Compliance Prediction for Structural Topology Optimization on the Basis of Moment Invariants and a Generalized Regression Neural Network.

Topology optimization techniques are essential for manufacturing industries, such as designing fiber-reinforced polymer composites (FRPCs) and structures with outstanding strength-to-weight ratios and light weights. In the SIMP approach, artificial intelligence algorithms are commonly utilized to enhance traditional FEM-based compliance minimization procedures. Based on an effective generalized regression neural network (GRNN), a new deep learning algorithm of compliance prediction for structural topology optimization is proposed. The algorithm learns the structural information using a fourth-order moment invariant analysis of the structural topology obtained from FEA at different iterations of classical topology optimization. A cantilever and a simply supported beam problem are used as ground-truth datasets, and the moment invariants are used as independent variables for input features. By comparing it with the well-known convolutional neural network (CNN) and deep neural network (DNN) models, the proposed GRNN model achieves a high prediction accuracy (R2 > 0.97) and drastically shortens the training and prediction cost. Furthermore, the GRNN algorithm exhibits excellent generalization ability on the prediction performance of the optimized topology with rotations and varied material volume fractions. This algorithm is promising for the replacement of the FEA calculation in the SIMP method, and can be applied to real-time optimization for advanced FRPC structure design.

Hybrid and adaptive control of functional electrical stimulation to correct hemiplegic gait for patients after stroke.

Introduction: Gait, as a fundamental human movement, necessitates the coordination of muscles across swing and stance phases. Functional electrical stimulation (FES) of the tibialis anterior (TA) has been widely applied to foot drop correction for patients with post-stroke during the swing phase. Although the gastrocnemius (GAS) during the stance phase is also affected, the Functional electrical stimulation of the gastrocnemius received less attention. Methods: To address this limitation, a timing- and intensity-adaptive Functional electrical stimulation control strategy was developed for both the TA and GAS. Each channel incorporates a speed-adaptive (SA) module to control stimulation timing and an iterative learning control (ILC) module to regulate the stimulation intensity. These modules rely on real-time kinematic or kinetic data during the swing or stance phase, respectively. The orthotic effects of the system were evaluated on eight patients with post-stroke foot drop. Gait kinematics and kinetics were assessed under three conditions: no stimulation (NS), Functional electrical stimulation to the ankle dorsiflexor tibialis anterior (SA-ILC DS) and FES to the tibialis anterior and the ankle plantarflexor gastrocnemius (SA-ILC DPS). Results: The ankle plantarflexion angle, the knee flexion angle, and the anterior ground reaction force (AGRF) in the SA-ILC DPS condition were significantly larger than those in the NS and SA-ILC DS conditions (p < 0.05). The maximum dorsiflexion angle during the swing phase in the SA-ILC DPS condition was similar to that in the SA-ILC DS condition, with both being significantly larger than the angle observed in the NS condition (p < 0.05). Furthermore, the angle error and force error relative to the set targets were minimized in the SA-ILC DPS condition. Discussion: The observed improvements can be ascribed to the appropriate stimulation timing and intensity provided by the SA-ILC DPS strategy. This study demonstrates that the hybrid and adaptive control strategy of functional electrical stimulation system offers a significant orthotic effect, and has considerable potential for future clinical application.

The Association Between PM2.5 and Depression in China.

While China has been experiencing unprecedented economic growth, depression is becoming one of the most striking social and mental health problems in recent years. Such a paradox to progress may partially be due to the notoriously poor air quality of the country. To verify this argument, we constructed an index of the prevalence of depression (IPD) using internet search query volumes in Baidu to proxy the potential depression and examined how IPD is associated with PM2.5, the major air pollutant in China. Our results from 2-way fixed effects models reveal that a 100 µg·m-3 increase in previous week's PM2.5 in a city is significantly associated with 0.279 increase in its IPD, comparable to 7.34 hours decrease in weekly daylight, and such relationship is particularly pronounced in the spring and summer and in East and South areas. Our findings of large-scale pattern suggest that PM2.5 at current levels in China poses serious mental health risks.

Impact of International Immigration on Life Satisfaction of Local Residents in England: Exploring the Differentiated Relationships across Socioeconomic Gradients.

Objectives: Large-scale influxes of international immigrants into England have stimulated heated debate about whether the increasing ethnic diversity has undermined local residents' life satisfaction and wellbeing. In this paper, we provide the first nationally representative evidence on the relationship between international immigration and local residents' life satisfaction in England. Methods: We used multilevel linear regression models to analyze nationally representative data (2011-2012) from 23,143 respondents and neighborhood level data from the 2011 Census. Results: The results show that the local share of international immigrants who arrived in 2010-2011, in particular the non-white immigrants, has a significantly adverse impact on local people's life satisfaction. Further analysis shows that the adverse impact of migration is particularly pronounced for local residents who do not have a job or from intermediate social class. Conclusions: This study enables a better understanding of the link between international immigration and life satisfaction, highlighting the need of public policies to be more targeted to areas that experienced great influxes of international immigrants by facilitating positive interactions and communication between international immigrants and the local residents.

