Miracle-dz/UniFAR-FTUs huggingface dataset:
A Compact Soft Robotic Wrist Brace With Origami Actuators

Wrist disability caused by a series of diseases or injuries hinders the patient’s capability to perform activities of daily living (ADL). Rehabilitation devices for the wrist motor function have gained popularity among clinics and researchers due to the convenience of self-rehabilitation. The inherent compliance of soft robots enabled safe human-robot interaction and light-weight characteristics, providing new possibilities to develop wearable devices. Compared with the conventional apparatus, soft robotic wearable rehabilitation devices showed advantages in flexibility, cost, and comfort. In this work, a compact and low-profile soft robotic wrist brace was proposed by directly integrating eight soft origami-patterned actuators on the commercially available wrist brace. The linear motion of the actuators was defined by their origami pattern. The extensions of the actuators were constrained by the brace fabrics, deriving the motions of the wrist joint, i.e., extension/flexion, ulnar/radial deviation. The soft actuators were made of ethylene-vinyl acetate by blow molding, achieving mass-production capability, low cost, and high repeatability. The design and fabrication of the soft robotic wrist brace are presented in this work. The experiments on the range of motion, output force, wearing position adaptivity, and performance under disturbance have been carried out with results analyzed. The modular soft actuator approach of design and fabrication of the soft robotic wrist brace has a wide application potential in wearable devices.
The Anti-Inflammatory Effect and Mucosal Barrier Protection of Clostridium butyricum RH2 in Ceftriaxone-Induced Intestinal Dysbacteriosis

This study aimed at determining the beneficial effect of Clostridium butyricum (CB) RH2 on ceftriaxone-induced dysbacteriosis. To this purpose, BALB/c mice were exposed to ceftriaxone (400 mg/ml) or not (control) for 7 days, and administered a daily oral gavage of low-, and high-dose CB RH2 (108 and 1010 CFU/ml, respectively) for 2 weeks. CB RH2 altered the diversity of gut microbiota, changed the composition of gut microbiota in phylum and genus level, decreased the F/B ratio, and decreased the pro-inflammatory bacteria (Deferribacteres, Oscillibacter, Desulfovibrio, Mucispirillum and Parabacteroides) in ceftriaxone-treated mice. Additionally, CB RH2 improved colonic architecture and intestinal integrity by improving the mucous layer and the tight junction barrier. Furthermore, CB RH2 also mitigated intestinal inflammation through decreasing proinflammatory factors (TNF-α and COX-2) and increasing anti-inflammatory factors (IL-10). CB RH2 had direct effects on the expansion of CD4+ T cells in Peyer’s patches (PPs) in vitro, which in turn affected their immune response upon challenge with ceftriaxone. All these data suggested that CB RH2 possessed the ability to modulate the intestinal mucosal and systemic immune system in limiting intestinal alterations to relieve ceftriaxone-induced dysbacteriosis.
Prolonged Exposure to Platelet Activating Factor Transforms Breast Epithelial Cells

Lipid species are known to have various biological functions owing to their structural differences, and each of them possesses a specific role to play depending upon their location and distribution in the cell. Some of these lipids interact with proteins on the cell membrane and acts as second messengers. The level of lipid mediators is generally maintained in the cell by feedback mechanisms; however, their improper degradation or enhanced production leads to their accumulation in the tumor microenvironment and disturbs the homeostasis of the cell. Platelet activating factor (PAF) is a known phospholipid mediator secreted upon immunological challenges by platelets, neutrophils, basophils, and macrophages. PAF, as a potent inflammatory molecule, is well studied, and its role in various cancers and cardiovascular diseases has also been investigated. Interestingly, increased levels of PAF have been found in the blood plasma of smokers, and breast cancer cells have shown the accumulation of PAF in presence of cigarette smoke extract. This accumulation was found to increase tumor cell motility that in turn could promote metastasis. Beyond this, however, the effect of PAF on tumorigenesis has not yet been well explored. Here, we show that the continuous exposure of 3D breast acinar cultures to PAF resulted in the activation of various oncogenic signaling pathways leading to transformation. We also found that the presence of PAF in the micro-environment increased the expression of PAF receptor (PAF-R), which corroborated with the higher expression of PAF-R detected in some epithelial cancers, as per literature. Thus, this study impresses on the fact that the presence of PAF alters the cellular microenvironment and eventually triggers irreversible effects that can cumulatively lead to transformation.
An Auroral Alfvén Wave Cascade

