Fluorescent, multifunctional anti-counterfeiting, fast response electrophoretic display based on TiO2/CsPbBr3 composite particles.

Traditional optical anti-counterfeiting (AC) is achieved by static printed images, which makes them susceptible to lower levels of security and easier replication. Therefore, it is essential to develop AC device with dynamic modulation for higher security. Electrophoretic display (EPD) has the advantages of low power consumption, high ambient contrast ratio, and capability of showing dynamic images which is suitable for dynamic AC applications. Herein, we prepared a dynamical AC device based on a fluorescent EPD, and achieving the image switch between black, white, and green fluorescence states under the dual-mode driving (electronic field and UV light). We loaded perovskite quantum dots (CsPbBr3) onto the TiO2 particles and further prepared fluorescent electrophoretic particles TiO2/CsPbBr3-3-PLMA (TiO/CPB-3) by grafting and polymerizing method. In addition, we fabricated the AC devices based on the fluorescent EPD, which exhibits the multifunctional AC, where the fluorescent EPD has a fast response time of 350 ms, a high contrast ratio of 17, and bright green fluorescence. This prototype demonstrates a new way for future dynamic AC and identification.

METI: deep profiling of tumor ecosystems by integrating cell morphology and spatial transcriptomics.

Recent advances in spatial transcriptomics (ST) techniques provide valuable insights into cellular interactions within the tumor microenvironment (TME). However, most analytical tools lack consideration of histological features and rely on matched single-cell RNA sequencing data, limiting their effectiveness in TME studies. To address this, we introduce the Morphology-Enhanced Spatial Transcriptome Analysis Integrator (METI), an end-to-end framework that maps cancer cells and TME components, stratifies cell types and states, and analyzes cell co-localization. By integrating spatial transcriptomics, cell morphology, and curated gene signatures, METI enhances our understanding of the molecular landscape and cellular interactions within the tissue. We evaluate the performance of METI on ST data generated from various tumor tissues, including gastric, lung, and bladder cancers, as well as premalignant tissues. We also conduct a quantitative comparison of METI with existing clustering and cell deconvolution tools, demonstrating METI's robust and consistent performance.

Profiling cell identity and tissue architecture with single-cell and spatial transcriptomics.

Single-cell transcriptomics has broadened our understanding of cellular diversity and gene expression dynamics in healthy and diseased tissues. Recently, spatial transcriptomics has emerged as a tool to contextualize single cells in multicellular neighbourhoods and to identify spatially recurrent phenotypes, or ecotypes. These technologies have generated vast datasets with targeted-transcriptome and whole-transcriptome profiles of hundreds to millions of cells. Such data have provided new insights into developmental hierarchies, cellular plasticity and diverse tissue microenvironments, and spurred a burst of innovation in computational methods for single-cell analysis. In this Review, we discuss recent advancements, ongoing challenges and prospects in identifying and characterizing cell states and multicellular neighbourhoods. We discuss recent progress in sample processing, data integration, identification of subtle cell states, trajectory modelling, deconvolution and spatial analysis. Furthermore, we discuss the increasing application of deep learning, including foundation models, in analysing single-cell and spatial transcriptomics data. Finally, we discuss recent applications of these tools in the fields of stem cell biology, immunology, and tumour biology, and the future of single-cell and spatial transcriptomics in biological research and its translation to the clinic.

A comparison of scRNA-seq annotation methods based on experimentally labeled immune cell subtype dataset.