Suppression of NLRP3 inflammasome attenuates stress-induced depression-like behavior in NLGN3-deficient mice.

Depression, regulated by central nervous system (CNS), is a significant inflammatory disorder. Neuroligin3 (NLGN3) has been implicated in brain functions. In the study, a chronic unpredictable mild stress (CUMS) model in wild type (WT) or NLGN3-knockout (KO) mice was established to explore the role of NLGN3 in regulating depression and to reveal the underlying molecular mechanism. The results indicated that NLGN3-knockout markedly reversed the loss of body weight, the reduction of sucrose consumption, the decrease of immobile time in the forced swimming tests (FST) and tail suspension tests (TST) induced by CUMS paradigm. CUMS up-regulated corticosterone (CORT) in serum, and down-regulated serotonin (5-HT), norepinephrine (NE) and brain-derived neurotrophic factor (BDNF) in hippocampus of mice, which were significantly reversed by NLGN3 deficiency. The results further demonstrated that NLGN3-knockout improved the degenerative neurons in cortex and hippocampus of CUMS-treated mice, accompanied with a significant decrease of ionized calciumbinding adapter molecule 1 (Iba-1) and glial fibrillary acidic protein (GFAP) expressions. Additionally, NLGN3-KO mice challenged with CUMS showed a significant reduction of pro-inflammatory cytokines and chemokine, including tumor necrosis factor-alpha (TNF-α), interleukin-18 (IL-18), interleukin-1 beta (IL-1ß), interleukin-4 (IL-4), CC-chemokine ligand-1 (CCL-1) and CXC-chemokine ligand-1 (CXCL-1), in cortex, hippocampus and amygdala tissue samples. Western blot analysis suggested that NLGN3-knockout inhibited the activation of nod-like receptor protein 3 (NLRP3) inflammasome and its adaptor of apoptosis-associated speck like protein (ASC), and reduced the expression of Caspase-1, along with the inactivation of nuclear factor-κB (NF-κB) in CUMS-challenged mice. The role of NLGN3 in regulating depression in mice was confirmed in vitro using astrocytes stimulated by LPS that NLGN3 knockdown reduced LPS-induced inflammation. Importantly, the suppressive effects of NLGN3-knockdown on inflammatory response were reversed by NLRP3 or ASC over-expression in AST exposed to LPS. In sum, our findings indicated that suppressing NLGN3 played a potential antidepressant role in CUMS animal model by inactivating NLRP3 inflammasome, providing a new therapeutic avenue for depression.

Acetylshikonin attenuates angiotensin II-induced proliferation and motility of human brain smooth muscle cells by inhibiting Wnt/ß-catenin signaling.

Cerebrovascular smooth muscle cell proliferation and migration contribute to hyperplasia in case of cerebrovascular remodeling and stroke. In the present study, we investigated the effects of acetylshikonin, the main ingredient of a Chinese traditional medicine Zicao, on human brain vascular smooth muscle cell (HBVSMCs) proliferation and migration induced by angiotensin II (AngII), and the underlying mechanisms. We found that acetylshikonin treatment significantly inhibited AngII-induced HBVSMCs proliferation and cell cycle transition from G1 to S phase. Wound-healing assay and Transwell assay showed that AngII-induced cell migration and invasion were markedly attenuated by acetylshikonin. In addition, AngII challenge significantly induced Wnt/ß-catenin signaling activation, as evidenced by increased ß-catenin phosphorylation and nuclear translocation and GSK-3ß phosphorylation. However, acetylshikonin treatment inhibited the activation of Wnt/ß-catenin signaling. Consequently, western blotting analysis revealed that acetylshikonin effectively reduced the expression of downstream target genes in AngII-treated cells, including c-myc, survivin and cyclin D1, which contributed to the inhibitory effect of acetylshikonin on HBVSMCs proliferation. Further, stimulation with recombinant Wnt3a dramatically reversed acetylshikonin-mediated inhibition of proliferation and cell cycle transition in HBVSMCs. Our study demonstrates that acetylshikonin prevents AngII-induced cerebrovascular smooth muscle cells proliferation and migration through inhibition of Wnt/ß-catenin pathway, indicating that acetylshikonin may present a potential option for the treatment of cerebrovascular remodeling.