Substance P (SP), a neuropeptide diffusely scattered in the nervous system and immune system, participates in various physiological and pathological processes, including pain perception and inflammatory response. However, the regulatory mechanisms of SP in itch perception and its downstream pathophysiological responses, such as the chronic itch-scratch vicious cycle, have not been systematically elucidated. Based on an analysis of the existing literature, this review summarizes the biological functions of substance P in the itch-scratch response, and explores its mechanism of action in signal transduction, inflammatory response and nerve sensitization.

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In the context of continuous social development and overnutrition, Alzheimer's disease, as a neurodegenerative disease, is becoming more and more common in the elderly and gradually younger, and there is currently no effective treatment. This article reviews the role of m6A as a target site for the treatment of Alzheimer's disease, discusses the main case characteristics of AD, including tau hyperphosphorylation, neuroinflammation, etc., and discusses the combination of m6A regulation and anti-Aβ/antitau drugs, m6A and anti-inflammatory treatment, etc., and reveals the new mechanism of AD pathogenesis after combining recent related research cases, and proposes that m6A can be used as a new target for AD, providing a new epitranscriptional perspective for the treatment of AD. In addition, it will promote the development of m6A-targeted drugs and provide relevant suggestions to solve the current treatment bottleneck.

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Objective: Adverse experiences in childhood may induce structural and functional changes in the brain, thereby affecting psychological phenotypes. This study aims to explore the relationship between small-world properties of brain networks and psychological resilience phenotypes in adults with left-behind experiences. Methods: A total of 145 adult volunteers with childhood left-behind experiences were recruited. All participants underwent resting-state functional magnetic resonance imaging (rs-fMRI) scanning. Data were processed using the GRETNA toolbox to obtain small-world properties (σ, γ, λ). Based on the median CD-RISC (Connor-Davidson Resilience Scale) score, participants were divided into a high-resilience group (n = 75) and a low-resilience group (n = 70). Statistical analyses were conducted to examine the relationships among left-behind experience, psychological resilience, and small-world properties of brain networks. Results: The high-resilience group showed significantly higher small-world coefficient (σ), normalized clustering coefficient (γ), global efficiency, and local efficiency than the low-resilience group. Degree centrality (Dc) and nodal efficiency (Ne) values in the right medial orbitofrontal superior frontal gyrus, left insula, and left anterior cingulate gyrus were positively correlated with psychological resilience scores, while Dc and Ne values in the left middle temporal gyrus were negatively correlated with resilience scores. Conclusion: Alterations in small-world properties of brain networks in adults with left-behind experiences are associated with psychological resilience.

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Chronic lymphocytic leukemia (CLL) is a hematologic malignancy originating from mature B cells, where the tumor microenvironment—particularly proliferation centers (PCs)—plays a pivotal role in disease progression and treatment resistance. PCs support tumor cell survival, proliferation, and therapy resistance through intercellular communication, metabolic reprogramming, and extracellular vesicle (EV)-mediated signaling. This study investigates the mechanisms by which the CLL microenvironment, especially PCs, contributes to drug resistance and disease evolution, with a particular focus on EVs and metabolic remodeling. A comprehensive literature review was conducted to synthesize current findings in this domain.. Key findings reveal that PCs mediate resistance through multiple interconnected mechanisms, including: (1) the CXCL12/CXCR4 retention axis; (2) CD40-CD40L-induced activation of the alternative NF-κB pathway; (3) metabolic reprogramming favoring anti-apoptotic profiles; and (4) EV-mediated communication that alters stromal cell behavior. CLL-derived EVs play a critical role in reshaping the bone marrow microenvironment by transferring miRNAs and proteins that alter stromal cell function and metabolism. Additionally, this study identifies a “dual metabolic shift” in CLL cells, characterized by the simultaneous enhancement of both glycolysis and oxidative phosphorylation, which is closely linked to microenvironmental dependency. Furthermore, the research uncovers metabolic regionalization within PCs and spatiotemporal heterogeneity in EV distribution.

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