α-CsPbI3 Quantum Dots ReRAM with High Air Stability Working by Valance Change Filamentary Mechanism.

The current memory system is facing obstacles to improvement, and ReRAM is considered a powerful alternative. All-inorganic α-CsPbI3 perovskite-based ReRAM working by electrochemical mechanism is reported, but the electrochemically active electrode raised difficulty in long-term stable operation, and bulk α-CsPbI3 device can not show resistive switching behavior with an inert metal top electrode. Herein, by making the α-CsPbI3 into QDs and applying it to the device with inert Au as the top electrode, the devices working by valence change mechanism are successfully fabricated. The large surface-to-volume ratio made an abundant amount of iodine vacancies and facile migration of vacancies allowed the device to work by valence change mechanism. The devices show reliable electrical characteristics, 800 cycles endurance and retention for over 4 × 104 s, and air stability for 1 month. This work demonstrates that applying the QDs can improve the stability and enable a new type of working mechanism in ReRAM.

Feasibility of Sarcopenia Diagnosis Using Stimulated Muscle Contraction Signal in Hemiplegic Stroke Patients.

Sarcopenia, a condition characterized by muscle weakness and mass loss, poses significant risks of accidents and complications. Traditional diagnostic methods often rely on physical function measurements like handgrip strength which can be challenging for affected patients, including those with stroke. To address these challenges, we propose a novel sarcopenia diagnosis model utilizing stimulated muscle contraction signals captured via wearable devices. Our approach achieved impressive results, with an accuracy of 93% and 100% in sarcopenia classification for male and female stroke patients, respectively. These findings underscore the significance of our method in diagnosing sarcopenia among stroke patients, offering a non-invasive and accessible solution.

Multiclassification of the symptom severity of social anxiety disorder using digital phenotypes and feature representation learning.

Objective: Social anxiety disorder (SAD) is characterized by heightened sensitivity to social interactions or settings, which disrupts daily activities and social relationships. This study aimed to explore the feasibility of utilizing digital phenotypes for predicting the severity of these symptoms and to elucidate how the main predictive digital phenotypes differed depending on the symptom severity. Method: We collected 511 behavioral and physiological data over 7 to 13 weeks from 27 SAD and 31 healthy individuals using smartphones and smartbands, from which we extracted 76 digital phenotype features. To reduce data dimensionality, we employed an autoencoder, an unsupervised machine learning model that transformed these features into low-dimensional latent representations. Symptom severity was assessed with three social anxiety-specific and nine additional psychological scales. For each symptom, we developed individual classifiers to predict the severity and applied integrated gradients to identify critical predictive features. Results: Classifiers targeting social anxiety symptoms outperformed baseline accuracy, achieving mean accuracy and F1 scores of 87% (with both metrics in the range 84-90%). For secondary psychological symptoms, classifiers demonstrated mean accuracy and F1 scores of 85%. Application of integrated gradients revealed key digital phenotypes with substantial influence on the predictive models, differentiated by symptom types and levels of severity. Conclusions: Leveraging digital phenotypes through feature representation learning could effectively classify symptom severities in SAD. It identifies distinct digital phenotypes associated with the cognitive, emotional, and behavioral dimensions of SAD, thereby advancing the understanding of SAD. These findings underscore the potential utility of digital phenotypes in informing clinical management.

CRISPR/Cas13a-assisted amplification-free miRNA biosensor via dark-field imaging and magnetic gold nanoparticles.

