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This study aimed to develop wearable robotic gloves that can provide comfort to logistics and transportation workers while providing hand assistance and addressing accumulated muscle fatigue caused by repetitive manual handling tasks. Two types of gloves, rivet-type and pouch-type were developed and evaluated using the nine-hole peg test (NHPT) and grip strength tests. Results showed rivet-type gloves had better dexterity, with an 8.14% faster NHPT time, and maintained 85% grip strength compared to 80% for pouch-type gloves, even after fatigue exercises. Wearability tests were conducted by measuring clothing pressure and brainwaves. In contrast to the functional experimental results, the pouch-type gloves exhibited significant decreases in clothing pressure during actuation. According to the difference in brain waves in the frontal lobe region, the beta and gamma waves observed when wearing pouch-type gloves were lower than those of rivet-type gloves, and pouch-type gloves exhibited higher alpha-wave results than rivet-type gloves. These results imply that participants were in a comparatively relaxed state when wearing pouch-type gloves. A wearer's evaluation survey on the overall design, function, comfort, safety, ease of use, usefulness, and use intention was conducted. In summary, the rivet-type gloves exhibited better results in hand performance while the pouch-type gloves showed advantages in wearability, suggesting a tradeoff relationship between force transmission and wearer comfort. The results of this study aimed to improve the work efficiency at logistics and transportation industry sites and help improve the welfare of workers. [ABSTRACT FROM AUTHOR]

Poly L-lactic acid (PLLA) fillers stimulate collagen synthesis by activating various immune cells and fibroblasts. Piezo1, an ion channel, responds to mechanical stimuli, including changes in extracellular matrix stiffness, by mediating Ca2+ influx. Given that elevated intracellular Ca2+ levels trigger signaling pathways associated with fibroblast proliferation, Piezo1 is a pivotal regulator of collagen synthesis and tissue fibrosis. The aim of the present study was to investigate the impact of PLLA on dermal collagen synthesis by activating Piezo1 in both an H2O2-induced cellular senescence model in vitro and aged animal skin in vivo. PLLA elevated intracellular Ca2+ levels in senescent fibroblasts, which was attenuated by the Piezo1 inhibitor GsMTx4. Furthermore, PLLA treatment increased the expression of phosphorylated ERK1/2 to total ERK1/2 (pERK1/2/ERK1/2) and phosphorylated AKT to total AKT (pAKT/AKT), indicating enhanced pathway activation. This was accompanied by upregulation of cell cycle-regulating proteins (CDK4 and cyclin D1), promoting the proliferation of senescent fibroblasts. Additionally, PLLA promoted the expression of phosphorylated mTOR/S6K1/4EBP1, TGF-β, and Collagen I/III in senescent fibroblasts, with GsMTx4 treatment mitigating these effects. In aged skin, PLLA treatment similarly upregulated the expression of pERK1/2/ERK1/2, pAKT/AKT, CDK4, cyclin D1, mTOR/S6K1/4EBP1, TGF-β, and Collagen I/III. In summary, our findings suggest Piezo1′s involvement in PLLA-induced collagen synthesis, mediated by heightened activation of cell proliferation signaling pathways such as pERK1/2/ERK1/2, pAKT/AKT, and phosphorylated mTOR/S6K1/4EBP1, underscoring the therapeutic potential of PLLA in tissue regeneration. [ABSTRACT FROM AUTHOR]

Solute carrier family 26 member 4 (SLC26A4) is a member of the SLC26A transporter family and is expressed in various tissues, including the airway epithelium, kidney, thyroid, and tumors. It transports various ions, including bicarbonate, chloride, iodine, and oxalate. As a multiple-ion transporter, SLC26A4 is involved in the maintenance of hearing function, renal function, blood pressure, and hormone and pH regulation. In this review, we have summarized the various functions of SLC26A4 in multiple tissues and organs. Moreover, the relationships between SLC26A4 and other channels, such as cystic fibrosis transmembrane conductance regulator, epithelial sodium channel, and sodium chloride cotransporter, are highlighted. Although the modulation of SLC26A4 is critical for recovery from malfunctions of various organs, development of specific inducers or agonists of SLC26A4 remains challenging. This review contributes to providing a better understanding of the role of SLC26A4 and development of therapeutic approaches for the SLC26A4-associated hearing loss and SLC26A4-related dysfunction of various organs. [ABSTRACT FROM AUTHOR]

