Biomedicines最新文献

{"title":"Interferon Regulator Factor 5: A Novel Inflammatory Marker and Promising Therapeutic Target in Ulcerative Colitis.","authors":"Karima Farrag, Aysegül Aksan, Marina Korotkova, Helena Idborg, Per-Johan Jakobsson, Andreas Weigert, Michael Vieth, Stefan Zeuzem, Irina Blumenstein, Jürgen Stein","doi":"10.3390/biomedicines13092251","DOIUrl":"10.3390/biomedicines13092251","url":null,"abstract":"<p><p><b>Background:</b> Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), is characterized by chronic inflammation affecting the gastrointestinal tract and extraintestinal organs. The etiology of IBD is multifactorial, involving genetic, immunological, and environmental factors. Over 200 genetic loci have been associated with the disease, indicating a significant genetic predisposition. Despite advances in understanding its genetic basis, clinical management remains challenging due to heterogeneity in disease presentation and variable treatment responses. Current therapies, such as 5-aminosalicylates and biologics, are not universally effective, underscoring the need for reliable biomarkers to predict therapeutic responses. <b>Objective:</b> This study investigates the potential role of interferon regulatory factor 5 (IRF5) in the pathogenesis of IBD, with a particular focus on UC. <b>Methods:</b> We conducted a systematic analysis of colon biopsies from 30 adult patients diagnosed with UC and from 8 non-IBD controls. Immunostaining was performed to assess IRF5 expression in colonic tissues using the primary IRF5 antibody (1:300, Abcam, ab181553). Statistical analyses evaluated the correlation between IRF5-positive cell counts, disease activity, and inflammatory markers such as calprotectin. <b>Results:</b> Our analysis revealed a significant increase in IRF5-positive macrophage-like cells in the inflamed mucosa of IBD patients compared to healthy controls. The number of IRF5-positive cells showed a positive correlation with disease activity and calprotectin levels, indicating that higher IRF5 expression is associated with increased inflammation. <b>Conclusions:</b> This study demonstrates a significant correlation between IRF5 expression and disease activity in UC, suggesting that IRF5 may play a crucial role in the inflammatory processes of the disease. The findings propose IRF5 as a novel biomarker for therapeutic intervention in IBD. Further research is needed to clarify the mechanisms by which IRF5 contributes to IBD pathogenesis and to explore the therapeutic potential of targeting this pathway in clinical settings.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 9","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Variants and Soluble Isoforms of PD-1/PD-L1 as Novel Biomarkers for Pancreatic Ductal Adenocarcinoma (PDAC) Susceptibility and Prognosis.","authors":"Marwa Hassan, Walaa H El-Maadawy, Yasmine Elhusseny, Fatma Elbatol Agamy, Sally A Fahim, Mahmoud Balata","doi":"10.3390/biomedicines13092246","DOIUrl":"10.3390/biomedicines13092246","url":null,"abstract":"<p><p><b>Background:</b> Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive neoplasm often diagnosed at advanced stages. Immune checkpoint molecules, particularly programmed cell death protein-1 (PD-1) and its ligand PD-L1, are pivotal in tumor immune evasion. Genetic polymorphisms in PD-1/PD-L1 and their soluble isoforms (sPD-1/sPD-L1) may influence individual susceptibility to cancer and disease progression. Therefore, this study was conducted to examine the correlation between PD-1/PD-L1 gene polymorphisms, serum levels of sPD-1/sPD-L1, and their association with PDAC susceptibility, severity, and prognostication. <b>Methods:</b> This case-control study was performed with 150 PDAC patients and 150 controls. Clinical and laboratory data, including tumor markers (CA19-9 and CEA), were recorded. Allele-specific PCR was utilized to genotype PD-1 (rs6749527 and rs7421861) and PD-L1 (rs2297136, and rs4143815). sPD-1/sPD-L1 were quantified with ELISA. Mapping of the Kaplan-Meier survival curve of mutant genes was performed. <b>Results:</b> The rs7421861 AG and GG and rs4143815 GG genotypes, together with their G-alleles, were linked to increased PDAC risk and greater tumor burden. In contrast, the rs2297136 GG genotype and G-allele conferred protection against PDAC development. Serum sPD-L1 levels, rather than sPD-1, were markedly elevated in PDAC patients, progressively increased with tumor grade, and correlated with tumor markers. Also, higher PD-L1 gene expression was associated with lower overall survival. <b>Conclusions:</b> PD-1/PD-L1 genetic variants, particularly rs7421861 and rs4143815, along with sPD-L1 levels, correlate with PDAC susceptibility and disease severity. These findings endorse the prospects of integrating immune checkpoint genetic variants and soluble biomarkers for early identification, risk stratification, prognostication, and personalized therapeutic strategies in PDAC management.