MicroRNAs (miRNAs) are short (about 18-24 nucleotides) non-coding RNAs and have emerged as potential biomarkers for various diseases, including cancers. Due to their short lengths, the specificity often becomes an issue in conventional amplification-based methods. Next-generation sequencing techniques could be an alternative, but the long analysis time and expensive costs make them less suitable for routine clinical diagnosis. Therefore, it is essential to develop a rapid, selective, and accurate miRNA detection assay using a simple, affordable system. In this work, we report a CRISPR/Cas13a-based miRNA biosensing using point-of-care dark-field (DF) imaging. We utilized magnetic-gold nanoparticle (MGNPs) complexes as signal probes, which consist of 200 nm-sized magnetic beads and 60 nm-sized gold nanoparticles (AuNPs) linked by DNA hybridization. Once the CRISPR/Cas13a system recognized the target miRNAs (miR-21-5p), the activated Cas13a cleaved the bridge linker containing RNA sequences, releasing 60 nm-AuNPs detected and quantified by a portable DF imaging system. The combination of CRISPR/Cas13a, MGNPs, and DF imaging demonstrated amplification-free detection of miR-21-5p within 30 min at a detection limit of 500 attomoles (25 pM) and with single-base specificity. The CRISPR/Cas13a-assisted MGNP-DF assay achieved rapid, selective, and accurate detection of miRNAs with simple equipment, thus providing a potential application for cancer diagnosis.

Comparative metabolomic analysis of mouse plasma in response to different dietary conditions.

Plasma metabolites offer insights into aging processes and aging-related biomarkers. Here, the dietary effects of various functional foods on older adult mice were evaluated using metabolomic techniques. Fifty-week-old mice were divided into four groups (n = 4 each) and fed either a normal diet (AC) or the diets from Triticum aestivum sprout (TA), Schisandra chinensis (SZ), or Pisum sativum sprout (PS) extracts. Additionally, a group of 8-week-old mice fed a normal diet (YC; n = 5) was included for the comparison. The PS group had a significantly lower free fatty acid content and higher ornithine, proline, citric acid, and oxalic acid contents than the AC group. The PS group also showed reduced oxidative stress and muscle damage, suggesting the higher anti-aging efficacy of P. sativum sprouts than the other diets. These findings suggest plasma metabolite profiling is an effective tool to assess the anti-aging effects of functional foods. Supplementary Information: The online version contains supplementary material available at 10.1007/s10068-023-01479-8.

1-palmitoyl-2-linoleoyl-3-acetyl-rac-glycerol treatment inhibits abnormal tumor growth by regulating neutrophil infiltration in a non-small cell lung carcinoma mouse model.

Excessive neutrophil infiltration into the tumor microenvironment (TME) is an important factor that contributes to tumor overgrowth and limited immunotherapy efficacy. Neutrophils activate various receptors involved in tumor progression, while suppressing the infiltration and activity of cytotoxic T cells and creating optimal conditions for tumor growth. Therefore, the appropriate control of neutrophil infiltration is an effective strategy for tumor treatment. In the present study, 1-palmitoyl-2-linoleoyl-3-acetyl-rac-glycerol (PLAG) inhibited tumor overgrowth by suppressing excessive neutrophil infiltration, resulting in >74.97 % reduction in tumor size in a Lewis lung carcinoma (LLC-1) mouse model. All subjects in the positive control group died during the 90-day survival period, whereas only four subjects in the PLAG treatment group survived. PLAG had a significantly higher tumor growth inhibitory effect and survival rate than other neutrophil infiltration-targeting inhibitors (e.g., Navarixin, lymphocyte antigen 6 complex locus G6D antibody [aLy6G]). The ability of PLAG to regulate neutrophil infiltration and inhibit tumor growth depends on thioredoxin-interacting protein (TXNIP). In tumors lacking TXNIP expression, PLAG failed to control neutrophil infiltration and infiltration-related factor release, and the inhibitory effect of PLAG on tumor growth was reduced. PLAG-mediated inhibition of neutrophil infiltration enhances the efficacy of immune checkpoint inhibitors (ICIs), increasing the antitumor efficacy and survival rate by 30 %. In conclusion, PLAG could be a novel alternative to anti-tumor drugs that effectively targets excessive neutrophil infiltration into cancer tissues.

Predicting avian diversity based on land use and cover on a national scale.

