Efficacy of Laurus nobilis L. for Tight Junction Protein Imbalance in Leaky Gut Syndrome.

Laurus nobilis L. (LNL) belongs to the evergreen Lauraceae family. It is native to the Mediterranean and widely distributed in the southern United States, Europe, and the Middle East. LNL is rich in active ingredients of the sesquiterpene lactone series and has been reported to have antioxidant, anti-inflammatory, and anticancer effects. And parthenolide, known as a sesquiterpene lactone-based compound, inhibits the activation of lipopolysaccharide-binding protein (LBP), which is a major trigger for leaky gut syndrome. However, the effectiveness of LNL in improving the state of increased intestinal permeability has not yet been reported. Therefore, we demonstrated the efficacy of LNL, which is known to be rich in parthenolide, in improving intestinal permeability induced by IL-13. We investigated the improvement in permeability and analyzed major tight junction proteins (TJs), permeability-related mechanisms, weight and disease activity indices, and corresponding cytokine mechanisms. LNL maintained TJs homeostasis and clinical improvement by reducing increased claudin-2 through the inhibition of IL-13/STAT6 activation in TJ-damaged conditions. These results are expected to be effective in preventing leaky gut syndrome through the TJ balance and to further improve intestinal-related diseases, such as inflammatory bowel disease.

Depletion of proteasome subunit PSMD1 induces cancer cell death via protein ubiquitination and DNA damage, irrespective of p53 status.

Hepatocellular carcinoma (HCC) is characterized by high incidence and fatality rates worldwide. In our exploration of prognostic factors in HCC, the 26s proteasome subunit, non-ATPase 1 (PSMD1) protein emerged as a significant contributor, demonstrating its potential as a therapeutic target in this aggressive cancer. PSMD1 is a subunit of the 19S regulatory particle in the 26S proteasome complex; the 19S particle controls the deubiquitination of ubiquitinated proteins, which are then degraded by the proteolytic activity of the complex. Proteasome-targeting in cancer therapy has received significant attention because of its practical application as an established anticancer agent. We investigated whether PSMD1 plays a critical role in cancer owing to its prognostic significance. PSMD1 depletion induced cell cycle arrest in G2/M phase, DNA damage and apoptosis of cancer cells, irrespective of the p53 status. PSMD1 depletion-mediated cell death was accompanied by an increase in overall protein ubiquitination. These phenotypes occurred exclusively in cancer cells, with no effects observed in normal cells. These findings indicate that PSMD1 depletion-mediated ubiquitination of cellular proteins induces cell cycle arrest and eventual death in cancer cells, emphasizing PSMD1 as a potential therapeutic target in HCC.

A Cell-Penetrant Peptide Disrupting the Transcription Factor CP2c Complexes Induces Cancer-Specific Synthetic Lethality.

Despite advances in precision oncology, cancer remains a global public health issue. In this report, proof-of-principle evidence is presented that a cell-penetrable peptide (ACP52C) dissociates transcription factor CP2c complexes and induces apoptosis in most CP2c oncogene-addicted cancer cells through transcription activity-independent mechanisms. CP2cs dissociated from complexes directly interact with and degrade YY1, leading to apoptosis via the MDM2-p53 pathway. The liberated CP2cs also inhibit TDP2, causing intrinsic genome-wide DNA strand breaks and subsequent catastrophic DNA damage responses. These two mechanisms are independent of cancer driver mutations but are hindered by high MDM2 p60 expression. However, resistance to ACP52C mediated by MDM2 p60 can be sensitized by CASP2 inhibition. Additionally, derivatives of ACP52C conjugated with fatty acid alone or with a CASP2 inhibiting peptide show improved pharmacokinetics and reduced cancer burden, even in ACP52C-resistant cancers. This study enhances the understanding of ACP52C-induced cancer-specific apoptosis induction and supports the use of ACP52C in anticancer drug development.

Indium-Gallium-Zinc Oxide-Based Synaptic Charge Trap Flash for Spiking Neural Network-Restricted Boltzmann Machine.

