bioRxiv - Physiology最新文献

{"title":"Amputation Triggers Long-Range Epidermal Permeability Changes in Evolutionarily Distant Regenerative Organisms","authors":"Kelly E. Dooling, Ryan T. Kim, Elane M. Kim, Erica Chen, Adnan Abouelela, Benjamin J. Tajer, Noah J. Lopez, Julia C. Paoli, Connor J. Powell, Anna G. Luong, S.Y. Celeste Wu, Kara N. Thornton, Hani D. Singer, Aaron M. Savage, Joel Bateman, Tia DiTommaso, Duygu Payzin-Dogru, Jessica L. Whited","doi":"10.1101/2024.08.29.610385","DOIUrl":"https://doi.org/10.1101/2024.08.29.610385","url":null,"abstract":"Previous studies have reported that amputation invokes body-wide responses in regenerative organisms, but most have not examined the implications of these changes beyond the region of tissue regrowth. Specifically, long-range epidermal responses to amputation are largely uncharacterized, with research on amputation-induced epidermal responses in regenerative organisms traditionally being restricted to the wound site. Here, we investigate the effect of amputation on long-range epidermal permeability in two evolutionarily distant, regenerative organisms: axolotls and planarians. We find that amputation triggers a long-range increase in epidermal permeability in axolotls, accompanied by a long-range epidermal downregulation in MAPK signaling. Additionally, we provide functional evidence that pharmacologically inhibiting MAPK signaling in regenerating planarians increases long-range epidermal permeability. These findings advance our knowledge of body-wide changes due to amputation in regenerative organisms and warrant further study on whether epidermal permeability dysregulation in the context of amputation may lead to pathology in both regenerative and non-regenerative organisms.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197784","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":"Adipose tissue protein kinase D (PKD): regulation of signalling networks and its sex-dependent effects on metabolism","authors":"Mark C Renton, Sean J Humphrey, Tim Connor, Sheree D Martin, Krystal Kremerer, Hilary Fernando, Chistopher S Shaw, David E James, Kirsten F Howlett, Sean L McGee","doi":"10.1101/2024.08.29.610294","DOIUrl":"https://doi.org/10.1101/2024.08.29.610294","url":null,"abstract":"The protein kinase D (PKD) family of three highly homologous isoforms (PKD1, PKD2, and PKD3) are implicated as nutrient sensing signalling kinases that regulate the response of adipose and other tissues to the nutrient environment. However, the physiological role of adipose tissue PKD and its downstream cellular signalling targets are not well characterised. Phosphoproteomics was performed to elucidate signalling events downstream of PKD activation in differentiated 3T3L1 adipocytes using a triple isoform siRNA knockdown model. This revealed PKD-regulated pathways including insulin and cAMP signalling, which control metabolic responses in adipose tissue. An adipose tissue-specific and inducible dominant negative PKD (atDNPKD) mouse model that achieves functional inhibition of all three PKD isoforms was generated to assess the function of adipose PKD on whole-body metabolism in vivo in both male and female mice. Insulin-stimulated suppression of lipolysis was blunted in male, but not female, atDNPKD mice compared to control mice. Female, but not male, atDNPKD mice had higher fasting insulin but normal insulin action. Male atDNPKD mice showed greater sensitivity to the β-adrenergic receptor agonist CL316,243 on measures of lipolysis and energy expenditure, and displayed greater fat oxidation during fasting. During refeeding, male atDNPKD mice consumed less food and took longer to regain body weight lost during fasting. These effects were not observed in female mice. These findings indicate that PKD provides sex-dependent fine-tuning control of cAMP signalling in adipose tissue that is important for the coordination of energy balance during fasting and refeeding.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"207 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197788","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":"Impaired S-nitrosylation of Cx43 prevents arrhythmogenicity and myocardial injury upon cardiac stress in Duchenne Muscular Dystrophy","authors":"Manuel F Muñoz, Jonathan J Quan, Thao T Nguyen, Janet Nuno, Adrian Sheehy, Pia C Burboa, Pablo S. Gaete, Mauricio A Lillo, Jorge E Contreras","doi":"10.1101/2024.08.29.610357","DOIUrl":"https://doi.org/10.1101/2024.08.29.610357","url":null,"abstract":"Connexin-43 (Cx43) plays a critical role in the propagation of action potentials and cardiac contractility. In healthy cardiomyocytes, Cx43 is mainly located at the intercalated disk; however, Cx43 remodeling is observed in cardiac pathologies and is linked with arrhythmogenesis and sudden cardiac death. Using a mouse model of Duchenne muscular dystrophy (DMD), we previously demonstrated that Cx43 localizes to the lateral side of dystrophic cardiomyocytes, forming undocked hemichannels. β-adrenergic signaling-induced cardiac stress promotes S-nitrosylation and the opening of undocked Cx43 hemichannels leading to disrupted cardiac membrane excitability and deadly arrhythmogenic behaviors. To establish