This study explores the relationship between landscape features and avian diversity in South Korea, examining both taxonomic and functional diversity. The Korean Peninsula serves as a pivotal habitat for resident bird species and a migratory pathway in the East Asia-Pacific flyway. Using a national dataset with block sizes ranging from 3.5 to 4.5 kilometers per side, we found that less urbanized open plains exhibit higher taxonomic diversity, while coastal regions with diverse water bird populations show higher functional diversity. These findings underscore the significance of conserving the existing land types and qualities in specific regions to substantially impact bird distribution and regional biodiversity. Remarkably, closed forests display diversity patterns akin to urban/built-up areas, despite their disparate land use characteristics. The stability of bird diversity indices across different land use types enables us to predict bird diversity indices based on the particular land use and land cover configurations. This study emphasizes the complementary nature of functional biodiversity indices in comprehending bird distribution patterns alongside taxonomic diversity indices.

The dopamine analogue CA140 alleviates AD pathology, neuroinflammation, and rescues synaptic/cognitive functions by modulating DRD1 signaling or directly binding to Abeta.

BACKGROUND: We recently reported that the dopamine (DA) analogue CA140 modulates neuroinflammatory responses in lipopolysaccharide-injected wild-type (WT) mice and in 3-month-old 5xFAD mice, a model of Alzheimer's disease (AD). However, the effects of CA140 on Aß/tau pathology and synaptic/cognitive function and its molecular mechanisms of action are unknown. METHODS: To investigate the effects of CA140 on cognitive and synaptic function and AD pathology, 3-month-old WT mice or 8-month-old (aged) 5xFAD mice were injected with vehicle (10% DMSO) or CA140 (30 mg/kg, i.p.) daily for 10, 14, or 17 days. Behavioral tests, ELISA, electrophysiology, RNA sequencing, real-time PCR, Golgi staining, immunofluorescence staining, and western blotting were conducted. RESULTS: In aged 5xFAD mice, a model of AD pathology, CA140 treatment significantly reduced Aß/tau fibrillation, Aß plaque number, tau hyperphosphorylation, and neuroinflammation by inhibiting NLRP3 activation. In addition, CA140 treatment downregulated the expression of cxcl10, a marker of AD-associated reactive astrocytes (RAs), and c1qa, a marker of the interaction of RAs with disease-associated microglia (DAMs) in 5xFAD mice. CA140 treatment also suppressed the mRNA levels of s100ß and cxcl10, markers of AD-associated RAs, in primary astrocytes from 5xFAD mice. In primary microglial cells from 5xFAD mice, CA140 treatment increased the mRNA levels of markers of homeostatic microglia (cx3cr1 and p2ry12) and decreased the mRNA levels of a marker of proliferative region-associated microglia (gpnmb) and a marker of lipid-droplet-accumulating microglia (cln3). Importantly, CA140 treatment rescued scopolamine (SCO)-mediated deficits in long-term memory, dendritic spine number, and LTP impairment. In aged 5xFAD mice, these effects of CA140 treatment on cognitive/synaptic function and AD pathology were regulated by dopamine D1 receptor (DRD1)/Elk1 signaling. In primary hippocampal neurons and WT mice, CA140 treatment promoted long-term memory and dendritic spine formation via effects on DRD1/CaMKIIα and/or ERK signaling. CONCLUSIONS: Our results indicate that CA140 improves neuronal/synaptic/cognitive function and ameliorates Aß/tau pathology and neuroinflammation by modulating DRD1 signaling in primary hippocampal neurons, primary astrocytes/microglia, WT mice, and aged 5xFAD mice.

Glutaminase-1 inhibition alleviates senescence of Wharton's jelly-derived mesenchymal stem cells via senolysis.

