Unveiling the role of HIST2H2AC in stroke through single-cell and transcriptome analysis.

Stroke is a leading cause of death and disability, and genetic risk factors play a significant role in its development. Unfortunately, effective therapies for stroke are currently limited. Early detection and diagnosis are critical for improving outcomes and developing new treatment strategies. In this study, we aimed to identify potential biomarkers and effective prevention and treatment strategies for stroke by conducting transcriptome and single-cell analyses. Our analysis included screening for biomarkers, functional enrichment analysis, immune infiltration, cell-cell communication, and single-cell metabolism. Through differential expression analysis, enrichment analysis, and protein-protein interaction (PPI) network construction, we identified HIST2H2AC as a potential biomarker for stroke. Our study also highlighted the diagnostic role of HIST2H2AC in stroke, its relationship with immune cells in the stroke environment, and our improved understanding of metabolic pathways after stroke. Overall, our research provided important insights into the pathogenesis of stroke, including potential biomarkers and treatment strategies that can be explored further to improve outcomes for stroke patients.

Polyethylene glycol crosslinked modified chitosan/halloysite nanotube composite aerogel microspheres for efficient adsorption of melanoidin.

Melanoidins are widely present in molasses wastewater and are dark-colored macromolecules that are hazardous to the environment. Currently, adsorption methods can effectively remove melanoidins from wastewater. However, existing adsorbents have shown unsatisfactory removal efficiency for melanoidins, making practical application challenging. Polyethylene glycol crosslinked modified chitosan/halloysite nanotube composite aerogel microspheres (PCAM@HNTs) were developed as a highly efficient adsorbent for melanoidins. The removal rate of PCAM@HNTs for melanoidins was 98.53 % at adsorbent dosage 0.4 mg/mL, pH 7, temperature 303 K and 450 mg/L initial melanoidins concentration, and the corresponding equilibrium adsorption capacity was 1108.49 mg/g. The analysis results indicate that the adsorption of melanoidins by PCAM@HNTs is a spontaneous and endothermic process. It fits well with pseudo-second-order kinetic models and the Freundlich isotherm equation. The adsorption of PCAM@HNT on melanoidins is primarily attributed to electrostatic and hydrogen bonding interactions. Furthermore, PCAM@HNTs exhibit excellent biocompatibility and are nonhazardous. Therefore, PCAM@HNTs proved to be an ideal adsorbent for the decolorization of molasses wastewater.

A promise for neuronal repair: reprogramming astrocytes into neurons in vivo.

Massive loss of neurons following brain injury or disease is the primary cause of central nervous system dysfunction. Recently, much research has been conducted on how to compensate for neuronal loss in damaged parts of the nervous system and thus restore functional connectivity among neurons. Direct somatic cell differentiation into neurons using pro-neural transcription factors, small molecules, or microRNAs, individually or in association, is the most promising form of neural cell replacement therapy available. This method provides a potential remedy for cell loss in a variety of neurodegenerative illnesses, and the development of reprogramming technology has made this method feasible. This article provides a comprehensive review of reprogramming, including the selection and methods of reprogramming starting cell populations as well as the signaling methods involved in this process. Additionally, we thoroughly examine how reprogramming astrocytes into neurons can be applied to treat stroke and other neurodegenerative diseases. Finally, we discuss the challenges of neuronal reprogramming and offer insights about the field.

Identification of disulfidptosis-related genes and analysis of immune infiltration characteristics in ischemic strokes.

Immune infiltration plays a pivotal role in the pathogenesis of ischemic stroke. A novel form of cell death known as disulfidptosis has emerged in recent studies. However, there is currently a lack of research investigating the regulatory mechanism of disulfidptosis-related genes in immune infiltration during ischemic stroke. Using machine learning methods, we identified candidate key disulfidptosis-related genes (DRGs). Subsequently, we performed an analysis of immune cell infiltration to investigate the dysregulation of immune cells in the context of ischemic stroke. We assessed their diagnostic value by employing receiver operating characteristic (ROC) curves. To gain further insights, we conducted functional enrichment analyses to elucidate the signaling pathways associated with these seven DRGs. We identified two distinct subclusters based on the expression patterns of these seven DRGs. The unique roles of these subclusters were further evaluated through KEGG analysis and immune infiltration studies. Furthermore, we validated the expression profiles of these seven DRGs using both single-cell datasets and external datasets. Lastly, molecular docking was performed to explore potential drugs for the treatment of ischemic stroke. We identified seven DRGs. The seven DRGs are related to immune cells. Additionally, these seven DRGs also demonstrate potential diagnostic value in ischemic stroke. Functional enrichment analysis highlighted pathways such as platelet aggregation and platelet activation. Two subclusters related to disulfidptosis were defined, and functional enrichment analysis of their differentially expressed genes (DEGs) primarily involved pathways like cytokine-cytokine receptor interaction. Single-cell analysis indicated that these seven DRGs were primarily distributed among immune cell types. Molecular docking results suggested that genistein might be a potential therapeutic drug. This study has opened up new avenues for exploring the causes of ischemic stroke and developing potential therapeutic targets.

