Journal of Physiology-London最新文献

{"title":"Cardiac sympathetic neurons are additional cells affected in genetically determined arrhythmogenic cardiomyopathy.","authors":"Induja Perumal Vanaja, Arianna Scalco, Marco Ronfini, Anna Di Bona, Camilla Olianti, Stefania Rizzo, Stephen P Chelko, Domenico Corrado, Leonardo Sacconi, Cristina Basso, Marco Mongillo, Tania Zaglia","doi":"10.1113/JP286845","DOIUrl":"https://doi.org/10.1113/JP286845","url":null,"abstract":"<p><p>Arrhythmogenic cardiomyopathy (AC) is a familial cardiac disease, mainly caused by mutations in desmosomal genes, which accounts for most cases of stress-related arrhythmic sudden death, in young and athletes. AC hearts display fibro-fatty lesions that generate the arrhythmic substrate and cause contractile dysfunction. A correlation between physical/emotional stresses and arrhythmias supports the involvement of sympathetic neurons (SNs) in the disease, but this has not been confirmed previously. Here, we combined molecular, in vitro and ex vivo analyses to determine the role of AC-linked DSG2 downregulation on SN biology and assess cardiac sympathetic innervation in desmoglein-2 mutant (Dsg2^mut/mut) mice. Molecular assays showed that SNs express DSG2, implying that DSG2-mutation carriers would harbour the mutant protein in SNs. Confocal immunofluorescence of heart sections and 3-D reconstruction of SN network in clarified heart blocks revealed significant changes in the physiologialc SN topology, with massive hyperinnervation of the intact subepicardial layers and heterogeneous distribution of neurons in fibrotic areas. Cardiac SNs isolated from Dsg2^mut/mut neonatal mice, prior to the establishment of cardiac innervation, show alterations in axonal sprouting, process development and distribution of varicosities. Consistently, virus-assisted DSG2 downregulation replicated, in PC12-derived SNs, the phenotypic alterations displayed by Dsg2^mut/mut primary neurons, corroborating that AC-linked Dsg2 variants may affect SNs. Our results reveal that altered sympathetic innervation is an unrecognized feature of AC hearts, which may result from the combination of cell-autonomous and context-dependent factors implicated in myocardial remodelling. Our results favour the concept that AC is a disease of multiple cell types also hitting cardiac SNs. KEY POINTS: Arrhythmogenic cardiomyopathy is a genetically determined cardiac disease, which accounts for most cases of stress-related arrhythmic sudden death. Arrhythmogenic cardiomyopathy linked to mutations in desmoglein-2 (DSG2) is frequent and leads to a left-dominant form of the disease. Arrhythmogenic cardiomyopathy has been approached thus far as a disease of cardiomyocytes, but we here unveil that DSG2 is expressed, in addition to cardiomyocytes, by cardiac and extracardiac sympathetic neurons, although not organized into desmosomes. AC-linked DSG2 downregulation primarily affect sympathetic neurons, resulting in the significant increase in cardiac innervation density, accompanied by alterations in sympathetic neuron distribution. Our data supports the notion that AC develops with the contribution of several 'desmosomal protein-carrying' cell types and systems.</p>","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141983758","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}

{"title":"Vaping for two: unravelling the mysteries of E-cigarettes and fetal vascular health","authors":"Beth J. Allison","doi":"10.1113/JP287313","DOIUrl":"10.1113/JP287313","url":null,"abstract":"&lt;p&gt;The negative impact of cigarettes on the health of the developing fetus was first recognized by Simpson (&lt;span&gt;1957&lt;/span&gt;). Since then, our understanding of the adverse impacts of smoking on fetal health has grown to include fetal growth restriction and preterm birth, in addition to organ-specific pathology in the lungs (chronic bronchitis and asthma), heart (hypertension and atherosclerosis) and brain (increased risk of poor neurodevelopmental outcomes). Cigarette smoking during pregnancy causes profound neuropathology, including abnormalities in brain structure, reduced cortical thickness and altered neurotransmitter release that are evident from birth (Slotkin et al., &lt;span&gt;2011&lt;/span&gt;).