Folding, kinking, curling and vortical optical forms are distinctive features of most bright auroral displays. These forms are symptomatic of non-linear forcing of the plasma above auroral arcs resulting from the intensification of electrical currents and Alfvén waves along high-latitude geomagnetic field-lines during periods of disturbed space weather. Electrons accelerated to energies sufficient to carry these currents impact the atmosphere and drive visible emission with spatial structure and dynamics that replicate the morphology and time evolution of the plasma region where the acceleration occurs. Movies of active auroral displays, particularly when combined with conjugate in-situ fields and plasma measurements, therefore capture the physics of a driven, non-linearly evolving space plasma system. Here a perspective emphasizing the utility of combining in-situ measurements through the auroral acceleration region with high time and spatial resolution auroral imaging for the study of space plasma turbulence is presented. It is demonstrated how this special capacity reveals the operation of a cascade of vortical flows and currents through the auroral acceleration region regulated by the physics of Alfvén waves similar to that thought to operate in the Solar wind.
Take a “Selfie”: Examining How Leaders Emerge From Leader Self-Awareness, Self-Leadership, and Self-Efficacy

It is important to understand the processes behind how and why individuals emerge as leaders, so that the best and most capable individuals may occupy leadership positions. So far, most literature in this area has focused on individual characteristics, such as personality or cognitive ability. While interactions between individuals and context do get research attention, we still lack a comprehensive understanding of how the social context at work may help individuals to emerge as leaders. Such knowledge could make an important contribution toward getting the most capable, rather than the most dominant or narcissistic individuals, into leadership positions. In the present work, we contribute toward closing this gap by testing a mediation chain linking a leader's leader self-awareness to a follower's leadership emergence with two time-lagged studies (nstudy1 = 449, nstudy2 = 355). We found that the leader's leader self-awareness was positively related to (a) the follower's leadership emergence and (b) the follower's nomination for promotion and that both relationships were serially mediated by the follower's self-leadership and the follower's leader self-efficacy. We critically discuss our findings and provide ideas for future research.
Protective or Harmful: The Dual Roles of Autophagy in Diabetic Retinopathy

Autophagy is a self-degradative pathway involving intracellular substance degradation and recycling. Recently, this process has attracted a great deal of attention for its fundamental effect on physiological processes in cells, tissues, and the maintenance of organismal homeostasis. Dysregulation of autophagy occurs in some diseases, including immune disease, cancer, and neurodegenerative conditions. Diabetic retinopathy (DR), as a serious microvascular complication of diabetes, is the main cause of visual loss in working-age adults worldwide. The pathogenic mechanisms of DR are thought to be associated with accumulation of oxidative stress, retinal cell apoptosis, inflammatory response, endoplasmic reticulum (ER) stress, and nutrient starvation. These factors are closely related to the regulation of autophagy under pathological conditions. Increasing evidence has demonstrated the potential role of autophagy in the progression of DR through different pathways. However, to date this role is not understood, and whether the altered level of autophagy flux protects DR, or instead aggravates the progression, needs to be explored. In this review, we explore the alterations and functions of autophagy in different retinal cells and tissues under DR conditions, and explain the mechanisms involved in DR progression. We aim to provide a basis on which DR associated stress-modulated autophagy may be understood, and to suggest novel targets for future therapeutic intervention in DR.
Regenerative Medicine of Epithelia: Lessons From the Past and Future Goals

