Pub Date : 2025-09-30DOI: 10.1016/j.conb.2025.103122
Zachary A. Knight, Stephen D. Liberles
{"title":"Interoception 2025","authors":"Zachary A. Knight, Stephen D. Liberles","doi":"10.1016/j.conb.2025.103122","DOIUrl":"10.1016/j.conb.2025.103122","url":null,"abstract":"","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"95 ","pages":"Article 103122"},"PeriodicalIF":5.2,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-13DOI: 10.1016/j.conb.2025.103111
Patrick T. O'Neill , Dayu Lin
Becoming a parent involves extraordinary changes that allow caregivers to attend to and nurture infants. Neural circuits must adapt to the demands of caregiving to orchestrate various complex nurturing behaviors. These changes occur between two opposing circuits: a circuit primed for the expression of parenting to execute caregiving, and a circuit that suppresses this behavioral expression when the timing is not appropriate. In this review, we provide an overview of the neural circuits supporting the positive and negative control of parental behaviors and discuss mechanisms by which these opposing circuits are altered to facilitate the onset of parental care.
{"title":"Neural plasticity supporting parental behaviors","authors":"Patrick T. O'Neill , Dayu Lin","doi":"10.1016/j.conb.2025.103111","DOIUrl":"10.1016/j.conb.2025.103111","url":null,"abstract":"<div><div>Becoming a parent involves extraordinary changes that allow caregivers to attend to and nurture infants. Neural circuits must adapt to the demands of caregiving to orchestrate various complex nurturing behaviors. These changes occur between two opposing circuits: a circuit primed for the expression of parenting to execute caregiving, and a circuit that suppresses this behavioral expression when the timing is not appropriate. In this review, we provide an overview of the neural circuits supporting the positive and negative control of parental behaviors and discuss mechanisms by which these opposing circuits are altered to facilitate the onset of parental care.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"95 ","pages":"Article 103111"},"PeriodicalIF":5.2,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145047458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-16DOI: 10.1016/j.conb.2025.103096
Nilay Yapici
Over the past decades, significant advancements have transformed our understanding of the gut-brain circuits in Drosophila melanogaster. In this review, we explore how mapping these circuits and signaling pathways has deepened our knowledge of the neural and hormonal pathways that regulate nutrient preference, feeding behavior, metabolism, and other homeostatic behaviors in flies. We summarize the recent breakthroughs in gut-brain communication and highlight how these advancements have provided valuable insights into the complex relationship between the gut and the brain. Finally, we emphasize the importance of Drosophila as a model system for investigating gut-brain communication. Insights from fly research not only enhance our understanding of fundamental gut-brain biology but also provide promising avenues for identifying molecular targets for therapeutic strategies in humans for gastrointestinal and metabolic disorders.
{"title":"Gut-brain communication in Drosophila melanogaster","authors":"Nilay Yapici","doi":"10.1016/j.conb.2025.103096","DOIUrl":"10.1016/j.conb.2025.103096","url":null,"abstract":"<div><div>Over the past decades, significant advancements have transformed our understanding of the gut-brain circuits in <em>Drosophila melanogaster</em>. In this review, we explore how mapping these circuits and signaling pathways has deepened our knowledge of the neural and hormonal pathways that regulate nutrient preference, feeding behavior, metabolism, and other homeostatic behaviors in flies. We summarize the recent breakthroughs in gut-brain communication and highlight how these advancements have provided valuable insights into the complex relationship between the gut and the brain. Finally, we emphasize the importance of <em>Drosophila</em> as a model system for investigating gut-brain communication. Insights from fly research not only enhance our understanding of fundamental gut-brain biology but also provide promising avenues for identifying molecular targets for therapeutic strategies in humans for gastrointestinal and metabolic disorders.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"94 ","pages":"Article 103096"},"PeriodicalIF":5.2,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144852823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-04-30DOI: 10.1016/j.conb.2025.103032
Kasey L. Brida, Jeremy J. Day
Drugs of abuse result in well-characterized changes in synapse function and number in brain reward regions such as the nucleus accumbens. However, recent reports demonstrate that only a small fraction of neurons in the nucleus accumbens are activated in response to psychostimulants such as cocaine. While these “ensemble” neurons are marked by drug-related transcriptional changes in immediate early genes, the mechanisms that ultimately link these early changes to enduring molecular alterations in the same neurons are less clear. In this review, we 1) describe potential mechanisms underlying regulation of diverse plasticity-related gene programs across drug-activated ensembles, 2) discuss factors conferring ensemble recruitment bias within seemingly homogeneous populations, and 3) speculate on the role of chromatin and epigenetic modifiers in gating metaplastic state transitions that contribute to addiction.
