Frontiers in bioscience (Landmark edition)最新文献

{"title":"Brain-targeting Nanoparticle Drug Delivery Systems for Brain Tumors.","authors":"Yi Zhao, Yamin Cui, Yuanyuan Sun","doi":"10.31083/FBL27934","DOIUrl":"https://doi.org/10.31083/FBL27934","url":null,"abstract":"","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 1","pages":"27934"},"PeriodicalIF":3.3,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: Ke <i>et al.</i> Resveratrol enhances chemosensitivity of renal cell carcinoma to paclitaxel. Frontiers in Bioscience (Landmark Edition). 2019; 24: 1452-1461.","authors":"","doi":"10.31083/FBL37283","DOIUrl":"10.31083/FBL37283","url":null,"abstract":"","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 1","pages":"37283"},"PeriodicalIF":3.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of NF-κB/MIR155HG in Regulating the Stemness and Radioresistance in Breast Cancer Stem Cells.","authors":"Yunbao Xu, Lu Yang, Guangming Li, Chuangzhou Rao","doi":"10.31083/FBL25810","DOIUrl":"https://doi.org/10.31083/FBL25810","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer stem cells (BCSCs) are instrumental in treatment resistance, recurrence, and metastasis. The development of breast cancer and radiation sensitivity is intimately pertinent to long non-coding RNA (lncRNA). This work is formulated to investigate how the lncRNA <i>MIR155HG</i> affects the stemness and radioresistance of BCSCs.</p><p><strong>Methods: </strong>Effects of <i>MIR155HG</i> knockdown on BCSCs were gauged in MCF-7 and MDA-MB-231 cell lines. <i>MIR155HG</i> expression was manipulated in cells, followed by an assessment of stemness, DNA damage repair, apoptosis, cell cycle, and the Wnt signaling pathway under radiation conditions. The interaction between nuclear factor kappa B (NF-κB) subunit RelA and <i>MIR155HG</i> was examined using a dual-luciferase reporter assay. To examine the binding interaction between RelA and <i>MIR155HG</i> promoter, chromatin immunoprecipitation was performed.</p><p><strong>Results: </strong>Breast cancer-derived stem cells exhibited a high level of <i>MIR155HG</i>. Knockdown of <i>MIR155HG</i> reduced stemness, enhanced radiosensitivity, induced apoptosis, and arrested cells in the G1 phase. Mechanistically, <i>MIR155HG</i> knockdown repressed Wnt/β-catenin signaling and mediated apoptosis-related protein expressions. NF-κB subunit RelA transcriptionally activated <i>MIR155HG</i>, thereby contributing to radioresistance in BCSCs.</p><p><strong>Conclusion: </strong>NF-κB regulates <i>MIR155HG</i> transcriptionally to activate the Wnt pathway, thus enhancing stemness and radioresistance in BCSCs. Targeting <i>MIR155HG</i> may enhance the susceptibility of cancer stem cells to radiation-induced cell death, potentially improving therapeutic outcomes. These findings underscore <i>MIR155HG</i> as a promising therapeutic target for breast cancer.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 1","pages":"25810"},"PeriodicalIF":3.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydroxyapatite Chitosan Gradient Pore Scaffold Activates Oxidative Phosphorylation Pathway to Induce Bone Formation.","authors":"Zeliang Zhang, Wei Shang, Lisong Lin","doi":"10.31083/FBL26299","DOIUrl":"https://doi.org/10.31083/FBL26299","url":null,"abstract":"<p><strong>Background: </strong>In this study, we prepared a porous gradient scaffold with hydroxyapatite microtubules (HAMT) and chitosan (CHS) and investigated osteogenesis induced by these scaffolds.</p><p><strong>Methods: </strong>The arrangement of wax balls in the mold can control the size and distribution of the pores of the scaffold, and form an interconnected gradient pore structure. The scaffolds were systematically evaluated <i>in vitro</i> and <i>in vivo</i> for biocompatibility, biological activity, and regulatory mechanisms.</p><p><strong>Results: </strong>The porosity of the four scaffolds was more than 80%. The 50% and 70% HAMT-CHS scaffolds formed an excellent gradient pore structure, with interconnected pores. Furthermore, the 70% HAMT-CHS scaffold showed better anti-compressive deformation ability. <i>In vitro</i> experiments indicated that the scaffolds had good biocompatibility, promoted the expression of osteogenesis-related genes and proteins, and activated the oxidative phosphorylation pathway to promote bone regeneration. Eight weeks after implanting the HAMT-CHS scaffold in rat skull defects, new bone formation was observed <i>in vivo</i> by micro-computed tomographic (CT) staining. The obtained data were statistically analyzed, and the <i>p-</i>value < 0.05 was statistically significant.</p><p><strong>Conclusion: </strong>HAMT-CHS scaffolds can accelerate osteogenesis in bone defects, potentially through the activation of the oxidative phosphorylation pathway. These results highlight the potential therapeutic application of HAMT-CHS scaffolds.