Differential Modulation Research Articles

Enhanced activation of retinal progenitor cells by zinc silicate bioceramics for effective functional restoration in retinal degenerative diseases

AbstractRetinal degenerative diseases, primarily owing to the gradual loss of neuronal cells, could lead to blindness. Transplantation of retinal progenitor cells (RPCs), which had the unique ability to differentiate into neuronal cells, offered promising therapeutic potential for these diseases. However, a critical challenge in stem cell therapy was the efficient promotion of the directed proliferation and differentiation of progenitor cells. To overcome this limitation, we formulated a zinc silicate bioceramic (ZS) composite hydrogel. The experimental outcomes demonstrated that this novel material possessed substantial advantages and immense possibilities for mimicking the extracellular matrix environment, thereby effectively modulating stem cell proliferation and differentiation. Notably, it enhanced the differentiation of RPCs into neurons while suppressing glial cell differentiation. In particular, ZS had an exceptional capacity to induce the differentiation of RPCs into photoreceptor cells, a specialized type of neuronal cell. It was important to highlight that the ZS composite hydrogel predominantly facilitated the differentiation of RPCs through activation of the Tiam2‐Rac signaling pathway. Concurrently, it stimulated proliferation via activation of the AKT and ERK signaling pathways. The Zn ions in the ZS composite hydrogel primarily promoted the proliferation of RPCs, while the synergistic effect of Zn ions and Si ions contributed to reducing inflammatory factor expression and promoting the neuronal differentiation of RPCs. In conclusion, the meticulous modulation of RPC proliferation and differentiation mediated by ZS bioceramics held promise for novel therapeutic strategies of retinal degenerative diseases and neurodegenerative disorders.

Duplexed direct RNA sequencing protocol using polyadenylation and polyuridylation.

Oxford Nanopore Technologies provides multiplexing options for DNA and cDNA sequencing, but not for direct RNA sequencing. Here we describe a duplexing approach and validate it by simultaneously sequencing the Saccharomyces cerevisiae rRNA from wild type and knockout that have differential rRNA modifications, successfully demultiplexing the data using bioinformatics approaches.

Suppression of METTL3 expression attenuated matrix stiffness-induced vaginal fibroblast-to-myofibroblast differentiation and abnormal modulation of the extracellular matrix in pelvic organ prolapse.

Fibrosis of the connective tissue in the vaginal wall predominates in pelvic organ prolapse (POP), which is characterized by excessive fibroblast-to-myofibroblast differentiation and abnormal deposition of the extracellular matrix (ECM). Our study aimed to investigate the effect of ECM stiffness on vaginal fibroblasts and to explore the role of methyltransferase 3 (METTL3) in the development of POP. Polyacrylamide hydrogels were applied to create an ECM microenvironment with variable stiffness to evaluate the effects of ECM stiffness on the proliferation, differentiation, and expression of ECM components in vaginal fibroblasts. METTL3small interfering RNA and an overexpression vector were transfected into vaginal fibroblasts to evaluate the effects of METTL3silencing and overexpression on matrix stiffness-induced vaginal fibroblast-to-myofibroblast differentiation and abnormal modulation of the ECM. Both procedures were detected by 5-ethynyl-2'-deoxyuridine (EdU) staining, Western blotting (WB), quantitative real-time polymerase chain reaction (RT-qPCR), and immunofluorescence (IF). Vaginal fibroblasts from POP patients exhibited increased proliferation ability, increased expression of α-smooth muscle actin (α-SMA), decreased expression of collagen I/III, and significantly decreased expression of tissue inhibitors of matrix metalloproteinases (TIMPs) in the stiff matrix (P<0.05). Compared with those from non-POP patients, vaginal wall tissues from POP patients demonstrated a significant increase in METTL3 content (P<0.05). However, silencing METTL3 expression in vaginal fibroblasts with high ECM stiffness resulted in decreased proliferation ability, decreased α-SMA expression, an increased ratio of collagen I/III, and increased TIMP1 and TIMP2 expression. Conversely, METTL3 overexpression significantly promoted the process of increased proliferation ability, increased α-SMA expression, decreased ratio of collagen I/III and decreased TIMP1 and TIMP2 expression in the soft matrix (P<0.05). Elevated ECM stiffness can promote excessive proliferation, differentiation, and abnormal ECM modulation, and the expression of METTL3 plays an important role in alleviating or aggravating matrix stiffness-induced vaginal fibroblast-to-myofibroblast differentiation and abnormal ECM modulation.

