Function最新文献

{"title":"Physiological Adaptations to Progressive Endurance Exercise Training in Adult And Aged Rats: Insights from The Molecular Transducers of Physical Activity Consortium (MoTrPAC)","authors":"Simon Schenk, Tyler J. Sagendorf, Gina Many, Ana K Lira, Gustavo DeSousa, Dam Bae, Michael Cicha, Kyle S Kramer, Michael Muehlbauer, Andrea L Hevener, R. Rector, John P Thyfault, John P Williams, Laurie J. Goodyear, Karyn A. Esser, Christopher B. Newgard, Sue C. Bodine, Joshua N Adkins, Brent G. Albertson, David Amar, M. A. Amper, Euan Ashley, Dam Bae, M. Bamman, Jerry Barnes, Bryan C Bergman, Daniel H. Bessesen, Sue C. Bodine, T. Buford, Charles F. Burant, Michael Cicha, G. Cutter, Luis Oliveria De Sousa, Karyn A. Esser, Facundo M. Fernández, David A. Gaul, Y. Ge, Bret H. Goodpaster, Laurie J. Goodyear, Kristen Guevara, Andrea L Hevener, M. Hirshman, Kim M. Huffman, Bailey E. Jackson, Catherine M. Jankowski, D. Jimenez-Morales, W. Kohrt, Kyle S Kramer, William E. Kraus, S. Lessard, Bridget Lester, Maléne E. Lindholm, Ana K Lira, Gina Many, Nada Marjanović, A. Marshall, Edward L. Melanson, Michael E Miller, K. Moreau, V. Nair, Christopher B. Newgard, E. Ortlund, Wei-Jun Qian, Blake B Rasmussen, R. Rector,","doi":"10.1093/function/zqae014","DOIUrl":"https://doi.org/10.1093/function/zqae014","url":null,"abstract":"\u0000 While regular physical activity is a cornerstone of health, wellness, and vitality, the impact of endurance exercise training on molecular signaling within and across tissues remains to be delineated. The Molecular Transducers of Physical Activity Consortium (MoTrPAC) was established to characterize molecular networks underlying the adaptive response to exercise. Here, we describe the endurance exercise training studies undertaken by the Preclinical Animal Sites Studies component of MoTrPAC, in which we sought to develop and implement a standardized endurance exercise protocol in a large cohort of rats. To this end, Adult (6-month) and Aged (18-month) female (n = 151) and male (n = 143) Fischer 344 rats were subjected to progressive treadmill training (5 days/week, ∼70–75% VO2max) for 1, 2, 4, or 8 weeks; sedentary rats were studied as the control group. Eighteen solid tissues, as well as blood, plasma, and feces, were collected to establish a publicly accessible biorepository and for extensive omics-based analyses by MoTrPAC. Treadmill training was highly effective, with robust improvements in skeletal muscle citrate synthase activity in as little as 1–2 weeks and improvements in maximum run speed and maximal oxygen uptake by 4–8 weeks. For body mass and composition, notable age- and sex-dependent responses were observed. This work in mature, treadmill-trained rats represents the most comprehensive and publicly accessible tissue biorepository, to date, and provides an unprecedented resource for studying temporal-, sex-, and age-specific responses to endurance exercise training in a pre-clinical rat model.","PeriodicalId":503843,"journal":{"name":"Function","volume":"119 12","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140380081","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 left-right side-specific neuroendocrine signaling from injured brain: an organizational principle","authors":"H. Watanabe, Yaromir Kobikov, O. Nosova, D. Sarkisyan, Vladimir Galatenko, Liliana Carvalho, Gisela H Maia, Nikolay Lukoyanov, Igor Lavrov, Michael H Ossipov, Mathias Hallberg, Jens Schouenborg, Mengliang Zhang, Georgy Bakalkin","doi":"10.1093/function/zqae013","DOIUrl":"https://doi.org/10.1093/function/zqae013","url":null,"abstract":"\u0000 A neurological dogma is that the contralateral effects of brain injury are set through crossed descending neural tracts. We have recently identified a novel topographic neuroendocrine system (T-NES) that operates via a humoral pathway and mediates the left-right side-specific effects of unilateral brain lesions. In rats with completely transected thoracic spinal cords, unilateral injury to the hindlimb sensorimotor cortex produced hindlimb postural asymmetry with contralateral hindlimb flexion, a proxy for neurological deficit. Here, we investigated in acute experiments whether T-NES