlated ...with expression of the SARS coronavirus receptor, angiotensin converting enzyme 2 (ACE2), in different organs, especially in the endocrine tissues of the pancreas, and to elucidate the pathogenesis of glucose intolerance in SARS patients. The effect of clinical variables on survival was estimated in 135 SARS patients who died, 385 hospitalized SARS patients who survived, and 19 patients with non-SARS pneumonia. A total of 39 SARS patients who had no previous diabetes and received no steroid treatment were compared to 39 matched healthy siblings during a 3-year follow-up period. The pattern of SARS coronavirus receptor-ACE2 proteins in different human organs was also studied. Significant elevations in oxygen saturation, serum creatinine, lactate dehydrogenase, creatine kinase MB isoenzyme, and fasting plasma glucose (FPG), but not in alanine transaminase were predictors for death. Abundant ACE2 immunostaining was found in lung, kidney, heart, and islets of pancreas, but not in hepatocytes. Twenty of the 39 followed-up patients were diabetic during hospitalization. After 3 years, only two of these patients had diabetes. Compared with their non-SARS siblings, these patients exhibited no significant differences in FPG, postprandial glucose (PPG), and insulin levels. The organ involvements of SARS correlated with organ expression of ACE2. The localization of ACE2 expression in the endocrine part of the pancreas suggests that SARS coronavirus enters islets using ACE2 as its receptor and damages islets causing acute diabetes.
Brain-derived neurotrophic factor (BDNF) is a key regulator of energy balance; however, its underlying mechanism remains unknown. By analyzing BDNF-expressing neurons in paraventricular hypothalamus ...(PVH), we have uncovered neural circuits that control energy balance. The Bdnf gene in the PVH was mostly expressed in previously undefined neurons, and its deletion caused hyperphagia, reduced locomotor activity, impaired thermogenesis, and severe obesity. Hyperphagia and reduced locomotor activity were associated with Bdnf deletion in anterior PVH, whereas BDNF neurons in medial and posterior PVH drive thermogenesis by projecting to spinal cord and forming polysynaptic connections to brown adipose tissues. Furthermore, BDNF expression in the PVH was increased in response to cold exposure, and its ablation caused atrophy of sympathetic preganglionic neurons. Thus, BDNF neurons in anterior PVH control energy intake and locomotor activity, whereas those in medial and posterior PVH promote thermogenesis by releasing BDNF into spinal cord to boost sympathetic outflow.
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•The PVH is a key structure that produces BDNF to control energy balance•The majority of BDNF neurons in the PVH are distinct from previously defined ones•BDNF neurons in the anterior PVH inhibit feeding and stimulate locomotor activity•BDNF neurons in the medial and posterior PVH drive adaptive thermogenesis
Distinct subsets of BDNF-expressing neurons in the paraventricular hypothalamus (PVH) control different aspects of energy balance, with those in the anterior PVH suppressing food intake and promoting locomotor activity and those in the medial and posterior PVH driving adaptive thermogenesis through polysynaptic connections to brown adipose tissues.
Genetic evidence indicates that brain-derived neurotrophic factor (BDNF) signaling through the TrkB receptor plays a critical role in the control of energy balance. Mutations in the BDNF or the ...TrkB-encoding NTRK2 gene have been found to cause severe obesity in humans and mice. However, it remains unknown which brain neurons express TrkB to control body weight. Here, we report that TrkB-expressing neurons in the dorsomedial hypothalamus (DMH) regulate food intake. We found that the DMH contains both glutamatergic and GABAergic TrkB-expressing neurons, some of which also express the leptin receptor (LepR). As revealed by Fos immunohistochemistry, a significant number of TrkB-expressing DMH (DMHTrkB) neurons were activated upon either overnight fasting or after refeeding. Chemogenetic activation of DMHTrkB neurons strongly suppressed feeding in the dark cycle when mice are physiologically hungry, whereas chemogenetic inhibition of DMHTrkB neurons greatly promoted feeding in the light cycle when mice are physiologically satiated, without affecting feeding in the dark cycle. Neuronal tracing revealed that DMHTrkB neurons do not innervate neurons expressing agouti-related protein in the arcuate nucleus, indicating that DMHTrkB neurons are distinct from previously identified LepR-expressing GABAergic DMH neurons that suppress feeding. Furthermore, selective Ntrk2 deletion in the DMH of adult mice led to hyperphagia, reduced energy expenditure, and obesity. Thus, our data show that DMHTrkB neurons are a population of neurons that are necessary and sufficient to suppress appetite and maintain physiological satiation. Pharmacological activation of these neurons could be a therapeutic intervention for the treatment of obesity.
The mechanism of local inflammation and systemic injury in chronic periodontitis is complicated, in which and exosomes play an important role. In our study, we found that T helper cell 17 ...(Th17)/regulatory T cell (Treg) balance is destabilized in the peripheral blood of patients with periodontitis, with upregulated Th17 or downregulated Treg, respectively. Porphyromonas gingivalis lipopolysaccharide (LPS) was used to simulate the inflammatory microenvironment of chronic periodontitis. The exosomes were extracted from periodontal ligament stem cells (PDLSCs) in LPS‐induced periodontitis environment, which inversely effected on CD4+ T cells under normal and inflammatory conditions. Furthermore, compared with exosomes from normal PDLSCs, lower expression of microRNA‐155‐5p (miR‐155‐5p) and higher expression of Sirtuin‐1 (SIRT1) were observed in exosomes from LPS‐stimulated PDLSCs. Exosomes from PDLSCs alleviated inflammatory microenvironment through Th17/Treg/miR‐155‐5p/SIRT1 regulatory network. This study aimed to find the “switching” factors that affected the further deterioration of periodontitis to maximally control the multiple downstream damage signal factors to further understand periodontitis and find new targets for its treatment.
The mechanism of how exosomes from periodontal ligament stem cells (PDLSCs) alleviated inflammatory microenvironment through T helper cell 17 (Th17)/regulatory T cell (Treg)/microRNA‐155‐5p (miR‐155‐5p)/Sirtuin‐1 (SIRT1) regulatory network. PDLSCs in the normal environment was favorable for the maintenance of Th17/Treg balance. The expression of miR‐155‐5p is decreased in exosomes released by PDLSCs in the inflammatory microenvironment. After ingestion by CD4+ T cells, the expression of SIRT1 in CD4+ T cells is increased, causing the upregulation of Th17 and the downregulation of Treg.
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