Cell-type annotation is a critical step in single-cell data analysis. With the development of numerous cell annotation methods, it is necessary to evaluate these methods to help researchers use them effectively. Reference datasets are essential for evaluation, but currently, the cell labels of reference datasets mainly come from computational methods, which may have computational biases and may not reflect the actual cell-type outcomes. This study first constructed an experimentally labeled immune cell-subtype single-cell dataset of the same batch and systematically evaluated 18 cell annotation methods. We assessed those methods under five scenarios, including intra-dataset validation, immune cell-subtype validation, unsupervised clustering, inter-dataset annotation, and unknown cell-type prediction. Accuracy and ARI were evaluation metrics. The results showed that SVM, scBERT, and scDeepSort were the best-performing supervised methods. Seurat was the best-performing unsupervised clustering method, but it couldn't fully fit the actual cell-type distribution. Our results indicated that experimentally labeled immune cell-subtype datasets revealed the deficiencies of unsupervised clustering methods and provided new dataset support for supervised methods.

Atlas of Metastatic Gastric Cancer Links Ferroptosis to Disease Progression and Immunotherapy Response.

BACKGROUND & AIMS: Metastases from gastric adenocarcinoma (GAC) lead to high morbidity and mortality. Developing innovative and effective therapies requires a comprehensive understanding of the tumor and immune biology of advanced GAC. Yet, collecting matched specimens from advanced, treatment-naïve patients with GAC poses a significant challenge, limiting the scope of current research, which has focused predominantly on localized tumors. This gap hinders deeper insight into the metastatic dynamics of GAC. METHODS: We performed in-depth single-cell transcriptome and immune profiling on 68 paired, treatment-naïve, primary metastatic tumors to delineate alterations in cancer cells and their tumor microenvironment during metastatic progression. To validate our observations, we conducted comprehensive functional studies both in vitro and in vivo, using cell lines and multiple patient-derived xenograft and novel mouse models of GAC. RESULTS: Liver and peritoneal metastases exhibited distinct properties in cancer cells and dynamics of tumor microenvironment phenotypes, supporting the notion that cancer cells and their local tumor microenvironments co-evolve at metastatic sites. Our study also revealed differential activation of cancer meta-programs across metastases. We observed evasion of cancer cell ferroptosis via GPX4 up-regulation during GAC progression. Conditional depletion of Gpx4 or pharmacologic inhibition of ferroptosis resistance significantly attenuated tumor growth and metastatic progression. In addition, ferroptosis-resensitizing treatments augmented the efficacy of chimeric antigen receptor T-cell therapy. CONCLUSIONS: This study represents the largest single-cell dataset of metastatic GACs to date. High-resolution mapping of the molecular and cellular dynamics of GAC metastasis has revealed a rationale for targeting ferroptosis defense in combination with chimeric antigen receptor T-cell therapy as a novel therapeutic strategy with potential immense clinical implications.

The U-shaped association between age at diagnosis and recurrence in patients with papillary thyroid carcinoma: A retrospective single-institution cohort study.

PURPOSE: Age is a significant predictor of papillary thyroid carcinoma (PTC). At present, the available evidence shows that age at diagnosis has an important impact on the recurrence of PTC. The objective of our investigation was to examine the relationship between age at diagnosis and recurrence in patients with PTC. METHODS: The medical records of patients with PTC who were treated between January 2010 and December 2018 at a single institute in a cancer referral center in China were retrospectively reviewed. The hazard ratios (HRs) and 95 % confidence intervals (CIs) for recurrence-free survival (RFS), locoregional recurrence-free survival (LRRFS) and distant metastasis-free survival (DMFS) were assessed using Cox proportional hazard models and restricted cubic splines (RCSs). RESULTS: A total of 13758 patients were included in the study. With a median follow-up of 60 months (range 12-277), a total of 687 patients experienced recurrence, and 90 patients died. The 5-year RFS, LRRFS and DMFS rates were 95.0 % (95 % CI 94.6%-95.4 %), 95.8 % (95 % CI 95.4%-96.2 %) and 98.8 % (95 % CI 98.6%-99.0 %), respectively. The adjusted smooth RCS curves revealed a U-shaped association between age at diagnosis and RFS, LRRFS, and DMFS. After adjusting for potential confounding variables, both younger (≤30 years) and older (≥55 years) patients exhibited significantly lower RFS and LRRFS rates than did middle-aged patients (31-54 years). Older patients had significantly lower DMFS rates. CONCLUSIONS: This study confirmed a U-shaped association between age at diagnosis and the risk of both locoregional recurrence and distant metastasis.