Recently, neuromorphic computing has been proposed to overcome the drawbacks of the current von Neumann computing architecture. Especially, spiking neural network (SNN) has received significant attention due to its ability to mimic the spike-driven behavior of biological neurons and synapses, potentially leading to low-power consumption and other advantages. In this work, we designed the indium-gallium-zinc oxide (IGZO) channel charge-trap flash (CTF) synaptic device based on a HfO2/Al2O3/Si3N4/Al2O3 layer. Our IGZO-based CTF device exhibits synaptic functions with 128 levels of synaptic weight states and spike-timing-dependent plasticity. The SNN-restricted Boltzmann machine was used to simulate the fabricated CTF device to evaluate the efficiency for the SNN system, achieving the high pattern-recognition accuracy of 83.9%. We believe that our results show the suitability of the fabricated IGZO CTF device as a synaptic device for neuromorphic computing.

Device-Algorithm Co-Optimization for an On-Chip Trainable Capacitor-Based Synaptic Device with IGZO TFT and Retention-Centric Tiki-Taka Algorithm.

Analog in-memory computing synaptic devices are widely studied for efficient implementation of deep learning. However, synaptic devices based on resistive memory have difficulties implementing on-chip training due to the lack of means to control the amount of resistance change and large device variations. To overcome these shortcomings, silicon complementary metal-oxide semiconductor (Si-CMOS) and capacitor-based charge storage synapses are proposed, but it is difficult to obtain sufficient retention time due to Si-CMOS leakage currents, resulting in a deterioration of training accuracy. Here, a novel 6T1C synaptic device using only n-type indium gaIlium zinc oxide thin film transistor (IGZO TFT) with low leakage current and a capacitor is proposed, allowing not only linear and symmetric weight update but also sufficient retention time and parallel on-chip training operations. In addition, an efficient and realistic training algorithm to compensate for any remaining device non-idealities such as drifting references and long-term retention loss is proposed, demonstrating the importance of device-algorithm co-optimization.

Unripe Rubus occidentalis, Ellagic Acid, and Urolithin A Attenuate Inflammatory Responses in IL-1ß-Stimulated A549 Cells and PMA-Stimulated Differentiated HL-60 Cells.

Unripe Rubus occidentalis (uRO) contains various natural polyphenols with beneficial physiological activities and is particularly rich in ellagic acid (EA). EA has ameliorated type 2 inflammation and airway hyperresponsiveness in animal models of eosinophilic asthma. EA is metabolized by the gut microbiota to urolithin A (UA), which exhibits anti-inflammatory properties. However, it remains unclear whether uRO, EA, and UA reduce inflammatory responses and oxidative stress in respiratory epithelial cells and neutrophils. In this study, inflammation was induced in A549 (human lung epithelial cells) and dHL-60 cells (neutrophil-like cells differentiated from human promyelocytic leukemia HL-60 cells) and treated with various concentrations of water extract of uRO (uRO-w), EA, and UA. EA, uRO-w and UA suppressed the inflammatory cytokine and chemokine levels and reduced the expression of matrix metalloproteinase-9 in A549 cells stimulated with IL-1ß. As a result of analyzing the mechanism by which these inflammatory molecules are expressed, it was found that EA, uRO-w, and UA regulated corticosteroid-sensitive mitogen activated protein kinase, nuclear factor κB, and corticosteroid-insensitive AKT. In addition, uRO-w, EA, and UA significantly reduced reactive oxygen species levels in phorbol 12-myristate 13-acetate-stimulated dHL-60 cells and inhibited neutrophil extracellular trap formation. Therefore, our results suggest that uRO-w, EA, and UA are potential therapeutic agents for preventing and treating inflammatory respiratory diseases.

A Comparative Analysis of Pain Control Methods after Ankle Fracture Surgery with a Peripheral Nerve Block: A Single-Center Randomized Controlled Prospective Study.