Replicative senescence of mesenchymal stem cells (MSCs) caused by repeated cell culture undermines their potential as a cell therapy because of the reduction in their proliferation and therapeutic potential. Glutaminase-1 (GLS1) is reported to be involved in the survival of senescent cells, and inhibition of GLS1 alleviates age-related dysfunction via senescent cell removal. In the present study, we attempted to elucidate the association between MSC senescence and GLS1. We conducted in vitro and in vivo experiments to analyze the effect of GLS1 inhibition on senolysis and the therapeutic effects of MSCs. Inhibition of GLS1 in Wharton's jelly-derived MSCs (WJ-MSCs) reduced the expression of aging-related markers, such as p16, p21, and senescence-associated secretory phenotype genes, by senolysis. Replicative senescence-alleviated WJ-MSCs, which recovered after short-term treatment with bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide 3 (BPTES), showed increased proliferation and therapeutic effects compared to those observed with senescent WJ-MSCs. Moreover, compared to senescent WJ-MSCs, replicative senescence-alleviated WJ-MSCs inhibited apoptosis in serum-starved C2C12 cells, enhanced muscle formation, and hindered apoptosis and fibrosis in mdx mice. These results imply that GLS1 inhibition can ameliorate the therapeutic effects of senescent WJ-MSCs in patients with muscle diseases such as Duchenne muscular dystrophy. In conclusion, GLS1 is a key factor in modulating the senescence mechanism of MSCs, and regulation of GLS1 may enhance the therapeutic effects of senescent MSCs, thereby increasing the success rate of clinical trials involving MSCs.

Comparative effectiveness of perioperative physical activity in older adults with lung cancer and their family caregivers: design of a multicenter pragmatic randomized trial.

BACKGROUND: With a median age at diagnosis of 70, lung cancer remains a significant public health challenge for older Americans. Surgery is a key component in treating most patients with non-metastatic lung cancer. These patients experience postoperative pain, fatigue, loss of respiratory capacity, and decreased physical function. Data on quality of life (QOL) in older adults undergoing lung cancer surgery is limited, and few interventions are designed to target the needs of older adults and their family caregivers (FCGs). The primary aim of this comparative effectiveness trial is to determine whether telephone-based physical activity coaching before and after surgery will be more beneficial than physical activity self-monitoring alone for older adults and their FCGs. METHODS: In this multicenter comparative effectiveness trial, 382 older adults (≥ 65 years) with lung cancer and their FCGs will be recruited before surgery and randomized to either telephone-based physical activity coaching or physical activity self-monitoring alone. Participants allocated to the telephone-based coaching comparator will receive five telephone sessions with coaches (1 pre and 4 post surgery), an intervention resource manual, and a wristband pedometer. Participants in the self-monitoring only arm will receive American Society of Clinical Oncology (ASCO) physical activity information and wristband pedometers. All participants will be assessed at before surgery (baseline), at discharge, and at days 30, 60, and 180 post-discharge. The primary endpoint is the 6-minute walk test (6MWT) at 30 days post-discharge. Geriatric assessment, lower extremity function, self-reported physical function, self-efficacy, and QOL will also be assessed. DISCUSSION: The trial will determine whether this telephone-based physical activity coaching approach can enhance postoperative functional capacity and QOL outcomes for older adults with lung cancer and their FCGs. Trial results will provide critical findings to inform models of postoperative care for older adults with cancer and their FCGs. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT06196008.

Association between gastrectomy and the risk of type 2 diabetes in gastric cancer survivors: a nationwide cohort study.

AIM: Postprandial glycemic fluctuations after gastrectomy are seen in patients with gastric cancer but, no studies have investigated the association between gastrectomy and type 2 diabetes mellitus (T2DM) in gastric cancer survivors. This study aimed to elucidate the relationship between gastrectomy (total or subtotal) and incident T2DM. In addition, we explored whether vitamin B12 supplementation modulates this risk among patients who have undergone total gastrectomy. METHODS: In this large nationwide population-based retrospective cohort study using the National Health Insurance Service database of South Korea, we identified patients aged >20 years who underwent gastrectomy from 2008 to 2015 (n=150,074) and age- and sex-matched controls without gastrectomy (n=301,508). A Cox proportional hazards model was used. RESULTS: During the median follow-up duration of 4.4 years after the 2-year time lag after gastrectomy, of the 78,006 subjects, 4,597 (5.9%) developed T2DM. Compared with matched controls, the adjusted hazard ratio (AHR[95% confidence interval]) for T2DM of patients with total gastrectomy was 1.34[1.23;1.47]. The corresponding AHR after subtotal gastrectomy was 0.81[0.76;0.86]. Among the patients with total gastrectomy, the risk of T2DM was significantly increased in those who did not receive any vitamin B12 supplementation (AHR=1.60[1.33;1.92]), whereas the risk of T2DM was lower (close to being statistically significant) in those who received continuous vitamin B12 supplementation after gastrectomy (AHR=0.70[0.49;1.01]). CONCLUSION: These results show a significantly reduced risk of T2DM in gastric cancer patients undergoing subtotal gastrectomy and a significantly increased risk of T2DM in gastric cancer patients undergoing total gastrectomy, which is mitigated by continuous vitamin B12 supplementation.

