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Objectives: This study aimed to elucidate the connection between osteoclastic forkhead transcription factor O1 (FoxO1) and periodontitis and explore the underlying mechanism by which FoxO1 knockdown regulates osteoclast formation. Materials and Methods: A conventional ligature‐induced periodontitis model was constructed to reveal the alterations in the proportion of osteoclastic FoxO1 in periodontitis via immunofluorescence staining. Additionally, RNA sequencing (RNA‐seq) was performed to explore the underlying mechanisms of FoxO1 knockdown‐mediated osteoclastogenesis, followed by western blotting, quantitative polymerase chain reaction, and enzyme‐linked immunosorbent assay. Results: FoxO1+ osteoclasts were enriched in the alveolar bone in experimental periodontitis. Moreover, FoxO1 knockdown led to impaired osteoclastogenesis with low expression of osteoclast differentiation‐related genes, accompanied by an insufficient osteoclast maturation phenotype. Mechanistically, RNA‐seq revealed that the nuclear factor kappa B (NF‐κB) and nucleotide‐binding oligomerization domain‐like receptor family pyrin domain containing 3 (NLRP3) inflammasome signaling pathways were inhibited in FoxO1‐knockdown osteoclasts. Consistent with this, MCC950, an effective inhibitor of the NLRP3 inflammasome, substantially attenuated osteoclast formation. Conclusions: FoxO1 knockdown contributed to the inhibition of osteoclastogenesis by effectively suppressing NF‐κB signaling and NLRP3 inflammasome activation. This prospective study reveals the role of FoxO1 in mediating osteoclastogenesis and provides a viable therapeutic target for periodontitis treatment. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC), characterized by significant morbidity and mortality rates, poses a substantial threat to human health. The expression of ligands and receptors within the classical and non-classical Wnt signaling pathways plays an important role in HCC. The Wnt signaling pathway is essential for regulating multiple biological processes in HCC, including proliferation, invasion, migration, tumor microenvironment modulation, epithelial–mesenchymal transition (EMT), stem cell characteristics, and autophagy. Molecular agents that specifically target the Wnt signaling pathway have demonstrated significant potential for the treatment of HCC. However, the precise mechanism by which the Wnt signaling pathway interacts with HCC remains unclear. In this paper, we review the alteration of the Wnt signaling pathway in HCC, the mechanism of Wnt pathway action in HCC, and molecular agents targeting the Wnt pathway. This paper provides a theoretical foundation for identifying molecular agents targeting the Wnt pathway in hepatocellular carcinoma. [ABSTRACT FROM AUTHOR]

Simple Summary: Inhibitors of Bruton's tyrosine kinase (BTK) have changed how we treat chronic lymphocytic leukemia (CLL), a B cell malignancy. These inhibitors are known for blocking signals in B cells that help cancers derived from these immune cells grow, but they also have important effects on the non-malignant immune system. This work explains how BTK inhibitors influence different components of the immune system, such as B cells, T cells, and macrophages. It also reviews their impact on the generation of immune-signaling molecules or their effect on the tumor microenvironment. We also explored how these effects might be useful in treating autoimmune diseases and infections. By understanding how BTK inhibitors can impact cancer cells and the immune system, this paper highlights the potential for these drugs to be used in a wider range of medical conditions. Bruton's tyrosine kinase (BTK), a cytoplasmic tyrosine kinase, plays a pivotal role in B cell biology and function. As an essential component of the B cell receptor (BCR) signaling pathway, BTK is expressed not only in B cells but also in myeloid cells, including monocytes/macrophages, dendritic cells, neutrophils, and mast cells. BTK inhibitors (BTKis) have revolutionized the treatment of chronic lymphocytic leukemia (CLL) and other B cell malignancies. Besides their well-characterized role in inhibiting BCR signaling, BTKis also exert significant immunological influences outside the tumor cell that extend their therapeutic potential and impact on the immune system in different ways. This work elucidates the immunomodulatory mechanisms associated with BTK inhibition, focusing on CLL and other clinical contexts. We discuss how BTK inhibition affects various immune cells, including B cells, T cells, and macrophages. The effects of BTKis on the profiles of cytokines, also fundamental parts of the tumor microenvironment (TME), are summarized here as well. This review also appraises the implications of these immunomodulatory actions in the management of autoimmune diseases and infections. Summarizing the dual role of BTK inhibition in modulating malignant lymphocyte and immune cell functions, this paper highlights the broader potential clinical use of compounds targeting BTK. [ABSTRACT FROM AUTHOR]

Febrile infection-related epilepsy syndrome (FIRES) is a rare epilepsy syndrome with unclear pathogenesis, characterized by fever-induced, super-refractory status epilepticus and high mortality. Studies have shown that ketogenic diet (KD) is effective in controlling convulsions in FIRES, but its mechanisms are unclear. This paper intends to summarize the mechanisms by which KD may exert effects against FIRES. Clinical studies have shown that patients with FIRES have elevated levels of various inflammatory factors such as interleukin (IL)-6, IL-8, IL-10, and so on. KD may exert anti-FIRES effects through several potential inflammatory pathways, including nuclear factor -κB (NF-κB) and NLR family pyrin domain containing 3 (NLRP3). Furthermore, the Kyoto Encyclopedia of Genes and Genomes (KEGG) network suggested that KD may play an anti-inflammatory role through several pathways such as cellular senescence and neutrophil extracellular trap formation. These mechanisms need to be further investigated. [ABSTRACT FROM AUTHOR]

The seed of Herpetospermum pedunculosum (Ser.) C.B. Clarke, known in Chinese as Bo-Leng-Gua-Zi and in Tibetan as Sejimedo, are here abbreviated as H. pedunculosum seeds. Herpetospermum pedunculosum seeds is a traditional Chinese medicine for protecting the liver, clearing heat, and detoxifying. A total of 125 chemical metabolites of H. pedunculosum seeds are found, including lignans, fatty acids, terpenes, coumarins, and others. The pharmacological activities of H. pedunculosum seeds are mainly in hepatoprotective, antioxidant, anti-cancer cells, and anticholestatic effects. In clinical application, it is mainly used in combination with other traditional Chinese medicines to play a key role in treating the liver disease. This paper gives a systematic review of above research aspects, proposes the potential limitations and put forward plausible solutions. Relevant literatures were searched in PubMed, Web of Science and Chinese National Knowledge Infrastructure with Herpetospermum as the key word. A number of studies have shown that H. pedunculosum seeds exert excellent hepatoprotective effects by acting on NF-κB, TGF-β, and Keap1-Nrf2 signaling pathways, which provide a solid base for its clinic application. However, more research is needed to explore the standard cultivation and quality evaluation of H. pedunculosum seeds and systematical structure-activity relationship of its active metabolites. [ABSTRACT FROM AUTHOR]