&lt;/p&gt;&lt;p&gt;Awareness of the overwhelmingly devastating impacts of cigarettes on the health of an individual and for both the mother and fetus during pregnancy has led to the implementation of regulations, health warnings, advertising restrictions and taxation to reduce smoking rates for the first time in history. In turn, the highly regulated consumption of cigarettes has prompted the tobacco industry to diversify into smokeless tobacco products. The emergence of E-cigarette devices occurred in 2003, initially intended for use as a product to help quit smoking. E-cigarettes, which deliver nicotine through aerosolized vapour rather than smoke, were then marketed as a smoking cessation aid and rapidly gained popularity. Since then, the uptake of E-cigarettes has increased rapidly, particularly for a younger demographic of previous non-smokers looking for a less harmful alternative to smoking. Current data indicate that 19−32% of people of reproductive age are using E-cigarettes and, in women of reproductive age, between 4 and 10% are daily users (Scully et al., &lt;span&gt;2023&lt;/span&gt;). Worryingly, the highest prevalence of individuals who use E-cigarettes are those of childbearing age. Unsurprisingly and concerningly, data are now emerging that E-cigarettes are as harmful, if not more harmful, than their cigarette predecessor. Conventional cigarettes contain tobacco and ≤600 other ingredients, whereas E-cigarettes have a unique composition of propylene glycol, vegetable glycerine, formaldehyde, acrolein, flavouring chemicals, heavy metals and other trace elements. They may or may not contain nicotine.&lt;/p&gt;&lt;p&gt;In this issue of &lt;i&gt;The Journal of Physiology&lt;/i&gt;, Mills et al. (&lt;span&gt;2024&lt;/span&gt;) report a significant step forwards in our understanding of the potential harm of E-cigarettes on the developing fetus. Using a model of rat pregnancy, Mills and colleagues exposed female rats to a whole-body chamber containing the base mixture upon which flavourings or tobacco are typically added to E-cigarettes, i.e. vegetable glycerol and propylene glycol. The study aimed to examine the timing of E-cigarette exposure on vascular and behavioural outcomes. The different periods of exposure examined included preconception, the first third of gestation, the second third of gestation, ","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1113/JP287313","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141977132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peer review: the imprimatur of scientific publication","authors":"Ronan M. G. Berg,&nbsp;Karyn L. Hamilton,&nbsp;Joanne Fiona Murray,&nbsp;Peying Fong","doi":"10.1113/JP286273","DOIUrl":"10.1113/JP286273","url":null,"abstract":"","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1113/JP286273","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141983760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiple layers of diversity govern the cell type specificity of GABAergic input received by mouse subicular pyramidal neurons","authors":"Nancy Castro Borjas,&nbsp;Max Anstötz,&nbsp;Gianmaria Maccaferri","doi":"10.1113/JP286679","DOIUrl":"10.1113/JP286679","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 \u0000 &lt;div&gt;The subiculum is a key region of the brain involved in the initiation of pathological activity in temporal lobe epilepsy, and local GABAergic inhibition is essential to prevent subicular-originated epileptiform discharges. Subicular pyramidal cells may be easily distinguished into two classes based on their different firing patterns. Here, we have compared the strength of the GABAa receptor-mediated inhibitory postsynaptic currents received by regular- &lt;i&gt;vs&lt;/i&gt;. burst-firing subicular neurons and their dynamic modulation by the activation of μ opioid receptors. We have taken advantage of the sequential re-patching of the same cell to initially classify pyramidal neurons according to their firing patters, and then to measure GABAergic events triggered by the optogenetic stimulation of parvalbumin- and somatostatin-expressing interneurons. Activation of parvalbumin-expressing cells generated larger responses in postsynaptic burst-firing neurons whereas the opposite was observed for currents evoked by the stimulation of somatostatin-expressing interneurons. In all cases, events depended critically on ω-agatoxin IVA- but not on ω-conotoxin GVIA-sensitive calcium channels. Optogenetic GABAergic input originating from both parvalbumin- and somatostatin-expressing cells was reduced in amplitude following the exposure to a μ opioid receptor agonist. The kinetics of this pharmacological sensitivity was different in regular- &lt;i&gt;vs&lt;/i&gt;. burst-firing neurons, but only when responses were evoked by the activation of parvalbumin-expressing neurons, whereas no differences were observed when somatostatin-expressing cells were stimulated. In conclusion, our results show that a high degree of complexity regulates the organizing principles of subicular GABAergic inhibition, with the interaction of pre- and postsynaptic diversity at multiple levels.