Background and Objectives: Patients experience severe pain after surgical correction of ankle fractures. Although their exact mechanism is unknown, dexamethasone and epinephrine increase the analgesic effect of anesthetics in peripheral nerve blocks. This study aimed to compare the postoperative pain control efficacy of peripheral nerve blocks with ropivacaine combined with dexamethasone/epinephrine and peripheral nerve blocks with only ropivacaine and added patient-controlled analgesia in patients with ankle fractures. Materials and Methods: This randomized, controlled prospective study included patients aged 18-70 years surgically treated for ankle fractures between December 2021 and September 2022. The patients were divided into group A (n = 30), wherein pain was controlled using patient-controlled analgesia after lower extremity peripheral nerve block, and group B (n = 30), wherein dexamethasone/epinephrine was combined with the anesthetic solution during peripheral nerve block. In both groups, ropivacaine was used as the anesthetic solution for peripheral nerve block, and this peripheral nerve block was performed just before ankle surgery for the purpose of anesthesia for surgery. Pain (visual analog scale), patient satisfaction, and side effects were assessed and compared between the two groups. Results: The patients' demographic data were similar between groups. Pain scores were significantly lower in group B than in group A postoperatively. Satisfaction scores were significantly higher in group B (p = 0.003). There were no anesthesia-related complications in either group. Conclusions: Dexamethasone and epinephrine as adjuvant anesthetic solutions can effectively control pain when performing surgery using peripheral nerve blocks for patients with ankle fractures.

Feasibility of 3D-Printed Locking Compression Plates with Polyether Ether Ketone (PEEK) in Tibial Comminuted Diaphyseal Fractures.

The applicability of a polyether ether ketone locking compression plate (PEEK LCP) fabricated using FDM (fused deposition modeling)-based 3D printing to treat actual patients was studied. Three different tests-bending, axial compression, and axial torsion-were conducted on tibial non-osteoporotic comminuted diaphyseal fracture samples fixed with the commercial titanium alloy LCP and 3D-printed PEEK LCP. Comparing the outcomes of these tests revealed that the commercial titanium alloy LCP underwent plastic deformation in the bending and axial torsion tests, though the LCP did not fail even when an external force greater than the maximum allowable load of the tibia fixture of the LCP was applied. Elastic deformation occurred in the 3D-printed PEEK LCP in the bending and axial torsion tests. However, deformation occurred even under a small external force, and its stiffness was 10% compared to commercial titanium alloy LCP. Thus, 3D-printed PEEK LCP can be applied to the fracture conditions in non-weight-bearing regions. The experimental results reveal detailed insights into the treatment of actual patients by considering the stiffness and high toughness of 3D-printed PEEK LCP.

Difference in Joint Stability Between Small Posterior Malleolar Fragments With Fixation and Those Without Fixation: A Biomechanical Cadaver Study.

The indication for the surgical treatment of ankle fractures that involve a posterior malleolar fragment remains controversial. This cadaver study assessed the biomechanical results of rotation stiffness of Haraguchi type 1 posterior malleolar fragments with or without cannulated screw fixation. Twelve anatomic lower-extremity specimens from 6 cadavers were tested. Six right legs were subjected to posterior malleolus osteotomy (Haraguchi type I) followed with (group A; n = 3) or without (group B; n = 3) fixation using a cannulated screw. Ankle joint stability was measured under both external rotation force and axial loading, and the passive resistive torque was measured in both groups. The mean torque value in group A was 0.1093 Nm/º, while that in group B was 0.0537 Nm/º. There was a significant intergroup difference (p = .004). In group B, the torque value was further increased in the latter rotation period (about 40-60 degrees). Group A proved more stable under experimental conditions than group B. Fixation in type I posterior malleolar fragments produced improved stability in ankle rotation, even for posterior malleolar fragments involving <25% of the articular surface, and has been considered an effective aid in treatment.

Anti-fibrotic effect of aurocyanide, the active metabolite of auranofin.