Tissue fibrosis is one of the important causes of disability and mortality in various chronic diseases, and its prevention and treatment are also major challenges in the medical field. Myofibroblasts are the core involved in the progression of tissue fibrosis. Glutaminolysis can provide energy for the activation and proliferation of myofibroblasts. Glutaminase is a key and initiating enzyme in the process of glutaminolysis and plays a crucial role in the realization of glutamine function. In this paper, the role of glutaminase in tissue fibrosis and related signaling pathways are introduced. In addition, the treatment strategies for tissue fibrosis targeting glutaminase are also analyzed. In conclusion, glutaminase is expected to be a key target for the treatment of tissue fibrosis, and this paper aims to provide some reference for research on tissue fibrosis. [ABSTRACT FROM AUTHOR]

Primary cilia (PC) are essential signaling hubs for proper epithelial formation and the maintenance of skin homeostasis. Found on most cells in the human body, including skin cells, PC facilitate signal transduction that allows ciliated cells to interact with the immune system via multiple pathways, helping to maintain immune system homeostasis. PC can be altered by various microenvironmental stimuli to develop corresponding regulatory functions. Both PC and ciliary signaling pathways have been shown to be involved in the immune processes of various skin lesions. However, the mechanisms by which PC regulate cellular functions and maintain immune homeostasis in tissues are highly complex, and our understanding of them in the skin remains limited. In this paper, we discuss key ciliary signaling pathways and ciliated cells in the skin, with a focus on their immunomodulatory functions. We have compiled evidence from various cells, tissues and disease models to help explore the potential immunomodulatory effects of PC in the skin and their molecular mechanisms. [ABSTRACT FROM AUTHOR]

Low back pain caused by intervertebral disc degeneration (IDD) has emerged as a significant global public health concern, with far-reaching consequences for patients' quality of life and healthcare systems. Although previous research have revealed that the mechanisms of intervertebral disc cell apoptosis, pyroptosis and necroptosis can aggravate IDD damage by mediating inflammation and promoting extracellular matrix degradation, but they cannot explain the connection between different cell death mechanisms and ion metabolism disorders. The latest study shows that cell death mechanisms such as cellular senescence, ferroptosis, and cuproptosis, and PANopotosis have similar roles in the progression of intervertebral disc degeneration, but not exactly the same damage mechanism. This paper summarizes the effects of various cell death patterns on the disease progression of IDD, related molecular mechanisms and signaling pathways, providing new perspectives and potential clinical intervention strategies for the prevention and treatment of IDD. [ABSTRACT FROM AUTHOR]

The high incidence, death, disability, and recurrence of ischemic stroke (CIS) place a significant cost on families and society. According to recent research on the condition, immune-related damage is a major contributor to the development and occurrence of CIS. Innate immunity and adaptive immunity are the two primary categories of the immune system in the body. The body's first line of defense is innate immunity, and immune cells play a role in every stage of the immune system. At the same time, protein molecules play a vital function in regulating and differentiating immune cells. It can be said that protein molecules are the foundation of immune regulation. Model mice are necessary for us to examine fixed compounds in our studies. Conditional deletion and overexpression mouse models are the two primary categories of model mice. Numerous model mice have been documented in CIS research. The study of innate immune responses following ischemic stroke will benefit more from the use of these transgenic mice that target innate immunity. This paper analyzes the literature on transgenic mice related to innate immune responses following ischemic stroke because of the significance of these responses. It is anticipated to produce novel medications, improve clinical treatment guidance, and undergo a metamorphosis and application in the clinic in the future. [ABSTRACT FROM AUTHOR]

Electrochemical biosensors have emerged as predominant devices for sensitive, rapid, and specific sensing of biomolecules, with significant applications in clinical diagnostics, environmental observation, and food processing. The improvement of inventive materials, especially carbon-based materials, and metal/metal oxide nanoparticles (M/MONPs), has changed the impact of biosensing, improving the performance and flexibility of electrochemical biosensors. Carbon-based materials, such as graphene, carbon nanotubes, and carbon nanofibers, have excellent electrical conductivity, a high surface area, large pore size, and good biocompatibility, making them ideal electrocatalysts for biosensor applications. Furthermore, M and MONPs have highly effective synergistic, electronic, and optical properties that influence signal transduction, selectivity, and sensitivity. This study completely explored continuous progressions and upgrades in carbonaceous materials (CBN materials) and M/MONPs for electrochemical biosensor applications. It analyzed the synergistic effects of hybrid nanocomposites that combine carbon materials with metal nanoparticles (MNPs) and their part in upgrading sensor performance. The paper likewise incorporated the surface alteration procedures and integration of these materials into biosensor models. The study examined difficulties, requirements, and possibilities for executing these innovative materials in practical contexts. This overview aimed to provide specialists with insights into the most recent patterns in the materials study of electrochemical biosensors and advance further progressions in this dynamic sector. [ABSTRACT FROM AUTHOR]

The extracellular matrix is an organized three-dimensional network of protein-based molecules and other macromolecules that provide structural and biochemical support to tissues. Depending on its biochemical and structural properties, the extracellular matrix influences cell adhesion and signal transduction and, in general, can influence cell differentiation and proliferation through specific mechanisms of chemical and mechanical sensing. The development of body tissues during ontogenesis is accompanied by changes not only in cells but also in the composition and properties of the extracellular matrix. Similarly, tumor development in carcinogenesis is accompanied by a continuous change in the properties of the extracellular matrix of tumor cells, called 'oncomatrix', as the tumor matures, from the development of the primary focus to the stage of metastasis. In this paper, the characteristics of the composition and properties of the extracellular matrix of tumor tissues are considered, as well as changes to the composition and properties of the matrix during the evolution of the tumor and metastasis. The extracellular matrix patterns of tumor tissues can be used as biomarkers of oncological diseases as well as potential targets for promising anti-tumor therapies. [ABSTRACT FROM AUTHOR]

In this paper, active polysaccharides were extracted from Brassica rapa L. polysaccharide (BRP), and structural characterization was preliminarily investigated. Its immunomodulatory activity and molecular biological mechanisms in cyclophosphamide‐induced immunosuppressed mice were also explored, as well as its effects on intestinal microbiota. Results indicate that BRP is an acidic heteropolysaccharide with the main components of Ara, GalA, and GlcA and has α‐ and β‐glycosidic linkages with pyranose bonds. The results of the study showed that BRP could effectively improve the thymus and spleen indices and repair Cy‐induced immune tissue damage in immunosuppressed mice. Meanwhile, BRP increased the immune cell activity and antioxidant levels in mice. In addition, BRP increased the secretion of cytokines (IL‐1β, IL‐6, IL‐10, and TNF‐α) and immunoglobulins (IgA, IgG) in mouse serum. It also regulates the relative expression of genes related to the TLR4/NF‐κB signaling pathways as well as regulates the diversity and composition of mouse intestinal microbiota. In conclusion, BRP was able to regulated the immune function in immunosuppressed mice, providing a theoretical basis for the development of immunomodulators. [ABSTRACT FROM AUTHOR]