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 1","pages":"26299"},"PeriodicalIF":3.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Vitamin D on Skin Aging, and Age-Related Dermatological Conditions.","authors":"Sankalya S Ambagaspitiya, Gayan A Appuhamillage, Sunil J Wimalawansa","doi":"10.31083/FBL25463","DOIUrl":"https://doi.org/10.31083/FBL25463","url":null,"abstract":"<p><p>Human skin is a physical and biochemical barrier that protects the internal body from the external environment. Throughout a person's life, the skin undergoes both intrinsic and extrinsic aging, leading to microscopic and macroscopic changes in its morphology. In addition, the repair processes slow with aging, making the older population more susceptible to skin diseases. Intrinsic factors associated with advanced age gradually degrade the dermal collagen matrix, resulting in fine wrinkles and reduced elasticity; this is accelerated in post-menopausal women due to estrogen deficiency. In contrast, extrinsic factors associated with advanced age, primarily caused by exposure to ultraviolet (UV) radiation, lead to coarse wrinkles, solar elastosis, hyperkeratosis, irregular pigmentation, and skin cancers. UVB radiation, while contributing to skin photo-aging, also induces the cutaneous synthesis of vitamin D. Vitamin D, in turn, protects the skin from oxidative stress, inflammation, and DNA damage, thereby delaying both chronological and photo-aging. Moreover, research has demonstrated an association between lower vitamin D levels and a higher prevalence of certain cutaneous diseases. This review explores and summarizes the critical role of vitamin D in skin aging and age-related skin diseases. The data presented highlight the importance of maintaining vitamin D adequacy throughout life.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 1","pages":"25463"},"PeriodicalIF":3.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thyroid Hormone Activation Regulates the Crosstalk between Breast Cancer and Mesenchymal Stem Cells.","authors":"Annarita Nappi, Vittoria D'Esposito, Caterina Miro, Alessia Parascandolo, Annunziata Gaetana Cicatiello, Serena Sagliocchi, Lucia Acampora, Sepehr Torabinejad, Federica Restolfer, Maddalena Raia, Melania Murolo, Emery Di Cicco, Pietro Formisano, Monica Dentice","doi":"10.31083/FBL26113","DOIUrl":"https://doi.org/10.31083/FBL26113","url":null,"abstract":"<p><strong>Background: </strong>Thyroid Hormones (THs) critically impact human cancer. Although endowed with both tumor-promoting and inhibiting effects in different cancer types, excess of THs has been linked to enhanced tumor growth and progression. Breast cancer depends on the interaction between bulk tumor cells and the surrounding microenvironment in which mesenchymal stem cells (MSCs) exert powerful pro-tumorigenic activities.</p><p><strong>Methods: </strong>Primary human MSCs from healthy female donors were co-cultured with DIO2 knock out (D2KO) and wild type (WT) MCF7 breast cancer cells to assess cell growth, migration, invasion and the expression of known epithelial-mesenchymal transition (EMT)- and inflammation-related markers. Furthermore, a surgery-free intraductal delivery model, i.e., the Mouse-INtraDuctal (MIND) injection method, was used as a tool for <i>in vivo</i> characterization of breast tumor formation and progression.</p><p><strong>Results: </strong>In this study, we uncovered a novel role of THs in regulating the tumor-stroma crosstalk. MCF7 cells enhanced the intracellular activation of THs through the TH-activating enzyme, D2, fostering their EMT properties and the dialogue with MSCs. D2 inactivation reduced the invasiveness of MCF7 cells and their responsiveness to the pro-tumorigenic induction via MSCs, both <i>in vivo</i> and <i>in vitro</i>.</p><p><strong>Conclusions: </strong>Thus, we argue that intracellular activation of THs via D2 is a critical requirement for invasive and metastatic conversion of breast cancer cells, advising the blocking of D2 as a potential therapeutic tool for cancer therapy.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 1","pages":"26113"},"PeriodicalIF":3.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative and Excitatory Neurotoxic Stresses in CRISPR/Cas9-Induced Kynurenine Aminotransferase Knockout Mice: A Novel Model for Despair-Based Depression and Post-Traumatic Stress Disorder.","authors":"Ágnes Szabó, Zsolt Galla, Eleonóra Spekker, Mónika Szűcs, Diána Martos, Keiko Takeda, Kinuyo Ozaki, Hiromi Inoue, Sayo Yamamoto, József Toldi, Etsuro Ono, László Vécsei, Masaru Tanaka","doi":"10.31083/FBL25706","DOIUrl":"https://doi.org/10.31083/FBL25706","url":null,"abstract":"<p><strong>Backgrounds: </strong>Memory and emotion are especially vulnerable to psychiatric disorders such as post-traumatic stress disorder (PTSD), which is linked to disruptions in serotonin (5-HT) metabolism. Over 90% of the 5-HT precursor tryptophan (Trp) is metabolized via the Trp-kynurenine (KYN) metabolic pathway, which generates a variety of bioactive molecules. Dysregulation of KYN metabolism, particularly low levels of kynurenic acid (KYNA), appears to be linked to neuropsychiatric disorders. The majority of KYNA is produced by the <i>aadat</i> (kat2) gene-encoded mitochondrial kynurenine aminotransferase (KAT) isotype 2. Little is known about the consequences of deleting the KYN enzyme gene.