Drug repositioning has gained significant attention over the past several years. The anti-rheumatoid arthritis drug auranofin has been investigated for the treatment of other diseases, including liver fibrosis. Because auranofin is rapidly metabolized, it is necessary to identify the active metabolites of auranofin that have detectable levels in the blood and reflect its therapeutic effects. In the present study, we investigated whether aurocyanide as an active metabolite of auranofin, can be used to evaluate the anti-fibrotic effects of auranofin. Incubation of auranofin with liver microsomes showed that auranofin was susceptible to hepatic metabolism. Previously, we found that the anti-fibrotic effects of auranofin are mediated via system xc--dependent inhibition of the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome. Therefore, we tried to identify active metabolites of auranofin based on their inhibitory effects on system xc- and NLRP3 inflammasome in bone marrow-derived macrophages. Among the seven candidate metabolites, 1-thio-ß-D-glycopyrano-sato-S-(triethyl-phosphine)-gold(I) and aurocyanide potently inhibited system xc- and NLRP3 inflammasome. A pharmacokinetics study on mice detected significant plasma levels of aurocyanide after auranofin administration. Oral administration of aurocyanide significantly prevented thioacetamide-induced liver fibrosis in mice. Moreover, the in vitro anti-fibrotic effects of aurocyanide were assessed in LX-2 cells, where aurocyanide significantly decreased the migratory ability of the cells. In conclusion, aurocyanide is metabolically stable and detectable in plasma, and has inhibitory effects on liver fibrosis, suggesting that it is a potential marker of the therapeutic effects of auranofin.

Alteration of Gut Microbes in Benign Prostatic Hyperplasia Model and Finasteride Treatment Model.

Gut microbes are closely associated with disease onset and improvement. However, the effects of gut microbes on the occurrence, prevention, and treatment of benign prostatic hyperplasia (BPH) are still unclear. We investigated the alteration of gut microbiota with implications for the diagnosis, prevention, and treatment of BPH and identified correlations among various indicators, including hormone indicators, apoptosis markers in BPH, and finasteride treatment models. BPH induction altered the abundance of Lactobacillus, Flavonifractor, Acetatifactor, Oscillibacter, Pseudoflavonifractor, Intestinimonas, and Butyricimonas genera, which are related to BPH indicators. Among these, the altered abundance of Lactobacillus and Acetatifactor was associated with the promotion and inhibition of prostate apoptosis, respectively. Finasteride treatment altered the abundance of Barnesiella, Acetatifactor, Butyricimonas, Desulfovibrio, Anaerobacterium, and Robinsoniella genera, which are related to BPH indicators. Among these, altered abundances of Desulfovibrio and Acetatifactor were associated with the promotion and inhibition of prostate apoptosis, respectively. In addition, the abundances of Lactobacillus and Acetatifactor were normalized after finasteride treatment. In conclusion, the association between apoptosis and altered abundances of Lactobacillus and Acetatifactor, among other gut microbes, suggests their potential utility in the diagnosis, prevention, and treatment of BPH.

Impact of Chronic Obstructive Pulmonary Disease on Outcomes After Total Joint Arthroplasty: A Meta-analysis and Systematic Review.