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 9","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of Cytokine Levels in Cardiac Transthyretin and Immunoglobulin Light Chain Amyloidosis and Their Correlation with Myocardial Inflammatory Cells and MACE.","authors":"Nicolas Musigk, Phillip Suwalski, Maximilian Müller, Michele Violano, Karin Klingel, January Weiner, Dieter Beule, Ulf Landmesser, Bettina Heidecker","doi":"10.3390/biomedicines13092254","DOIUrl":"10.3390/biomedicines13092254","url":null,"abstract":"<p><p><b>Aims:</b> Myocardial inflammation in cardiac amyloidosis is associated with poor clinical outcomes. This study aimed to (a) investigate the relationship between peripheral blood cytokine levels and the presence of inflammatory cells within the myocardium, and to (b) evaluate the potential of cytokines as predictors of major adverse cardiovascular events (MACE) in transthyretin (ATTR) and immunoglobulin light chain (AL) cardiac amyloidosis. <b>Methods:</b> Peripheral blood samples were collected from 50 patients with cardiac ATTR or AL amyloidosis between 2018 and 2023 at baseline and every three months during follow-up visits. Cytokine analysis was performed using Olink's Proximity Extension Assay. For MACE prediction analysis, only patients with MACE occurring within ±14 days of a study visit were included (<i>n</i> = 16). Associations were evaluated using linear models. <b>Results:</b> No significant associations were identified between the EMB-confirmed myocardial presence of inflammatory cells and cytokine levels. There was a trend of weak-to-moderate associations between serial blood cytokine levels and MACE, albeit this was non-significant after adjustment for multiple testing (FDR): r² = 0.28 for PON3 (<i>p</i> = 0.00075, FDR = 0.28), SIGLEC1 (<i>p</i> = 0.00077, FDR = 0.28), and IL-6 (<i>p</i> = 0.00086, FDR = 0.31). <b>Conclusions:</b> Peripheral blood cytokine levels were not reliable biomarkers for the myocardial presence of inflammatory cells. PON3, SIGLEC1, and IL-6 demonstrated a statistically non-significant trend of a weak-to-moderate association with MACE in cardiac amyloidosis. Since we recently demonstrated that amyloidosis with an inflammatory component is associated with poor outcomes, these additional findings underscore the need for alternative approaches to identify and manage inflammation in this patient population.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 9","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of HTR1F with Prognosis, Tumor Immune Microenvironment, and Drug Sensitivity in Cancer: A Multi-Omics Perspective.","authors":"Yanjun Gao, Ziyue Zhang, Dafu Ye, Qingqing Li, Yingmei Wen, Shaowen Ma, Bo Zheng, Lei Chen, Yi Yao","doi":"10.3390/biomedicines13092238","DOIUrl":"10.3390/biomedicines13092238","url":null,"abstract":"<p><p><b>Background:</b><i>HTR1F</i> (5-Hydroxytryptamine Receptor 1F) encodes a G protein-coupled receptor involved in serotonin signaling. Although dysregulated <i>HTR1F</i> expression has been implicated in certain malignancies, its biological functions and clinical significance across cancer types remain largely unexplored. <b>Methods:</b> We performed an integrative pan-cancer analysis of transcriptomic and pharmacogenomic datasets covering 34 cancer types (PAN-CAN cohort, N = 19,131; normal tissues, G = 60,499). Drug sensitivity and molecular docking analyses were conducted using the GSCALite database. The protein-protein interaction (PPI) network of <i>HTR1F</i> was constructed via the STRING database. Additionally, we evaluated the effects of <i>HTR1F</i> overexpression on proliferation and invasion in human lung squamous cell carcinoma (LUSC) cell lines NCI-H520 and NCI-H226. <b>Results:</b><i>HTR1F</i> expression was significantly upregulated in 17 cancer types and was associated with poor prognosis, with LUSC showing an AUC of 0.912 for 1-year survival prediction. In LUSC, 695 genes were upregulated and 67 downregulated in response to <i>HTR1F</i> overexpression. <i>HTR1F</i> expression correlated