Automated identification of thrombectomy amenable vessel occlusion on computed tomography angiography using deep learning.

Introduction: We developed and externally validated a fully automated algorithm using deep learning to detect large vessel occlusion (LVO) in computed tomography angiography (CTA). Method: A total of 2,045 patients with acute ischemic stroke who underwent CTA were included in the development of our model. We validated the algorithm using two separate external datasets: one with 64 patients (external 1) and another with 313 patients (external 2), with ischemic stroke. In the context of current clinical practice, thrombectomy amenable vessel occlusion (TAVO) was defined as an occlusion in the intracranial internal carotid artery (ICA), or in the M1 or M2 segment of the middle cerebral artery (MCA). We employed the U-Net for vessel segmentation on the maximum intensity projection images, followed by the application of the EfficientNetV2 to predict TAVO. The algorithm's diagnostic performance was evaluated by calculating the area under the receiver operating characteristics curve (AUC), sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV). Results: The mean age in the training and validation dataset was 68.7 ± 12.6; 56.3% of participants were men, and 18.0% had TAVO. The algorithm achieved AUC of 0.950 (95% CI, 0.915-0.971) in the internal test. For the external datasets 1 and 2, the AUCs were 0.970 (0.897-0.997) and 0.971 (0.924-0.990), respectively. With a fixed sensitivity of 0.900, the specificities and PPVs for the internal test, external test 1, and external test 2 were 0.891, 0.796, and 0.930, and 0.665, 0.583, and 0.667, respectively. The algorithm demonstrated a sensitivity and specificity of approximately 0.95 in both internal and external datasets, specifically for cases involving intracranial ICA or M1-MCA occlusion. However, the diagnostic performance was somewhat reduced for isolated M2-MCA occlusion; the AUC for the internal and combined external datasets were 0.903 (0.812-0.944) and 0.916 (0.816-0.963), respectively. Conclusion: We developed and externally validated a fully automated algorithm that identifies TAVO. Further research is needed to evaluate its effectiveness in real-world clinical settings. This validated algorithm has the potential to assist early-career physicians, thereby streamlining the treatment process for patients who can benefit from endovascular treatment.

Immobilization and Catalytic Conversion of Polysulfide by In-Situ Generated Nickel in Hollow Carbon Fibers for High-Rate Lithium-Sulfur Batteries.

Lithium-sulfur (Li-S) batteries are considered promising energy-storage systems because of their high theoretical energy density, low cost, and eco-friendliness. However, problems such as the shuttle effect can result in the loss of active materials, poor cyclability, and rapid capacity degradation. The utilization of a structural configuration that enhances electrochemical performance via dual adsorption-catalysis strategies can overcome the limitations of Li-S batteries. In this study, an integrated interlayer structure, in which hollow carbon fibers (HCFs) were modified with in-situ-generated Ni nanoparticles, was prepared by scalable one-step carbonization. Highly hierarchically porous HCFs act as the carbon skeleton and provide a continuous three-dimensional conductive network that enhances ion/electron diffusion. Ni nanoparticles with superior anchoring and catalytic abilities can prevent the shuttle effect and increase the conversion rate, thereby promoting the electrochemical performance. This synergistic effect resulted in a high capacity retention of 582 mAh g-1 at 1 C after 100 cycles, providing an excellent rate capability of up to 3 C. The novel structure, wherein Ni nanoparticles are embedded in cotton-tissue-derived HCFs, provides a new avenue for enhancing electrochemical performance at high C rates. This results in a low-cost, sustainable, and high-performance hybrid material for the development of practical Li-S batteries.