Background: Comorbid chronic obstructive pulmonary disease (COPD) is increasingly common and may have an adverse impact on outcomes in patients undergoing total joint arthroplasty (TJA) of lower extremity. The purpose of this meta-analysis is to compare the postoperative complications between COPD and non-COPD patients undergoing primary TJA including total hip and knee arthroplasty. Methods: PubMed, EMBASE, and Cochrane Library were systematically searched for relevant studies published before December 2021. Postoperative outcomes were compared between patients with COPD versus those without COPD as controls. The outcomes were mortality, re-admission, pulmonary, cardiac, renal, thromboembolic complications, surgical site infection (SSI), periprosthetic joint infection (PJI), and sepsis. Results: A total of 1,002,779 patients from nine studies were finally included in this meta-analysis. Patients with COPD had an increased risk of mortality (OR [odds ratio] = 1.69, 95% confidence interval [CI] 1.42-2.02), re-admission (OR = 1.54, 95% CI 1.38-1.71), pulmonary complications (OR = 2.73, 95% CI 2.26-3.30), cardiac complications (OR = 1.40, 95% CI 1.15-1.69), thromboembolic complications (OR = 1.21, 95% CI 1.15-1.28), renal complications (OR = 1.50, 95% CI 1.14-1.26), SSI (OR = 1.23, 95% CI 1.18-1.30), PJI (OR = 1.26, 95% CI 1.15-1.38), and sepsis (OR = 1.36, 95% CI 1.22-1.52). Conclusion: Patients with comorbid COPD showed an increased risk of mortality and postoperative complications following TJA compared with patients without COPD. Therefore, orthopedic surgeons can use the study to adequately educate these potential complications when obtaining informed consent. Furthermore, preoperative evaluation and medical optimization are crucial to minimizing postoperative complications from arising in this difficult-to-treat population. Level of evidence: Level III. Registration: None. Supplementary Information: The online version contains supplementary material available at 10.1007/s43465-022-00794-2.

NPFFR2 Contributes to the Malignancy of Hepatocellular Carcinoma Development by Activating RhoA/YAP Signaling.

G protein-coupled receptors (GPCRs) are a diverse family of cell surface receptors implicated in various physiological functions, making them common targets for approved drugs. Many GPCRs are abnormally activated in cancers and have emerged as therapeutic targets for cancer. Neuropeptide FF receptor 2 (NPFFR2) is a GPCR that helps regulate pain and modulates the opioid system; however, its function remains unknown in cancers. Here, we found that NPFFR2 is significantly up-regulated in liver cancer and its expression is related to poor prognosis. Silencing of NPFFR2 reduced the malignancy of liver cancer cells by decreasing cell survival, invasion, and migration, while its overexpression increased invasion, migration, and anchorage-independent cell growth. Moreover, we found that the malignant function of NPFFR2 depends on RhoA and YAP signaling. Inhibition of Rho kinase activity completely restored the phenotypes induced by NPFFR2, and RhoA/F-Actin/YAP signaling was controlled by NPFFR2. These findings demonstrate that NPFFR2 may be a potential target for the treatment of hepatocellular carcinoma.

Functional outcomes of residual varus alignment versus mechanical alignment in total knee arthroplasty for varus osteoarthritis: A preferred reporting items for systematic reviews and meta-analyses-compliant meta-analysis.

BACKGROUND: One in five patients with mechanical alignment (MA) after total knee arthroplasty (TKA) was reportedly dissatisfied. As constitutional varus knees are common, restoring the patients' natural residual varus (RV) alignment is as an appealing alternative to neutral MA. This meta-analysis aimed to evaluate the effects of RV alignment on the functional outcomes compared with those of MA in TKA for the knees with varus osteoarthritis. METHODS: The MEDLINE/PubMed, Cochrane Library, and EMBASE databases were comprehensively searched for papers comparing the effects of RV alignment and MA on the functional outcomes from the time of inception of the databases to July 2020. Studies comparing the functional outcomes in the knees subjected to TKA with RV alignment (case group) and MA (control group) were included. The Knee Society knee and functional scores (KSKS and KSFS, respectively), Western Ontario and McMaster University Osteoarthritis Index (WOMAC), Oxford knee score (OKS), and forgotten joint score (FJS) were compared. RESULTS: Seven studies were finally included; all studies showed a low risk of selection bias and provided detailed demographic data. The pooled mean difference in the KSKS (0.06, 95% confidence interval [CI]: -0.14 to 0.27; p = 0.55) and KSFS (0.08, 95% CI: -0.08 to 0.35; p = 0.56) between RV alignment and MA did not significantly differ. The pooled mean differences in the WOMAC (-0.25, 95% CI: -0.57 to 0.07; p = 0.12), OKS (0.06, 95% CI: -0.15 to 0.27; p = 0.56), and FJS (0.41, 95% CI: -0.18 to 1.00; p = 0.18) between the groups were not significant. CONCLUSION: The beneficial effects of RV alignment on the functional outcomes are limited compared to those of MA in TKA for varus osteoarthritis to date. Currently, TKA with neutral MA should be considered as the gold standard.