</p><p><strong>Methods: </strong>In CRISPR/Cas9-induced <i>aadat</i> knockout (<i>kat2</i>^-/-) mice, we examined the effects on emotion, memory, motor function, Trp and its metabolite levels, enzyme activities in the plasma and urine of 8-week-old males compared to wild-type mice.</p><p><strong>Results: </strong>Transgenic mice showed more depressive-like behaviors in the forced swim test, but not in the tail suspension, anxiety, or memory tests. They also had fewer center field and corner entries, shorter walking distances, and fewer jumping counts in the open field test. Plasma metabolite levels are generally consistent with those of urine: antioxidant KYNs, 5-hydroxyindoleacetic acid, and indole-3-acetic acid levels were lower; enzyme activities in KATs, kynureninase, and monoamine oxidase/aldehyde dehydrogenase were lower, but kynurenine 3-monooxygenase was higher; and oxidative stress and excitotoxicity indices were higher. Transgenic mice displayed depression-like behavior in a learned helplessness model, emotional indifference, and motor deficits, coupled with a decrease in KYNA, a shift of Trp metabolism toward the KYN-3-hydroxykynurenine pathway, and a partial decrease in the gut microbial Trp-indole pathway metabolite.</p><p><strong>Conclusions: </strong>This is the first evidence that deleting the <i>aadat</i> gene induces depression-like behaviors uniquely linked to experiences of despair, which appear to be associated with excitatory neurotoxic and oxidative stresses. This may lead to the development of a double-hit preclinical model in despair-based depression, a better understanding of these complex conditions, and more effective therapeutic strategies by elucidating the relationship between Trp metabolism and PTSD pathogenesis.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 1","pages":"25706"},"PeriodicalIF":3.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Primer on the Role of TP53 Mutation and Targeted Therapy in Endometrial Cancer.","authors":"Bohao Zhang, Haozhe Zhang, Yanru Qin","doi":"10.31083/FBL25447","DOIUrl":"https://doi.org/10.31083/FBL25447","url":null,"abstract":"<p><p>Endometrial Cancer (EC) is one of the most common gynecological malignancies, ranking first in developed countries and regions. The occurrence and development of EC is closely associated with genetic mutations. <i>TP53</i> mutation, in particular, can lead to the dysfunction of numerous regulatory factors and alteration of the tumor microenvironment (TME). The changes in the TME subsequently promote the development of tumors and assist in immune escape by tumor cells, making it more challenging to treat EC and resulting in a poor prognosis. Therefore, it is important to understand the effects of <i>TP53</i> mutation in EC and to conduct further research in relation to the targeting of <i>TP53</i> mutations. This article reviews current research progress on the role of <i>TP53</i> mutations in regulating the TME and in the mechanism of EC tumorigenesis, as well as progress on drugs that target <i>TP53</i> mutations.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 1","pages":"25447"},"PeriodicalIF":3.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trimetazidine: Activating AMPK Signal to Ameliorate Coronary Microcirculation Dysfunction after Myocardial Infarction.","authors":"Xiaolong Qu, Pan Yang, Li Jiao, Yuehui Yin","doi":"10.31083/FBL25565","DOIUrl":"https://doi.org/10.31083/FBL25565","url":null,"abstract":"<p><strong>Background: </strong>Myocardial ischemia-reperfusion (I/R) injury and coronary microcirculation dysfunction (CMD) are observed in patients with myocardial infarction after vascular recanalization. The antianginal drug trimetazidine has been demonstrated to exert a protective effect in myocardial ischemia-reperfusion injury.</p><p><strong>Objectives: </strong>This study aimed to investigate the role of trimetazidine in endothelial cell dysfunction caused by myocardial I/R injury and thus improve coronary microcirculation.