consists of left and right counterparts and whether they differ in neural and molecular mechanisms and their operating patterns, which may be ipsi- or contra-lateral relative to the side of brain injury. We demonstrated that left and right-sided hormonal signaling is differentially blocked by the selective opioid antagonists. The effects of the left-brain lesion were inhibited by antagonists of the δ- and κ-opioid receptors, whereas those of the right brain lesion were inhibited by a µ-opioid antagonist. Left and right neurohormonal signaling differed in targeting the afferent spinal mechanisms. Bilateral deafferentation of the lumbar spinal cord abolished the hormone-mediated effects of the left-brain injury but not the right-sided lesion. The sympathetic nervous system was ruled out as a brain-to-spinal cord signaling pathway since the hindlimb responses were induced in rats with cervical spinal cord transections that were rostral to the preganglionic sympathetic neurons. Analysis of gene-gene co-expression patterns identified the left- and right-side-specific gene regulatory networks that were coordinated via the humoral pathway across the hypothalamus and lumbar spinal cord. The coordination was ipsilateral and disrupted by brain injury. These findings suggest that T-NES is bipartite, and that its left and right counterparts contribute to contralateral neurological deficits through distinct neural mechanisms, and may enable ipsilateral regulation of molecular and neural processes across distant neural areas along the neuraxis.","PeriodicalId":503843,"journal":{"name":"Function","volume":"11 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140243588","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":"Long-term musculoskeletal consequences of chemotherapy in pediatric mice","authors":"J. Huot, Patrick D Livingston, Fabrizio Pin, Connor R Thomas, Nicholas A Jamnick, Chandler S Callaway, A. Bonetto","doi":"10.1093/function/zqae011","DOIUrl":"https://doi.org/10.1093/function/zqae011","url":null,"abstract":"\u0000 Thanks to recent progress in cancer research, most children treated for cancer survive into adulthood. Nevertheless, the long-term consequences of anticancer agents are understudied, especially in the pediatric population. We and others have shown that routinely administered chemotherapeutics drive musculoskeletal alterations, which contribute to increased treatment-related toxicity and long-term morbidity. Yet, the nature and scope of these enduring musculoskeletal defects following anticancer treatments and whether they can potentially impact growth and quality of life in young individuals remain to be elucidated. Here, we aimed at investigating the persistent musculoskeletal consequences of chemotherapy in young (pediatric) mice. Four-week-old male mice were administered a combination of 5-FU, leucovorin, irinotecan (a.k.a., Folfiri) or the vehicle for up to 5 weeks. At time of sacrifice, skeletal muscle, bones, and other tissues were collected, processed, and stored for further analyses. In another set of experiments, chemotherapy-treated mice were monitored for up to 4 weeks after cessation of treatment. Overall, the growth rate was significantly slower in the chemotherapy-treated animals, resulting in diminished lean and fat mass, as well as significantly smaller skeletal muscles. Interestingly, 4 weeks after cessation of the treatment, the animals exposed to chemotherapy showed persistent musculoskeletal defects, including muscle innervation deficits and abnormal mitochondrial homeostasis. Altogether, our data supports that anticancer treatments may lead to long-lasting musculoskeletal complications in actively growing pediatric mice and support the need for further studies to determine the mechanisms responsible for these complications, so that new therapies to prevent or diminish chemotherapy-related toxicities can be identified.","PeriodicalId":503843,"journal":{"name":"Function","volume":"48 18","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140259210","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":"Hypertension Increases Susceptibility to Experimental Malaria in Mice","authors":"Mrunmayee R