Ubiquitin-like modifier-activating enzyme 6 (UBA6) is a member of the E1 enzyme family, which initiates the ubiquitin–proteasome system (UPS). The UPS plays critical roles not only in protein degradation but also in various cellular functions, including neuronal signaling, myocardial remodeling, immune cell differentiation, and cancer development. However, the specific role of UBA6 in cellular functions is not fully elucidated in comparison with the roles of the UPS. It has been known that the E1 enzyme is associated with the motility of cancer cells. In this study, we verified the physiological roles of UBA6 in lung cancer cells through gene-silencing siRNA targeting UBA6 (siUBA6). The siUBA6 treatment attenuated the migration of H1975 cells, along with a decrease in lysosomal Ca2+ release. While autophagosomal proteins remained unchanged, lysosomal proteins, including TRPML1 and TPC2, were decreased in siUBA6-transfected cells. Moreover, siUBA6 induced the production of multivesicular bodies (MVBs), accompanied by an increase in MVB markers in siUBA6-transfected H1975 cells. Additionally, the expression of the exosomal marker CD63 and extracellular vesicles was increased by siUBA6 treatment. Our findings suggest that knock-down of UBA6 induces lysosomal TRPML1 depletion and inhibits endosomal trafficking to lysosome, and subsequently, leads to the accumulation of MVBs and enhanced exosomal secretion in lung cancer cells. [ABSTRACT FROM AUTHOR]

Cholesterol trafficking is initiated by the endocytic pathway and transported from endo/lysosomes to other intracellular organelles. Deficiencies in cholesterol-sensing and binding proteins NPC1 and NPC2 induce accumulation in lysosomes and the malfunction of trafficking to other organelles. Each organelle possesses regulatory factors to induce cholesterol trafficking. The mutation of NPC1 and NPC2 genes induces Niemann-Pick disease type C (NPDC), which is a hereditary disease and causes progressive neurodegeneration, developmental disability, hypotonia, and ataxia. Oxidative stress induces damage in NPDC-related intracellular organelles. Although studies on the relationship between NPDC and oxidation are relatively rare, several studies have reported the therapeutic potential of antioxidants in treating NPDC. Investigating antioxidant drugs to relieve oxidative stress and cholesterol accumulation is suggested to be a powerful tool for developing treatments for NPDC. Understanding NPDC provides challenging issues in understanding the oxidative stress–lysosome metabolism of the lipid axis. Thus, we elucidated the relationship between complexes of intracellular organelles and NPDC to develop our knowledge and suggested potential antioxidant reagents for NPDC therapy. [ABSTRACT FROM AUTHOR]

Lysosomes are responsible for protein degradation and clearance in cellular recycling centers. It has been known that the lysosomal chloride level is enriched and involved in the intrinsic lysosomal function. However, the mechanism by which chloride levels can be sensed and that of the chloride-mediated lysosomal function is unknown. In this study, we verified that reduced chloride levels acutely induced lysosomal calcium release through TRPML1 and lysosomal repositioning toward the juxtanuclear region. Functionally, low chloride-induced lysosomal calcium release attenuated cellular migration. In addition, spontaneous exposure to low chloride levels dysregulated lysosomal biogenesis and subsequently induced delayed migration and promoted apoptosis. Two chloride-sensing GXXXP motifs in the TRPML1 were identified. Mutations in the GXXXP motif of TRPML1 did not affect chloride levels, and there were no changes in migratory ability. In this study, we demonstrated that the depletion of chloride induces reformation of the lysosomal calcium pool and subsequently dysregulated cancer progression, which will assist in improving therapeutic strategies for lysosomal accumulation-associated diseases or cancer cell apoptosis. [ABSTRACT FROM AUTHOR]

Dexmedetomidine (Dex) has analgesic and sedative properties and anti-inflammatory functions. Although the effects of Dex on arthritis have been revealed, the physiological mechanism underlying the interaction between Dex and rheumatoid arthritis (RA)-mediated inflammatory cytokines has not been fully studied. Inflamed and migrated fibroblast-like synoviocytes (FLSs) are involved in RA severity. Thus, we aimed to determine the effects of Dex on RA-FLSs treated with inflammatory cytokines and a growth factor as multiple stimulating inputs. TNF-α, IL-6, and EGF as multiple stimulating inputs increased the cAMP concentration of RA-FLSs, while Dex treatment reduced cAMP concentration. Dex reduced electroneutral sodium-bicarbonate cotransporter 1 (NBCn1) expression, NBC activity, and subsequent RA-FLS migration. The mRNA expression levels of RA-related factors, such as inflammatory cytokines and osteoclastogenesis factors, were enhanced by multiple-input treatment. Notably, Dex effectively reduced these expression levels in RA-FLSs. These results indicate that multiple inflammatory or stimulating inputs enhance RA-FLS migration, and treatment with Dex relieves activated RA-FLSs, suggesting that Dex is a potential therapeutic drug for RA. [ABSTRACT FROM AUTHOR]