This article explores examples of successful and unsuccessful regenerative medicine on human epithelia. To evaluate the applications of the first regenerated tissues, the analysis of the past successes and failures addresses some pending issues and lay the groundwork for developing new therapies. Research should still be encouraged to fill the gap between pathologies, clinical applications and what regenerative medicine can attain with current knowledge.
Medial Parabrachial Nucleus Is Essential in Controlling Wakefulness in Rats

Activation of the parabrachial nucleus (PB) in the brainstem induced wakefulness in rats, suggesting which is an important nucleus that controls arousal. However, the sub-regions of PB in regulating sleep-wake cycle is still unclear. Here, we employ chemogenetics and optogenetics strategies and find that activation of the medial part of PB (MPB), but not the lateral part, induces continuous wakefulness for 10 h without sleep rebound in neither sleep amount nor the power spectra. Optogenetic activation of glutamatergic MPB neurons in sleeping rats immediately wake rats mediated by the basal forebrain (BF) and lateral hypothalamus (LH), but not the ventral medial thalamus. Most importantly, chemogenetic inhibition of PB neurons decreases wakefulness for 10 h. Conclusively, these findings indicate that the glutamatergic MPB neurons are essential in controlling wakefulness, and that MPB-BF and MPB-LH pathways are the major neuronal circuits.
Alterations in CD8+ Tregs, CD56+ Natural Killer Cells and IL-10 Are Associated With Invasiveness of Nonfunctioning Pituitary Adenomas (NFPAs)

Invasive nonfunctioning pituitary adenomas (NFPAs) grow rapidly and the mechanisms are unclear. Among many complex mechanisms, the role of immunity in the development of NFPAs has not been fully explored. Here, we analyzed the clinical features 146 NFPA patients who underwent trans-sphenoidal surgery or craniotomy and examined the effects of immune tolerance in invasiveness of NFPA patients using fluorescence-activated cell sorting and immunohistochemical methods. We found patients with invasive NFPAs had more visual deficits and defective fields, higher tumor size, and lower white blood cell count compared with patients with noninvasive NFPAs. Additionally, compared with patients with noninvasive NFPAs, patients with invasive NFPAs had conspicuously lower CD3−CD56+ natural killer (NK) cells and significantly higher levels of CD3+CD8+CD28-T cells (CD8+ Tregs) and interleukin-10 (IL-10) in peripheral blood. Moreover, patients with invasive NFPAs had lower infiltrated CD56+ cells, less infiltrated CD28+ cells, and significantly greater IL-10 expression. These results demonstrated that low CD56+ cells infiltration and CD28+ cells infiltration, as well as high IL-10 expression in pituitary tumor tissues, were related with increased invasiveness of NFPAs. Levels of CD3−CD56+ NK cells, CD8+ Tregs and IL-10 in the peripheral blood could be feasible diagnostic markers for invasive NFPAs.
The Benefits of Unnatural Amino Acid Incorporation as Protein Labels for Single Molecule Localization Microscopy

Single Molecule Localization Microscopy (SMLM) is an imaging method that allows for the visualization of structures smaller than the diffraction limit of light (~200 nm). This is achieved through techniques such as stochastic optical reconstruction microscopy (STORM) and photoactivated localization microscopy (PALM). A large part of obtaining ideal imaging of single molecules is the choice of the right fluorescent label. An upcoming field of protein labeling is incorporating unnatural amino acids (UAAs) with an attached fluorescent dye for precise localization and visualization of individual molecules. For this technique, fluorescent probes are conjugated to UAAs and are introduced into the protein of interest (POI) as a label. Here we contrast this labeling method with other commonly used protein-based labeling methods such as fluorescent proteins (FPs) or self-labeling tags such as Halotag, SNAP-tags, and CLIP-tags, and highlight the benefits and shortcomings of the site-specific incorporation of UAAs coupled with fluorescent dyes in SMLM.
Editorial: Terahertz Radiation: Materials and Applications