</p><p><strong>Methods: </strong>The myocardial I/R mouse model was established, and trimetazidine was administered for 7 days before myocardial I/R model establishment. Echocardiography, 2,3,5-triphenyltetrazolium chloride (TTC) staining, hematoxylin-eosin (H&E) staining, and thioflavin S staining were applied to assess myocardial injury and microvascular function. Additionally, the oxygen-glucose deprivation/reperfusion (OGD/R) model was developed in endothelial cells to simulate myocardial I/R injury <i>in vitro</i>. Griess reaction method, immunofluorescence, and western blotting (WB) were employed to detect the expressions of nitric oxide (NO), platelet endothelial cell adhesion molecule-1 (CD31) and vascular endothelial (VE)-cadherin, zonula occludens protein 1 (ZO-1), occludin, vascular endothelial growth factor (VEGF) and adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling-related proteins in endothelial cells and mouse cardiomyocytes. AMPK pathway inhibitor compound C was used for further mechanism validation.</p><p><strong>Results: </strong>Our research demonstrated that trimetazidine can alleviate myocardial pathological injury and cardiac function injury during myocardial I/R. Trimetazidine was observed to improve microvascular reflux phenomenon and microvascular function and barrier injury in myocardial I/R and OGD/R models. Additionally, the expressions of AMPK signal-related proteins were found to be inhibited in myocardial I/R and OGD/R models, which were then activated in mice administered trimetazidine. However, the effects of trimetazidine on endothelial cell function and barrier damage were attenuated after co-treatment with compound C and trimetazidine.</p><p><strong>Conclusion: </strong>Trimetazidine ameliorated myocardial I/R-induced CMD by activating AMPK signaling.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 1","pages":"25565"},"PeriodicalIF":3.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular Cholesterol Loss Impairs Synaptic Vesicle Mobility via the CAMK2/Synapsin-1 Signaling Pathway.","authors":"Atikam Qurban, Mengqi Zhang, Hengbing Zu, Kai Yao","doi":"10.31083/FBL27111","DOIUrl":"https://doi.org/10.31083/FBL27111","url":null,"abstract":"<p><strong>Background: </strong>Neuronal cholesterol deficiency may contribute to the synaptopathy observed in Alzheimer's disease (AD). However, the underlying mechanisms remain poorly understood. Intact synaptic vesicle (SV) mobility is crucial for normal synaptic function, whereas disrupted SV mobility can trigger the synaptopathy associated with AD. In this study, we investigated whether cellular cholesterol deficiency affects SV mobility, with the aim of identifying the mechanism that links cellular cholesterol loss to synaptopathy in AD.</p><p><strong>Methods: </strong>Lentiviruses carrying 3β-hydroxysteroid-Δ24 reductase-complementary DNA (<i>DHCR24-cDNA</i>), <i>DHCR24</i>-short hairpin RNA (<i>DHCR24- shRNA</i>) or empty lentiviral vectors were transfected into SHSY-5Y cells in order to construct DHCR24 knock-down and knock-in models, along with corresponding controls. Filipin III cholesterol staining was employed to visualize membrane and intracellular cholesterol in the different cell models, and fluorescence intensity was assessed using confocal microscopy. Additionally, we performed immunoblotting to quantify the expression of DHCR24, total calmodulin-dependent protein kinase 2 (CAMK-2), p-CAMK2 (T286), caveolin-1, total synapsin-1, phosphorylated synapsin-1 (p-synapsin-1; S605), and synaptophysin in each experimental group.</p><p><strong>Results: </strong>In DHCR24-silenced cells, the loss of cellular cholesterol caused by knock-down of DCHR24 resulted in a significant decrease in the levels of phosphorylated CAMK2 (p-CAMK2) and phosphorylated synapsin-1 (p-synapsin-1) compared to control cells. The reduction in p-CAMK2 and p-synapsin-1 could disrupt SV mobility, thereby reducing replenishment of the readily releasable pool (RRP) from the reserve pool (RP). Furthermore, cells with DHCR24 knock-down showed downregulation of caveolin-1, a crucial lipid raft marker, compared to control cells. Conversely, elevated cellular cholesterol levels caused by knock-in of DHCR24 reversed the effects of cholesterol deficiency, suggesting that CAMK2-mediated synapsin-1 phosphorylation may be regulated in a lipid raft-associated manner. Additionally, we found that cellular cholesterol loss could significantly downregulate the expression of synaptophysin protein, which is vital for SV biogenesis and synaptic plasticity.</p><p><strong>Conclusion: </strong>These results suggest that depletion of cellular cholesterol following knock-down of DHCR24 can decrease synaptophysin protein expression and impair SV mobility by regulating the CAMK2-meditated synapsin-1 phosphorylation pathway, potentially via a lipid raft-associated mechanism. Our study indicates a critical role for cellular cholesterol deficiency in AD-related synaptopathy, thus highlighting the potential for targeting cellular cholesterol metabolism in therapeutic strategies.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 1","pages":"27111"},"PeriodicalIF":3.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143061083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}