Cluster-type analogue memristor by engineering redox dynamics for high-performance neuromorphic computing.

Memristors, or memristive devices, have attracted tremendous interest in neuromorphic hardware implementation. However, the high electric-field dependence in conventional filamentary memristors results in either digital-like conductance updates or gradual switching only in a limited dynamic range. Here, we address the switching parameter, the reduction probability of Ag cations in the switching medium, and ultimately demonstrate a cluster-type analogue memristor. Ti nanoclusters are embedded into densified amorphous Si for the following reasons: low standard reduction potential, thermodynamic miscibility with Si, and alloy formation with Ag. These Ti clusters effectively induce the electrochemical reduction activity of Ag cations and allow linear potentiation/depression in tandem with a large conductance range (~244) and long data retention (~99% at 1 hour). Moreover, according to the reduction potentials of incorporated metals (Pt, Ta, W, and Ti), the extent of linearity improvement is selectively tuneable. Image processing simulation proves that the Ti4.8%:a-Si device can fully function with high accuracy as an ideal synaptic model.

Risk factors for postoperative pneumonia in patients undergoing hip fracture surgery: a systematic review and meta-analysis.

BACKGROUND: Postoperative pneumonia (POP) is a devastating complication that can frequently occur after hip fracture surgery. This study aimed to quantitatively and comprehensively summarize the risk factors for POP following hip fracture surgery. METHODS: PubMed, Embase, and Cochrane Library were systematically searched for studies assessing risk factors for POP following hip fracture surgery. The pooled odds ratio (OR) and standardized mean difference (SMD) between patients with and without POP were calculated. Evidence was assessed using the Newcastle-Ottawa scale. RESULTS: Ten studies including 37,130 patients with hip fractures were selected. POP occurred in 1768 cases with an accumulated incidence of 7.8% (95% confidence interval [CI]: 0.061-0.094). Advanced age (SMD: 0.50, 95% CI: 0.10-0.90), male sex (OR: 1.50, 95% CI: 1.12-2.01), American Society of Anesthesiologists physical status scale ≥3 (OR: 3.17, 95% CI: 1.25-8.05), chronic obstructive pulmonary disease (OR: 2.05, 95% CI: 1.43-2.94), coronary heart disease (OR: 1.82, 95% CI: 1.27-2.60), arrhythmia (OR: 1.49, 95% CI: 1.04-2.15), congestive heart failure (OR: 1.41, 95% CI: 1.14-1.75), chronic kidney disease (OR: 2.09, 95% CI: 1.28-3.41), and cerebrovascular accident (OR: 2.14, 95% CI: 1.60-2.85) were risk factors for POP. Hemoglobin (SMD: -0.14, 95% CI: - 0.25 to - 0.03), albumin (SMD: -0.97, 95% CI: - 1.54--0.41), blood urea nitrogen (SMD: 0.20, 95% CI: 0.03-0.37), alanine aminotransferase (SMD: 0.27, 95% CI: 0.10-0.44), arterial oxygen pressure (SMD: -0.49, 95% CI: - 0.71--0.27), time from injury to surgery (SMD: 0.13, 95% CI: 0.08-0.17), and surgery within 48 h (OR: 3.74, 95% CI: 2.40-5.85) were associated with the development of POP. CONCLUSION: Patients with the aforementioned risk factors should be identified preoperatively, and related prophylaxis strategies should be implemented to prevent POP following hip fracture surgery.

Determining the Anticancer Activity of Sphingosine Kinase Inhibitors Containing Heteroatoms in Their Tail Structure.