Targeting focal adhesion kinase (FAK) in cancer therapy: A recent update on inhibitors and PROTAC degraders.

Focal adhesion kinase (FAK) is considered as a pivotal intracellular non-receptor tyrosine kinase, and has garnered significant attention as a promising target for anticancer drug development. As of early 2024, a total of 12 drugs targeting FAK have been approved for clinical or preclinical studies worldwide, including three PROTAC degraders. In recent three years (2021-2023), significant progress has been made in designing targeted FAK anticancer agents, including the development of a novel benzenesulfofurazan type NO-releasing FAK inhibitor and the first-in-class dual-target inhibitors simultaneously targeting FAK and HDACs. Given the pivotal role of FAK in the discovery of anticancer drugs, as well as the notable advancements achieved in FAK inhibitors and PROTAC degraders in recent years, this review is underbaked to present a comprehensive overview of the function and structure of FAK. Additionally, the latest findings on the inhibitors and PROTAC degraders of FAK from the past three years, along with their optimization strategies and anticancer activities, were summarized, which might help to provide novel insights for the development of novel targeted FAK agents with promising anticancer potential and favorable pharmacological profiles.

Strategies that regulate Hippo signaling pathway for novel anticancer therapeutics.

As a highly conserved signaling network across different species, the Hippo pathway is involved in various biological processes. Dysregulation of the Hippo pathway could lead to a wide range of diseases, particularly cancers. Extensive researches have demonstrated the close association between dysregulated Hippo signaling and tumorigenesis as well as tumor progression. Consequently, targeting the Hippo pathway has emerged as a promising strategy for cancer treatment. In fact, there has been an increasing number of reports on small molecules that target the Hippo pathway, exhibiting therapeutic potential as anticancer agents. Importantly, some of Hippo signaling pathway inhibitors have been approved for the clinical trials. In this work, we try to provide an overview of the core components and signal transduction mechanisms of the Hippo signaling pathway. Furthermore, we also analyze the relationship between Hippo signaling pathway and cancers, as well as summarize the small molecules with proven anti-tumor effects in clinical trials or reported in literatures. Additionally, we discuss the anti-tumor potency and structure-activity relationship of the small molecule compounds, providing a valuable insight for further development of anticancer agents against this pathway.

Two nomograms constructed for predicting the efficacy and prognosis of advanced non­small cell lung cancer patients treated with anti­PD­1 inhibitors based on the absolute counts of lymphocyte subsets.

BACKGROUND: Patients treated with immune checkpoint inhibitors (ICIs) are at risk of considerable adverse events, and the ongoing struggle is to accurately identify the subset of patients who will benefit. Lymphocyte subsets play a pivotal role in the antitumor response, this study attempted to combine the absolute counts of lymphocyte subsets (ACLS) with the clinicopathological parameters to construct nomograms to accurately predict the prognosis of advanced non-small cell lung cancer (aNSCLC) patients treated with anti-PD-1 inhibitors. METHODS: This retrospective study included a training cohort (n = 200) and validation cohort (n = 100) with aNSCLC patients treated with anti-PD-1 inhibitors. Logistic and Cox regression were conducted to identify factors associated with efficacy and progression-free survival (PFS) respectively. Nomograms were built based on independent influencing factors, and assessed by the concordance index (C-index), calibration curve and receiver operating characteristic (ROC) curve. RESULT: In training cohort, lower baseline absolute counts of CD3+ (P < 0.001) and CD4+ (P < 0.001) were associated with for poorer efficacy. Hepatic metastases (P = 0.019) and lower baseline absolute counts of CD3+ (P < 0.001), CD4+ (P < 0.001), CD8+ (P < 0.001), and B cells (P = 0.042) were associated with shorter PFS. Two nomograms to predict efficacy at 6-week after treatment and PFS at 4-, 8- and 12-months were constructed, and validated in validation cohort. The area under the ROC curve (AUC-ROC) of nomogram to predict response was 0.908 in training cohort and 0.984 in validation cohort. The C-index of nomogram to predict PFS was 0.825 in training cohort and 0.832 in validation cohort. AUC-ROC illustrated the nomograms had excellent discriminative ability. Calibration curves showed a superior consistence between the nomogram predicted probability and actual observation. CONCLUSION: We constructed two nomogram based on ACLS to help clinicians screen of patients with possible benefit and make individualized treatment decisions by accurately predicting efficacy and PFS for advanced NSCLC patient treated with anti-PD-1 inhibitors.