Posttranscriptional Control of Neural Progenitors Temporal Dynamics During Neocortical Development by Syncrip.

The development of the mammalian neocortex is precisely regulated by temporal gene expression, yet the temporal regulatory mechanisms of cortical neurogenesis, particularly how radial glial cells (RGCs) sequentially generate deep to superficial neurons, remain unclear. Here, the hnRNP family member Syncrip (hnRNP Q) is identified as a key modulator of superficial neuronal differentiation in neocortical neurogenesis. Syncrip knockout in RGCs disrupts differentiation and abnormal neuronal localization, ultimately resulting in superficial cortical layer defects as well as learning and memory impairments in mice. Single-cell RNA sequencing analysis demonstrated that the knockout of Syncrip disrupts the late-stage neurogenesis, stalling transcriptional progression in RGCs. Mechanistically, Syncrip maintains the transcription of temporal process-related transcription factors by recruiting stabilization complexes through phase separation, crucially regulating the Notch signaling pathway that determines the fate of RGCs. Furthermore, pathogenic human mutations in Syncrip weaken its phase-separation capability, failing to form stable complexes normally. Thus, Syncrip acts as a mediator of posttranscriptional regulatory mechanisms, governing the fate progression of RGCs and the advancement of intrinsic temporal programs. This study establishes an intracellular mechanism for posttranscriptional regulation of progressive fate determination in cortical neurogenesis.

The analysis of gene co-expression network and immune infiltration revealed biomarkers between triple-negative and non-triple negative breast cancer.

Triple-negative breast cancer (TNBC) is a heterogeneous disease with a worse prognosis. Despite ongoing efforts, existing therapeutic approaches show limited success in improving early recurrence and survival outcomes for TNBC patients. Therefore, there is an urgent need to discover novel and targeted therapeutic strategies, particularly those focusing on the immune infiltrate in TNBC, to enhance diagnosis and prognosis for affected individuals. The gene co-expression network and gene ontology analyses were used to identify the differential modules and their functions based on the GEO dataset of GSE76275. The Weighted Gene Co-Expression Network Analysis (WGCNA) was used to describe the correlation patterns among genes across multiple samples. Subsequently, we identified key genes in TNBC by assessing genes with an absolute correlation coefficient greater than 0.80 within the eigengene of the enriched module that were significantly associated with breast cancer subtypes. The diagnostic potential of these key genes was evaluated using receiver operating characteristic (ROC) curve analysis with three-fold cross-validation. Furthermore, to gain insights into the prognostic implications of these key genes, we performed relapse-free survival (RFS) analysis using the Kaplan-Meier plotter online tool. CIBERSORT analysis was used to characterize the composition of immune cells within complex tissues based on gene expression data, typically derived from bulk RNA sequencing or microarray datasets. Therefore, we explored the immune microenvironment differences between TNBC and non-TNBC by leveraging the CIBERSORT algorithm. This enabled us to estimate the immune cell compositions in the breast cancer tissue of the two subtypes. Lastly, we identified key transcription factors involved in macrophage infiltration and polarization in breast cancer using transcription factor enrichment analysis integrated with orthogonal omics. The gene co-expression network and gene ontology analyses revealed 19 modules identified using the dataset GSE76275. Of these, modules 5, 11, and 12 showed significant differences between in breast cancer tissue between TNBC and non-TNBC. Notably, module 11 showed significant enrichment in the WNT signaling pathway, while module 12 demonstrated enrichment in lipid/fatty acid metabolism pathways. Subsequently, we identified SHC4/KCNK5 and ABCC11/ABCA12 as key genes in module 11 and module 12, respectively. These key genes proved to be crucial in accurately distinguishing between TNBC and non-TNBC, as evidenced by the promising average AUC value of 0.963 obtained from the logistic regression model based on their combinations. Furthermore, we found compelling evidence indicating the prognostic significance of three key genes, KCNK5, ABCC11, and ABCA12, in TNBC. Finally, we also identified the immune cell compositions in breast cancer tissue between TNBC and non-TNBC. Our findings revealed a notable increase in M0 and M1 macrophages in TNBC compared to non-TNBC, while M2 macrophages exhibited a significant reduction in TNBC. Particularly intriguing discovery emerged with respect to the transcription factor FOXM1, which demonstrated a significant regulatory role in genes positively correlated with the proportions of M0 and M1 macrophages, while displaying a negative correlation with the proportion of M2 macrophages in breast cancer tissue. Our research provides new insight into the biomarkers and immune infiltration of TNBC, which could be useful for clinical diagnosis of TNBC.