N-acetylcysteine (NAC), a compound known for its cysteine and glutathione precursor properties, has been used in therapeutic applications for many years. Recently, there has been increasing interest in exploring the potential benefits of NAC in addressing polycystic ovary syndrome (PCOS). However, the exact mechanisms underlying NAC's therapeutic and clinical uses remain not fully understood. This review aims to specifically investigate how NAC offers protection against PCOS. This involved an extensive systematic review of the literature, and it made use of PubMed, Embase, and Web of Science databases. By analyzing key findings from over 100 research papers, the potential mechanisms through which NAC produces its effects were explored and summarized. Most studies suggest that NAC, whether used on its own or in combination with other medications, has the potential to counteract oxidative stress, utilize its anti-inflammatory and anti-apoptotic properties, and offer benefits in managing PCOS. Moreover, NAC might have the potential to influence specific signaling pathways in insulin target cells and β cells. Diverse biological effects of NAC indicate its potential usefulness as a supplementary or therapeutic approach for managing PCOS. As a result, additional research is required to explore its potential in addressing PCOS. [ABSTRACT FROM AUTHOR]

Simple Summary: Myeloproliferative neoplasms (MPNs) are exceedingly rare in children, adolescents, and young adults. The current literature focuses mainly on older patients, so the purpose of the review is to present the genetic landscape of pediatric patients. Modern genetic diagnostics makes it possible to identify genetic markers involved in the pathomechanisms of these uncommon clonal marrow disorders. Excluding driver gene mutations (JAK2, MPL, CALR), over 20 other mutations have been described as of significance to MPNs. The aim of the review is to improve and present knowledge of MPNs and genetic targets for diagnosis and therapy in children, adolescents, and young adults. Myeloproliferative neoplasms (MPNs) are clonal hematopoietic cancers characterized by hyperproliferation of the myeloid lineages. These clonal marrow disorders are extremely rare in pediatric patients. MPN is reported to occur 100 times more frequently in adults, and thus research is primarily focused on this patient group. At present, modern diagnostic techniques, primarily genetic, facilitate the identification of the biology of these diseases. The key genes are JAK2, MPL, and CALR, namely, driver mutations, which are present in approximately 90% of patients with suspected MPN. Moreover, there are more than 20 other mutations that affect the development of these hematological malignancies, as evidenced by a review of the literature. The pathogenic mechanism of MPNs is characterized by the dysregulation of the JAK/STAT signaling pathway (JAK2, MPL, CALR), DNA methylation (TET2, DNMT3A, IDH1/2), chromatin structure (ASXL1, EZH2), and splicing (SF3B1, U2AF2, SRSF2). Although rare, myeloproliferative neoplasms can involve young patients and pose unique challenges for clinicians in diagnosis and therapy. The paper aims to review the biological markers of MPNs in pediatric populations—a particular group of patients that has been poorly studied due to the low frequency of MPN diagnosis. [ABSTRACT FROM AUTHOR]

Simple Summary: Hepatocellular carcinoma (HCC), the primary liver cancer arising from hepatocytes, the predominant cell constituting the liver, accounts for ~90% of all liver cancers. HCC is characterized by activation of receptors on tumor cell surface which regulates tumor cell proliferation and spread to distant organs (metastasis). The class of drugs which predominantly inhibits these receptors are collectively known as tyrosine kinase inhibitors (TKIs). Among them sorafenib, lenvatinib, regorafenib, and cabozantinib have been approved either as the first or as the second line of treatment for advanced HCC. In general, ~30% of HCC patients respond to TKIs, and those that respond invariably develop resistance in ~6 months. This review paper addresses the potential molecular mechanisms by which resistance to TKIs develop and enumerates potential strategies to overcome them thereby providing prolonged survival benefit to HCC patients. Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths worldwide, and the development of effective treatment strategies remains a significant challenge in the management of advanced HCC patients. The emergence of tyrosine kinase inhibitors (TKIs) has been a significant advancement in the treatment of HCC, as these targeted therapies have shown promise in prolonging the survival of patients with advanced disease. Although immunotherapy is currently considered as the first line of treatment for advanced HCC patients, many such patients do not meet the clinical criteria to be eligible for immunotherapy, and in many parts of the world there is still lack of accessibility to immunotherapy. As such, TKIs still serve as the first line of treatment and play a major role in the treatment repertoire for advanced HCC patients. However, the development of resistance to these agents is a major obstacle that must be overcome. In this review, we explore the underlying mechanisms of resistance to TKIs in HCC, the clinical implications of this resistance, and the potential strategies to overcome or prevent the emergence of resistance. [ABSTRACT FROM AUTHOR]

Hair is an intricate biological structure that originates from hair follicles (HFs), which are complex mini‐organs embedded in the skin. Each HF undergoes continuous cycles of growth (anagen), regression (catagen), and rest (telogen), driven by intricate signaling pathways and interactions between epithelial and mesodermal cells. The development of HFs requires the interplay of several key signaling pathways, including Wnt, Shh, Notch, and BMP. The Wnt pathway is primarily involved in induction, Shh is essential for early organogenesis and later stages of cytodifferentiation, Notch signaling governs the fate of HF stem cells, and BMP plays a role in cytodifferentiation. Hair health is closely associated with psychological well‐being and personal distress. While hair loss (alopecia) does not impact biological health, it significantly affects social well‐being. Therefore, a deep understanding of the molecular mechanisms underlying HF development is crucial for developing treatments for hair‐related problems and improving hair health. This knowledge has led to significant advancements in therapeutic applications, particularly in treating hair loss disorders, enhancing wound healing, and developing cosmetic treatments. This paper aims to review the molecular mechanisms involved in HF development, with an emphasis on their potential impact on human health and well‐being. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes joint inflammation and gradual tissue destruction. New research has shown how important noncoding RNAs (ncRNAs) are for changing immune and inflammatory pathways, such as the WNT signaling pathway, which is important for activating synovial fibroblasts and osteoblasts to work. This article examines the current understanding of several ncRNAs, such as miRNAs, lncRNAs, and circRNAs, that influence NF-κB signaling in the pathogenesis of RA. We investigate how these ncRNAs impact NF-κB signaling components, altering cell proliferation, differentiation, and death in joint tissues. The paper also looks at how ncRNAs can be used as potential early detection markers and therapeutic targets in RA because they can change important pathogenic pathways. This study highlights the therapeutic potential of targeting ncRNAs in RA therapy techniques, with the goal of reducing inflammation and stopping disease progression. This thorough analysis opens up new possibilities for understanding the molecular foundations of RA and designing novel ncRNA-based treatments. [ABSTRACT FROM AUTHOR]

Cancer remains one of the leading causes of death worldwide. Despite advances in medical treatments, current therapeutic strategies, including radiotherapy, chemotherapy, targeted therapy, and surgical resection, have not significantly reduced the global incidence and mortality rates of cancer. Oncologists face considerable challenges in devising effective treatment plans due to the adverse side effects associated with standard therapies. Therefore, there is an urgent need for more effective and well-tolerated cancer treatments. Curcumin, a naturally occurring compound, has garnered significant attention for its diverse biological properties. Both preclinical studies and clinical trials have highlighted curcumin's potential in cancer treatment, demonstrating its ability to inhibit the proliferation of various cancer cell types through multiple cellular and molecular pathways. This paper examines the antineoplastic properties, and the therapeutic mechanisms including cell signalling pathways targeted by curcumin that are implicated in cancer development and explores the challenges in advancing curcumin as a viable anticancer therapy. [ABSTRACT FROM AUTHOR]