Department of Electrical & Electronic Engineering, Southern University of Science and Technology, Shenzhen, China, Division of Physics and Applied Physics, School of Physical and Mathematical Sciences, Nanyang Technological University, Singapore, Singapore, 3 Key Laboratory of In-Fiber Integrated Optics of Ministry of Education, College of Physics and Optoelectronic Engineering, Harbin Engineering University, Harbin, China, Center for Terahertz Waves, Key Laboratory of
Multi-Dimensional Gene Regulation in Innate and Adaptive Lymphocytes: A View From Regulomes

The precise control of cytokine production by innate lymphoid cells (ILCs) and their T cell adaptive system counterparts is critical to mounting a proper host defense immune response without inducing collateral damage and autoimmunity. Unlike T cells that differentiate into functionally divergent subsets upon antigen recognition, ILCs are developmentally programmed to rapidly respond to environmental signals in a polarized manner, without the need of T cell receptor (TCR) signaling. The specification of cytokine production relies on dynamic regulation of cis-regulatory elements that involve multi-dimensional epigenetic mechanisms, including DNA methylation, transcription factor binding, histone modification and DNA-DNA interactions that form chromatin loops. How these different layers of gene regulation coordinate with each other to fine tune cytokine production, and whether ILCs and their T cell analogs utilize the same regulatory strategy, remain largely unknown. Herein, we review the molecular mechanisms that underlie cell identity and functionality of helper T cells and ILCs, focusing on networks of transcription factors and cis-regulatory elements. We discuss how higher-order chromatin architecture orchestrates these components to construct lineage- and state-specific regulomes that support ordered immunoregulation.
Toward Augmented Reality in Museums: Evaluation of Design Choices for 3D Object Pose Estimation

The solutions to many computer vision problems, including that of 6D object pose estimation, are dominated nowadays by the explosion of the learning-based paradigm. In this paper, we investigate 6D object pose estimation in a practical, real-word setting in which a mobile device (smartphone/tablet) needs to be localized in front of a museum exhibit, in support of an augmented-reality application scenario. In view of the constraints and the priorities set by this particular setting, we consider an appropriately tailored classical as well as a learning-based method. Moreover, we develop a hybrid method that consists of both classical and learning based components. All three methods are evaluated quantitatively on a standard, benchmark dataset, but also on a new dataset that is specific to the museum guidance scenario of interest.
Peripheral Electrical Stimulation Modulates Cortical Beta-Band Activity

Low-frequency peripheral electrical stimulation using a matrix electrode (PEMS) modulates spinal nociceptive pathways. However, the effects of this intervention on cortical oscillatory activity have not been assessed yet. The aim of this study was to investigate the effects of low-frequency PEMS (4 Hz) on cortical oscillatory activity in different brain states in healthy pain-free participants. In experiment 1, PEMS was compared to sham stimulation. In experiment 2, motor imagery (MI) was used to modulate the sensorimotor brain state. PEMS was applied either during MI-induced oscillatory desynchronization (concurrent PEMS) or after MI (delayed PEMS) in a cross-over design. For both experiments, PEMS was applied on the left forearm and resting-state electroencephalography (EEG) was recording before and after each stimulation condition. Experiment 1 showed a significant decrease of global resting-state beta power after PEMS compared to sham (p = 0.016), with a median change from baseline of −16% for PEMS and −0.54% for sham. A cluster-based permutation test showed a significant difference in resting-state beta power comparing pre- and post-PEMS (p = 0.018) that was most pronounced over bilateral central and left frontal sensors. Experiment 2 did not identify a significant difference in the change from baseline of global EEG power for concurrent PEMS compared to delayed PEMS. Two cluster-based permutation tests suggested that frontal beta power may be increased following both concurrent and delayed PEMS. This study provides novel evidence for supraspinal effects of low-frequency PEMS and an initial indication that the presence of a cognitive task such as MI may influence the effects of PEMS on beta activity. Chronic pain has been associated with changes in beta activity, in particular an increase of beta power in frontal regions. Thus, brain state-dependent PEMS may offer a novel approach to the treatment of chronic pain. However, further studies are warranted to investigate optimal stimulation conditions to achieve a reduction of pain.
Structural and Functional Features of the P2X4 Receptor: An Immunological Perspective