{"title":"Molecular and genetic mechanisms of plasticity in addiction","authors":"Kasey L. Brida, Jeremy J. Day","doi":"10.1016/j.conb.2025.103032","DOIUrl":"10.1016/j.conb.2025.103032","url":null,"abstract":"<div><div>Drugs of abuse result in well-characterized changes in synapse function and number in brain reward regions such as the nucleus accumbens. However, recent reports demonstrate that only a small fraction of neurons in the nucleus accumbens are activated in response to psychostimulants such as cocaine. While these “ensemble” neurons are marked by drug-related transcriptional changes in immediate early genes, the mechanisms that ultimately link these early changes to enduring molecular alterations in the same neurons are less clear. In this review, we 1) describe potential mechanisms underlying regulation of diverse plasticity-related gene programs across drug-activated ensembles, 2) discuss factors conferring ensemble recruitment bias within seemingly homogeneous populations, and 3) speculate on the role of chromatin and epigenetic modifiers in gating metaplastic state transitions that contribute to addiction.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103032"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143885948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-04-09DOI: 10.1016/j.conb.2025.103020
Aaron R. Seitz
Do we choose what we learn? On the contrary, research suggests that much of learning is incidental. The present article reviews frameworks of incidental statistical and perceptual learning and discusses implications of these frameworks to memory. This research supports the premise that much of what we know is shaped by statistical regularities in the environment, how our attention is directed, and what reinforcement we receive from successes and failures. This incidental learning shapes what we perceive and what we remember. This idea that we don’t control when and what we learn, instead we at best trick our brain into states that will lead to desired learning outcomes, has important implications both to individuals and society.
{"title":"Tricking our brains to learn and remember; is all learning incidental?","authors":"Aaron R. Seitz","doi":"10.1016/j.conb.2025.103020","DOIUrl":"10.1016/j.conb.2025.103020","url":null,"abstract":"<div><div>Do we choose what we learn? On the contrary, research suggests that much of learning is incidental. The present article reviews frameworks of incidental statistical and perceptual learning and discusses implications of these frameworks to memory. This research supports the premise that much of what we know is shaped by statistical regularities in the environment, how our attention is directed, and what reinforcement we receive from successes and failures. This incidental learning shapes what we perceive and what we remember. This idea that we don’t control when and what we learn, instead we at best trick our brain into states that will lead to desired learning outcomes, has important implications both to individuals and society.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103020"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143808619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-04-22DOI: 10.1016/j.conb.2025.103029
Benjamin J. Menarchek, Michelle C.D. Bridi
Sleep is thought to serve an important role in learning and memory, but the mechanisms by which sleep promotes plasticity remain unclear. Even in the absence of plastic changes in neuronal function, many molecular, cellular, and physiological processes linked to plasticity are upregulated during sleep. Therefore, sleep may be a state in which latent plasticity mechanisms are poised to respond following novel experiences during prior wake. Many of these plasticity-related processes can promote both synaptic strengthening and weakening. Signaling pathways activated during sleep may interact with complements of proteins, determined by the content of prior waking experience, to establish the polarity of plasticity. Furthermore, precise reactivation of neuronal spiking patterns during sleep may interact with ongoing neuromodulatory, dendritic, and network activity to strengthen and weaken synapses. In this review, we will discuss the idea that sleep elevates latent plasticity mechanisms, which drive bidirectional plasticity depending on prior waking experience.
{"title":"Latent mechanisms of plasticity are upregulated during sleep","authors":"Benjamin J. Menarchek, Michelle C.D. Bridi","doi":"10.1016/j.conb.2025.103029","DOIUrl":"10.1016/j.conb.2025.103029","url":null,"abstract":"<div><div>Sleep is thought to serve an important role in learning and memory, but the mechanisms by which sleep promotes plasticity remain unclear. Even in the absence of plastic changes in neuronal function, many molecular, cellular, and physiological processes linked to plasticity are upregulated during sleep. Therefore, sleep may be a state in which latent plasticity mechanisms are poised to respond following novel experiences during prior wake. Many of these plasticity-related processes can promote both synaptic strengthening and weakening. Signaling pathways activated during sleep may interact with complements of proteins, determined by the content of prior waking experience, to establish the polarity of plasticity. Furthermore, precise reactivation of neuronal spiking patterns during sleep may interact with ongoing neuromodulatory, dendritic, and network activity to strengthen and weaken synapses. In this review, we will discuss the idea that sleep elevates latent plasticity mechanisms, which drive bidirectional plasticity depending on prior waking experience.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103029"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143860335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-06-25DOI: 10.1016/j.conb.2025.103067
Rose Z. Hill
The kidneys filter the blood and balance fluid and electrolytes to keep the composition of the internal environment within the narrow parameters essential for life. A perturbation to the internal state, such as a sudden loss of blood or dehydration, engages autonomic efferent and neuroendocrine pathways to adjust kidney function rapidly and robustly. The mechanisms of these multiorgan pathways are extensively studied. By contrast, the roles of sensory afferent nerves in regulating renal function are just beginning to be understood. In this review, we examine recent advances in understanding the morphology, identity, and functions of the renal sensory nerves that form the first node in the interoceptive pathways that update the kidney on its own internal state. We end by highlighting open questions in the field, influenced by recent work in other areas of interoception neuroscience, and the outstanding gaps in our knowledge of kidney biology.