with immune-related genes, immune checkpoints, tumor-infiltrating immune cells, tumor mutation burden (TMB), microsatellite instability (MSI), and drug responses. Genomic alterations, including amplification and deletion, were positively associated with <i>HTR1F</i> expression. Drug sensitivity analysis identified compounds such as sotrastaurin (-10.2 kcal/mol), austocystin D (-9.7 kcal/mol), and tivozanib (-9.3 kcal/mol) as potentially effective inhibitors based on predicted binding affinity. Functional enrichment analyses (GO, KEGG) and GSEA revealed that <i>HTR1F</i> is primarily involved in cell cycle regulation, DNA replication, cellular senescence, and immune-related pathways. Functional validation showed that <i>HTR1F</i> overexpression promotes proliferation of LUSC cells via the MAPK signaling pathway. <b>Conclusions:</b> Our integrative analysis highlights <i>HTR1F</i> as a potential biomarker associated with prognosis, immune modulation, and drug sensitivity across multiple cancer types. These findings provide a foundation for future experimental and clinical studies to explore <i>HTR1F</i>-targeted therapies.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 9","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467612/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of <i>LPCAT1</i>*rs9728 Variant with Reduced Susceptibility to Neonatal Respiratory Distress Syndrome.","authors":"Shimaa Dorgham, Sohier Yahia, Doaa Shahin, Ahmad M Eita, Eman A Toraih, Rami M Elshazli","doi":"10.3390/biomedicines13092237","DOIUrl":"10.3390/biomedicines13092237","url":null,"abstract":"<p><p><b>Background/Objectives</b>: Neonatal respiratory distress syndrome (NRDS) is a heterogenous respiratory illness that mainly affects preterm neonates. It is characterized by insufficient production of pulmonary surfactant and impaired lung compliance. The lysophosphatidylcholine acyltransferase 1 (LPCAT1) enzyme has a crucial function in lipid remodeling through the conversion of lysophosphatidylcholine to phosphatidylcholine, the major component of pulmonary surfactant. In this research, we aimed to investigate the association of the <i>LPCAT1</i>*rs9728 variant with NRDS susceptibility using hereditary analysis and bioinformatic approaches. <b>Methods</b>: The <i>LPCAT1</i> (rs9728; c.*1668T>C) variant was characterized among 100 preterm neonates with RDS and 100 non-RDS neonates utilizing the TaqMan SNP genotyping assay. Logistic regression analysis was performed to identify the risk factors of respiratory distress syndrome. The functional mechanism of the <i>LPCAT1</i> gene was elucidated using bioinformatic approaches. <b>Results</b>: The <i>LPCAT1*</i>rs9728 C/C genotype was significantly associated with a 78% reduced risk of NRDS (OR = 0.22, <i>p</i> = 0.027), although the minor C allele did not attain a significant finding (OR = 0.83, <i>p</i> = 0.416). Apgar score and Silverman-Andersen respiratory severity score (RSS) were statistically significant with prematurity classes (<i>p</i> < 0.05). Additionally, gestational age and birth weight were considered independent risk factors in the progression of RDS among preterm neonates. <b>Conclusions</b>: This research exhibited a significant difference between the <i>LPCAT1</i> (rs9728; c.*1668T>C) variant and reduced risk against the development of RDS among preterm neonates. The rs9728*C/C genotype revealed a significant association with decreased risk of NRDS compared to non-RDS neonates.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 9","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial of the Special Issue: Extracellular Vesicles and Exosomes as Therapeutic Agents.","authors":"David J Rademacher","doi":"10.3390/biomedicines13092234","DOIUrl":"10.3390/biomedicines13092234","url":null,"abstract":"<p><p>Membrane-enclosed particles, known as extracellular vesicles (EVs), are ubiquitously present in organisms, including animals, plants, and microorganisms [...].