Extracellular nucleotides are important mediators of activation, triggering various responses through plasma membrane P2 and P1 receptors. P2 receptors are further subdivided into ionotropic P2X receptors and G protein-coupled P2Y receptors. P2X4 is an ATP-gated cation channel broadly expressed in most tissues of the body. Within the P2X family, P2X4 has a unique subcellular distribution, being preferentially localized in lysosomes. In these organelles, high ATP concentrations do not trigger P2X4 because of the low pH. However, when the pH increases to 7.4, P2X4 can be stimulated by intra-lysosomal ATP, which is in its active, tetra-anionic form. Elucidation of P2X4, P2X3 and P2X7 structures has shed some light on the functional differences between these purinergic receptors. The potential interaction between P2X4 and P2X7 has been extensively studied. Despite intensive effort, it has not been possible yet to determine whether P2X4 and P2X7 interact as heterotrimers or homotrimers at the plasma membrane. However, several publications have shown that functional interactions between P2X4 and P2X7 do occur. Importantly, these studies indicate that P2X4 potentiates P2X7-dependent activation of inflammasomes, leading to increased release of IL-1β and IL-18. The role of P2X4 in various diseases could be beneficial or deleterious even though the pathophysiological mechanisms involved are still poorly defined. However, in diseases whose physiopathology involves activation of the NLRP3 inflammasome, P2X4 was found to exacerbate severity of disease. The recent production of monoclonal antibodies specific for the human and mouse P2X4, some of which are endowed with agonist or antagonist properties, raises the possibility that they could be used therapeutically. Analysis of single nucleotide polymorphisms of the human P2RX4 gene has uncovered the association of P2RX4 gene variants with susceptibility to several human diseases.
Cholesterol, Atherosclerosis, and APOE in Vascular Contributions to Cognitive Impairment and Dementia (VCID): Potential Mechanisms and Therapy

Vascular contributions to cognitive impairment and dementia (VCID) are a common cause of cognitive decline, yet limited therapies exist. This cerebrovascular disease results in neurodegeneration via acute, chronic, local, and systemic mechanisms. The etiology of VCID is complex, with a significant impact from atherosclerosis. Risk factors including hypercholesterolemia and hypertension promote intracranial atherosclerotic disease and carotid artery stenosis (CAS), which disrupt cerebral blood flow and trigger ischemic strokes and VCID. Apolipoprotein E (APOE) is a cholesterol and phospholipid carrier present in plasma and various tissues. APOE is implicated in dyslipidemia and Alzheimer disease (AD); however, its connection with VCID is less understood. Few experimental models for VCID exist, so much of the present information has been drawn from clinical studies. Here, we review the literature with a focus on the clinical aspects of atherosclerotic cerebrovascular disease and build a working model for the pathogenesis of VCID. We describe potential intermediate steps in this model, linking cholesterol, atherosclerosis, and APOE with VCID. APOE4 is a minor isoform of APOE that promotes lipid dyshomeostasis in astrocytes and microglia, leading to chronic neuroinflammation. APOE4 disturbs lipid homeostasis in macrophages and smooth muscle cells, thus exacerbating systemic inflammation and promoting atherosclerotic plaque formation. Additionally, APOE4 may contribute to stromal activation of endothelial cells and pericytes that disturb the blood-brain barrier (BBB). These and other risk factors together lead to chronic inflammation, atherosclerosis, VCID, and neurodegeneration. Finally, we discuss potential cholesterol metabolism based approaches for future VCID treatment.