Clinical and pathological significance of Orai1 channel expression in human diabetic nephropathy.

Background: Targeted therapies for diabetic nephropathy (DN) are lacking, partly due to their irreversible nature. The role of Orai1, a store-operated Ca2+ channel, in DN remains debated, with conflicting evidence on its effect on proteinuria in animal models. We aimed to elucidate the functional relevance of Orai1 expression for clinicopathological parameters in patients with DN. Methods: In this study, we included 93 patients diagnosed with DN between 2009 and 2019. Immunohistochemical staining for Orai1 was performed on paraffin-embedded kidney sections. The significance of Orai1 expression in human DN was assessed by examining its correlation with DN's pathological and clinical parameters using Pearson's correlation coefficient and univariate logistic regression. Results: Orai1 was significantly overexpressed in DN patients compared to control. A strong correlation was observed between increased Orai1 expression and higher Renal Pathology Society DN classification, enhanced interstitial fibrosis and tubular atrophy scores. Positive correlations with serum creatinine levels and prognosis of chronic kidney disease (CKD) by glomerular filtration rate (GFR) and albuminuria category were noted but the estimated GFR was inversely related to Orai1 expression. Orai1's association with advanced CKD stages persisted even after adjusting for confounding variables in multivariate logistic regression analysis. Conclusion: Orai1 expression is closely associated with histological and clinical severities of DN, suggesting its potential as a predictive biomarker for disease progression and prognosis. These findings provide new perspectives on therapeutic interventions targeting Orai1 in DN.

Serum cortisol and neuroticism for post-traumatic stress disorder over 2 years in patients with physical injuries.

AIM: This study aimed to explore the relationships between serum cortisol levels, personality traits, and the development of Post-Traumatic Stress Disorder (PTSD) over 2 years among individuals with physical injuries. METHODS: Participants were consecutively recruited from a trauma center and followed prospectively for 2 years. At baseline, serum cortisol levels were measured, and personality traits were categorized into five dimensions (Extraversion, Agreeableness, Conscientiousness, Neuroticism, and Openness), using the Big Five Inventory-10. The diagnosis of PTSD during follow-up (at 3, 6, 12, and 24 months post-injury) was determined using the Clinician-Administered PTSD Scale for DSM-5. Binary and multinomial logistic regression analyses were conducted to examine the interactions between cortisol levels, personality traits, and PTSD development. RESULTS: Among 923 patients analyzed, 112 (12.1%) were diagnosed with PTSD at some point during the study period, with prevalence rates decreasing from 8.8% at 3 months to 3.7% at 24 months post-injury. Direct associations between cortisol levels or personality traits and PTSD were not observed. However, a significant interaction between lower cortisol levels and higher Neuroticism in relation to PTSD risk was identified, especially during the early follow-up periods (3 to 6 months), but this association waned from the 12-month follow-up onward. CONCLUSION: Our findings reveal Neuroticism-dependent associations between serum cortisol levels and PTSD development, exhibiting temporal variations. These results suggest that PTSD development may be influenced by a complex, time-sensitive interplay of biological and psychosocial factors, underscoring the importance of considering individual differences in stress reactivity and personality in PTSD research and treatment.

Activity-based protein profiling and global proteome analysis reveal MASTL as a potential therapeutic target in gastric cancer.