</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 9","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467427/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Arthrospira platensis</i> and Its Potential for Skin Regeneration in Animal Models as Support for Initiating Clinical Trials in Humans: A Systematic Review.","authors":"Sara Isabel Fernández, María Estefanía Hernández, Lina Andrea Gómez","doi":"10.3390/biomedicines13092239","DOIUrl":"10.3390/biomedicines13092239","url":null,"abstract":"<p><p><b>Background/Objectives:</b> The search for natural alternatives to enhance wound healing has driven the investigation of bioactive compounds, such as <i>Spirulina</i>. This microalga, rich in antioxidant, anti-inflammatory, and antimicrobial properties, contains compounds like phycocyanin (C-PC), which promote cell repair, reduce inflammatory markers, and combat bacteria. Although its effects are promising, its efficacy still requires validation through human clinical trials. This article aims to review scientific publications on the use of <i>Spirulina</i> in skin regeneration using animal wound models. <b>Methods:</b> A database search was conducted for studies published between 2017 and 2024 on the effects of <i>Spirulina</i> on tissue regeneration in rats, chosen for their genetic similarity to humans. In vitro studies, those using other animal models, or studies published in languages other than Spanish or English were excluded. The review followed the PRISMA 2020 guidelines. <b>Results:</b> Four studies were analyzed, all of which demonstrated promising results in wound healing in rats. <i>Spirulina</i> was administered through oral supplements, hydrogels, and nanophytosomal formulations. These treatments accelerated wound closure and improved granulation tissue formation, vascularization, and epithelialization. Additionally, they exhibited antihyperglycemic effects in diabetic rats. <b>Conclusions:</b> The reviewed studies highlight the potential of <i>Spirulina platensis</i> to enhance wound healing, particularly in cases of diabetes and burns. Its antioxidant and anti-inflammatory properties play a crucial role in accelerating cellular regeneration and reducing inflammation, contributing to faster and more effective recovery. However, further research in humans is necessary to confirm its safety and clinical efficacy.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 9","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA Landscape in Hepatocellular Carcinoma: Metabolic Re-Wiring, Predictive and Diagnostic Biomarkers, and Emerging Therapeutic Targets.","authors":"Dimitris Liapopoulos, Panagiotis Sarantis, Theodora Biniari, Thaleia-Eleftheria Bousou, Eleni-Myrto Trifylli, Ioanna A Anastasiou, Stefania Kokkali, Dimitra Korakaki, Spyridon Pantzios, Evangelos Koustas, Ioannis Elefsiniotis, Michalis V Karamouzis","doi":"10.3390/biomedicines13092243","DOIUrl":"10.3390/biomedicines13092243","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality, in part due to late diagnosis and limited prognostic tools. In recent years, microRNAs, small, non-coding regulators of gene expression, have emerged as key modulators of tumor metabolism, microenvironmental crosstalk, and therapeutic response in HCC. This narrative review synthesizes evidence published from January 2000 through April 2025, focusing on four interrelated themes: (1) miRNA-driven metabolic rewiring; (2) circulating and exosomal miRNAs as diagnostic and (3) predictive biomarkers; (4) miRNA-based therapeutic strategies. We conducted a targeted PubMed search using terms related to HCC, miRNA biology, biomarkers, metabolism, and therapy, supplemented by manual reference mining. Preclinical and clinical studies reveal that loss of tumor-suppressor miRNAs and gain of oncomiRs orchestrate glycolysis, lipid and glutamine metabolism, and stromal-immune remodeling. Circulating miRNA signatures, including single- and multimarker panels, demonstrate diagnostic AUCs up to 0.99 for early-stage HCC and distinguish HCC from cirrhosis more accurately than alpha-fetoprotein. Predictively, miRNAs such as miR-21 and miR-486-3p correlate with sorafenib resistance, while tissue and exosomal miRNAs forecast recurrence and survival after curative therapy. Therapeutic manipulation, restoring tumor-suppressor miRNAs via mimics or AAV vectors and inhibiting oncomiRs with antagomirs or LNA oligonucleotides, yields potent anti-tumor effects in models, affecting cell cycle, apoptosis, angiogenesis, and immune activation. Despite technical and delivery challenges, early-phase trials validate target engagement and inform safety optimization. In this review, we highlight opportunities to integrate miRNA biomarkers into surveillance algorithms and combine miRNA therapeutics with existing modalities, charting a roadmap toward precision-guided management of HCC.