the direct role of S-nitrosylated Cx43 in DMD cardiomyopathy, we generated knockin DMD^mdx mice with reduced levels of S-nitrosylated Cx43, by replacing cysteine 271 with a serine in one Cx43 of the unique site for S-nitrosylation of Cx43 (DMD^mdx:C271S^+/-). Immunofluorescence analysis revealed that cardiac Cx43 lateralization in DMD^mdx:C271S^+/- mice was similar to DMD^mdx mice, indicating that the genetic modification did not prevent Cx43 remodeling. Upon isoproterenol treatment, DMD^mdx mice displayed a higher incidence of arrhythmogenic events when compared to DMD^mdx:C271S^+/- mice, which more closely resemble wild-type mice. Optical mapping imaging in isolated hearts showed that DMD^mdx mice displayed aberrant Ca²⁺ signaling and prolonged action potentials, which is restored in DMD^mdx:C271S^+/- mice. Isoproterenol treatment evoked severe myocardial injury in DMD^mdx mice, which was significantly attenuated in DMD^mdx:C271S^+/- mice. Notably, DMD^mdx mice treated with Gap19, a Cx43 hemichannel blocker, exhibited cardioprotection against myocardial injury. We concluded that S-nitrosylation of Cx43 proteins is a fundamental NO-mediated mechanism involved in arrhythmias and myocardial injury in DMD^mdx, occurring through the opening of hemichannels following β-adrenergic stress.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"128 11 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142225333","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":"An active model for the basilar membrane and the outer hair cells","authors":"Jorge Berger, Jacob Rubinstein","doi":"10.1101/2024.08.29.610286","DOIUrl":"https://doi.org/10.1101/2024.08.29.610286","url":null,"abstract":"A model for the joint motion of the basilar membrane (BM) and the outer hair cells (OHC) in the cochlea is presented. The model consists of two one-imensional mass distributions, one along the OHC and outer hair bundle (OHB) interface, and one along the BM. The motion of these masses is driven by the forces exerted on them by the elastic bodies connecting them and by the pressure difference in the fluids separated by the BM. The model includes a nonlinear motility of the OHC and its coupling with the vibrations of the BM. The model implies a Hopf bifurcation for the dynamical system governing the two coupled distributed oscillators. It is shown that when the system operates near the bifurcation point the BM motion is amplified up to a saturation level. The model provides very sharp frequency decomposition of the incident audio signal according to the place principle. It also acts as a powerful filter that distinguishes pure tones even in the presence of louder noisy background. In addition to simulations of the model, the unusual role played by the OHC friction is studied. Energy estimates are derived for the model functions.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197789","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":"Muscle Type-Specific Modulation of Autophagy Signaling in Obesity: Effects of Caloric Restriction and Exercise","authors":"Fujue Ji, Jong-Hee Kim","doi":"10.1101/2024.08.29.610325","DOIUrl":"https://doi.org/10.1101/2024.08.29.610325","url":null,"abstract":"Background: Obesity is a global health issue that contributes to the development of various diseases through metabolic dysregulation. Recent findings indicate that obesity leads to autophagy dysregulation, a cellular degradation process. Caloric restriction (CR) and CR combined with exercise (CR+Ex) are effective strategies for managing obesity and modulating autophagy. However, the regulation of autophagy and its signaling pathways in skeletal muscle under conditions of obesity, CR, and CR+Ex remains poorly understood.\u0000Method: Mice were divided into six groups: normal diet, normal diet CR, normal die CR+Ex, high-fat diet, high-fat diet CR, and high-fat diet CR+Ex. All mice were fed ad libitum with either a normal or high-fat diet for the first four months, followed by the respective interventions for the subsequent four months. We examined body composition, skeletal muscle functions, and expression of autophagy signaling pathway in these mice.\u0000Result: Obesity resulted in increased body weight, lean mass, fat mass, and fat mass in tissue; decreased grip strength and endurance (P < 0.05). CR+Ex decreased body weight, lean mass, and fat mass in obese mice (P < 0.05). In red muscle, P62, LC3B-I and LC3B-II levels were elevated (P < 0.05), regardless of dietary conditions. High-fat diet induced Cathepsin L was reduced in red muscle (P < 0.05).\u0000Conclusion: Obesity leads to altered body composition and impaired skeletal muscle function, which are partially improved by CR+Ex. The modulation of the autophagy pathway was more pronounced in red muscle compared to white muscle, irrespective of the intervention. Autophagic activity was higher in red muscle compared to white muscle.