{"title":"Renal interoception: form, function, and open questions","authors":"Rose Z. Hill","doi":"10.1016/j.conb.2025.103067","DOIUrl":"10.1016/j.conb.2025.103067","url":null,"abstract":"<div><div>The kidneys filter the blood and balance fluid and electrolytes to keep the composition of the internal environment within the narrow parameters essential for life. A perturbation to the internal state, such as a sudden loss of blood or dehydration, engages autonomic efferent and neuroendocrine pathways to adjust kidney function rapidly and robustly. The mechanisms of these multiorgan pathways are extensively studied. By contrast, the roles of sensory afferent nerves in regulating renal function are just beginning to be understood. In this review, we examine recent advances in understanding the morphology, identity, and functions of the renal sensory nerves that form the first node in the interoceptive pathways that update the kidney on its own internal state. We end by highlighting open questions in the field, influenced by recent work in other areas of interoception neuroscience, and the outstanding gaps in our knowledge of kidney biology.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103067"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144470338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The reciprocal regulation of the neural ensemble and vascular network within the mammalian central nervous system (CNS) is crucial for its development and functionality. Neuron-derived pro-angiogenic factors, such as growth factors, morphogens, and guidance cues, play a key role in forming stereotypical vascular architectures in the cortex, spinal cord, and cerebellum during development. Notably, the CNS vasculature forms distinct 3D lattice structures composed of laminar vascular networks interconnected by penetrating vessels. This contrasts with the more random 3D arborizations found in tumors. While the morphogen gradients for vascular network growth have been well-studied, the mechanisms contributing to vascular patterning and lattice maintenance in 3D are not fully understood. The mammalian retina provides an ideal model for studying these mechanisms, given its laminar organization of neurons and plexus organization of vessels, allowing for the investigation of 2D growth to 3D lattice establishment in a stepwise manner. Notably, recent studies have highlighted the roles of neurons and glia in retinal vascular patterning in 2D, as well as the involvement of neurotransmitters in regulating vascular growth. Additionally, direct neuron-to-vessel interactions have been found to contribute to 3D retinal vascular lattice formation. As emerging technologies provide new insights into retinal vascular assembly in 3D, understanding the developmental regulation and the physiological and pathophysiological effects of 3D lattice disruption remains a fertile field of research.
{"title":"A neurobiology perspective on the assembly of retinal vasculature from 2D to 3D","authors":"Mahima Bose , Mengya Zhao , Kenichi Toma , Xin Ye , Xin Duan","doi":"10.1016/j.conb.2025.103085","DOIUrl":"10.1016/j.conb.2025.103085","url":null,"abstract":"<div><div>The reciprocal regulation of the neural ensemble and vascular network within the mammalian central nervous system (CNS) is crucial for its development and functionality. Neuron-derived pro-angiogenic factors, such as growth factors, morphogens, and guidance cues, play a key role in forming stereotypical vascular architectures in the cortex, spinal cord, and cerebellum during development. Notably, the CNS vasculature forms distinct 3D lattice structures composed of laminar vascular networks interconnected by penetrating vessels. This contrasts with the more random 3D arborizations found in tumors. While the morphogen gradients for vascular network growth have been well-studied, the mechanisms contributing to vascular patterning and lattice maintenance in 3D are not fully understood. The mammalian retina provides an ideal model for studying these mechanisms, given its laminar organization of neurons and plexus organization of vessels, allowing for the investigation of 2D growth to 3D lattice establishment in a stepwise manner. Notably, recent studies have highlighted the roles of neurons and glia in retinal vascular patterning in 2D, as well as the involvement of neurotransmitters in regulating vascular growth. Additionally, direct neuron-to-vessel interactions have been found to contribute to 3D retinal vascular lattice formation. As emerging technologies provide new insights into retinal vascular assembly in 3D, understanding the developmental regulation and the physiological and pathophysiological effects of 3D lattice disruption remains a fertile field of research.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103085"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144631574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-06-23DOI: 10.1016/j.conb.2025.103069
Inês C. Dias , Nicolas Gutierrez-Castellanos , Constanze Lenschow , Susana Q. Lima
Female sexual behavior is essential for reproduction and species survival. It is orchestrated by hormonal and neuronal mechanisms that coordinate sexual maturation, reproductive cycle, and the copulatory sequence, preparing the female for pregnancy. These mechanisms synchronize behavioral receptivity with reproductive capacity, ensuring that copulation occurs during optimal reproductive windows while actively suppressing sexual behavior outside fertile periods.