Cation-Modified Poly(vinyl alcohol) Film to Optimize the Bistability of Transparent Electrophoretic Display Based on Charge Adsorption Behavior in Nonpolar Solvent.

Electrophoretic displays (EPDs) utilize the electrophoretic particles in electronic ink (e-ink) to display different color states with bistability. Bistability of EPDs is achieved by placing colloidal particles in a highly viscous solvent to keep the distribution of colloidal particles stable without sustaining the external field, so it only consumes power when updating the image. The feature of low power consumption makes it suitable for applications such as advertising boards, price tags, etc. Apart from these applications, recent research on lateral-driving EPDs extends its applications to smart windows, privacy control, and so on. However, achieving bistability by simply increasing the viscosity of solvent is inefficient in the case of lateral driving operation. Therefore, it is deserving to have intensive study on the mechanism of bistability from other aspects. Herein, we propose a mechanism to investigate the charge adsorption behavior on the electrode to affect the bistability of particles, which is based on the "Stern layer adsorption/desorption" model. Based on the above mechanism, we further fabricated a hexadecyl trimethylammonium bromide (CTAB)/poly(vinyl alcohol) (PVA) composite film on the electrode to improve the bistability of lateral-driving EPD by reducing the diffusion current caused by unabsorbed charges. This developed lateral-driving EPD can significantly improve the bistability, which is enhanced from 40 s to 7 min, an increase by a factor of approximately 10. This work gives a way to consider the bistability of colloidal particles in nonpolar solvent.

An atlas of epithelial cell states and plasticity in lung adenocarcinoma.

Understanding the cellular processes that underlie early lung adenocarcinoma (LUAD) development is needed to devise intervention strategies1. Here we studied 246,102 single epithelial cells from 16 early-stage LUADs and 47 matched normal lung samples. Epithelial cells comprised diverse normal and cancer cell states, and diversity among cancer cells was strongly linked to LUAD-specific oncogenic drivers. KRAS mutant cancer cells showed distinct transcriptional features, reduced differentiation and low levels of aneuploidy. Non-malignant areas surrounding human LUAD samples were enriched with alveolar intermediate cells that displayed elevated KRT8 expression (termed KRT8+ alveolar intermediate cells (KACs) here), reduced differentiation, increased plasticity and driver KRAS mutations. Expression profiles of KACs were enriched in lung precancer cells and in LUAD cells and signified poor survival. In mice exposed to tobacco carcinogen, KACs emerged before lung tumours and persisted for months after cessation of carcinogen exposure. Moreover, they acquired Kras mutations and conveyed sensitivity to targeted KRAS inhibition in KAC-enriched organoids derived from alveolar type 2 (AT2) cells. Last, lineage-labelling of AT2 cells or KRT8+ cells following carcinogen exposure showed that KACs are possible intermediates in AT2-to-tumour cell transformation. This study provides new insights into epithelial cell states at the root of LUAD development, and such states could harbour potential targets for prevention or intervention.

Experimental Investigation of the Size Effect on Roller-Compacted Hydraulic Asphalt Concrete under Different Strain Rates of Loading.