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"171 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197787","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 gut microbiota is a determinant of sexual dimorphism in ALS-linked TDP43 mice","authors":"Evandro J Beraldi, Sukyoung Lee, Yulan Jiang, Isabel M Rea, Rushda Phull, Catherine M Keenan, Matthew Stephens, Martin Bardhi, Oluwamolakun Bankole, Gerald Pfeffer, Jeff Biernaskie, Kathy D McCoy, Eran Elinav, Keith A Sharkey, Minh Dang Nguyen","doi":"10.1101/2024.08.29.610355","DOIUrl":"https://doi.org/10.1101/2024.08.29.610355","url":null,"abstract":"The mechanisms underlying the earlier onset and male predominance of amyotrophic lateral sclerosis (ALS), the most common form of human motoneuron disease, are poorly understood. Here we show that the gut microbiota protects against TDP43 toxicity and contributes to the sexual dimorphism in mice expressing a mutant form of TDP43 (A315T) linked to ALS. TDP43 mice raised under germ-free conditions, or treated with antibiotics to deplete the gut microbiota, develop motoneuron disease earlier and show no sex differences in onset and lifespan. Behavioral and histopathological analyses confirm the exacerbation in neurodegeneration caused by the absence of gut microbiota. Castration did not alter disease course of male TDP43 mice, suggesting that male sex hormones do not interact with the gut microbiota to confer disease phenotype. Future identification of gut bacteria species and their mechanisms of action offers a unique opportunity to understand sexual dimorphism in ALS, with the ultimate goal to develop non-invasive and sex-specific treatments for ALS.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197790","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":"Immune aging impairs muscle regeneration via macrophage-derived anti-oxidant selenoprotein P","authors":"Dieu-Huong Hoang, Jessica Bouvière, Johanna Galvis, Pauline Moullé, Eugenia Migliavacca, Gaetan Juban, Sophie Liot, Pascal Stuelsatz, Fabien Le Grand, Jerome N Feige, Rémi Mounier, Bénédicte Chazaud","doi":"10.1101/2024.08.28.610036","DOIUrl":"https://doi.org/10.1101/2024.08.28.610036","url":null,"abstract":"Muscle regeneration is impaired in the aged organism, due to both intrinsic defects of muscle stem cells (MuSCs) and alterations of their environmental niche. However, the latter has still been poorly explored. Here, we compared and analyzed the time course of the various cell types constituting the MuSC niche during muscle generation in young and old mice. Aging altered the amplification of all niche cells with particularly prominent phenotypes in macrophages that impaired the resolution of inflammation in the old regenerating muscle. RNAsequencing of FACs-isolated MuSCs and non-myogenic niche cells during regeneration uncovered specific profiles and kinetics of genes and molecular pathways differentially regulated in old versus young regenerating muscle, indicating that each cell type responded to aging in a specific manner. Through this, we discovered that macrophages have a strong signature of aging with altered the activation of Selenoprotein P (Sepp1) expression in macrophages during the resolution of inflammation in regenerating muscle. Macrophage-specific deletion of Sepp1 gene was sufficient to impair the acquisition of the repair inflammatory profile, perturbed the support of macrophages to MuSCs in vitro and in vivo, and to cause inefficient skeletal muscle regeneration. When transplanted in aged mice, bone marrow from young WT mice, but not Sepp1 KOs, restored muscle regeneration to youthful levels. Altogether this work provides a unique resource to study the aging of the MuSC niche, reveals that aging of niche cells is asynchronous and establishes impaired macrophage dynamics/polarization and the anti-oxidant Selenoprotein P expression as drivers of age-related decline of muscle regeneration.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"44 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197765","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":"Hawkmoth pheromone transduction involves G protein-dependent phospholipase Cβ signaling","authors":"Anna C Schneider, Katrin Schroeder, Yajun Chang, Andreas Nolte, Petra Gawalek, Monika Stengl","doi":"10.1101/2024.08.29.610295","DOIUrl":"https://doi.org/10.1101/2024.08.29.610295","url":null,"abstract":"Evolutionary pressures adapted insect chemosensation to the respective insect's physiological needs and tasks in their ecological niches. Solitary nocturnal moths rely on their acute olfactory sense to find mates at night. Pheromones are detected with maximized sensitivity and high temporal resolution through mechanisms that are mostly unknown. While the inverse topology of insect olfactory receptors and heteromerization with the coreceptor Orco suggest ionotropic transduction via odorant-gated receptor-ion channel complexes, contradictory data propose amplifying G protein-coupled transduction. Here, we used <em>in vivo</em> tip-recordings of pheromone-sensitive sensilla of male <em>Manduca sexta</em> hawkmoths at specific times of day (rest vs. activity). Since the olfactory receptor neurons distinguish signal parameters in three consecutive temporal windows of their pheromone response (phasic; tonic; late, long-lasting), respective response parameters were analyzed separately. Disruption of G protein-coupled transduction and block of phospholipase C decreased and slowed the phasic response component during the activity phase of hawkmoths without affecting any other component of the response during activity and rest. A more targeted disruption of Gα subunits by blocking G_αo or sustained activation of G_αs using bacterial toxins affected the phasic pheromone response, while toxins targeting G_αq and G_α12/13 were ineffective. Consistent with these data, the expression of phospholipase Cβ4 depended on zeitgeber time, which indicates circadian clock-modulated metabotropic pheromone transduction cascades that maximize sensitivity and temporal resolution of pheromone transduction during the hawkmoth's activity phase. Thus, discrepancies in the literature on insect olfaction may be resolved by considering circadian timing and the distinct odor response components.