Kandalgaonkar, B. Yeoh, B. Joe, Nathan W. Schmidt, M. Vijay-Kumar, P. Saha","doi":"10.1093/function/zqae009","DOIUrl":"https://doi.org/10.1093/function/zqae009","url":null,"abstract":"\u0000 Global prevalence of hypertension is on the rise, burdening healthcare, especially in developing countries where infectious diseases, such as malaria, are also rampant. Whether hypertension could predispose or increase susceptibility to malaria, however, has not been extensively explored. Previously, we reported that hypertension is associated with abnormal red blood cell (RBC) physiology and anemia. Since RBC are target host cells for malarial parasite, Plasmodium, we hypothesized that hypertensive patients with abnormal RBC physiology are at greater risk or susceptibility to Plasmodium infection. To test this hypothesis, normotensive (BPN/3 J) and hypertensive (BPH/2 J) mice were characterized for their RBC physiology and subsequently infected with Plasmodium yoelii (P. yoelii), a murine-specific non-lethal strain. When compared to BPN mice, BPH mice displayed microcytic anemia and their RBC were highly resistant to osmotic hemolysis. Further, BPH RBC exhibited an increase in membrane rigidity and an altered lipid composition, as evidenced by higher levels of phospholipids and saturated fatty acid, such as stearate (C18:0), along with lower levels of polyunsaturated fatty acid like arachidonate (C20:4). Moreover, BPH mice had significantly greater circulating Ter119+ CD71+ reticulocytes, or immature RBC, prone to P. yoelii infection. Upon infection with P. yoelii, BPH mice experienced significant body weight loss accompanied by sustained parasitemia, indices of anemia, and substantial increase in systemic pro-inflammatory mediators, compared to BPN mice, indicating that BPH mice were incompetent to clear P. yoelii infection. Collectively, these data demonstrate that aberrant RBC physiology observed in hypertensive BPH mice contributes to an increased susceptibility to P. yoelii infection and malaria-associated pathology.","PeriodicalId":503843,"journal":{"name":"Function","volume":"278 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140420940","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":"Carotid Body Function in Tyrosine Hydroxylase Conditional Olfr78 Knockout Mice","authors":"Olalla Colinas, Peter Mombaerts, J. López-Barneo, Patricia Ortega-Sáenz","doi":"10.1093/function/zqae010","DOIUrl":"https://doi.org/10.1093/function/zqae010","url":null,"abstract":"\u0000 The Olfr78 gene encodes a G-protein coupled receptor that is expressed in olfactory sensory neurons, where it functions as a conventional odorant receptor, and also in several ectopic sites, where its function is not well understood. Olfr78 is one of the most highly expressed mRNA species in glomus cells of the carotid body (CB). These cells are the prototypical oxygen (O2) sensitive arterial chemoreceptors, which, in response to lowered O2 tension (hypoxia), activate the respiratory centers to induce hyperventilation. It has been proposed that Olfr78 is a lactate receptor and that glomus cell activation by the increase in blood lactate mediates the hypoxic ventilatory response (HVR). However, this proposal has been challenged by several groups showing that Olfr78 is not a physiologically relevant lactate receptor and that the O2-based regulation of breathing is not affected in Olfr78 knockout mice. In another study, Olfr78 knockout mice were reported to have altered systemic and CB responses to mild hypoxia. These organismal phenotypes could result from pleiotropic effects of the constitutive Olfr78 knockout mutations in the various CB cell types and/or various organs where this gene is expressed. Therefore, to further characterize the functional role of Olfr78 in CB glomus cells, we here generated a conditional Olfr78 knockout mouse strain and then restricted the knockout to glomus cells and other catecholaminergic cells by crossing with a tyrosine hydroxylase-specific Cre driver strain (TH-Olfr78 KO mice). We find that TH-Olfr78 KO mice have a normal HVR. Interestingly, glomus cells of TH-Olfr78 KO mice exhibit molecular and electrophysiological alterations as well as a reduced