Aging-Related Gene-Based Prognostic Model for Lung Adenocarcinoma: Insights into Tumor Microenvironment and Therapeutic Implications.

Lung cancer remains the leading cause of cancer-related mortality globally, with a poor prognosis primarily due to late diagnosis and limited treatment options. This research highlights the critical demand for advanced prognostic tools by creating a model centered on aging-related genes (ARGs) to improve prediction and treatment strategies for lung adenocarcinoma (LUAD). By leveraging datasets from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), we developed a prognostic model that integrates 14 ARGs using the least absolute shrinkage and selection operator (LASSO) alongside Cox regression analyses.

Senescent Macrophages and the Lung Cancer Microenvironment: A New Perspective on Tumor Immune Evasion.

Lung cancer treatment is evolving, and the role of senescent macrophages in tumor immune evasion has become a key focus. This study explores how senescent macrophages interact with lung cancer cells, contributing to tumor progression and immune dysfunction. As aging impairs macrophage functions, including phagocytosis and metabolic signaling, it promotes chronic inflammation and cancer development.

Dissecting the functions and regulatory mechanisms of disulfidoptosis-related RPN1 in pan-cancer: modulation of immune microenvironment and cellular senescence.

Introduction: Cancer's inherent heterogeneity, marked by diverse genetic and molecular alterations, presents significant challenges for developing effective treatments. One such alteration is the regulation of disulfidoptosis, a recently discovered programmed cell death pathway. RPN1, a key regulator associated with disulfidoptosis, may influence various aspects of tumor biology, including immune evasion and cellular senescence.

PCAS: An Integrated Tool for Multi-Dimensional Cancer Research Utilizing Clinical Proteomic Tumor Analysis Consortium Data.

Proteomics offers a robust method for quantifying proteins and elucidating their roles in cellular functions, surpassing the insights provided by transcriptomics. The Clinical Proteomic Tumor Analysis Consortium database, enriched with comprehensive cancer proteomics data including phosphorylation and ubiquitination profiles, alongside transcriptomics data from the Genomic Data Commons, allow for integrative molecular studies of cancer. The ProteoCancer Analysis Suite (PCAS), our newly developed R package and Shinyapp, leverages these resources to facilitate in-depth analyses of proteomics, phosphoproteomics, and transcriptomics, enhancing our understanding of the tumor microenvironment through features like immune infiltration and drug sensitivity analysis.

Identifying and assessing a prognostic model based on disulfidptosis-related genes: implications for immune microenvironment and tumor biology in lung adenocarcinoma.

Introduction: Lung cancer, with the highest global mortality rate among cancers, presents a grim prognosis, often diagnosed at an advanced stage in nearly 70% of cases. Recent research has unveiled a novel mechanism of cell death termed disulfidptosis, which is facilitated by glucose scarcity and the protein SLC7A11.

Methods: Utilizing the least absolute shrinkage and selection operator (LASSO) regression analysis combined with Cox regression analysis, we constructed a prognostic model focusing on disulfidptosis-related genes.

Constructing and Evaluating a Mitophagy-Related Gene Prognostic Model: Implications for Immune Landscape and Tumor Biology in Lung Adenocarcinoma.

Mitophagy, a conserved cellular mechanism, is crucial for cellular homeostasis through the selective clearance of impaired mitochondria. Its emerging role in cancer development has sparked interest, particularly in lung adenocarcinoma (LUAD). Our study aimed to construct a risk model based on mitophagy-related genes (MRGs) to predict survival outcomes, immune response, and chemotherapy sensitivity in LUAD patients.

Homocysteine Modulates Social Isolation-Induced Depressive-Like Behaviors Through BDNF in Aged Mice.

Social isolation is an unpleasant experience associated with an increased risk of mental disorders. Exploring whether these experiences affect behaviors in aged people is particularly important, as the elderly is very likely to suffer from periods of social isolation during their late-life. In this study, we analyzed the depressive-like behaviors, plasma concentrations of homocysteine (Hcy), and brain-derived neurotropic factor (BDNF) levels in aged mice undergoing social isolation.

