Owing to the mixed electron/hole and ion transport in the aqueous environment, poly(3,4-ethylenedioxythiophene):poly(styrenesulfonate)-based organic electrochemical transistor has been regarded as one of the most promising device platforms for bioelectronics. Nonetheless, there exist very few in-depth studies on how intrinsic channel material properties affect their performance and long-term stability in aqueous environments. Herein, we investigated the correlation among film microstructural crystallinity/composition, device performance, and aqueous stability in poly(3,4-ethylenedioxythiophene):poly(styrenesulfonate) films. The highly organized anisotropic ordering in crystallized conducting polymer films led to remarkable device characteristics such as large transconductance (∼20 mS), extraordinary volumetric capacitance (113 F·cm−3), and unprecedentedly high [μC*] value (∼490 F·cm−1V−1s−1). Simultaneously, minimized poly(styrenesulfonate) residues in the crystallized film substantially afforded marginal film swelling and robust operational stability even after >20-day water immersion, >2000-time repeated on-off switching, or high-temperature/pressure sterilization. We expect that the present study will contribute to the development of long-term stable implantable bioelectronics for neural recording/stimulation.

Surface-architecture-controlled ZnO nanowires were grown using a vapor transport method on various ZnO buffer film coated c-plane sapphire substrates with or without Au catalysts. The ZnO nanowires that were grown showed two different types of geometric properties: corrugated ZnO nanowires having a relatively smaller diameter and a strong deep-level emission photoluminescence (PL) peak and smooth ZnO nanowires having a relatively larger diameter and a weak deep-level emission PL peak. The surface morphology and size-dependent tunable electronic transport properties of the ZnO nanowires were characterized using a nanowire field effect transistor (FET) device structure. The FETs made from smooth ZnO nanowires with a larger diameter exhibited negative threshold voltages, indicating n-channel depletion-mode behavior, whereas those made from corrugated ZnO nanowires with a smaller diameter had positive threshold voltages, indicating n-channel enhancement-mode behavior.

Despite the great potential of polymer microfibers in human-friendly wearable electronics, most previous polymeric electronics have been limited to thin-film-based devices due to practical difficulties in fabricating microfibrillar devices, as well as defining the active channel dimensions in a reproducible manner. Herein, we report on conducting polymer microfiber-based organic electrochemical transistors (OECTs) and their application in single-strand fiber-type wearable ion concentration sensors. We developed a simple wet-spinning process to form very conductive poly(3,4ethylenedioxythiophene):poly(styrene sulfonate) (PEDOT:PSS) microfibers using aqueous sulfuric acid solutions and carefully examined their electrical/electrochemical properties. In conjunction with fabricating substrate-free PEDOT:PSS microfiber-based OECT devices, the proposed novel characterization method demonstrated that the current variation ratio can be a reliable method for evaluating the device performance for sensing ion concentrations, regardless of the actual channel dimensions. Finally, we developed single-strand fiber-type skin-mountable OECTs by introducing a source-gate hybrid electrode and demonstrated that the resultant microfiber sensors can perform real-time repetitive measurements of the ion concentration in human sweat.

Monohydroxyethyl terephthalate (MHET) hydrolase (MHE-Tase) is an enzyme known to be involved in the final degradation step of poly(ethylene terephthalate) (PET) by hydrolyzing MHET into terephthalic acid and ethylene glycol in Ideonella sakaiensis. Here, we report the extracellular production of MHETase in an active form with a proper folding. Based on the structural observations and biochemical experiments, we reveal that MHETase also functions as exo-PETase by hydrolyzing the synthesized PET pentamer. We further present that MHETase has a hydrolysis activity against the termini-generated PET film, demonstrating the exo-PETase function of the enzyme. We also develop a MHETase R411K/S416A/F424I variant with a higher BHET activity, and the variant exhibits an enhanced degradation activity against the PET film. Based on these results, we propose that MHETase plays several roles in the biodegradation of PET using the BHETase and exo-PETase activities as well as the MHET hydrolysis function.

Although several crystalline materials have been developed as Li-ion conductors for use as solid electrolytes in all-solid-state batteries (ASSBs), producing materials with high Li-ion conductivities is timeconsuming and cost-intensive. Herein, we introduce a superionic halogen-rich Li-argyrodite (HRLA) and demonstrate its innovative synthesis using ultimate-energy mechanical alloying (UMA) and rapid thermal annealing (RTA). UMA with a 49 G-force milling energy provides a one-pot process that includes mixing, glassification, and crystallization, to produce as-milled HRLA powder that is ∼70% crystallized; subsequent RTA using an infrared lamp increases this crystallinity to ∼82% within 25 min. Surprisingly, this HRLA exhibits the highest Li-ion conductivity among Li-argyrodites (10.2 mS cm −1 at 25 °C, cold-pressed powder compact) reported so far. Furthermore, we confirm that this superionic HRLA works well as a promising solid electrolyte without a decreased intrinsic electrochemical window in various electrode configurations and delivers impressive cell performance (114.2 mAh g −1 at 0.5 C).

Adult thyroid dysfunction is a common endocrine disorder associated with an increased risk of cardiovascular disease and mortality. A recent epidemiologic study revealed a link between obesity and increased prevalence of hypothyroidism. It is conceivable that excessive adiposity in obesity might lead to expansion of the interfollicular adipose (IFA) depot or steatosis in thyroid follicular cells (thyroid steatosis, TS). In this study, we investigated the morphological and functional changes in thyroid glands of obese humans and animal models, diet-induced obese (DIO), ob/ob, and db/db mice. Expanded IFA depot and TS were observed in obese patients. Furthermore, DIO mice showed increased expression of lipogenesis-regulation genes, such as sterol regulatory element binding protein 1 (SREBP-1), peroxisome proliferator-activated receptor γ (PPARγ), acetyl coenzyme A carboxylase (ACC), and fatty acid synthetase (FASN) in the thyroid gland. Steatosis and ultrastructural changes, including distension of the endoplasmic reticulum (ER) and mitochondrial distortion in thyroid follicular cells, were uniformly observed in DIO mice and genetically obese mouse models, ob/ob and db/db mice. Obese mice displayed a variable degree of primary thyroid hypofunction, which was not corrected by PPARγ agonist administration. We propose that systemically increased adiposity is associated with characteristic IFA depots and TS and may cause or influence the development of primary thyroid failure.

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Activated macrophages have a greater ability of phagocytosis against pathogens that is mediated by large-scale actin rearrangement. However, molecular machineries that conduct this task have not been fully identified. Here, we demonstrate an unanticipated role of TAGLN2, a 22-kDa actin-binding protein, in Toll-like receptor (TLR)-stimulated phagocytosis. TAGLN2 was greatly induced in macrophages in response to lipopolysaccharide (LPS), a ligand for TLR4, partly via the NF-κB pathway. TAGLN2-deficient macrophages (TAGLN2 −/−) showed defective phagocytic functions of IgM- and IgG-coated sheep red blood cells as well as bacteria. Cell signaling pathways involved in actin rearrangement—PI3 kinase/AKT and Ras-ERK—were also down-regulated in LPS-stimulated TAGLN2-deficient macrophages. Moreover, TAGLN2 −/− mice showed higher mortality after bacterial infection than wild-type littermates. Thus, our results revealed a novel function of TAGLN2 as a molecular armament required for host defense.