Sphingosine kinase (SK) enzyme, a central player of sphingolipid rheostat, catalyzes the phosphorylation of sphingosine to the bioactive lipid mediator sphingosine 1 phosphate (S1P), which regulates cancer cell proliferation, migration, differentiation, and angiogenesis through its extracellular five G protein-coupled S1P receptors (S1PR1-5). Recently, several research studies on SK inhibitors have taken place in order use them for the development of novel anticancer-targeted therapy. In this study, we designed and synthesized analog derivatives of known SK1 inhibitors, namely RB005 and PF-543, by introducing heteroatoms at their tail structure, as well as investigated their anticancer activities and pharmacokinetic parameters in vitro. Compounds 1-20 of RB005 and PF-543 derivatives containing an aliphatic chain or a tail structure of benzenesulfonyl were synthesized. All compounds of set 1 (1-10) effectively reduced cell viability in both HT29 and HCT116 cells, whereas set 2 derivatives (11-20) showed poor anticancer effect. Compound 10, having the highest cytotoxic effect (48 h, HT29 IC50 = 6.223 µM, HCT116 IC50 = 8.694 µM), induced HT29 and HCT116 cell death in a concentration-dependent manner through the mitochondrial apoptotic pathway, which was demonstrated by increased annexin V-FITC level, and increased apoptotic marker cleaved caspase-3 and cleaved PARP. Compound 10 inhibited SK1 by 20%, and, thus, the S1P level decreased by 42%. Unlike the apoptosis efficacy, the SK1 inhibitory effect and selectivity of the PF-543 derivative were superior to that of the RB005 analog. As a result, compounds with an aliphatic chain tail exhibited stronger apoptotic effects. However, this ability was not proportional to the degree of SK inhibition. Compound 10 increased the protein phosphatase 2A (PP2A) activity (1.73 fold) similar to FTY720 (1.65 fold) and RB005 (1.59 fold), whereas compounds 11 and 13 had no effect on PP2A activation. Since the PP2A activity increased in compounds with an aliphatic chain tail, it can be suggested that PP2A activation has an important effect on anticancer and SK inhibitory activities.

ZnO-Impregnated Polyacrylonitrile Nanofiber Filters against Various Phases of Air Pollutants.

The incorporation of metal oxide nanoparticles (NPs) in fiber filters is an effective approach to enhance the specific surface area and surface roughness of the fiber, hence improving their efficiency for fine dust capture and other gas treatment or biological applications. Nevertheless, uneven distribution of NPs limits their practical applications. In this study, a commercial silane coupling agent (3-methacryloxypropyltrimethoxysilane) was used to improve the dispersion of zinc oxide (ZnO) NPs in thin polyacrylonitrile fibers. Scanning electron microscopy (SEM) revealed that the fibers incorporating the silane-modified NPs exhibited better distribution of NPs than those prepared with pristine ZnO NPs. The silane modification enhanced the specific surface area, surface roughness, and fiber porosity. In particular, the nanofiber filter incorporating 12 wt% ZnO NPs modified with 0.5 g silane per g of ZnO NPs maintained a filtration efficiency of 99.76% with a low pressure drop of 44 Pa, excellent antibacterial activity, and could decompose organic methylene blue dye with an efficiency of 85.11% under visible light.

Nanofiber Channel Organic Electrochemical Transistors for Low-Power Neuromorphic Computing and Wide-Bandwidth Sensing Platforms.

Organic neuromorphic computing/sensing platforms are a promising concept for local monitoring and processing of biological signals in real time. Neuromorphic devices and sensors with low conductance for low power consumption and high conductance for low-impedance sensing are desired. However, it has been a struggle to find materials and fabrication methods that satisfy both of these properties simultaneously in a single substrate. Here, nanofiber channels with a self-formed ion-blocking layer are fabricated to create organic electrochemical transistors (OECTs) that can be tailored to achieve low-power neuromorphic computing and fast-response sensing by transferring different amounts of electrospun nanofibers to each device. With their nanofiber architecture, the OECTs exhibit a low switching energy of 113 fJ and operate within a wide bandwidth (cut-off frequency of 13.5 kHz), opening a new paradigm for energy-efficient neuromorphic computing/sensing platforms in a biological environment without the leakage of personal information.