Innate immunity is the first line of the host cell defensing against viral infection, in which the pattern recognition re-ceptors (PRRs) such as Toll-like receptors (TLRs) and retinoic acid induces gene I -like receptors (RLRs) play an important role. After virus infection, mitochondrial antiviral signaling protein (MAVS) in PRRs-mediated signaling pathway, which are of the common linker molecule for downstream signal transmission, can receive signals transmitted by upstream TLR and RIG-I, activate downstream NF-κB and IRF3/7 signaling pathways leading to the activation of interferon (IFN) expression. Therefore MAVS acts as a bridge in the innate immune signaling pathway. More and more studies have shown that viruses have evolved a series of mechanism to escape the innate immune response over the long course of their evolution, and evaded the host's antiviral immune response by interfering with multiple sites in the MAVS-mediated signaling pathway so as to complete its own replication and proliferation. In this paper, the role of MAVS in IFN- I pathway and its latest research progress in the mechanism of anti-DNA viruses and anti-RNA viruses reaction are reviewed, providing theoretical basis for further studying the detailed mechanism of anti-virus of MAVS. [ABSTRACT FROM AUTHOR]

Diabetic foot ulcer (DFU) is a chronic and serious complication of diabetes mellitus. It is mainly caused by hyperglycaemia, diabetic peripheral vasculopathy and diabetic peripheral neuropathy. These conditions result in ulceration of foot tissues and chronic wounds. If left untreated, DFU can lead to amputation or even endanger the patient's life. Single‐cell RNA sequencing (scRNA‐seq) is a technique used to identify and characterise transcriptional subpopulations at the single‐cell level. It provides insight into cellular function and the molecular drivers of disease. The objective of this paper is to examine the subpopulations, genes and molecules of cells associated with chronic wounds of diabetic foot by using scRNA‐seq. The paper aims to explore the wound‐healing mechanism of DFU from three aspects: inflammation, angiogenesis and extracellular matrix remodelling. The goal is to gain a better understanding of the mechanism of DFU wound healing and identify possible DFU therapeutic targets, providing new insights for the application of DFU personalised therapy. [ABSTRACT FROM AUTHOR]

The aim of this paper was to investigate the transcriptomic and metabolomic differences in Populus cathayana × canadasis 'Xinlin1' (P. cathayana × canadasis 'Xinlin 1') under varying irrigation and fertilization conditions. Ten-year-old P. cathayana × canadasis 'Xinlin 1' was selected as the test subject in this study; different irrigation and fertilization treatments were set up, and DEGs and DAMs in response to water and fertilizer regulation were identified. Transcriptomic and metabolomic profiles were analyzed from both leaves and roots. A total of 22,870 DEGs were identified in response to water and fertilizer treatments, predominantly belonging to 48 transcription factor families, including MYB, ERF, and MYB-related ones. Additionally, 2432 DAMs were detected and categorized into 18 metabolite classes, with flavonoids being the most abundant (342 metabolites), followed by terpenoids, lipids, and others. KEGG enrichment analysis revealed that DEGs and DAMs were significantly associated with pathways such as plant hormone signal transduction and starch and sucrose metabolism pathways. The levels of ABA exhibited an initial decrease followed by an increase, with several key genes, including PYR/PYL, PP2C, SnRK2, and ABF, also differentially expressed in the plant hormone signal transduction pathway. In the starch and sucrose metabolic pathways, sucrose was more hydrolyzed into D-fructose, which gradually translocated from roots to leaves. DEGs were significantly involved in sucrose synthesis and decomposition into D-fructose and 1,3-β-glucose, as well as starch synthesis and starch decomposition into cellulose dextrin, which underwent complete hydrolysis to glucose. In the starch hydrolysis process, 29 DEGs were involved, with 12 down-regulated and 17 up-regulated. [ABSTRACT FROM AUTHOR]

Simple Summary: Head and neck squamous cell carcinoma (HNSCC) is a deadly form of cancer, affecting areas like the mouth, throat, and larynx. This review explores the complex molecular pathways involved in HNSCC development and progression, focusing on the role of microRNAs (miRNAs)—small molecules that regulate gene expression. We aim to provide a comprehensive overview of how miRNAs influence HNSCC, their potential as diagnostic and prognostic markers, and their use in developing new targeted therapies. We also discuss promising nanotechnology-based approaches for delivering miRNA therapies more effectively. By synthesizing the current knowledge on miRNAs in HNSCC, this research may help identify new biomarkers for early detection and prognosis, as well as novel therapeutic targets. Ultimately, these insights could lead to improved personalized treatments and better outcomes for HNSCC patients. This paper presents a comprehensive comparative analysis of biomarkers for head and neck cancer (HNC), a prevalent but molecularly diverse malignancy. We detail the roles of key proteins and genes in tumourigenesis and progression, emphasizing their diagnostic, prognostic, and therapeutic relevance. Our bioinformatic validation reveals crucial genes such as AURKA, HMGA2, MMP1, PLAU, and SERPINE1, along with microRNAs (miRNA), linked to HNC progression. OncomiRs, including hsa-miR-21-5p, hsa-miR-31-5p, hsa-miR-221-3p, hsa-miR-222-3p, hsa-miR-196a-5p, and hsa-miR-200c-3p, drive tumourigenesis, while tumour-suppressive miRNAs like hsa-miR-375 and hsa-miR-145-5p inhibit it. Notably, hsa-miR-155-3p correlates with survival outcomes in addition to the genes RAI14, S1PR5, OSBPL10, and METTL6, highlighting its prognostic potential. Future directions should focus on leveraging precision medicine, novel therapeutics, and AI integration to advance personalized treatment strategies to optimize patient outcomes in HNC care. [ABSTRACT FROM AUTHOR]

Semiconductor nanocrystals (NCs) can function as efficient gain materials with chemical versatility because of their surface ligands. Because the properties of NCs in solution are sensitive to ligand–environment interactions, local chemical changes can result in changes in the optical response. However, amplification of the optical response is technically challenging because of colloidal instability at NC concentrations needed for sufficient gain to overcome losses. This paper demonstrates liquid lasing from plasmonic lattice cavities integrated with ligand-engineered CdZnS/ZnS NCs dispersed in toluene and water. By taking advantage of calcium ion-induced aggregation of NCs in aqueous solutions, we show how lasing threshold can be used as a transduction signal for ion detection. Our work highlights how NC solutions and plasmonic lattices with open cavity architectures can serve as a biosensing platform for lab-on-chip devices. [ABSTRACT FROM AUTHOR]