PyK2 is a member of the proline-rich tyrosine kinase and focal adhesion kinase families and is ubiquitously expressed. PyK2 is mainly activated by stimuli, such as activated Src kinases and intracellular acidic pH. The mechanism of PyK2 activation in cancer cells has been addressed extensively. The up-regulation of PyK2 through overexpression and enhanced phosphorylation is a key feature of tumorigenesis and cancer migration. In this review, we summarized the cancer milieu, including acidification and cancer-associated molecules, such as chemical reagents, interactive proteins, chemokine-related molecules, calcium channels/transporters, and oxidative molecules that affect the fate of PyK2. The inhibition of PyK2 leads to a beneficial strategy to attenuate cancer cell development, including metastasis. Thus, we highlighted the effect of PyK2 on various cancer cell types and the distribution of molecules that affect PyK2 activation. In particular, we underlined the relationship between PyK2 and cancer metastasis and its potential to treat cancer cells. [ABSTRACT FROM AUTHOR]

The ubiquitin–proteasome system (UPS) is the main proteolytic pathway by which damaged target proteins are degraded after ubiquitination and the recruit of ubiquitinated proteins, thus regulating diverse physiological functions and the maintenance in various tissues and cells. Ca2+ signaling is raised by oxidative or ER stress. Although the basic function of the UPS has been extensively elucidated and has been continued to define its mechanism, the precise relationship between the UPS and Ca2+ signaling remains unclear. In the present review, we describe the relationship between the UPS and Ca2+ signaling, including Ca2+-associated proteins, to understand the end point of oxidative stress. The UPS modulates Ca2+ signaling via the degradation of Ca2+-related proteins, including Ca2+ channels and transporters. Conversely, the modulation of UPS is driven by increases in the intracellular Ca2+ concentration. The multifaceted relationship between the UPS and Ca2+ plays critical roles in different tissue systems. Thus, we highlight the potential crosstalk between the UPS and Ca2+ signaling by providing an overview of the UPS in different organ systems and illuminating the relationship between the UPS and autophagy. [ABSTRACT FROM AUTHOR]

The twisted string actuator (TSA) has been extensively studied as an alternative to metallic gear reducers due to its low-cost, lightweight, compliance, and highly adjustable actuation characteristics. Owing to these advantages, TSAs are utilized to realize lightweight human–robot interactive robots requiring safe interaction, such as wearables and prosthetics, at a relatively low cost. However, because its force transmission ratio is almost proportional to the length of the string, the string of the conventional TSA must be elongated to achieve high force output. Thus, it is difficult to obtain high force capacity while maintaining a small size. To overcome this limitation, in this article, we propose a novel TSA based on parallel bundle-driven actuation to significantly reduce the length of the TSA while achieving high force output. Furthermore, in order to boost the proposed TSA performance, we also present a passive mechanism of an asymmetric behavior compensator. The experimental results show that the force transmission ratio of the proposed TSA is increased by 21%, compared with that of the conventional TSA. Consequently, the proposed TSA has a 44% higher torque capacity with a 37% shorter string than those of theconventional TSA. [ABSTRACT FROM AUTHOR]

Twisted string actuation is an actuation concept which uses the twisting motion of strings to convert the rotational motion of a motor into a linear motion. By replacing the heavy, high friction, and high-cost gearheads with light, silent, compliant, and low-cost strings, twisted string actuators (TSAs) can provide powerful tendon-based transmission, making it a unique solution for human–robot interactive tasks. Despite such advantages, TSAs exhibit highly nonlinear force/displacement characteristics when compared to conventional geared motors, thus limiting their performance in bidirectional joints. In order to implement TSAs in a bidirectional joint, two motors had to be used to compensate for the nonlinearities, which eventually increased the control complexity, weight, and overall cost of the robotic system. In addition, TSAs show poor durability, which also limits its applicability. To address these issues, a high-performance bidirectional joint has been proposed by implementing optimized TSAs with lubrication, and a variable radius pulley (VRP). By implementation of specially designed TSAs, we achieved 1) extended service time of the strings. Furthermore, by replacing the conventional circular pulley with a VRP, we achieved 2) improved range of motion; 3) increased payload; and 4) better tracking performance, even with a single motor. [ABSTRACT FROM AUTHOR]