Cross-modal feature interaction network for heterogeneous change detection

ABSTRACT Heterogeneous change detection is a task of considerable practical importance and significant challenge in remote sensing. Heterogeneous change detection involves identifying change areas using remote sensing images obtained from different sensors or imaging conditions. Recently, research has focused on feature space translation methods based on deep learning technology for heterogeneous images. However, these types of methods often lead to the loss of original image information, and the translated features cannot be efficiently compared, further limiting the accuracy of change detection. For these issues, we propose a cross-modal feature interaction network (CMFINet). Specifically, CMFINet introduces a cross-modal interaction module (CMIM), which facilitates the interaction between heterogeneous features through attention exchange. This approach promotes consistent representation of heterogeneous features while preserving image characteristics. Additionally, we design a differential feature extraction module (DFEM) to enhance the extraction of true change features from spatial and channel dimensions, facilitating efficient comparison after feature interaction. Extensive experiments conducted on the California, Toulouse, and Wuhan datasets demonstrate that CMFINet outperforms eight existing methods in identifying change areas in different scenes from multimodal images. Compared to the existing methods applied to the three datasets, CMFINet achieved the highest F1 scores of 83.93%, 75.65%, and 95.42%, and the highest mIoU values of 85.38%, 78.34%, and 94.87%, respectively. The results demonstrate the effectiveness and applicability of CMFINet in heterogeneous change detection.

The Dual Role of ADAMTS9-AS1 in Various Human Cancers: Molecular Pathogenesis and Clinical Implications.

Long non-coding RNA (lncRNA) is a type of non-coding RNA distinguished by a length exceeding 200 nucleotides. Recent studies indicated that lncRNAs participate in various biological processes, such as chromatin remodeling, transcriptional and post-transcriptional regulation, and the modulation of cell proliferation, death, and differentiation, hence influencing gene expression and cellular function. ADAMTS9-AS1, an antisense long non-coding RNA situated on human chromosome 3p14.1, has garnered significant interest due to its pivotal involvement in the advancement and spread of diverse malignant tumors. ADAMTS9-AS1 functions as a competitive endogenous RNA (ceRNA) that interacts with multiple microRNAs (miRNAs) and plays a crucial role in regulating gene expression and cellular functions by modulating essential signaling pathways, including PI3K/AKT/mTOR, Wnt/β-catenin, and Ras/MAPK pathways. Dysregulation of this factor has been linked to tumor development, migration, invasion, and resistance to apoptotic mechanisms, including as iron-induced apoptosis, underscoring its intricate function in cancer pathology. While current research has clarified certain pathways involved in cancer formation, additional clinical and in vivo investigations are necessary to enhance comprehension of its specific involvement across various cancer types. This review encapsulates the recent discoveries on the correlation of ADAMTS9-AS1 with numerous malignancies, clarifying its molecular mechanisms and its prospective role as a therapeutic target in oncology. Furthermore, it identifies ADAMTS9-AS1 as a potential early diagnostic biomarker and therapeutic target, offering novel opportunities for targeted intervention in oncology.

Single-cell morphological tracking of cell states to identify small-molecule modulators of liver differentiation

Single-cell morphological tracking of cell states to identify small-molecule modulators of liver differentiation

Rosavin derived from Rhodiola alleviates colitis in mice through modulation of Th17 differentiation