Asphalt concrete is widely used in hydraulic structure facilities as an impermeable structure in alpine cold regions, and its dynamic mechanical properties are influenced by the strain rate and specimen size. However, the specimen size has an important effect on mechanical properties; few systematic studies have investigated on the size effect of hydraulic asphalt concrete (HAC) under dynamic or static loading rates. In the present study, four sizes of cylindrical roller-compacted hydraulic asphalt concrete (RCHAC) specimens with heights of 50 mm, 100 mm, 150 mm, and 200 mm were prepared and tested under different loading rates ranging from 10-5 s-1 to 10-2 s-1 to investigate the size effects of mechanical properties and failure modes at the temperature of 5 °C. The effect of strain rate on the size effects of the compressive strength and the elastic modulus of RCHAC have also been explored. These tests indicate that when the specimen size increases, the compressive strength and failure degree decrease, while the elastic modulus increases. When the height increases from 50 mm to 200 mm, the compressive strength at different strain rates decreased by more than 50%. Furthermore, the elastic modulus increased by about 211.8% from 0.51 GPa to 1.59 GPa at a strain rate of 10-5 s-1, and increased by 150% from 5.08 GPa to 12.71 GPa at a strain rate of 10-2 s-1. As the strain rate increases, the variation trends with the size of the compressive strength, elastic modulus, and failure degree are distinctly intensified. A modified dynamic size effect law, which incorporates both the specimen size and strain rate, is proposed and verified to illustrate the dynamic size effect for the RCHAC under different loading rates.

Design, synthesis and biological evaluation of 1,2,3-triazole benzothiazole derivatives as tubulin polymerization inhibitors with potent anti-esophageal cancer activities.

In this work, we utilized the molecular hybridization strategy to design and synthesize novel 1,2,3-triazole benzothiazole derivatives K1-26. The antiproliferative activities against MGC-803, Kyse30 and HCT-116 cells were explored, and their structure-activity relationship were preliminarily conducted and summarized. Among them, compound K18, exhibited the strongest proliferation inhibitory activity, with esophageal cancer cells Kyse30 and EC-109 being the most sensitive to its effects (IC50 values were 0.042 and 0.038 µM, respectively). Compound K18 effectively inhibited tubulin polymerization (IC50 = 0.446 µM), thereby hindering tubulin polymerize into filamentous microtubules in Kyse30 and EC-109 cells. Additionally, compound K18 induced the degradation of oncogenic protein YAP via the UPS pathway. Based on these dual molecular-level effects, compound K18 could induce G2/M phase arrest and cell apoptosis in Kyse30 and EC-109 cells, as well as regulate the expression levels of cell cycle and apoptosis-related proteins. In summary, our findings highlight a novel 1,2,3-triazole benzothiazole derivative K18, which possesses significant potential for treating esophageal cancers.

(-)-Syringaresinol attenuates ulcerative colitis by improving intestinal epithelial barrier function and inhibiting inflammatory responses.