Nanoparticles (NPs) have been studied as therapeutic drug-delivery agents for promising clinical trial outcomes. Nanomaterial-based drugs can transfer conventional drugs to target lesions, such as tumors, with increasing efficiency by enhancing drug-cell interaction or drug absorption. Although they are favorable as efficient drug transfer systems, NPs also exhibit cytotoxicity that affects nonpathological regions. Here, we review the basic information behind NP-induced Ca2+ signaling and its participation in channel physiology and pathology. NPs are observed to demonstrate inhibitory or active effects on Ca2+ signaling. Thus, understanding Ca2+ signaling by NPs as a key mechanism in signal transduction will progress the application of nano-drugs in various diseases without deleterious effect. [ABSTRACT FROM AUTHOR]

Estrogen therapy has used to prevent bone loss in postmenopausal women. Although therapeutically enhanced estrogen levels have been suggested, patients are exposed to greater risks of nephrolithiasis and cancer. It has been known that oxalate or bicarbonate transporter SLC26A6 is involved in oxalate homeostasis and its deletion results in kidney stone formation and addressed that patients with kidney stones possess higher cancer risk. Thus, the mechanism of the interaction between estrogen and SLC26A6 and the effect of SLC26A6 on cancer cells should be elucidated. In this study, we investigated whether β-estradiol treatment modulates SLC26A6 expression and its bicarbonate or oxalate transporting activity and affects the proliferative and migratory ability of A549 cells. The β-estradiol stimulation attenuated oxalate or bicarbonate transporting activities through SLC26A6. Knockdown of SLC26A6 reduced transporter activity whereas enhanced cellular migration. β-estradiol-mediated cellular migration was independent of SLC26A6 transporter activity, whereas enhanced SLC26A6 expression attenuated cellular migration even in the presence of β-estradiol treatment. These results indicate β-estradiol treatment enhances cancer cell migration and dysregulates oxalate transport by inhibiting SLC26A6 activity, suggesting reduced oxalate transporting activity may involve in the oxalate homeostasis. • The treatment of β-estradiol attenuates oxalate transporting activity. • SLC26A6 expression involves in the inhibition of cellular migration. • The negative effect of estrogen on activity of chloride oxalate exchanger SLC26A6 in lung cancer cells reflects modulation of estrogen on oxalate homeostasis of lung cancer cell. [ABSTRACT FROM AUTHOR]

In Table I, the dXmax was writtenas \begin{equation*} d{X_{\text{max}}} = \ {C_{dx}}\ \cdot L. \end{equation*} [ABSTRACT FROM AUTHOR]

With the ongoing research on soft robots, the performance of soft actuators needs to be enhanced for more wide robotic applications. Currently, most soft robots based on pneumatic actuation are capable of assisting small systems, but they are not fully suited for supporting joints requiring large force and range of motion. This is due to the actuation characteristics of the pneumatic artificial muscle (PAM); they are relatively slow, inefficient, and experience a significant force reduction when the PAM contracts. Hence, we propose a novel PAM based on a spring-frame collateral compression mechanism. With only a single compressed air source, the external mesh-covered and inner spring-frame actuators of the proposed PAM operate simultaneously to generate considerable force. Additionally, the design of the internal actuator within the void space of PAM reduces the air consumption and consequently improves the actuator's operating speed and efficiency. We experimentally confirmed that the proposed PAM exhibited 31.2% greater force, was 25.6% faster, and consumed 21.5% lower air compared to the conventional McKibben muscles. The performance enhancement of the proposed PAM improves the performance of soft robots, allowing the development of more compact robots with greater assistive range. [ABSTRACT FROM AUTHOR]

