Given a set of calibrated images, Multiple View Stereo (MVS) applies end-to-end depth inference network to recover scene structure. However, previous methods designed pixel-visibility modules to aggregate cross-view cost, ignoring the consistency assumption of 2D contextual features in the 3D depth direction. The current multi-stage depth inference model also relies on intensive depth samples, which requires high memory consumption. To alleviate these problems, this work exploits edge-assisted epipolar Transformer for multi-view depth inference. The improvements of this work are summarized as follows: 1) The epipolar Transformer block is developed for reliable cross-view cost aggregation, and the edge detection branch is designed to constrain the consistency of epipolar geometry and edge features. 2) The dynamic depth range sampling mechanism based on probability volume is adopted to improve the accuracy of uncertain areas. Comprehensive comparisons with the state-of-the-art works indicate that our work can reconstruct dense scene representations with limited memory bottleblock Note to Practitioners —Learning-based MVS can obtain dense point clouds with accurate depth map estimation, which are widely applied in the fields of unmanned driving, battlefield environment perception and robot navigation. MVS-based scene reconstruction technology is the premise of the subsequent planning, decision-making and control of the human-machine system. To obtain dense scene representation with limited memory and runtime, this work proposes a multi-view stereo network with edge-assisted epipolar Transformer. Experiments on public benchmarks verify the feasibility and effectiveness of our model, which has good potential in battlefield environment reconstruction and human-computer interaction fields, and can provide intuitive and dense scene representation for decision-making assistance.

Previous studies have demonstrated activation of the local renin-angiotensin system in hindlimb unweighting (HU) rat vasculature. The present study intended to identify the effects of blockade of angiotensin II (ANG II) type 1 (AT₁) receptors with losartan on vascular reactivity, nitric oxide synthase (NOS) expression, and superoxide anion (O₂^•−) levels in 3-wk HU rat cerebral and carotid arteries. Three weeks later, vasoconstriction, vasodilatation, endothelial NOS (eNOS) and inducible NOS (iNOS) protein, as well as O₂^•− levels in rat cerebral and carotid arteries were examined. We found that HU enhanced maximal response to KCl/5-hydroxytryptamine ( P < 0.01) in basilar arteries and KCl/phenylephrine ( P < 0.05) in common carotid arteries from HU rats. Acetylcholine induced concentration-dependent vasodilatation in all the artery rings, but with significantly smaller amplitude in basilar ( P < 0.01) and common carotid ( P < 0.05) arteries from HU rats than those from control rats. Chronic treatment with losartan partially restored response to vasoconstrictors and acetylcholine-induced vasodilatation in basilar ( P < 0.01) and common carotid ( P < 0.05) arteries from losartan-treated HU rats. Furthermore, iNOS content in cerebral arteries and eNOS/iNOS content in carotid arteries were significantly ( P < 0.01) increased in HU rats. Meanwhile, HU increased O₂^•− levels in all the layers of these arteries. However, losartan restored NOS content and O₂^•− levels toward normal. These results suggested that the HU-induced enhancement of vasoconstriction and reduction in endothelium-dependent relaxation involved alterations in O₂^•− and NOS content through an ANG II/AT₁ receptor signaling pathway.

Wearable exoskeleton robots can promote the rehabilitation of patients with physical dysfunction. And improving human-computer interaction performance is a significant challenge for exoskeleton robots. The traditional feature extraction process based on surface Electromyography(sEMG) is complex and requires manual intervention, making real-time performance difficult to guarantee. In this study, we propose an end-to-end method to predict human knee joint angles based on sEMG signals using a tightly coupled convolutional transformer (TCCT) model. We first collected sEMG signals from 5 healthy subjects. Then, the envelope was extracted from the noise-removed sEMG signal and used as the input to the model. Finally, we developed the TCCT model to predict the knee joint angle after 100 ms. For the prediction performance, we used the Root Mean Square Error(RMSE), Pearson Correlation Coefficient(CC), and Adjustment R ² as metrics to evaluate the error between the actual knee angle and the predicted knee angle. The results show that the model can predict the human knee angle quickly and accurately. The mean RMSE, Adjustment R ² , and (CC) values of the model are 3.79°, 0.96, and 0.98, respectively, which are better than traditional deep learning models such as Informer (4.14, 0.95, 0.98), CNN (5.56, 0.89, 0.96) and CNN-BiLSTM (3.97, 0.95, 0.98). In addition, the prediction time of our proposed model is only 11.67±0.67 ms, which is less than 100 ms. Therefore, the real-time and accuracy of the model can meet the continuous prediction of human knee joint angle in practice.