BackgroundRosavin (RSV) is a naturally occurring compound isolated from Rhodiola species. Although RSV has been reported with pharmacological activities of anti-oxidation, anti-inflammation, anti-stress and immunomodulation, its effect on colitis relieving and the underlying mechanism remains unclear. PurposeThis study aims to investigate whether and how RSV alleviated colitis in mice. Study Design and MethodsThe protective effect of RSV (50, 100, 200 mg/kg, p.o.) was investigated on dextran sulfate sodium (DSS) mediated mouse models of acute and chronic colitis. Alterations in fecal microbiota was evaluated by 16S rRNA sequencing. Pseudo germ-free mice by antibiotics treatment was applied to evaluate the RSV-mediated functional role of gut microbiota on colitis. RNA sequencing was performed to determine RSV-induced colonic response. Primary T cell culture was conducted to see the effect of RSV on Th17 and Treg differentiation. Whole blood assay, dual luciferase reporter assay and molecular docking method were applied to investigate the mechanism and target of RSV in Th17 regulation. ResultsOral RSV significantly relieved DSS-mediated acute and chronic colitis in mice, which recovered body weight loss, reduced disease activity index, alleviated colon injury, inhibited inflammation, suppressed the apoptosis of intestinal epithelia and maintained intestinal barrier function. Moreover, RSV specifically regulated intestinal microbiota by recovering DSS-mediated microbial changes and elevating beneficial microbes of Lactobacillus and Akkermansia. Antibiotics treatment experiment showed that the protective role of RSV was at least partially dependent on gut microbiota; however, in vitro incubation showed that RSV did not directly promote the growth of Lactobacillus and Akkermansia strains. Further analysis showed that RSV-mediated genetic alteration in colon was enriched in lymphocyte regulation. Moreover, RSV regulated the balance of Th17/Treg in colitis mice. Importantly, RSV inhibited the differentiation of Th17 cell in vitro, suppressed the generation of IL-17 by Th17 cells, and downregulated Rorc encoding RORγt and the downstream Il17. RSV significantly inhibited the RORγt transcription activity, and bound to the RORγt ligand binding domain. ConclusionRSV alleviates murine colitis through regulating intestinal immunity. Notably, RSV is identified as a novel Th17 regulator that inhibits RORγt-mediated Th17 differentiation. The results potentiate the Rhodiola-derived chemical as novel anti-colitis agents.

Low-Complexity Maximum-Likelihood Detectors Incorporating Pre-calculated Symbol Metrics for Differential Spatial Modulation

Low-Complexity Maximum-Likelihood Detectors Incorporating Pre-calculated Symbol Metrics for Differential Spatial Modulation

Quantum Machine Learning for Video Compression: An Optimal Video Frames Compression Model using Qutrits Quantum Genetic Algorithm for Video multicast over the Internet

The transmission of video is greatly aided by video compression. Redundancy (spatial, temporal, statistical, and psycho-visual) within and between video frames is something that video compression approaches aim to get rid of. The degree to which similarity-based redundancy exists between consecutive frames, however, is a function of how often the frames are sampled and how the objects in the scene are moving. Existing neural network-based video compression approaches rely on a static codebook to perform compression, which prevents them from adapting to new video’s data. In order to create an optimal codebook for vector quantization, which is then employed as an activation function inside a neural network's hidden layer, this research offers a modified video compression method based on a Qutrits based Quantum Genetic Algorithm (QQGA). Using quantum parallelization and entanglement of the quantum state, QQGA is capable of solving the same set of problems as a traditional genetic algorithm while considerably accelerating the evolutionary process. The technique is built on the concept of utilizing Qutrits (three-level quantum system) to represent population individuals. The evolution operator, which is responsible for the updates to the quantum system state, has been constructed using a straightforward approach that does not need a lookup table. Compared to qubit, qudit provides a larger state space to store and process information, and thus can enhance the algorithm’s efficiency. To create the context-based initial codebook, the background subtraction algorithm is used to extract moving objects from frames. Moreover, important wavelet coefficients are compressed losslessly using Differential Pulse Code Modulation (DPCM), whereas low energy coefficients are compressed lossy using Learning Vector Quantization neural networks (LVQ). To obtain a high compression ratio, Run-Length Encoding is then used to encode the quantized coefficients. In comparison to the conventional evolutionary algorithm-based video compression method, experiments have shown that the quantum-inspired system may achieve a greater compression ratio with acceptable efficiency as evaluated by PSNR.

The Promise of Epigenetic Editing for Treating Brain Disorders.