Simple Summary: Intracellular Ca2+ signaling is a critical factor in breast cancer metastasis. In the proliferation stage, increases in intracellular Ca2+ concentration through voltage-dependent Ca2+ channels, P2Y2 channels, transient receptor potential (TRP) channels, store-operated Ca2+ channels (SOCCs), and IP3 receptors and a decrease in intracellular Ca2+ concentration through plasma membrane Ca2+ ATPases and secretory pathway Ca2+ ATPases (SPCA) activate breast cancer cell proliferation. TRPM7, SOCC, inositol trisphosphate receptor (IP3R), ryanodine receptor (RyR), and sarco-/endo-plasmic reticulum Ca2+-ATPase (SERCA) increase the expression of epithelial-to-mesenchymal transition (EMT)-related proteins; meanwhile, SPCA and the Na+/Ca2+ exchanger (NCX) control the activation of EMT-related proteins. Increased Ca2+ through TRPC1, TRPM7/8, P2X7, and SOCC enhances breast cancer cell migration. The stromal interaction molecule (STIM)-Orai complex, P2X7, and Ca2+ sensing receptors are involved in invadopodia. Various pharmacological agents for Ca2+ channels have been proposed against breast cancer and have provided potential strategies for treating metastatic processes. Metastatic features of breast cancer in the brain are considered a common pathology in female patients with late-stage breast cancer. Ca2+ signaling and the overexpression pattern of Ca2+ channels have been regarded as oncogenic markers of breast cancer. In other words, breast tumor development can be mediated by inhibiting Ca2+ channels. Although the therapeutic potential of inhibiting Ca2+ channels against breast cancer has been demonstrated, the relationship between breast cancer metastasis and Ca2+ channels is not yet understood. Thus, we focused on the metastatic features of breast cancer and summarized the basic mechanisms of Ca2+-related proteins and channels during the stages of metastatic breast cancer by evaluating Ca2+ signaling. In particular, we highlighted the metastasis of breast tumors to the brain. Thus, modulating Ca2+ channels with Ca2+ channel inhibitors and combined applications will advance treatment strategies for breast cancer metastasis to the brain. [ABSTRACT FROM AUTHOR]

As robots are becoming more accessible in our daily lives, the interest in physical human–robot interaction (HRI) is rapidly increasing. An electric bicycle (E-bike) is one of the best examples of HRI, because a rider simultaneously actuates the rear wheel of the E-bike in close proximity. Most commercially available E-bikes employ a control methodology known as a power assistant system (PAS). However, this type of system cannot offer fully efficient power assistance for E-bikes since it does not account for the biomechanics of riders. In order to address this issue, we propose a control algorithm to increase the efficiency and enhance the riding experience of E-bikes by implementing the control parameters acquired from analyses of human leg kinematics and muscular dynamics. To validate the proposed algorithm, we have evaluated and compared the performance of E-bikes in three different conditions: (1) without power assistance, (2) assistance with a PAS algorithm, and (3) assistance with the proposed algorithm. Our algorithm required 5.09% less human energy consumption than the PAS algorithm and 11.01% less energy consumption than a bicycle operated without power assistance. Our algorithm also increased velocity stability by 11.89% and acceleration stability by 27.28%, and decreased jerk by 12.36% in comparison to the PAS algorithm. [ABSTRACT FROM AUTHOR]

Applications of nanoparticles in various fields have been addressed. Nanomaterials serve as carriers for transporting conventional drugs or proteins through lysosomes to various cellular targets. The basic function of lysosomes is to trigger degradation of proteins and lipids. Understanding of lysosomal functions is essential for enhancing the efficacy of nanoparticles-mediated therapy and reducing the malfunctions of cellular metabolism. The lysosomal function is modulated by the movement of ions through various ion channels. Thus, in this review, we have focused on the recruited ion channels for lysosomal function, to understand the lysosomal modulation through the nanoparticles and its applications. In the future, lysosomal channels-based targets will expand the therapeutic application of nanoparticles-associated drugs. [ABSTRACT FROM AUTHOR]

The bicarbonate ion has a fundamental role in vital systems. Impaired bicarbonate transport leads to various diseases, including immune disorders, cystic fibrosis, tumorigenesis, kidney diseases, brain dysfunction, tooth fracture, ischemic reperfusion injury, hypertension, impaired reproductive system, and systemic acidosis. Carbonic anhydrases are involved in the mechanism of bicarbonate movement and consist of complex of bicarbonate transport systems including bicarbonate transporters. This review focused on the convergent regulation of ion homeostasis through various ion transporters including bicarbonate transporters, their regulatory enzymes, such as carbonic anhydrases, pH regulatory role, and the expression pattern of ion transporters in non-secretory systems throughout the body. Understanding the correlation between these systems will be helpful in order to obtain new insights and design potential therapeutic strategies for the treatment of pH-related disorders. In this review, we have discussed the broad prospects and challenges that remain in elucidation of bicarbonate-transport-related biological and developmental systems. [ABSTRACT FROM AUTHOR]

Highlights: [•] Carbon coated TiO2-Li4Ti5O12 hierarchical spheres are fabricated by a simplistic hydrothermal procedures. [•] TiO2-Li4Ti5O12@C spheres were investigated as anode materials for Li-ion batteries. [•] These unique mosoporous composite spheres demonstrated improvements to the anode capacity and cycle life while providing inherent advantages in terms of safety. [ABSTRACT FROM AUTHOR]