dopamine content in secretory vesicles and neurosecretory activity. These functional characteristics resemble those of CB neuroblasts in wild-type mice. We suggest that, although Olfr78 is not essential for CB O2 sensing, activation of Olfr78-dependent pathways is required for the phenotypic specification of mature glomus cells.","PeriodicalId":503843,"journal":{"name":"Function","volume":"60 5","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140439590","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 Warburg Effect Reinterpreted, 100 Years on: A First-principles Stoichiometric Analysis, and Interpretation from the Perspective of ATP Metabolism in Cancer Cells","authors":"Sunil Nath, Rudi Balling","doi":"10.1093/function/zqae008","DOIUrl":"https://doi.org/10.1093/function/zqae008","url":null,"abstract":"\u0000 The Warburg Effect is a longstanding enigma in cancer biology. Despite the passage of 100 years since its discovery, and the accumulation of a vast body of research on the subject, no convincing biochemical explanation has been given for the original observations of aerobic glycolysis in cancer cell metabolism. Here we have worked out a first-principles quantitative analysis of the problem from the principles of stoichiometry and available electron balance. The results have been interpreted using Nath's unified theory of energy coupling and ATP synthesis, and the original data of Warburg and colleagues have been analyzed from this new perspective. Use of the biomass yield based on ATP consumed, ${Y}_{X/S} ATP$ has been shown to excellently model the original data on the Warburg Effect with very small standard deviation values, and without employing additional fitted or adjustable parameters. Based on the results of the quantitative analysis, a novel conservative mechanism of synthesis, utilization, and recycling of ATP and other key metabolites (for example, lactate) is proposed. The mechanism offers fresh insights into metabolic symbiosis and coupling within and/or among proliferating cells. The fundamental understanding gained using our approach should help in catalyzing the development of more efficient metabolism-targeting anticancer drugs.","PeriodicalId":503843,"journal":{"name":"Function","volume":"3 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140443139","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 Reappraisal of The Reappraisal - CRAC Channels Are Activated by L-Type Ca2+ Channel Blockers, Reply to Bird et al.","authors":"Mohamed Trebak, Khaled Machaca, Patrick G Hogan","doi":"10.1093/function/zqae007","DOIUrl":"https://doi.org/10.1093/function/zqae007","url":null,"abstract":"","PeriodicalId":503843,"journal":{"name":"Function","volume":"16 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139870263","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 Reappraisal of The Reappraisal - CRAC Channels Are Activated by L-Type Ca2+ Channel Blockers, Reply to Bird et al.","authors":"Mohamed Trebak, Khaled Machaca, Patrick G Hogan","doi":"10.1093/function/zqae007","DOIUrl":"https://doi.org/10.1093/function/zqae007","url":null,"abstract":"","PeriodicalId":503843,"journal":{"name":"Function","volume":"50 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139810377","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":"Pro-BDNF, but Not Mature BDNF, Is Expressed in Human Skeletal Muscle: Implications for Exercise-Induced Neuroplasticity","authors":"Sebastian Edman, Oscar Horwath, Thibaux Van der Stede, Sarah Joan Blackwood, Isabel Moberg, Henrik Strömlind, Fabian Nordström, M. Ekblom, A. Katz, W. Apró, Marcus Moberg","doi":"10.1093/function/zqae005","DOIUrl":"https://doi.org/10.1093/function/zqae005","url":null,"abstract":"\u0000 Exercise promotes brain plasticity partly by stimulating increases in mature brain-derived neurotrophic factor (mBDNF), but the role of the pro-BDNF isoform in the regulation of BDNF metabolism in humans is unknown. We quantified the expression of pro-BDNF and mBDNF in human skeletal muscle and plasma at rest, after acute exercise (+/- lactate infusion), and after fasting. Pro-BDNF and mBDNF were analyzed with immunoblotting, ELISA, immunohistochemistry, and qPCR.