Pancreatic cancer is known to be the most lethal cancer. Fewer new treatments are being developed for pancreatic cancer as compared to other cancers. The bioactive lipid S1P, which is mainly regulated by sphingosine kinase 1 (SK1) and sphingosine kinase 2 (SK2) enzymes, plays significant roles in pancreatic cancer initiation and exacerbation. S1P controls many signaling pathways to modulate the progression of pancreatic cancer through the G-coupled receptor S1PR1-5. Several papers reporting amelioration of pancreatic cancer via modulation of S1P levels or downstream signaling pathways have previously been published. In this paper, for the first time, we have reviewed the results of previous studies to understand how S1P and its receptors contribute to the development of pancreatic cancer, and whether S1P can be a therapeutic target. In addition, we have also reviewed papers dealing with the effects of SK1 and SK2, which are kinases that regulate the level of S1P, on the pathogenesis of pancreatic cancer. We have also listed available drugs that particularly focus on S1P, S1PRs, SK1, and SK2 for the treatment of pancreatic cancer. Through this review, we would like to suggest that the SK/S1P/S1PR signaling system can be an important target for treating pancreatic cancer, where a new treatment target is desperately warranted. [ABSTRACT FROM AUTHOR]

Systematic inflammatory response syndrome (SIRS) and the accompanying sepsis pose a huge threat to human health worldwide. Heparin is a part of the standard supportive care for the disease. However, the molecular mechanism is not fully understood yet, and the potential signaling pathways that play key roles have not yet been elucidated. In this paper, the main findings regarding the molecular mechanisms associated with the beneficial effects of heparin, including inhibiting HMGB-1-driven inflammation reactions, histone-induced toxicity, thrombo-inflammatory response control and the new emerging mechanisms are concluded. To set up the link between the preclinical research and the clinical effects, the outcomes of the clinical trials are summarized. Then, the structure and function relationship of heparin is discussed. By providing an updated analysis of the above results, the paper highlights the feasibility of heparin as a possible alternative for sepsis prophylaxis and therapy. [ABSTRACT FROM AUTHOR]

Conventional biochemical methods for studying cellular signaling cascades have relied on destructive cell disruption. In contrast, the live cell imaging of fluorescent-tagged transfected proteins offers a non-invasive approach to understanding signal transduction events. One strategy involves monitoring the phosphorylation-dependent shuttling of a fluorescent-labeled kinase between the nucleus and cytoplasm using nuclear localization, export signals, or both. In this paper, we introduce a simple method to visualize intracellular signal transduction in live cells by exploring the translocation properties of PKC from the cytoplasm to the membrane. We fused bait protein to PKC, allowing the bait (RFP-labeled) and target (GFP-labeled) proteins to co-translocate from the cytoplasm to the membrane. However, in non-interacting protein pairs, only the bait protein was translocated to the plasma membrane. To verify our approach, we examined the Raf–MEK–ERK signaling cascade (ERK pathway). We successfully visualized direct Raf1/MEK2 interaction and the KSR1-containing ternary complex (Raf1/MEK2/KSR1). However, the interaction between MEK and ERK was dependent on the presence of the KSR1 scaffold protein under our experimental conditions. [ABSTRACT FROM AUTHOR]

Background: Cystic Fibrosis (CF) is a monogenic disease caused by mutations in the gene coding the Cystic Fibrosis Transmembrane Regulator (CFTR) protein, but its overall physio-pathology cannot be solely explained by the loss of the CFTR chloride channel function. Indeed, CFTR belongs to a yet not fully deciphered network of proteins participating in various signalling pathways. Methods: We propose a systems biology approach to study how the absence of the CFTR protein at the membrane leads to perturbation of these pathways, resulting in a panel of deleterious CF cellular phenotypes. Results: Based on publicly available transcriptomic datasets, we built and analyzed a CF network that recapitulates signalling dysregulations. The CF network topology and its resulting phenotypes were found to be consistent with CF pathology. Conclusion: Analysis of the network topology highlighted a few proteins that may initiate the propagation of dysregulations, those that trigger CF cellular phenotypes, and suggested several candidate therapeutic targets. Although our research is focused on CF, the global approach proposed in the present paper could also be followed to study other rare monogenic diseases. [ABSTRACT FROM AUTHOR]

Throughout development, complex networks of cell signaling pathways drive cellular decision-making across different tissues and contexts. The transforming growth factor β (TGF-β) pathways, including the BMP/Smad pathway, play crucial roles in determining cellular responses. However, as the Smad pathway is used reiteratively throughout the life cycle of all animals, its systems-level behavior varies from one context to another, despite the pathway connectivity remaining nearly constant. For instance, some cellular systems require a rapid response, while others require high noise filtering. In this paper, we examine how the BMP-Smad pathway balances trade-offs among three such systems-level behaviors, or "Performance Objectives (POs)": response speed, noise amplification, and the sensitivity of pathway output to receptor input. Using a Smad pathway model fit to human cell data, we show that varying non-conserved parameters (NCPs) such as protein concentrations, the Smad pathway can be tuned to emphasize any of the three POs and that the concentration of nuclear phosphatase has the greatest effect on tuning the POs. However, due to competition among the POs, the pathway cannot simultaneously optimize all three, but at best must balance trade-offs among the POs. We applied the multi-objective optimization concept of the Pareto Front, a widely used concept in economics to identify optimal trade-offs among various requirements. We show that the BMP pathway efficiently balances competing POs across species and is largely Pareto optimal. Our findings reveal that varying the concentration of NCPs allows the Smad signaling pathway to generate a diverse range of POs. This insight identifies how signaling pathways can be optimally tuned for each context. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Tumor immunotherapy is an emerging and promising therapeutic modality. Mesothelin, a cell surface membrane protein anchored by glycosylated phosphatidylinositol, is highly expressed in a variety of malignant solid tumors and hematological malignancies, but lowly expressed in the mesothelial cells of a few normal tissues, making it a promising target for tumor immunotherapy. High mesothelin expression is closely associated with poor prognosis patients, and soluble mesothelin has become a diagnostic biomarker for a variety of tumors. Immunotherapeutic strategies, such as antibody-drug conjugates and CAR-T cell therapy, are undergoing translational research for mesothelin-positive solid tumors, achieving preliminary progress. This paper systematically describes the structure, in vivo distribution, biological functions, and intracellular signaling mechanisms of mesothelin in tumor cells. It also covers targeted imaging and therapeutic strategies based on nuclides, antibody-drug conjugates and CAR-T cells, along with the associated challenges. These insights provide a new perspective for further exploration of mesothelin-targeted immunotherapies. [ABSTRACT FROM AUTHOR]