Brain disorders, especially neurodegenerative diseases, affect millions of people worldwide. There is no causal treatment available; therefore, there is an unmet clinical need for finding therapeutic options for these diseases. Epigenetic research has resulted in identification of various genomic loci with differential disease-specific epigenetic modifications, mainly DNA methylation. These biomarkers, although not yet translated into clinically approved options, offer therapeutic targets as epigenetic modifications are reversible. Indeed, clinical trials are designed to inhibit epigenetic writers, erasers, or readers using epigenetic drugs to interfere with epigenetic dysregulation in brain disorders. However, since such drugs elicit genome-wide effects and potentially cause toxicity, the recent developments in the field of epigenetic editing are gaining widespread attention. In this review, we provide examples of epigenetic biomarkers and epi-drugs, while describing efforts in the field of epigenetic editing, to eventually make a difference for the currently incurable brain disorders.

Unveiling the Prevalence and Impact of Silent Rhinovirus Infection in Chronic Rhinosinusitis with Nasal Polyps.

Chronic rhinosinusitis with nasal polyps (CRSwNP) involves persistent sinus inflammation, with emerging evidence suggesting a potential role of rhinovirus (RV) in its pathophysiology. However, whether RV exists in nasal tissues and affects the nasal mucosa after infection symptoms resolve remains unknown. This study aimed to investigate the prevalence and impact of silent RV infection in nasal tissues. RV loads were detected in nasal tissues from 47 controls and 101 CRSwNP patients without respiratory infection. Participants were categorized into RV-positive (+), RV-negative (-), and the "gray zone" groups. Quantitative PCR (qPCR), Western Blot, and immunofluorescence assays were employed to analyze the impact of silent RV infection on the immune status of nasal tissues. Silent RV infection was prevalent in both control (34%) and CRSwNP (30.7%) tissues, with higher viral loads observed in nasal polyps. In controls, it was associated with high expression of type Ⅰ and Ⅱ interferon, type 2 inflammation, interleukin-17A, and interleukin-10. In CRSwNP patients, silent RV infection was associated with lower type I IFN, IL-17A, type 2 inflammation, and IL-10, but higher type II IFN compared to those without RV infection. Meanwhile, RV (+) nasal polyps exhibited fewer tissue eosinophils and neutrophils than RV (-) nasal polyps. Silent RV infection was prevalent in nasal tissues, with a higher viral load detected in nasal polyps. This silent rhinovirus infection was associated with distinct immune responses in healthy controls and CRSwNP patients, involving differential modulation of IFNs, Th2 cytokines, IL-17A, IL-10, as well as eosinophil and neutrophil levels.

Adverse effects of environmentally relevant microplastics on in vivo endpoints, oxidative stress, and mitogen-activated protein kinase signaling pathway and multixenobiotic resistance system in the marine rotifer Brachionus plicatilis.

This study compared the toxicological effects of environmentally relevant microplastics (MPs) on the marine rotifer Brachionus plicatilis, focusing on MPs derived from various sources, including fossil fuel-based low-density polyethylene, bio-based polylactic acid (PLA), biodegradable poly(butylene adipate-co-terephthalate), and a novel PLA modified with β-cyclodextrin. We assessed in vivo effects such as reproductive output and mortality, alongside in vitro oxidative stress responses, including oxidative stress, antioxidant enzyme activities, and activation of the mitogen-activated protein kinase (MAPK) signaling pathway and the multixenobiotic resistance (MXR) system. Reproductive output and lifespan reduced significantly across all MP types, ranging from 0.5 to 10mgL-1, indicating compromised reproductive fitness and life maintenance. At an environmentally relevant concentration of 0.5mgL-1, in vitro assessments revealed differential modulation of reactive oxygen species levels and antioxidant enzyme activities, contingent upon the specific MP type. Moreover, MAPK signaling pathway and MXR assays showed changes in phosphorylation and detoxification proteins depending on the type of MPs. This study highlights the ecological risks that various MPs, including bio-based, biodegradable, and petrochemical-based MPs, could pose in marine environments.

