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This document is an editorial for a special issue of the journal Micromachines on the topic of exploring IoT sensors and their applications in smart environments. The editor highlights the importance of IoT sensors in various fields and discusses the advancements and challenges in this area. The editorial introduces ten research contributions that cover a range of applications and technologies, including wearable health monitoring systems, gesture recognition devices, low-light pedestrian detection systems, and gas sensors. The editor emphasizes the need for interdisciplinary collaboration, scalability of sensors, and data security in future research. Overall, this special issue provides valuable insights into the current state of IoT sensors and sets the stage for future innovations in this field. [Extracted from the article]

Dysregulation of Toll-like receptor (TLR) signaling contributes to the pathogenesis of autoimmune diseases. Here, we provide genetic evidence that tankyrase, a member of the poly(ADP-ribose) polymerase (PARP) family, negatively regulates TLR2 signaling. We show that mice lacking tankyrase in myeloid cells developed severe systemic inflammation with high serum inflammatory cytokine levels. We provide mechanistic evidence that tankyrase deficiency resulted in tyrosine phosphorylation and activation of TLR2 and show that phosphorylation of tyrosine 647 within the TIR domain by SRC and SYK kinases was critical for TLR2 stabilization and signaling. Last, we show that the elevated cytokine production and inflammation observed in mice lacking tankyrase in myeloid cells were dependent on the adaptor protein 3BP2, which is required for SRC and SYK activation. These data demonstrate that tankyrase provides a checkpoint on the TLR-mediated innate immune response., Introduction The Toll-like receptors (TLRs) recognize pathogen-associated molecular patterns (PAMPs) derived from microbes to drive the innate immune response (1-3). TLR activation induces NF-[kappa]B, a master transcription factor that controls [...]

Cleidocranial dysplasia (CCD) is an autosomal dominant human disorder characterized by abnormal bone development that is mainly due to defective intramembranous bone formation by osteoblasts. Here, we describe a mouse strain lackingthe E3 ubiquitin ligase RNF146 that shows phenotypic similarities to CCD. Loss of RNF146 stabilized its substrate AXIN1, leading to impairment of WNT3a-induced [beta]-catenin activation and reduced Fgf18 expression in osteoblasts. We showthat FGF18 induces transcriptional coactivator with PDZ-binding motif (TAZ) expression, which is required for osteoblast proliferation and differentiation through transcriptional enhancer associate domain (TEAD) and runt-related transcription factor 2 (RUNX2) transcription factors, respectively. Finally, we demonstrate that adipogenesis is enhanced in [Rnf146.sup.-/-] mouse embryonic fibroblasts. Moreover, mice with loss of RNF146 within the osteoblast lineage had increased fat stores and were glucose intolerant with severe osteopenia because of defective osteoblastogenesis and subsequent impaired osteocalcin production. These findings indicate that RNF146 is required to coordinate [beta]-catenin signaling within the osteoblast lineage during embryonic and postnatal bone development., Introduction Cleidocranial dysplasia (CCD) is an autosomal dominant skeletal disorder characterized by short stature, hypoplasia of facial bones and clavicles, and open fontanelles due to defective bone formation (1,2). Previous [...]

Bone undergoes continuous remodeling due to balanced bone formation and resorption mediated by osteoblasts and osteoclasts, respectively. Osteoclasts arise from the macrophage lineage, and their differentiation is dependent on RANKL, a member of the TNF family of cytokines. Here, we have provided evidence that RANKL controls the expression of 3BP2, an adapter protein that is required for activation of SRC tyrosine kinase and simultaneously coordinates the attenuation of [beta]-Catenin, both of which are required to execute the osteoclast developmental program. We found that RANKL represses the transcription of the E3 ubiquitin ligase RNF146 through an NF-[kappa]B-related inhibitory element in the RNF146 promoter. RANKL-mediated suppression of RNF146 results in the stabilization of its substrates, 3BP2 and AXIN1, which consequently triggers the activation of SRC and attenuates the expression of [beta]-Catenin, respectively. Depletion of RNF146 caused hypersensitivity to LPS-induced TNF-[alpha] production in vivo. RNF146 thus acts as an inhibitory switch to control osteoclastogenesis and cytokine production and may be a control point underlying the pathogenesis of chronic inflammatory diseases., Introduction RANKL, a member of the TNF superfamily of cytokines, is an obligate factor required for osteoclast differentiation and survival, lymph node organogenesis, lymphocyte development, and breast epithelial proliferation (1-6). [...]

Objectives Although personality characteristics of patients with SLE affect their disease activity and damage, it is unclear whether those of attending physicians affect the outcomes of patients with SLE. Grit is a personality trait for achieving long-term goals that may influence the decision-making for continuing treatment plans for patients. We aimed to evaluate the relationship between the grit of attending physicians and achievement of treatment goals in patients with SLE. Methods This cross-sectional study was conducted at five referral hospitals. The main exposure was 'consistency of interest' and 'perseverance of effort' of the attending physicians, measured by the Short Grit Scale. The primary outcome was achievement of a lupus low disease activity state (LLDAS). The association between physicians' grit score and LLDAS was analysed by generalized estimating equation (GEE) logistic regression with cluster robust variance estimation, with adjustment for confounders. Results The median (interquartile range) total, consistency and perseverance scores of 37 physicians were 3.1 (2.9–3.6), 3.3 (2.8–3.8) and 3.3 (3.0–3.5), respectively. Among the 386 patients, 154 (40%) had achieved LLDAS. Low consistency score (≤2.75) in physicians was related to LLDAS achievement independently using GEE logistic regression. The score of the question 'I often set a goal but later choose to pursue a different one' was significantly higher in patients achieving LLDAS. Conclusions Difficulty of attending physicians to change treatment goals might be related to lower LLDAS achievement in patients with SLE. [ABSTRACT FROM AUTHOR]