Physicochemical property and antioxidant activity of polysaccharide from the seed cakes of Abel.

Seed cake refers to the food by-product of Abel, and its insufficient utilization can cause serious environment pollution and resource waste. This study aimed to investigate antioxidant activities of the polysaccharide from the seed cakes of Abel (COCP) in vitro and in vivo. The physicochemical property of COCP was also determined.

Claudin-5 relieves cognitive decline in Alzheimer's disease mice through suppression of inhibitory GABAergic neurotransmission.

Alzheimer's disease (AD) is characterized by progressive cognitive decline, which is considered as the most common form of dementia in the elderly. Recently, it is suggested that impaired cerebrovascular function may precede the onset of AD. Claudin-5, which is the most enriched tight junction protein, has been reported to prevent the passage of damaging material at the blood-brain barrier.

Knockdown of astrocytic TREM2 in the hippocampus relieves cognitive decline in elderly male mice.

With the lengthening of the human lifespan, an increasing proportion of the population is subject to age-related cognitive impairments, making it important to investigate ways to confront the effects of aging. Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune receptor that is expressed mainly on the surfaces of microglia. Previous studies have found a significant positive correlation between age and TREM2 levels.

Ketamine reverses the impaired fear memory extinction and accompanied depressive-like behaviors in adolescent mice.

Post-traumatic stress disorder (PTSD) is a chronic and disabling condition arising after exposure to a severe traumatic event, which affects approximately eight percent of the population. The underlying neurobiology of PTSD, however, has only been partially understood. The exploration of fear memory and its extinction has been the subject to increase our understanding of PTSD.

Impaired fear memory extinction during adolescence is accompanied by the depressive-like behaviors.

Fear is the emotion that is best understood in terms of brain mechanisms. And the management of fear memories is important when facing mental health disorders such as post-traumatic stress. Adolescence is a transitional stage of physical and psychological human development and the ability to deal with the fear memory in adolescence may be a potent factor for developing mental disorders in adulthood.

Roflumilast ameliorates cognitive impairment in APP/PS1 mice via cAMP/CREB/BDNF signaling and anti-neuroinflammatory effects.

Phosphodiesterase type 4 (PDE4) inhibitors can prevent the breakdown of the second messenger cyclic adenosine monophosphate (cAMP) and improve cognitive performances in several animal models of cognition. However, the clinical development of PDE4 inhibitors has been seriously hampered by severe side effects, such as vomiting and nausea. In this study, we investigated the effect and mechanism of roflumilast, an FDA-approved PDE4 inhibitor for treatment of chronic obstructive pulmonary disease (COPD), on learning and memory abilities in the APP/PS1 mouse model of Alzheimer's disease (AD).

Huperzine A protects neural stem cells against Aβ-induced apoptosis in a neural stem cells and microglia co-culture system.

Objectives: This study aims to explore whether Huperzine A (HupA) could protect neural stem cells against amyloid beta-peptide Aβ induced apoptosis in a neural stem cells (NSCs) and microglia co-culture system.

Methods: Rat NSCs and microglial cells were isolated, cultured and identified with immunofluorescence Assays (IFA). Co-culture systems of NSCs and microglial cells were employed using Transwell Permeable Supports.

Nicotine contributes to the neural stem cells fate against toxicity of microglial-derived factors induced by Aβ via the Wnt/β-catenin pathway.

Recent studies have demonstrated that the molecules secreted from microglias play important roles in the cell fate determination of neural stem cells (NSCs), and nicotinic acetylcholine receptor agonist treatment could reduce neuroinflammation in some neurodegenerative disease models, such as Alzheimer's disease (AD). However, it is not clear how nicotine plays a neuroprotective role in inflammation-mediated central nervous diseases, and its possible mechanisms in the process remain largely elusive. The aim of this study is to improve the survival microenvironment of NSCs co-cultured with microglias in vitro by weakening inflammation that mediated by accumulation of β-amyloid peptide (Aβ).