THE ROLE OF EDUCATION ON BRAIN PATHOLOGY AND COGNITIVE DECLINE ACROSS WOMEN AND MEN IN THE US

Abstract Women have a higher risk of developing Alzheimer’s disease and related dementia (ADRD) than men. Education, as a key contributor to cognitive reserve, might protect the ADRD onset. While existing evidence suggests that increased educational attainment may attenuate the negative impact of neuropathology on cognitive function, these studies focused primarily on average cognitive function, and little is known about whether education similarly attenuates the relationship between neuropathology and cognitive decline among those with high or low levels of cognitive outcomes or sex/gender. Using the Alzheimer’s Disease Neuroimaging Initiative sample (772 male and 627 female participants, who were cognitively normal or had mild cognitive impairment at baseline), we investigated education attainment modified the association between anatomical reduction in the brain and cognitive decline in sex-stratified models. We applied quantile regression with a three-way interaction term (education x cortical thickness x years) against 10-year cognitive function, an established specification for testing the cognitive reserve mechanism. We included a robust set of biological and contextual confounders. Primary results showed that, among males, education had attenuated the relationship between brain pathology and cognitive decline at lower levels of cognitive function distribution. Among females, education attenuates brain pathology and cognitive decline in all levels of outcome distribution with large confidence intervals. We will discuss potential explanations for differential effect modification by education on the brain pathology-cognition relationship across sex/gender and expand its implications for future research and policy/practice intervention.

Reprogramming patient-iPSC specific retinal organoids for deciphering epigenetic modifications of RNA methylation.

Induced pluripotent stem cell (iPSC) technology has emerged as a powerful tool for disease modeling, providing an innovative platform for investigating disease mechanisms. iPSC-derived organoids, including retinal organoids, offer patient-specific models that closely replicate in vivo cellular environments, making them ideal for studying retinal neurodegenerative diseases where retinal ganglion cells (RGCs) are impacted. N6-methyladenosine (m6A), a prevalent internal modification in eukaryotic mRNAs, plays a critical role in RNA metabolic processes such as splicing, stability, translation, and transport. Given the high energy demands of RGCs, mitochondrial dysfunction, which leads to impaired ATP production and increased ROS levels, is often central to the progression of retinal neurodegenerative disorders. However, the epigenetic mechanisms underlying m6A modification and their contributions to these conditions remain unclear. Patient-specific iPSCs were generated from individuals with Leber's hereditary optic neuropathy (LHON) and differentiated into retinal ganglion cells (RGCs) within retinal organoids. To analyze m6A methylation, we employed quantitative PCR and focused on differential expression of key m6A-modifying enzymes. iPSC-derived retinal organoids are adaptable for studying and investigating the epigenetic mechanisms of retinal neurodegenerative diseases. Our data demonstrated the profiling of global m6A-related gene expression levels in LHON patient-derived iPSC-RGCs compared with controls, highlighting specific disruptions in m6A modification pathways. These findings suggest that differential m6A modifications may play pivotal roles in the pathogenesis of retinal neurodegenerative diseases and affect the progression of the disease in affected individuals.

Immunometabolic reprogramming in macrophages infected with active and dormant Cryptococcus neoformans: differential modulation of respiration, glycolysis, and fatty acid utilization.

Dormancy is an adaptation in which cells reduce their metabolism, transcription, and translation to stay alive under stressful conditions, preserving the capacity to reactivate once the environment reverts to favorable conditions. Dormancy and reactivation of Cryptococcus neoformans (Cn) are closely linked to intracellular residency within macrophages. Our previous work showed that in vitro murine macrophages rely on the viable but not cultivable (VBNC-a dormancy phenotype) fungus from active Cn, with striking differences in immunometabolic gene expression. Here, we analyzed the influence of VBNC and active Cn on the immunometabolism of infected macrophages, combining metabolic gene expression, mitochondrial membrane potential (ΔΨm), oxygen consumption analysis, and uptake of glucose and fatty acids. The active fungus induced mitochondrial depolarization, and increased glycolysis and mitochondrial oxygen consumption. VBNC infection in bone marrow-derived macrophage (BMDM) caused an attenuated modification in mitochondrial metabolism. However, we found differences in BMDM infected with VBNC vs those infected with active fungus, where VBNC induced an increment in fatty acid uptake in M0 and M1 BMDM, measured by incorporation of BODIPY-palmitate, accompanied by an increase in expression of fatty acid transporters Fabp1 and Fabp4. Overall, distinct fatty acid-related responses induced by VBNC and active Cn suggest different immunomodulatory reactions, depending on the microbial growth stage. We posit that, for VBNC, some of these macrophage metabolic responses reflect the establishment of prolonged microbial intracellular residency and possibly initial stages of granuloma formation.