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Simple Summary: Colorectal cancer (CRC) is one of the most common causes of death worldwide. Today, this disease does not have an effective treatment, leading to the exploration of novel pharmacological molecules. In this paper, we design and synthesize with a new synthetic route the lipophilic cation derived from gallic acid (TPP+C10) and gentisic acid (GA-TPP+C10), both able to reach mitochondria and uncouple the electron transport chain. Our results show that combining 5-fluorouracil with GA-TPP+C10 has a synergistic cytotoxic effect on CRC cells. Both compounds show antimigratory effects, decreasing signaling pathways and biomarkers. Our results show that mitochondrial agents could be an alternative to standard CRC drugs against this disease. Colorectal cancer (CRC) is the third leading cause of cancer deaths in the world. Standard drugs currently used for the treatment of advanced CRC—such as 5-fluorouracil (5FU)—remain unsatisfactory in their results due to their high toxicity, high resistance, and adverse effects. In recent years, mitochondria have become an attractive target for cancer therapy due to higher transmembrane mitochondrial potential. We synthesized gallic acid derivatives linked to a ten-carbon aliphatic chain associated with triphenylphosphonium (TPP+C10), a lipophilic cationic molecule that induces the uncoupling of the electron transport chain (ETC). Other derivatives, such as gentisic acid (GA-TPP+C10), have the same effects on colorectal cancer cells. Although part of our group had previously reported preparing these structures by a convergent synthesis route, including their application via flow chemistry, there was no precedent for a new methodology for preparing these compounds. In this scenario, this study aims to develop a new linear synthesis strategy involving an essential step of Steglich esterification under mild conditions (open flask) and a high degree of reproducibility. Moreover, the study seeks to associate GA-TPP+C10 with 5FU to evaluate synergistic antineoplastic effects. In addition, we assess the antimigratory effect of GA-TPP+C10 and TPP+C10 using human and mouse metastatic CRC cell lines. The results show a new and efficient synthesis route of these compounds, having synergistic effects in combination with 5FU, increasing apoptosis and enhancing cytotoxic properties. Additionally, the results show a robust antimigratory effect of GATPP+C10 and TPP+C10, reducing the activation pathways linked to tumor progression and reducing the expression of VEGF and MMP-2 and MMP-9, common biomarkers of advanced CRC. Moreover, TPP+C10 and GA-TPP+C10 increase the activity of metabolic signaling pathways through AMPK activation. The data allow us to conclude that these compounds can be used for in vivo evaluations and are a promising alternative associated with conventional therapies for advanced colorectal cancer. Additionally, the reported intermediates of the new synthesis route could give rise to analog compounds with improved therapeutic activity. [ABSTRACT FROM AUTHOR]

Background: Dauricine (DAU), a benzyl tetrahydroisoquinoline alkaloid isolated from the root of Menispermum dauricum DC, exhibits promising anti-Alzheimer's disease (AD) effects, but its underlying mechanisms remain inadequately investigated. This paper aims to identify potential targets and molecular mechanisms of DAU in AD treatment. Methods: Network pharmacology and molecular docking simulation method were used to screen and focus core targets. Various transgenic Caenorhabditis elegans models were chosen to validate the anti-AD efficacy and mechanism of DAU. Results: There are 66 potential DAU-AD target intersections identified from 100 DAU and 3036 AD-related targets. Subsequent protein-protein interaction (PPI) network analysis identified 16 core targets of DAU for anti-AD. PIK3CA, AKT1 and mTOR were predicted to be the central targets with the best connectivity through the analysis of "compound-target-biological process-pathway network". Molecular docking revealed strong binding affinities between DAU and PIK3CA, AKT1, and mTOR. In vivo experiments demonstrated that DAU effectively reduced paralysis in AD nematodes caused by Aβ aggregation toxicity, downregulated expression of PIK3CA, AKT1, and mTOR homologues (age-1, akt-1, let-363), and upregulated expression of autophagy genes and the marker protein LGG-1. Simultaneously, DAU increased lysosomal content and enhanced degradation of the autophagy-related substrate protein P62. Thioflavin T（Th-T）staining experiment revealed that DAU decreased Aβ accumulation in AD nematodes. Further experiments also confirmed DAU's protein scavenging activity in polyglutamine (polyQ) aggregation nematodes. Conclusion: Collectively, the mechanism of DAU against AD may be related to the activation of the autophagy-lysosomal protein clearance pathway, which contributes to the decrease of Aβ aggregation and the restoration of protein homeostasis. [ABSTRACT FROM AUTHOR]

Colorectal cancer is a common malignant tumor of the digestive system. Its morbidity and mortality rank among the highest in the world. Cancer development is associated with aberrant signaling pathways. Autophagy is a process of cell self-digestion that maintains the intracellular environment and has a bidirectional regulatory role in cancer. Apoptosis is one of the important death programs in cancer cells and is able to inhibit cancer development. Studies have shown that a variety of substances can regulate autophagy and apoptosis in colorectal cancer cells through signaling pathways, and participate in the regulation of autophagy on apoptosis. In this paper, we focus on the relevant research on autophagy in colorectal cancer cells based on the involvement of related signaling pathways in the regulation of apoptosis in order to provide new research ideas and therapeutic directions for the treatment of colorectal cancer. [ABSTRACT FROM AUTHOR]

TANK-binding kinase 1 (TBK1) is a member of the IKK family and plays a crucial role in the activation of non-canonical NF-kB signaling and type I interferon responses. The aberrant activation of TBK1 contributes to the proliferation and survival of various types of tumor cells, particularly in specific mutational or tumorous contexts. Inhibitors targeting TBK1 are under development and application in both in vivo and in vitro settings, yet their clinical efficacy remains limited. Numerous literatures have shown that TBK1 can exhibit both tumor promoting and tumor inhibiting effects. TBK1 acts as a pivotal node within the innate immune pathway, mediating anti-tumor immunity through the activation of innate immune responses. Facilitating interferon-I (IFN-I) production represents a critical mechanism through which TBK1 bridges these processes. IFN has been shown to exert both beneficial and detrimental effects on tumor progression. Hence, the paradoxical role of TBK1 in tumor development may necessitate acknowledgment in light of its downstream IFNI signaling cascade. In this paper, we review the signaling pathways mediated by TBK1 in various tumor contexts and summarize the dual roles of TBK1 and the TBK1-IFN pathways in both promoting and inhibiting tumor progression. Additionally, we highlight the significance of the TBK1-IFN pathway in clinical therapy, particularly in the context of immune response. We anticipate further advancements in the development of TBK1 inhibitors as part of novel cancer treatment strategies. [ABSTRACT FROM AUTHOR]

Medicinal food varieties developed according to the theory of medical and edible homologues are effective at preventing and treating chronic diseases and in health care. As of 2022, 110 types of traditional Chinese medicines from the same source of medicine and food have been published by the National Health Commission. Inflammation is the immune system's first response to injury, infection, and stress. Chronic inflammation is closely related to many diseases such as atherosclerosis and cancer. Therefore, timely intervention for inflammation is the mainstay treatment for other complex diseases. However, some traditional anti-inflammatory drugs on the market are commonly associated with a number of adverse effects, which seriously affect the health and safety of patients. Therefore, the in-depth development of new safe, harmless, and effective anti-inflammatory drugs has become a hot topic of research and an urgent clinical need. Polysaccharides, one of the main active ingredients of medical and edible homologous traditional Chinese medicines (MEHTCMs), have been confirmed by a large number of studies to exert anti-inflammatory effects through multiple targets and are considered potential natural anti-inflammatory drugs. In addition, the structure of medical and edible homologous traditional Chinese medicines' polysaccharides (MEHTCMPs) may be the key factor determining their anti-inflammatory activity, which makes the underlying the anti-inflammatory effects of polysaccharides and their structure–efficacy relationship hot topics of domestic and international research. However, due to the limitations of the current analytical techniques and tools, the structures have not been fully elucidated and the structure–efficacy relationship is relatively ambiguous, which are some of the difficulties in the process of developing and utilizing MEHTCMPs as novel anti-inflammatory drugs in the future. For this reason, this paper summarizes the potential anti-inflammatory mechanisms of MEHTCMPs, such as the regulation of the Toll-like receptor-related signaling pathway, MAPK signaling pathway, JAK-STAT signaling pathway, NLRP3 signaling pathway, PI3K-AKT signaling pathway, PPAR-γ signaling pathway, Nrf2-HO-1 signaling pathway, and the regulation of intestinal flora, and it systematically analyzes and evaluates the relationships between the anti-inflammatory activity of MEHTCMPs and their structures. [ABSTRACT FROM AUTHOR]