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"99 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197764","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":"Six months of physical inactivity is insufficient to cause chronic kidney disease in C57BL/6J mice","authors":"Precious C Opurum, Stephen T Decker, Deborah Stuart, Alek D Peterlin, Venisia L Paula, Piyarat Siripoksup, Micah J Drummond, Alejandro Sanchez, Nirupama Ramkumar, Katsuhiko Funai","doi":"10.1101/2024.08.29.610415","DOIUrl":"https://doi.org/10.1101/2024.08.29.610415","url":null,"abstract":"Chronic kidney disease (CKD) is a progressive disorder marked by a decline in kidney function. Obesity and sedentary behavior contribute to the development of CKD, though mechanisms by which this occurs are poorly understood. This knowledge gap is worsened by the lack of a reliable murine CKD model that does not rely on injury, toxin, or gene deletion to induce a reduction in kidney function. High-fat diet (HFD) feeding alone is insufficient to cause reduced kidney function until later in life. Here, we employed a small mouse cage (SMC), a recently developed mouse model of sedentariness, to study its effect on kidney function. Wildtype C57BL/6J male mice were housed in sham or SMC housing for six months with HFD in room (22 degrees C) or thermoneutral (30 degrees C) conditions. Despite hyperinsulinemia induced by the SMC+HFD intervention, kidneys from these mice displayed normal glomerular filtration rate (GFR). However, the kidneys showed early signs of kidney injury, including increases in Col1a1 and NGAL transcripts, as well as fibrosis by histology, primarily in the inner medullary/papilla region. High-resolution respirometry and fluorometry experiments showed no statistically significant changes in the capacities for respiration, ATP synthesis, or electron leak. These data confirm the technical challenge in modeling human CKD. They further support the notion that obesity and a sedentary lifestyle make the kidneys more vulnerable, but additional insults are likely required for the pathogenesis of CKD.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"399 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197785","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":"Role of AMPK in Atrial Metabolic Homeostasis and Substrate Preference","authors":"Zeren Toksoy, Yina Ma, Leigh Goedeke, Wenxue V Li, Xiaoyue Hu, Xiaohong Wu, Marine Cacheux, Yansheng Liu, Fadi G Akar, Gerald I Shulman, Lawrence H Young","doi":"10.1101/2024.08.29.608789","DOIUrl":"https://doi.org/10.1101/2024.08.29.608789","url":null,"abstract":"Atrial fibrillation is the most common clinical arrhythmia and may be due in part to metabolic stress. Atrial specific deletion of the master metabolic sensor, AMP-activated protein kinase (AMPK), induces atrial remodeling culminating in atrial fibrillation in mice, implicating AMPK signaling in the maintenance of atrial electrical and structural homeostasis. However, atrial substrate preference for mitochondrial oxidation and the role of AMPK in regulating atrial metabolism are unknown. Here, using LC-MS/MS methodology combined with infusions of [¹³C₆]glucose and [¹³C₄]β-hydroxybutyrate in conscious mice, we demonstrate that conditional deletion of atrial AMPK catalytic subunits shifts mitochondrial atrial metabolism away from fatty acid oxidation and towards pyruvate oxidation. LC-MS/MS-based quantification of acyl-CoAs demonstrated decreased atrial tissue content of long-chain fatty acyl-CoAs. Proteomic analysis revealed a broad downregulation of proteins responsible for fatty acid uptake (LPL, CD36, FABP3), acylation and oxidation. Atrial AMPK deletion reduced expression of atrial PGC1-α and downstream PGC1-α/PPARα/RXR regulated gene transcripts. In contrast, atrial [¹⁴C]2-deoxyglucose uptake and GLUT1 expression increased with fasting in mice with AMPK deletion, while the expression of glycolytic enzymes exhibited heterogenous changes. Thus, these results highlight the crucial homeostatic role of AMPK in the atrium, with loss of atrial AMPK leading to downregulation of the PGC1-α/PPARα pathway and broad metabolic reprogramming with a loss of fatty acid oxidation, which may contribute to atrial remodeling and arrhythmia.","PeriodicalId":501557,"journal":{"name":"bioRxiv - Physiology","volume":"27 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142197791","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}