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 9","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modalities Differentiation of Pain Perception Following Ischemic Stroke: Decreased Pressure Pain Perception.","authors":"Yongkang Zhi, Chen Zhao, Yu Zhang, Jianzhang Ni, Ming Zhang, Dongsheng Fan, Yazhuo Kong","doi":"10.3390/biomedicines13092241","DOIUrl":"10.3390/biomedicines13092241","url":null,"abstract":"<p><p><b>Background/Objectives</b>: Ischemic stroke frequently leads to somatosensory impairments and abnormal pain perception. Meanwhile, pain perception can be evoked through multiple somatosensory modalities, each mediated by distinct neural pathways. Despite this understanding, current research investigating stroke-induced alterations in pain perception across different modalities of noxious stimulation remains insufficient, particularly concerning responses to varying stimulus intensities (including both sub-threshold and supra-threshold levels). <b>Methods</b>: In this study (March 2023 to July 2024), we enrolled 30 ischemic stroke patients and 35 matched controls and employed two modalities of noxious stimuli (e.g., heat stimuli were delivered using the Medoc CHEPS and pressure stimuli were administered via an MRI-Compatible Foot-Sole Stimulator) to systematically evaluate post-stroke changes in pain perception through two experiments. We compared self-reported pain sensitivity, somatosensory thresholds (i.e., warmth and pressure), and pain thresholds (i.e., heat and pressure pain) between ischemic stroke patients and healthy controls in Experiment 1. We focused on pain perception when participants simultaneously experienced heat and pressure in Experiment 2. <b>Results</b>: Experiment 1 showed an absence of a significant correlation between heat and pressure pain thresholds in stroke patients, but this correlation could be observed in healthy controls. Notably, stroke patients had an impairment in pain perception of pressure stimulation at supra-threshold intensities. Experiment 2 observed a similar facilitative pain integration in patients as healthy controls when they perceived heat and pressure stimuli jointly and simultaneously. <b>Conclusions</b>: These findings provide valuable insights into pain perception following a stroke, highlighting the need for tailored evaluation strategies considering the differences in somatosensory modality damage.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 9","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12466989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sweet Relief? Short-Term Post-Traumatic High-Sucrose Intake Attenuates Acute but Not Long-Term Fear Responses in Mice.","authors":"Prabhat Kumar, Pedro Correia, Imola Plangár, Dóra Zelena","doi":"10.3390/biomedicines13092233","DOIUrl":"10.3390/biomedicines13092233","url":null,"abstract":"<p><p>People often turn to sweet foods for comfort during times of stress, as energy imbalance is implicated in several neuropsychiatric disorders including post-traumatic stress disorder (PTSD). Although acute sucrose consumption may improve cognitive capabilities, its long-term effectiveness has been debated. <b>Objectives</b>: In a widely used mouse model, we examined the effect of sucrose drinking on conditioned fear-induced freezing (as a model of PTSD), with emphasis on the concentrations and timing of the intervention as well as sex differences. We aimed to develop a low-cost, widely accessible therapeutic option. <b>Methods</b>: A short electric foot shock was used for trauma, and freezing was detected 24 h (mimicking acute stress disorder, ASD) or 14 days (PTSD-like symptoms) later in the trauma context and with trauma cues. <b>Results</b>: First, we confirmed that our trauma increased freezing, independent of previous habituation to sucrose drinking. Next, we confirmed that 16% and 32%, but not 2% sucrose drinking for 24 h (but not 3 h) immediately after trauma, diminished freezing behavior the next day. However, the same intervention did not influence behavior 14 days later. Moreover, we could not find any curative effect of 24 h of 16% sucrose consumption before testing remote fear memory 14 days after trauma. <b>Conclusions</b>: Consuming a high-calorie solution immediately following trauma for 24 h may influence ASD but does not necessarily alter the development of PTSD symptoms. Here, we offer a new perspective on energy regulation in neuropsychiatric disorders.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 9","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12467851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145173195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}