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As the field of wearable electronics continues to expand, the integration of inorganic thermoelectric (TE) materials into fabrics has emerged as a promising development due to their excellent TE properties. However, conventional thermal methods for fabricating TE fabrics are unsuitable for wearable applications because of their high temperatures, resulting in rigid TE materials. Herein, a nonthermally fabricated silver selenide (Ag2Se) TE fabric is developed that can be effectively integrated into wearable applications. Ag2Se nanoparticles are densely formed within the fabric through a simple in situ chemical reduction process, resulting in remarkable electrical stability even after 10 000 cycles of mechanical deformation, such as stretching and compression. Notably, the fabricated Ag2Se TE fabric exhibits superior stretchability, stretching ≈1.36 times more than the thermally treated Ag2Se TE fabrics, while retaining its excellent electrical conductivity. Moreover, the TE unit exhibits 9.80 μW m−1 K−2 power factor, 134.45 S cm−1 electrical conductivity, and −26.98 μV K−1 Seebeck coefficient at 370 K. A haptic sensing glove based on the Ag2Se TE fabric as a sensor for detecting potential hazards is demonstrated. The glove effectively distinguishes between simple touch, physical pain, and high‐temperature hazards, ensuring user safety and prompt response.

IntroductionIn patients with idiopathic normal pressure hydrocephalus (iNPH), the characteristics of balance disturbance are not as well understood as those related to gait. This study examined changes in postural stability in quiet standing after the cerebrospinal fluid tap test (CSFTT) in these patients. Furthermore, the study explored the relationship between the amount of spontaneous body sway and both gait and executive function.Materials and methodsAll patients diagnosed with iNPH underwent CSFTT. We evaluated their center of pressure (COP) measurements on a force plate during quiet standing, both pre- and post-CSFTT. Following the COP measurements, we calculated COP parameters using time and frequency domain analysis and assessed changes in these parameters after CSFTT. At pre-CSFTT, we assessed the Timed Up and Go (TUG) and the Frontal Assessment Battery (FAB). We investigated the relationship between COP parameters and the TUG and FAB scores at pre-CSFTT.ResultsA total of 72 patients with iNPH were initially enrolled, and 56 patients who responded positively to CSFTT were finally included. Post-CSFTT, significant improvements were observed in COP parameters through time domain analysis. These included the velocity of COP (vCOP), root-mean-square of COP (rmsCOP), turn index, torque, and base of support (BOS), compared to the pre-CSFTT values (p

Background: Keloids are a common fibrotic disease of the skin, with the pathological hallmark of excessive extracellular matrix synthesis due to abnormal fibroblast activity. Since keloids clinically arise in areas of high mechanical tension, the mechanotransductory pathway may be attributed to its pathogenesis. We aimed to establish a preclinical platform to elucidate the underlying mechanism of keloid development and its clinical persistence. Methods: We fabricated a mechanically stretchable polydimethylsiloxane cell culture platform; with its mimicry of the in vivo cyclic stretch of skeletal muscles, cells showed higher proliferation compared with conventional modalities. Results: In response to mechanical strain, TGF-β and type 1 collagen showed significant increases, suggesting possible TGF-β/Smad pathway activation via mechanical stimulation. Protein candidates selected by proteomic analysis were evaluated, indicating that key molecules involved in cell signaling and oxidative stress were significantly altered. Additionally, the cytoskeletal network of keloid fibroblasts showed increased expression of its components after periodic mechanical stimulation. Conclusions: Herein, we demonstrated and validated the existing body of knowledge regarding profibrotic mechanotransduction signaling pathways in keloid fibroblasts. Cyclic stretch, as a driving force, could help to decipher the tension-mediated biomechanical processes, leading to the development of optimized therapeutic targets.

Background: In previous studies, denosumab, a RANKL human monoclonal antibody used in osteoporosis treatment, has shown efficacy in tendon healing after rotator cuff repair. This prospective study investigated the effects of denosumab on tendon healing, re-tear rates, and clinical outcomes post rotator cuff repair in women with osteoporosis. Method: This was a prospective, observational study, employing propensity score matching for the control group. From March 2018 to March 2023, female patients over the age of 60 with normal bone density undergoing arthroscopic rotator cuff repair were selected as controls through propensity score matching (PSM) and compared with female patients of the same age group with osteoporosis who were receiving denosumab treatment. The control group was matched using 1-to-2 propensity score matching. Radiological examinations and functional outcomes were assessed preoperatively and at 6 months postoperatively. Results: In the final analysis, the study comprised 34 patients in the denosumab treatment group (Group 1) and 68 patients in the control group (Group 2). The functional scores showed significant improvement at 6 months post-surgery in both groups. No significant difference in the functional scores was observed among the groups. The re-tear rate, defined according to Sugaya’s classification (types IV and V) as re-tear, was slightly higher in Group 1 at 16.7% (6 of 34) compared to Group 2 at 11.7% (8 of 68), but the difference was not statistically significant (p = 0.469). The re-tear patterns, classified according to Rhee’s classification, also showed no significant difference among the groups (Group 1: 2/4 of 6; Group 2: 4/4 of 8; p = 0.571). The occurrence of type I re-tear exhibited no significant difference between the two groups (5.9% vs. 5.9%; p = 1.000). Conclusions: The administration of denosumab following arthroscopic rotator cuff repair in women aged 60 and over with osteoporosis resulted in a re-tear rate that was similar to that observed in patients without osteoporosis. This result suggests that denosumab administration might be beneficial for rotator cuff healing, particularly in the context of osteoporosis, a known risk factor for increased retear rates. Therefore, comprehensive osteoporosis screening and treatment should be considered in conjunction with rotator cuff repair surgery in middle-aged women.

Posttranslational modifications regulate the properties and abundance of synaptic α- amino- 3- hydroxy- 5- methyl- 4- isoxazolepropionic acid (AMPA) receptors that mediate fast excitatory synaptic transmission and synaptic plasticity in the central nervous system. During long- term depression (LTD), protein tyrosine phosphatases (PTPs) dephosphorylate tyrosine residues in the C- terminal tail of AMPA receptor GluA2 subunit, which is essential for GluA2 endocytosis and group I metabotropic glutamate receptor (mGluR)- dependent LTD. However, as a selective downstream effector of mGluRs, the mGluR- dependent PTP responsible for GluA2 tyrosine dephosphorylation remains elusive at Schaffer collateral (SC)- CA1 synapses. In the present study, we find that mGluR5 stimulation activates Src homology 2 (SH2) domain- containing phosphatase 2 (SHP2) by increasing phospho- Y542 levels in SHP2. Under steady- state conditions, SHP2 plays a protective role in stabilizing phospho- Y869 of GluA2 by directly interacting with GluA2 phosphorylated at Y869, without affecting GluA2 phospho- Y876 levels. Upon mGluR5 stimulation, SHP2 dephosphorylates GluA2 at Y869 and Y876, resulting in GluA2 endocytosis and mGluR- LTD. Our results establish SHP2 as a downstream effector of mGluR5 and indicate a dual action of SHP2 in regulating GluA2 tyrosine phosphorylation and function. Given the implications of mGluR5 and SHP2 in synaptic pathophysiology, we propose SHP2 as a promising therapeutic target for neurodevelopmental and autism spectrum disorders. [ABSTRACT FROM AUTHOR]