Transcriptomic analysis reveals the potential biological mechanism of AIS and lung adenocarcinoma.

Introduction: Acute ischemic stroke (AIS) and lung adenocarcinoma (LUAD) are associated with some of the highest morbidity and mortality rates worldwide. Despite reports on their strong correlation, the causal relationship is not fully understood. The study aimed to identify and annotate the biological functions of hub genes with clinical diagnostic efficacy in AIS and LUAD. Methods: Transcriptome and single-cell datasets were obtained from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA). We identified the differentially expressed genes (DEGs) upregulated in AIS and LUAD and found 372 genes intersecting both datasets. Hub genes were identified using protein-protein interaction (PPI) networks, and the diagnostic and prognostic utility of these hub genes was then investigated using receiver operating characteristic (ROC) curves, survival analysis, and univariable Cox proportional hazard regression. Single-cell analysis was used to detect whether the hub genes were expressed in tumor epithelial cells. The immune microenvironment of AIS and LUAD was assessed using the CIBERSORT algorithm. The protein expression of these hub genes was tracked using the Human Protein Atlas (HPA). We calculated the number of positive cells using the digital pathology software QuPath. Finally, we performed molecular docking after using the Enrichr database to predict possible medicines. Results: We identified the molecular mechanisms underlying hub genes in AIS and LUAD and found that CCNA2, CCNB1, CDKN2A, and CDK1 were highly expressed in AIS and LUAD tissue samples compared to controls. The hub genes were mainly involved in the following pathways: the cell cycle, cellular senescence, and the HIF-1 signaling pathway. Using immunohistochemical slices from the HPA database, we confirmed that these hub genes have a high diagnostic capability for AIS and LUAD. Further, their high expression is associated with poor prognosis. Finally, curcumin was tested as a potential medication using molecular docking modeling. Discussion: Our findings suggest that the hub genes we found in this study contribute to the development and progression of AIS and LUAD by altering the cellular senescence pathway. Thus, they may be promising markers for diagnosis and prognosis.

Somatic Cell Reprogramming for Nervous System Diseases: Techniques, Mechanisms, Potential Applications, and Challenges.

Nervous system diseases present significant challenges to the neuroscience community due to ethical and practical constraints that limit access to appropriate research materials. Somatic cell reprogramming has been proposed as a novel way to obtain neurons. Various emerging techniques have been used to reprogram mature and differentiated cells into neurons. This review provides an overview of somatic cell reprogramming for neurological research and therapy, focusing on neural reprogramming and generating different neural cell types. We examine the mechanisms involved in reprogramming and the challenges that arise. We herein summarize cell reprogramming strategies to generate neurons, including transcription factors, small molecules, and microRNAs, with a focus on different types of cells.. While reprogramming somatic cells into neurons holds the potential for understanding neurological diseases and developing therapeutic applications, its limitations and risks must be carefully considered. Here, we highlight the potential benefits of somatic cell reprogramming for neurological disease research and therapy. This review contributes to the field by providing a comprehensive overview of the various techniques used to generate neurons by cellular reprogramming and discussing their potential applications.

Flexible translucent chitosan-glycerin/QD nanocomposite glue for anti-counterfeiting films with strong adhesion and stability.

With the rapid development of commodity circulation, more attention has been paid to the anticounterfeiting technology of commodities, including stability, universality and ease of distinguishing. The authors report the use of gelatin-chitosan-glycerin/QD nanocomposite-functionalized glue for luminescent anti-counterfeiting labels. As the blend and plasticizer, the addition of chitosan and glycerin effectively improved the flexibility and formability of the gelatin-chitosan-glycerin/QD composite films, which show excellent mechanical properties, including high transparency, luminescence and flexibility, and they are easy to prepare on a large scale, providing certain reference values for new anticounterfeiting technology applying a variety of morphologies.