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With the sustained growth of economy and significant changes in social demographics, the issue of elderly-related diseases has increasingly drawn attention particularly. Alzheimer's disease (AD),as a representative disease of neurodegenerative diseases has become a major challenge, affecting the health and quality of life among the elderly population severely. In recent years, the incidence, prevalence, and mortality rate of AD increase in China, imposing substantial economic burdens on families, society, and the entire healthcare system. To proactively address this challenge and respond to the national 'Healthy China Action' initiative, leading experts from Renji Hospital, Shanghai Jiao Tong University School of Medicine,and Chinese Center for Disease Control and Prevention Chronic Non-communicable Disease Control Center, Fudan University School of Public Health, Shanghai Mental Health Center, Ruijin Hospital,Shanghai Jiao Tong University School of Medicine, Fujian Medical University, and other authoritative institutions, have jointly authored the 'China Alzheimer Disease Report 2024'. Building upon previous editions of 2021, 2022, and 2023, this report updates epidemiological data on AD in China, thoroughly analyzes the latest economic burdens of the disease, and comprehensively evaluates the current status of AD diagnosis and treatment services, as well as the allocation of public health resources in our country. The release of the 'China Alzheimer Disease Report 2024' not only reflects China's progress and efforts in AD research and prevention, but also underscores the social heightened concern for elderly health issues. It aims to provide scientific and technical guidance and robust data support for the prevention, diagnosis, and treatment of AD, offering a professional basis for the government and relevant departments to formulate targeted health policies and intervention measures. Furthermore, it serves as a platform for promoting academic exchanges and cooperation in this field domestically and internationally. Through the dissemination and application of this report, we anticipate it will not only serve as a reference for professionals but also enhance public awareness of AD, promote active participation across various sectors of society, and jointly advance the development of elderly health care in China, empowering us towards achieving 'healthy aging'.

AP000695.2 is a novel long non-coding RNA (lncRNA). Its aberrant high expression is remarkably associated with poor prognosis of patients with lung adenocarcinoma (LUAD). However, its role and underlying mechanism in LUAD remains unclear. Previous bioinformatics analysis indicated that AP000695.2 may be closely related to the glycolysis of LUAD. This study aims to verify and explore the mechanism of AP000695.2 in glycolysis of LUAD. Overexpression plasmid and siRNA are used to construct cell models of upregulation and downregulation of AP000695.2, respectively. AP000695.2 is highly expressed in lung cancer cell lines as revealed by qPCR. Western blot analysis, FDG uptake, lactate production assay and ECAR determination results show that high expression of AP000695.2 facilitates glycolysis of LUAD cells. CCK-8, EdU staining, Transwell and wound healing assays show that high expression of AP000695.2 promotes cell growth and migration of LUAD. The relationship between AP000695.2 and miR-335-3p is confirmed by bioinformatics analysis and dual-luciferase reporter assays. Through the dual-luciferase reporter assay, TEA domain transcription factor 1 (TEAD1) is identified as a target gene of miR-335-3p. Rescue experiments are applied to verify the relationship among AP000695.2, miR-335-3p and TEAD1. Our study indicates that AP000695.2 is involved in the mechanism of LUAD through functioning as a ceRNA to competitively sponge miR-335-3p, thereby regulating the expression of TEAD1. In the in vivo models, AP000695.2 depletion restrains tumor growth and glycolysis. AP000695.2 promotes the glycolysis of LUAD by regulating the miR-335-3p/TEAD1 axis, and it may serve as a potential target of anti-tumor energy metabolism therapy.

Background: Lung cancer is the most common malignancy in the world and a growing number of researches have focused on its metabolic characteristics. Studies have shown that the long non‐coding RNA (lncRNA) HOXA11‐AS is aberrantly expressed in many tumors. However, the role of HOXA11‐AS in lung adenocarcinoma (LUAD) glycolysis and other energy metabolism pathways has not been characterized. Method: The mRNA levels of HOXA11‐AS, microRNA‐148b‐3p (miR‐148b‐3p), and pyruvate kinase M2 (PKM2) were detected using qRT‐PCR. The expression levels of proteins were measured using immunohistochemistry and western blot. The CCK‐8, EdU, and colony formation assays were used to assess proliferation. Glycolytic changes were assessed by measuring lactate production, ATP production, and 18F‐FDG uptake. Bioinformatics analysis and dual‐luciferase reporter assays were used to characterize the relationship between HOXA11‐AS, miR‐148b‐3p, and PKM2. Proliferation and glycolytic changes were analyzed in xenograft tumor experiments using Micro‐PET imaging after downregulation of HOXA11‐AS in vivo. Results: The expression of HOXA11‐AS was markedly increased in LUAD, and was strongly associated with a poor prognosis. In addition, HOXA11‐AS promoted proliferation and glycolysis in LUAD, and miR‐148b‐3p inhibited proliferation and glycolysis in LUAD. Mechanistically, HOXA11‐AS positively regulated PKM2 expression by binding to miR‐148b‐3p, thereby promoting LUAD proliferation and glycolysis. In addition, HOXA11‐AS inhibited LUAD xenograft growth and glycolysis via upregulation of miR‐148b‐3p expression and downregulation of PKM2 expression in vivo. Conclusions: These results showed that HOXA11‐AS enhanced LUAD proliferation and glycolysis via the miR‐148b‐3p/PKM2 axis. The findings in this paper expanded our understanding of the molecular mechanisms of LUAD tumorigenesis and glycolysis and showed that HOXA11‐AS could be useful as a diagnostic and prognostic marker for LUAD. 18F‐FDG PET/CT can be used to visually evaluate the therapeutic effect of targeting HOXA11‐AS. [ABSTRACT FROM AUTHOR]

A hydrogel with bioadhesive function has high water content, inherent flexibility, adjustable mechanical strength, adequate biocompatibility, and a wide range of application prospects in the field of biomedicine. However, achieving reversible and robust adhesion between the hydrogel and the biological interface remains a challenge, including slow adhesive formation, weak adhesion, low biocompatibility, poor mechanical matching with tissues, and the lack of a benign detachment that can be triggered. Bioadhesive hydrogels adhere to distinct biological tissues and are used in biomedicine through the interaction between interfaces. The adhesion mechanism is usually a combination of multiple interactions in which one interaction is dominant. This article summarizes the preparation of bioadhesive hydrogels, the characteristics of biological interfaces, the methods of enhancing adhesion, and measuring the adhesion of hydrogels. These will assist researchers in developing adhesion strategies and accurately measuring adhesive forces according to contrasting biological interfaces. [ABSTRACT FROM AUTHOR]