BACKGROUND: Gastric cancer (GC) is a prevalent malignancy with limited therapeutic options for advanced stages. This study aimed to identify novel therapeutic targets for GC by profiling HSP90 client kinases. METHODS: We used mass spectrometry-based activity-based protein profiling (ABPP) with a desthiobiotin-ATP probe, combined with sensitivity analysis of HSP90 inhibitors, to profile kinases in a panel of GC cell lines. We identified kinases regulated by HSP90 in inhibitor-sensitive cells and investigated the impact of MASTL knockdown on GC cell behavior. Global proteomic analysis following MASTL knockdown was performed, and bioinformatics tools were used to analyze the resulting data. RESULTS: Four kinases-MASTL, STK11, CHEK1, and MET-were identified as HSP90-regulated in HSP90 inhibitor-sensitive cells. Among these, microtubule-associated serine/threonine kinase-like (MASTL) was upregulated in GC and associated with poor prognosis. MASTL knockdown decreased migration, invasion, and proliferation of GC cells. Global proteomic profiling following MASTL knockdown revealed NEDD4-1 as a potential downstream mediator of MASTL in GC progression. NEDD4-1 was also upregulated in GC and associated with poor prognosis. Similar to MASTL inhibition, NEDD4-1 knockdown suppressed migration, invasion, and proliferation of GC cells. CONCLUSIONS: Our multi-proteomic analyses suggest that targeting MASTL could be a promising therapy for advanced gastric cancer, potentially through the reduction of tumor-promoting proteins including NEDD4-1. This study enhances our understanding of kinase signaling pathways in GC and provides new insights for potential treatment strategies.

Real-Time Tunable Gas Sensing Platform Based on SnO2 Nanoparticles Activated by Blue Micro-Light-Emitting Diodes.

Micro-light-emitting diodes (µLEDs) have gained significant interest as an activation source for gas sensors owing to their advantages, including room temperature operation and low power consumption. However, despite these benefits, challenges still exist such as a limited range of detectable gases and slow response. In this study, we present a blue µLED-integrated light-activated gas sensor array based on SnO2 nanoparticles (NPs) that exhibit excellent sensitivity, tunable selectivity, and rapid detection with micro-watt level power consumption. The optimal power for µLED is observed at the highest gas response, supported by finite-difference time-domain simulation. Additionally, we first report the visible light-activated selective detection of reducing gases using noble metal-decorated SnO2 NPs. The noble metals induce catalytic interaction with reducing gases, clearly distinguishing NH3, H2, and C2H5OH. Real-time gas monitoring based on a fully hardware-implemented light-activated sensing array was demonstrated, opening up new avenues for advancements in light-activated electronic nose technologies.

Licochalcone A attenuates NMDA-induced neurotoxicity.

This study investigates the effect of Licochalcone A (Lico-A), a flavonoid from licorice roots known for its anti-inflammatory, anti-cancer, and antioxidant properties, on NMDA-induced neurotoxicity in primary cultured rat hippocampal neurons. The study measured cell survival following NMDA and Lico-A exposure, revealing that Lico-A at a 2.5 µg/ml significantly improved cell viability, countering the detrimental effects of NMDA. The study also analyzed synaptic changes by examining both postsynaptic density 95 (PSD95) and synaptophysin-targeted imaging, showing that Lico-A treatment resulted in a significant increase in synaptic puncta, contrasting with the reduction observed under NMDA exposure. Furthermore, levels of phosphorylated mixed lineage kinase domain-like pseudokinase (P-MLKL) and phosphorylated receptor-interacting serine/threonine-protein kinase 3 (P-RIP3), key necroptosis regulators, were measured using Western blotting. The results showed an increase in P-MLKL and P-RIP3 in neurons exposed to NMDA, which was reduced following Lico-A treatment. The response of astrocyte and microglia was also evaluated by immunostaining for glial fibrillary acidic protein (GFAP), ionized calcium-binding adaptor molecule 1 (IBA-1) and tumor necrosis factor alpha (TNF-α). These markers exhibited heightened expression in the NMDA group, which was substantially reduced by Lico-A treatment. These findings suggest that Lico-A has neuroprotective effects against NMDA-induced neurotoxicity, potentially contributing to synaptic preservation, inhibition of neuronal necroptosis, and modulation of glial activation. Therefore, Lico-A shows promise as a neuroprotective agent for conditions associated with NMDA-related neurotoxicity.