BACKGROUND: (-)-Syringaresinol (SYR), a natural lignan with significant antioxidant and anti-inflammatory activities, possesses various pharmacological benefits including cardio-protective, antibacterial, anticancer, and anti-aging effects. It was shown that the effectiveness of (+)-syringaresinol diglucoside on the ulcerative colitis (UC) was attributed to the active metabolite (+)-syringaresinol (the enantiomor of SYR). However, the efficacy of SYR against UC remains unclear, and the associated molecular mechanism has not been revealed yet PURPOSE: This study aimed to assess the protective effect of SYR in UC and its underlying mechanism STUDY DESIGN AND METHODS: We examined SYR's protective impact on the intestinal epithelial barrier and its ability to inhibit inflammatory responses in both a lipopolysaccharide (LPS)-induced Caco-2 cell model and a dextran sodium sulfate (DSS)-induced UC mouse model. We also explored the potential signaling pathways regulated by SYR using transcriptome analysis and western blot assay RESULTS: In Caco-2 cells, SYR significantly increased trans-epithelial electrical resistance, reduced tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interferon-γ (IFN-γ), and cyclooxygenase-2 (COX-2) levels, and enhanced cellular tight junction protein expression and distribution. In mice with UC, oral treatment with SYR (10, 20, 40 mg·kg-1) dose-dependently increased body weight, colon length, and expression of tight junction proteins, decreased disease activity index score, spleen coefficient, cytokine serum levels, bacterial translocation, and intestinal damage, and also preserved the ultrastructure of colonic mucosal cells. Transcriptomics indicated that the anti-UC effect of SYR is mediated via the PI3K-Akt/MAPK/Wnt signaling pathway. CONCLUSION: In summary, SYR effectively mitigated the development of UC by enhancing the intestinal epithelial barrier function and attenuating the inflammatory response. The plant-derived product SYR might be a potentially effective therapeutical agent against UC.

Low-voltage electrostatic field enhances the frozen force of -12 ℃ to suppress oxidative denaturation of the lamb protein during the subsequent frozen storage process after finishing initial freezing.

The effect of low-voltage electrostatic field (LVEF) assisted -9 °C (LVEF-9) and -12 °C (LVEF-12) frozen, non-LVEF-assisted -9 °C (NLVEF-9) and -12 °C (NLVEF-12) frozen, and conventional frozen (CF-18, -18 °C) storage on the muscle microstructure and the oxidative denaturation of the lamb protein during the subsequent frozen storage process after finishing initial freezing was investigated. Compared with NLVEF-9, LVEF-9, and NLVEF-12, LVEF-12 maintained the better integrity of muscle microstructure, demonstrated by smaller holes, more complete Z-line and M-line, and no significant difference with CF-18 (P > 0.05). Furthermore, LVEF-12 effectively inhibited protein oxidative denaturation as shown by the lower carbonyl content, surface hydrophobicity, and higher total/active sulfhydryl groups and Ca2+-ATPase activity. Moreover, LVEF-12 effectively maintained the integrity of the secondary and tertiary structure of proteins, reduced cross-linking aggregation of proteins, and sustained better functional properties, as shown by higher α-helix content, fluorescence intensity, protein solubility, and lower R-value, disulfide bonds.

The frequency of risk pathological characteristics in clinically low-risk papillary thyroid microcarcinoma suitable for active surveillance.

PURPOSE: Active surveillance has emerged as an initial management strategy for patients with low-risk papillary thyroid microcarcinoma (PTMC). The main objective of this research was to investigate the frequency of risk pathological characteristics among patients with clinically low-risk PTMC who are suitable for Active Surveillance. METHODS: A retrospective review was conducted on patients who underwent lobectomy for PTMC between January 2013 and December 2018. Patients with bilateral tumors, macroscopic multifocal tumors, macroscopic extrathyroidal extension (ETE), clinical lymph node metastases, macroscopic extranodal extension (ENE), distant metastases, a history of neck radiation or familial thyroid cancer were excluded. Pathological characteristics were collected from the postoperative pathological results. Aggressive variants, multifocality, ETE, lymphovascular invasion (LVI), perineural invasion (PNI), metastatic lymph nodes (LNs) ≥ 5, and ENE were defined as risk characteristics. RESULTS: The study included 4923 patients, of whom 1229 (25.0%) were male. The mean age was 43 years. A total of 2250 patients (45.7%) exhibited risk characteristics. Among them, 15 patients presented with aggressive variants, and 1813 patients (36.8%) had ETE. Multifocality, LVI, and PNI were observed in 551 (11.2%), 21 (0.4%), and 40 (0.8%) patients, respectively. A total of 139 patients (2.8%) had five or more metastatic LNs, and ENE was identified in 140 patients. Notably, 172 patients (3.5%) fulfilled the criteria for completion thyroidectomy, as they had aggressive variants, LVI, or five or more metastatic LNs. CONCLUSIONS: Nearly half of the patients diagnosed with clinically low-risk PTMC exhibited risk pathological characteristics, and a small proportion of patients met the criteria for completion thyroidectomy.