\u0000 Pro-BDNF was consistently and clearly detected in skeletal muscle (40-250 pg × mg−1 dry muscle), whereas mBDNF was not. All methods showed a 4-fold greater pro-BDNF expression in type I muscle fibers compared to type II fibers. Exercise resulted in elevated plasma levels of mBDNF (55%) and pro-BDNF (20%), as well as muscle levels of pro-BDNF (∼10%, all P < 0.05). Lactate infusion during exercise-induced a significantly greater increase in plasma mBDNF (115%, P < 0.05) compared to control (saline infusion), with no effect on pro-BDNF levels in plasma or muscle. A 3-day fast resulted in a small increase in plasma pro-BDNF (∼10%, P < 0.05), with no effect on mBDNF.\u0000 Pro-BDNF is highly expressed in human skeletal muscle, particularly in type I fibers, and is increased after exercise. While exercising with higher lactate augmented levels of plasma mBDNF, exercise-mediated increases in circulating mBDNF likely derives, partly, from release and cleavage of pro-BDNF from skeletal muscle, and partly from neural and other tissues. These findings have implications for pre-clinical and clinical work related to a wide range of neurological disorders such as Alzheimer's, clinical depression, and Amyotrophic lateral sclerosis.","PeriodicalId":503843,"journal":{"name":"Function","volume":"52 12","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140492151","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":"Phosphodiesterases Mediate The Augmentation of Myogenic Constriction by Inhibitory G Protein Signaling And Is Negatively Modulated by The Dual Action of RGS2 And 5","authors":"Bo Sun, Nia Smith, Alethia J. Dixon, Patrick Osei-Owusu","doi":"10.1093/function/zqae003","DOIUrl":"https://doi.org/10.1093/function/zqae003","url":null,"abstract":"\u0000 G protein regulation by regulators of G protein signaling (RGS) proteins of the R4/B family plays a key role in vascular tone maintenance; However, the regulatory mechanisms are poorly understood. Previous studies showed that the loss of Gi/o and Gq/11 regulation by RGS2 and RGS5 is involved in augmented vascular tone and decreased uterine blood flow in mice. RGS2 and 5 are structurally and functionally closely related and are co-expressed in the resistance vasculature, including the uterine vascular bed. However, whether and how RGS2 and 5 coordinate their regulatory activities to finetune G protein signaling and regulate vascular tone are unclear. Here, we tested the hypothesis that the integrated activity of RGS2 and 5 modulates vascular tone by negatively regulating Gi/o signaling to promote cAMP-dependent attenuation of uterine artery (UA) myogenic tone (MT). Using pressure myography, we examined MT of UA segments isolated from non-pregnant wild type (WT), Rgs2−/−, Rgs5−/−, and Rgs2/5 dbKO mice in the absence and presence of exogenous cAMP or chemical inhibition of Gi/o signaling, while nitric oxide tone was continuously suppressed with the eNOS inhibitor, L-NAME. We found that MT was reduced in Rgs5−/− relative to WT or Rgs2−/− UA in the absence or presence of L-NAME. Activating Gi/o with dopamine increased, whereas exogenous cAMP decreased MT in Rgs5−/− UA to similar levels in WT UA. Dual deletion of Rgs2 and 5 abolished the reduction of MT due to the absence of only Rgs5 and enhanced dopamine-induced Gi/o effects in Rgs2/5 dbKO UA. Conversely, and as in WT UA, Gi/o inhibition with pertussis toxin or the application of exogenous cAMP decreased MT in Rgs2/5 dbKO to similar levels in Rgs5−/− UA. Application of the pan-phosphodiesterase (PDE) inhibitor, IBMX, concentration dependently decreased and normalized MT in all genotypes, and blocked dopamine-mediated MT augmentation in Rgs2−/−, Rgs5−/−, and Rgs2/5 dbKO UA. These results indicate that activated Gi/o augments MT by promoting PDE-mediated inhibition of cAMP-dependent vasodilatation; and while both RGS2 and 5 negatively regulate this novel Gi/o-PDE-cAMP signaling pathway, RGS5 dampens the inhibitory efficacy of RGS2 towards Gi/o in uterine arteries.","PeriodicalId":503843,"journal":{"name":"Function","volume":"6 16","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139525694","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}