Atractylodin is one of the main active ingredients of Atractylodis Rhizoma. It has various pharmacological properties, such as antigastric ulcer, immune regulation, antibacterial, anti-inflammatory, antitumor, anti-oxidant, and neuroprotective properties. In the past few decades, atractylodin has attracted the attention of researchers due to its excellent therapeutic effects. This paper aims to review the pharmacology of atractylodin, focusing mainly on its pharmacological effects in tumor treatment. Atractylodin exerts its antitumor effect by regulating different signaling pathways to induce important biological events such as apoptosis, cell cycle arrest, and autophagy, inhibiting cancer cell invasion and metastasis. In the process of cell apoptosis, atractylodin mainly induces cancer cell apoptosis by downregulating the Notch signaling pathway, affecting multiple upstream and downstream targets. In addition, atractylodin induces autophagy in cancer cells by regulating various signaling pathways such as PI3K/AKT/mTOR, p38MAPK, and hypothalamic Sirt1 and p-AMPK. Atractylodin effectively induces G1/M and G2/M phase arrest under the action of multiple signaling pathways. Among them, the pathways related to G1/M are more widely stagnated. In inhibiting the migration and invasion of cancer cells, atractylodin mainly regulates the Wnt signaling pathway, downregulates the expression of N-cadherin in cancer cells, and then blocks the PI3K/AKT/mTOR signaling pathway, inhibiting the phosphorylation of PI3K, AKT, and mTOR proteins, thereby having a significant impact on the invasion and migration of cancer cells. This paper systematically reviews the research progress on the antitumor effects and mechanisms of atractylodin, hoping to provide a reference and theoretical basis for its clinical application and new drug development. [ABSTRACT FROM AUTHOR]

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Spinal cord injury (SCI) denotes damage to both the structure and function of the spinal cord, primarily manifesting as sensory and motor deficits caused by disruptions in neural transmission pathways, potentially culminating in irreversible paralysis. Its pathophysiological processes are complex, with numerous molecules and signaling pathways intricately involved. Notably, the pronounced upregulation of the Wnt signaling pathway post-SCI holds promise for neural regeneration and repair. Activation of the Wnt pathway plays a crucial role in neuronal differentiation, axonal regeneration, local neuroinflammatory responses, and cell apoptosis, highlighting its potential as a therapeutic target for treating SCI. However, excessive activation of the Wnt pathway can also lead to negative effects, highlighting the need for further investigation into its applicability and significance in SCI. This paper provides an overview of the latest research advancements in the Wnt signaling pathway in SCI, summarizing the recent progress in treatment strategies associated with the Wnt pathway and analyzing their advantages and disadvantages. Additionally, we offer insights into the clinical application of the Wnt signaling pathway in SCI, along with prospective avenues for future research direction. [ABSTRACT FROM AUTHOR]

The liver possesses a distinctive capacity for regeneration within the human body. Under normal circumstances, liver cells replicate themselves to maintain liver function. Compensatory replication of healthy hepatocytes is sufficient for the regeneration after acute liver injuries. In the late stage of chronic liver damage, a large number of hepatocytes die and hepatocyte replication is blocked. Liver regeneration has more complex mechanisms, such as the transdifferentiation between cell types or hepatic progenitor cells mediated. Dysregulation of liver regeneration causes severe chronic liver disease. Gaining a more comprehensive understanding of liver regeneration mechanisms would facilitate the advancement of efficient therapeutic approaches. This review provides an overview of the signalling pathways linked to different aspects of liver regeneration in various liver diseases. Moreover, new knowledge on cellular interactions during the regenerative process is also presented. Finally, this paper explores the potential applications of new technologies, such as nanotechnology, stem cell transplantation and organoids, in liver regeneration after injury, offering fresh perspectives on treating liver disease. [ABSTRACT FROM AUTHOR]

Wnts are secreted, lipid-modified proteins that bind to different receptors on the cell surface to activate canonical or non-canonical Wnt signaling pathways, which control various biological processes throughout embryonic development and adult life. Aberrant Wnt signaling pathway underlies a wide range of human disease pathogeneses. In this review, we provide an update of Wnt/β-catenin signaling components and mechanisms in bone formation, homeostasis, and diseases. The Wnt proteins, receptors, activators, inhibitors, and the crosstalk of Wnt signaling pathways with other signaling pathways are summarized and discussed. We mainly review Wnt signaling functions in bone formation, homeostasis, and related diseases, and summarize mouse models carrying genetic modifications of Wnt signaling components. Moreover, the therapeutic strategies for treating bone diseases by targeting Wnt signaling, including the extracellular molecules, cytosol components, and nuclear components of Wnt signaling are reviewed. In summary, this paper reviews our current understanding of the mechanisms by which Wnt signaling regulates bone formation, homeostasis, and the efforts targeting Wnt signaling for treating bone diseases. Finally, the paper evaluates the important questions in Wnt signaling to be further explored based on the progress of new biological analytical technologies. [ABSTRACT FROM AUTHOR]

Background: Ferroptosis, a newly proposed concept of programmed cell death, has garnered significant attention in research across different diseases in the last decade. Despite thorough citation analyses in neuroscience, there is a scarcity of information on ferroptosis research specifically related to neurodegenerative diseases. Method: The Web of Science Core Collection database retrieved relevant articles and reviews. Data on publications, countries, institutions, authors, journals, citations, and keywords in the included studies were systematically analyzed using Microsoft Excel 2019 and CiteSpace 6.2.R7 software. Result: A comprehensive analysis and visualization of 563 research papers on ferroptosis in neurodegenerative diseases from 2014 to 2023 revealed emerging research hotspots and trends. The number of annual publications in this field of study has displayed a pattern of stabilization in the early years of the decade, followed by a notable increase in the later years and peaking in 2023 with 196 publications. Regarding publication volume and total citations, notable research contributions were observed from countries, institutions, and authors in North America, Western Europe, and China. Current research endeavors primarily focus on understanding the intervention mechanisms of neurodegenerative diseases through the ferroptosis pathway and exploring and identifying potential therapeutic targets. Conclusion: The study highlights key areas of interest and emerging trends in ferroptosis research on neurodegenerative diseases, offering valuable insights for further exploration and potential directions for diagnosing and treating such conditions. [ABSTRACT FROM AUTHOR]