STFNet: A Spatiotemporal Fusion Network for Forest Change Detection Using Multi-Source Satellite Images

Forest resources have important ecological and environmental values, and monitoring forest changes using remote sensing images is essential for resource management and ecological protection. However, current forest change detection methods fail to simultaneously integrate fine spatial information with temporal dynamic data, making them susceptible to pseudo changes induced by seasonal factors. In this paper, we propose a forest change detection method called STFNet that integrates multi-source spatiotemporal information. By combining fine spatial details of high-resolution images with dynamic information from time-series images, STFNet enhances the accuracy of forest change detection, alleviating the problem of information fusion difficulties caused by inconsistent granularity in spatiotemporal spectral features from different sources. In STFNet, we propose a cross-attention-based temporal differential feature fusion module (CATFF) to capture spatiotemporal dependencies within time-series images and a multiresolution contextual differential feature fusion module (MCDF) to achieve efficient spatial contexture fusion across multiresolution images. To validate our method, we conduct experiments using Gaofen and Sentinel-2 satellite images. Experimental results demonstrate that STFNet achieves excellent performance with an F1-score of 87.65%, outperforming state-of-the-art methods by at least 2.02%. Our ablation study further confirms the effectiveness of our method in leveraging time-series information to detect forest changes and suppress seasonal interference.

A pan-cancer analysis of the oncogenic role of N-acetyltransferase 8 like in human cancer

BackgroundN-Acetyltransferase 8 Like (NAT8L) inhibits natural killer (NK)/T-cell cytotoxicity by impairing the formation of the immunological synapse via N-acetylaspartate (NAA). Existing research has predominantly focused on the metabolic functions of NAT8L, particularly in adipose tissues and myelination in the brain. However, in contrast to other N-acetyltransferases such as NAT1 and NAT2, the role of NAT8L in cancer has been less extensively studied. In this study, we conducted a comprehensive pan-cancer analysis to investigate the carcinogenic role of NAT8L in human cancers.MethodsWe utilized the standardized TCGA pan-cancer dataset to analyze differential expression, clinical prognosis, gene mutation, immune infiltration, epigenetic modification, tumor stemness, and heterogeneity. Additionally, we evaluated the sensitivity of NAT8L to small molecule drugs using the GDSC and CTRP databases.ResultsIn this study, we identified that NAT8L expression was upregulated in 6 cancers and downregulated in 12 compared to normal tissues. We analyzed its prognostic value in 5 tumor types (KIRP, COAD, COADREAD, GBMLGG, LUSC) and found correlations with overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI). Furthermore, NAT8L expression was significantly correlated with levels of most immune checkpoints, immunomodulators, and immune cell infiltration. The mutation frequencies for bladder cancer (BLCA), glioblastoma multiforme and glioma (GBMLGG), lower-grade glioma (LGG), and KIRP were 1.2%, 0.9%, 0.8%, and 0.4%, respectively.ConclusionOur findings suggest that NAT8L may serve as a potential prognostic marker and therapeutic target across a variety of cancers, particularly in KIRP, COAD, COADREAD, GBMLGG, and lung squamous cell carcinoma (LUSC).

Graded Hecke algebras and equivariant constructible sheaves on the nilpotent cone

Abstract Graded Hecke algebras can be constructed geometrically, with constructible sheaves and equivariant cohomology. The input consists of a complex reductive group G (possibly disconnected) and a cuspidal local system on a nilpotent orbit for a Levi subgroup of G. We prove that every such “geometric” graded Hecke algebra is naturally isomorphic to the endomorphism algebra of a certain $G \times \mathbb{C}^\times$-equivariant semisimple complex of sheaves on the nilpotent cone $\mathfrak g_N$ in the Lie algebra of G. From there we provide an algebraic description of the $G \times \mathbb{C}^\times$-equivariant bounded derived category of constructible sheaves on $\mathfrak g_N$. Namely, it is equivalent with the bounded derived category of finitely generated differential graded modules of a suitable direct sum of graded Hecke algebras. This can be regarded as a categorification of graded Hecke algebras. This paper prepares for a study of representations of reductive p-adic groups with a fixed infinitesimal central character. In sequel papers [34, 35], that will lead to proofs of the generalized injectivity conjecture and of the Kazhdan–Lusztig conjecture for p-adic groups.