The migration and transformation mechanism of vanadium in a soil-pore water-maize system.

The migration mechanism of vanadium (V) in the soil-pore water-maize system has not been revealed. This study conducted pot experiments under artificial control conditions to reveal V's distribution and transport mechanism under different growth stages and V content gradient stress. The V content in the soil pore water gradually increased by an order of magnitude. The V content of pore water in the no-plant group was higher than that in the plant group, indicating that the maize roots absorbed V. The V exists in the form of pentavalent oxygen anions, in which H2VO4- occupies the most significant proportion. With increasing V content, the root area, root number, root length, and tip number decreased significantly. The malondialdehyde content in maize leaves showed an increasing trend, indicating the degree of lipid peroxidation was gradually enhanced. The V content was in the order of root > leaf > stem > fruit and maturity stage > flowering stage > jointing stage, respectively. The transfer coefficient reached a maximum under natural conditions, and increased gradually with the growth. The results of synchrotron radiation X-ray absorption near edge structure (XANES) analysis showed that Fe in maize roots mainly comprised of Fe2O3 and Fe3O4. The Fe in the soil is primarily existed in lepidocrocite and Fe2O3. The µ-XRF analysis showed that V and Fe enriched in the roots with a positive relationship, indicating the synergistic absorption of V and Fe by roots. Part of the Fe2+ reduced V5+ to V4+ or V3+ in the forms of VO2+, V(OH)2+, or V(OH)3 (s), and fixed V at the root. Soil weak acid-soluble fraction V and soil total V were vital factors to maize extraction. This study provides new insights into V biogeochemical behavior and a scientific basis for correctly evaluating its ecological and human health risks.

Active matrix driven electrophoretic display with in-plane switching layout and driving waveform for reflective and transparent modes.

In-plane switching electrophoretic display (IPS-EPD) is an emerging field of display technology which achieves particles moving horizontally through a lateral electric field. Compared to vertically driven electrophoretic display (V-EPD), IPS-EPD exhibits the feasibility of transparent display function. However, most of the previous research was hindered by long response time, low optical transmittance, or complex structures. In this paper, we have proposed a newly developed electrode layout and driving waveform for IPS-EPD, achieving a device with fast response time of 0.32 s, high transmittance of 58.07%, good transmittance-contrast ratio of 11.25, and simple structure, which show a significant improvement over other related research. Additionally, we elucidated the physical mechanism for the device through developing a particles motion simulation. Finally, we presented a prototype of an IPS-EPD with TFT panel, which exhibits excellent performance in various application scenarios, making it a possible application prospect in mobile phone cases, glasses, windows, and so on.

OGT-1 regulates synaptic assembly through the insulin signaling pathway.

The formation and maintenance of synapses are precisely regulated, and the misregulation often leads to neurodevelopmental or neurodegenerative disorders. Besides intrinsic genetically encoded signaling pathways, synaptic structure and function are also regulated by extrinsic factors, such as nutrients. O-GlcNAc transferase (OGT), a nutrient sensor, is abundant in the nervous system and required for synaptic plasticity, learning, and memory. However, whether OGT is involved in synaptic development and the mechanism underlying the process are largely unknown. In this study, we found that OGT-1, the OGT homolog in C. elegans, regulates the presynaptic assembly in AIY interneurons. The insulin receptor DAF-2 acts upstream of OGT-1 to promote the presynaptic assembly by positively regulating the expression of ogt-1. This insulin-OGT-1 axis functions most likely by regulating neuronal activity. In this study, we elucidated a novel mechanism for synaptic development, and provided a potential link between synaptic development and insulin-related neurological disorders.