This review explores recent advances in neural mechanisms that integrate sensory, hormonal, and social cues in the female brain. We examine the main phases of sexual behavior: appetitive, consummatory, and refractory, focusing on the neural basis of sexual rejection during non-fertile periods. We also discuss studies using intersectional genetics and neural activity analysis to uncover the circuits underlying sexual receptivity and recent findings on how the female brain processes male ejaculation to trigger the refractory period. Altogether, this review sheds light on the orchestration of mating and reproductive readiness in female mice.
{"title":"Ready or not: Neural mechanisms regulating female sexual behavior","authors":"Inês C. Dias , Nicolas Gutierrez-Castellanos , Constanze Lenschow , Susana Q. Lima","doi":"10.1016/j.conb.2025.103069","DOIUrl":"10.1016/j.conb.2025.103069","url":null,"abstract":"<div><div>Female sexual behavior is essential for reproduction and species survival. It is orchestrated by hormonal and neuronal mechanisms that coordinate sexual maturation, reproductive cycle, and the copulatory sequence, preparing the female for pregnancy. These mechanisms synchronize behavioral receptivity with reproductive capacity, ensuring that copulation occurs during optimal reproductive windows while actively suppressing sexual behavior outside fertile periods.</div><div>This review explores recent advances in neural mechanisms that integrate sensory, hormonal, and social cues in the female brain. We examine the main phases of sexual behavior: appetitive, consummatory, and refractory, focusing on the neural basis of sexual rejection during non-fertile periods. We also discuss studies using intersectional genetics and neural activity analysis to uncover the circuits underlying sexual receptivity and recent findings on how the female brain processes male ejaculation to trigger the refractory period. Altogether, this review sheds light on the orchestration of mating and reproductive readiness in female mice.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103069"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144364951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-07-07DOI: 10.1016/j.conb.2025.103086
Madison T. Gray , Julie L. Lefebvre
Synaptic partner recognition and precise connectivity are essential components of neural circuit formation and function. Cell adhesion molecules with selective binding properties provide instructive cues for synapse specificity. Yet, we know little about how they guide the stereotyped organization of neural circuits. Advances in transcriptomics, genetic manipulations, neural tracing and imaging in intact nervous systems enable new avenues to identify mechanisms by which adhesion molecules regulate synapse specificity. Here we discuss the Cadherin superfamily, which forms one of the most functionally versatile families of cell adhesion molecules. Focusing on the classical cadherins and clustered protocadherins, we discuss recent findings that demonstrate roles in regulating synaptic partnerships and signaling properties, and optimizing neurite wiring. We highlight studies that demonstrate instructive roles through genetic manipulations with assays of synaptic connectivity. Understanding how neurons leverage a Cadherin code for specifying neural connectivity provides insights into the broader principles of circuit assembly and function.
{"title":"Cracking the cadherin codes that wire the nervous system","authors":"Madison T. Gray , Julie L. Lefebvre","doi":"10.1016/j.conb.2025.103086","DOIUrl":"10.1016/j.conb.2025.103086","url":null,"abstract":"<div><div>Synaptic partner recognition and precise connectivity are essential components of neural circuit formation and function. Cell adhesion molecules with selective binding properties provide instructive cues for synapse specificity. Yet, we know little about how they guide the stereotyped organization of neural circuits. Advances in transcriptomics, genetic manipulations, neural tracing and imaging in intact nervous systems enable new avenues to identify mechanisms by which adhesion molecules regulate synapse specificity. Here we discuss the Cadherin superfamily, which forms one of the most functionally versatile families of cell adhesion molecules. Focusing on the classical cadherins and clustered protocadherins, we discuss recent findings that demonstrate roles in regulating synaptic partnerships and signaling properties, and optimizing neurite wiring. We highlight studies that demonstrate instructive roles through genetic manipulations with assays of synaptic connectivity. Understanding how neurons leverage a Cadherin code for specifying neural connectivity provides insights into the broader principles of circuit assembly and function.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103086"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144570878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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