The functional and structural adaptations in cerebral arteries could be one of the fundamental causes in the occurrence of orthostatic intolerance after space flight. In addition, emerging studies have found that many cardiovascular functions exhibit circadian rhythm. Several lines of evidence suggest that space flight might increase an astronaut’s cardiovascular risks by disrupting circadian rhythm. However, it remains unknown whether microgravity disrupts the diurnal variation in vascular contractility and whether microgravity impacts on circadian clock system. Sprague-Dawley rats were subjected to 28-day hindlimb-unweighting to simulate the effects of microgravity on vasculature. Cerebrovascular contractility was estimated by investigating vasoconstrictor responsiveness and myogenic tone. The circadian regulation of Ca_V1.2 channel was determined by recording whole-cell currents, evaluating protein and mRNA expressions. Then the candidate miRNA in relation with Ca²⁺ signal was screened. Lastly, the underlying pathway involved in circadian regulation of cerebrovascular contractility was determined. The major findings of this study are: (1) The clock gene BMAL1 could induce the expression of miR-103, and in turn modulate the circadian regulation of Ca_V1.2 channel in rat cerebral arteries at post-transcriptional level; and (2) simulated microgravity disrupted intrinsic diurnal oscillation in rat cerebrovascular contractility by altering circadian regulation of BMAL1/miR-103/Ca_V1.2 signal pathway.

Cerebral arterial remodeling is one of the critical factors in the occurrence of postspaceflight orthostatic intolerance. We hypothesize that large-conductance calcium-activated K⁺ (BK_Ca) channels in vascular smooth muscle cells (VSMCs) may play an important role in regulating cerebrovascular adaptation during microgravity exposure. The aim of this work was to investigate whether activation of BK_Ca channels is involved in regulation of apoptotic remodeling of cerebral arteries in simulated microgravity rats. In animal studies, Sprague-Dawley rats were subjected to 1-wk hindlimb unweighting to simulate microgravity. Alterations of BK_Ca channels in cerebral VSMCs were investigated by patch clamp and Western blotting; apoptosis was assessed by electron microscopy and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick-end labeling (TUNEL). To evaluate the correlation of BK_Ca channel and apoptosis, channel protein and cell nucleus were double-stained. In cell studies, hSloα+β1 channel was coexpressed into human embryonic kidney 293 (HEK293) cells to observe the effects of BK_Ca channels on apoptosis. In rats, enhanced activities and expression of BK_Ca channels were found to be correlated with increased apoptosis in cerebral VSMCs after simulated microgravity. In transfected HEK293 cells, activation of cloned BK_Ca channel induced apoptosis, whereas inhibition of cloned BK_Ca channel decreased apoptosis. In conclusion, activation of BK_Ca channels is associated with increased apoptosis in cerebral VSMCs of simulated microgravity rats.

The mechanisms that drive placental dysfunction in pregnancies complicated by hypoxia and fetal growth restriction remain poorly understood. Changes to mitochondrial respiration contribute to cellular dysfunction in conditions of hypoxia and have been implicated in the pathoaetiology of pregnancy complications, such as pre‐eclampsia. We used bespoke isobaric hypoxic chambers and a combination of functional, molecular and imaging techniques to study cellular metabolism and mitochondrial dynamics in sheep undergoing hypoxic pregnancy. We show that hypoxic pregnancy in sheep triggers a shift in capacity away from β‐oxidation and complex I‐mediated respiration, while maintaining total oxidative phosphorylation capacity. There are also complex‐specific changes to electron transport chain composition and a switch in mitochondrial dynamics towards fission. Hypoxic placentas show increased activation of the non‐canonical mitochondrial unfolded protein response pathway and enhanced insulin like growth factor 2 signalling. Combined, therefore, the data show that the hypoxic placenta undergoes significant metabolic and morphological adaptations to maintain cellular energy balance. Chronic hypoxia during pregnancy in sheep activated placental mitochondrial stress pathways, leading to alterations in mitochondrial respiration, mitochondrial energy metabolism and mitochondrial dynamics, as seen in the placenta of women with pre‐eclampsia. image Key points: Hypoxia shifts mitochondrial respiration away from β‐oxidation and complex I. Complex‐specific changes occur in the electron transport chain composition. Activation of the non‐canonical mitochondrial unfolded protein response pathway is heightened in hypoxic placentas. Enhanced insulin like growth factor 2 signalling is observed in hypoxic placentas. Hypoxic placentas undergo significant functional adaptations for energy balance.