As one of the most prevalent chronic inflammatory skin diseases, atopic dermatitis (AD) increasingly affects the aging population. Amid the ongoing global aging trend, it's essential to recognize the intricate relationship between AD and aging. This paper reviews existing knowledge, summarizing clinical observations of associations between AD and aging-related diseases in various systems, including endocrine, cardiovascular, and neurological. Additionally, it discusses major theories explaining the correlation, encompassing skin-mucosal barriers, systemic inflammation and stress, genes, signal transduction, and environmental and behavioral factors. The association between AD and aging holds significant importance, both in population and basic perspectives. While further research is warranted, this paper aims to inspire deeper exploration of inflammation/allergy-aging dynamics and the timely management of elderly patients with AD. [ABSTRACT FROM AUTHOR]

Natural language processing (NLP) has become an essential technique in various fields, offering a wide range of possibilities for analyzing data and developing diverse NLP tasks. In the biomedical domain, understanding the complex relationships between compounds and proteins is critical, especially in the context of signal transduction and biochemical pathways. Among these relationships, protein–protein interactions (PPIs) are of particular interest, given their potential to trigger a variety of biological reactions. To improve the ability to predict PPI events, we propose the protein event detection dataset (PEDD), which comprises 6823 abstracts, 39 488 sentences and 182 937 gene pairs. Our PEDD dataset has been utilized in the AI CUP Biomedical Paper Analysis competition, where systems are challenged to predict 12 different relation types. In this paper, we review the state-of-the-art relation extraction research and provide an overview of the PEDD's compilation process. Furthermore, we present the results of the PPI extraction competition and evaluate several language models' performances on the PEDD. This paper's outcomes will provide a valuable roadmap for future studies on protein event detection in NLP. By addressing this critical challenge, we hope to enable breakthroughs in drug discovery and enhance our understanding of the molecular mechanisms underlying various diseases. [ABSTRACT FROM AUTHOR]

Cinnamon is one of the world's oldest and most popular spices, and is derived from the inner bark of several tree species from the genus Cinnamomum. During the last two decades, cinnamon has demonstrated beneficial metabolic effects not only in animal experiments but also in clinical trials. Even recent meta-analyses have shown the protective effects of cinnamon on different components of metabolic syndrome and their complications. In the last 5 years, several experimental studies have unraveled the intricate molecular mechanisms underlying the antihypertensive, antihyperglycemic, lipid-lowering, weight-lowering, and cardioprotective properties of cinnamon. This review paper will discuss how cinnamon and its active components, particularly cinnamaldehyde, suppress inflammation and oxidative stress, modulate mitochondrial dysfunction, and regulate glucose uptake, insulin resistance, lipogenesis, beta-oxidation, Ca2+ signaling, and other cellar events at the molecular level. Specifically, we will delve into the molecular mechanisms involved in the metabolic effects of cinnamon to provide a deeper insight into how cinnamon can bring such beneficial effects. This review hopes to encourage the use of cinnamon in clinical settings, guide the combination of cinnamon with other drugs used to treat different components of metabolic syndrome based on their mechanism of action, and support the concept of complementary medicine for metabolic diseases. [ABSTRACT FROM AUTHOR]

The flavonoid compound chinonin is one of the main active components of Rhizoma anemarrhena with multiple activities, including anti-inflammatory and antioxidant properties, protection of mitochondrial function and regulation of immunity. In this paper, we reviewed recent research progress on the protective effect of chinonin on brain injury in neurological diseases. "Chinonin" OR "Mangiferin" AND "Nervous system diseases" OR "Neuroprotection" was used as the terms for search in PumMed. After discarding duplicated and irrelevant articles, a total of 23 articles relevant to chinonin published between 2012 and 2023 were identified in our study. [ABSTRACT FROM AUTHOR]

DNA circuits, as a crucial tool for processing molecular information, achieve precise control of complex molecular reactions within biological systems, demonstrating significant potential in gene expression regulation, molecular computing, and biosensing. Here, we developed a G-quadruplex-regulated (G4-regulated) exonuclease cooperative hydrolysis signal transduction strategy with the advantages of excellent sequence orthogonality, simple modular reaction units, signal amplification capability, and no excess by-products. The reaction principle of this strategy is to use G4 as a switch to regulate signal transduction, and by controlling the conformational change of G4, regulate the cooperative hydrolysis of Exonuclease III (Exo III) and Exonuclease λ (Exo λ), thereby treating the molecular conformation as functional signals for information processing. Based on this strategy, we constructed fan-out and fan-in circuits to perform signal transduction tasks. We also extended them to design a DNA signal network to process temporal information. This work shows the multifunctionality of G4, providing an effective way to regulate enzyme hydrolysis while also offering new ideas and methods for understanding and constructing molecular networks for processing temporal information. This regulation approach and signaling strategy will have future applications in DNA computing, biosensing and nanomachines. [ABSTRACT FROM AUTHOR]

Mammals induce an innate aversive response by sensing H+ dissociated from sour substances to prevent the ingestion of harmful substances. Several sour taste candidate receptors have been ruled out over the past decades, only in recent years Otopetrinl (Otop1) has been identified as a sour taste receptor, and sour taste neurotransmitters and sensing pathways have been discovered. This paper reviewed three sour taste perception pathways, detailing the structure of the Otop1 sour taste receptor and its function. The Otop1 signaling pathway was explained with emphasis on the H+ inward flow blocking the inwardly-rectifying potassium channel 2.1 (Kir2.1) to enhance cell depolarization, the release of the activating sour taste neurotransmitter serotonin (5-hydroxytryptamine, 5-HT), and the pathway of sour taste information from the periphery to the centre via. The effects of specific diet, individual differences, transmembrane state perception, and disease on sour taste perception were discussed. The aim was to understand the causes of changes in personal sour taste perception, to provide a theoretical reference for the development of sour foods for different populations and looked forward to future research on unknown signaling pathways in sour taste transmission. [ABSTRACT FROM AUTHOR]

Peanut is one of the eight kinds of allergens, which can cause a variety of allergic reactions in the human body, and even endanger the lives of peanut allergy patients. Currently, the most effective treatment for peanut allergy is to avoid contact with products containing peanut matrix. Plant polyphenols may reduce the sensitization of peanut protein from two aspects: On the one hand, plant polyphenols can directly interfere with the mechanism of peanut allergy by affecting related signal transduction and gene expression in the process of allergic reaction. On the other hand, the IgE binding epitopes of peanut sensitized proteins can be masked or destroyed by the interaction of plant polyphenols with peanut proteins, so that they cannot be recognized by IgE antibodies. At present, the treatment of peanut protein with plant polyphenols is considered to be an effective and feasible strategy to reduce its sensitization. In this paper, the types and sequence length of peanut sensitizing proteins and the sensitization mechanism of peanut proteins were reviewed, the factors affecting peanut protein sensitization were summarized, and two desensitization mechanisms of plant polyphenols were introduced, providing theoretical reference for reducing peanut protein sensitization by plant polyphenols. [ABSTRACT FROM AUTHOR]