\u0000\u0000 &lt;figure&gt;\u0000 &lt;div&gt;&lt;picture&gt;\u0000 &lt;source&gt;&lt;/source&gt;&lt;/picture&gt;&lt;p&gt;&lt;/p&gt;\u0000 &lt;/div&gt;\u0000 &lt;/figure&gt;\u0000 &lt;/div&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Key points&lt;/h3&gt;\u0000 \u0000 &lt;div&gt;\u0000 &lt;ul&gt;\u0000 \u0000 &lt;li&gt;Optogenetic stimulation of parvalbumin- and somatostatin-expressing interneurons (PVs and SOMs) triggers inhibitory postsynaptic currents (IPSCs) in both regular- and burst-firing (RFs and BFs) subicular pyramidal cells.&lt;/li&gt;\u0000 \u0000 &lt;li&gt;The amplitude of optogenetically evoked IPSCs from PVs (PV-opto IPSCs) is larger in BFs whereas IPSCs generated by the light activation of SOMs (SOM-opto IPSCs) are larger in RFs.&lt;/li&gt;\u0000 \u0000 &lt;li&gt;Both PV- and SOM-opto IPSCs critically depend on ω-agatoxin IVA-sensitive P/Q type voltage-gated calcium channel","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1113/JP286679","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141983759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Persistence of quantal synaptic vesicle recycling in virtual absence of dynamins.","authors":"Olusoji A T Afuwape, Natali L Chanaday, Merve Kasap, Lisa M Monteggia, Ege T Kavalali","doi":"10.1113/JP286711","DOIUrl":"https://doi.org/10.1113/JP286711","url":null,"abstract":"<p><p>Dynamins are GTPases required for pinching vesicles off the plasma membrane once a critical curvature is reached during endocytosis. Here, we probed dynamin function in central synapses by depleting all three dynamin isoforms in postnatal hippocampal neurons down to negligible levels. We found a decrease in the propensity of evoked neurotransmission as well as a reduction in synaptic vesicle numbers. Recycling of synaptic vesicles during spontaneous or low levels of evoked activity were largely impervious to dynamin depletion, while retrieval of synaptic vesicle components at higher levels of activity was partially arrested. These results suggest the existence of balancing dynamin-independent mechanisms for synaptic vesicle recycling at central synapses. Classical dynamin-dependent mechanisms are not essential for retrieval of synaptic vesicle proteins after quantal single synaptic vesicle fusion, but they become more relevant for membrane retrieval during intense, sustained neuronal activity. KEY POINTS: Loss of dynamin 2 does not impair synaptic transmission. Loss of all three dynamin isoforms mostly affects evoked neurotransmission. Excitatory synapse function is more susceptible to dynamin loss. Spontaneous neurotransmission is only mildly affected by loss of dynamins. Single synaptic vesicle endocytosis is largely dynamin independent.</p>","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141983761","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}

{"title":"Physiological mechanisms contributing to human exercise performance","authors":"Scott K. Powers","doi":"10.1113/JP287382","DOIUrl":"10.1113/JP287382","url":null,"abstract":"&lt;p&gt;Interest in the physiological factors that contribute to human exercise performance spans many decades of research. In this special issue of the &lt;i&gt;Journal of Physiology&lt;/i&gt;, the Journal provides readers with two reviews related to the biological factors that contribute to human exercise performance. An overview of each review follows.&lt;/p&gt;&lt;p&gt;The first of these two outstanding review papers is authored by Dr Andy Jones from the University of Exeter, UK (Jones, &lt;span&gt;2024&lt;/span&gt;). This report provides a summary of Dr Jones’ keynote lecture presented at the Integrative Physiology of Exercise meeting in Baltimore, MD (USA) in 2022. In this interesting and well-crafted review, Dr Jones emphasizes that endurance exercise performance is associated with three key physiological factors: (1) maximal oxygen uptake (VO&lt;sub&gt;2&lt;/sub&gt; max); (2) economy or efficiency during exercise; and (3) the fraction of VO&lt;sub&gt;2&lt;/sub&gt; max that can be maintained during prolonged exercise. Professor Jones emphasizes that during prolonged endurance exercise, these variables are not static and are subject to deterioration as exercise proceeds. In particular, the fraction of VO&lt;sub&gt;2&lt;/sub&gt; max that can be maintained during fatiguing endurance exercise often decreases by 10% or more as the exercise bout proceeds. Therefore, Jones argues that ‘resilience’ (defined as the ability to resist fatigue during endurance exercise) should be considered as a fourth physiological factor that determines human endurance performance. The report debates the possible physiological mechanisms that contribute to physiological resilience and identifies several important topics for future research. Clearly, this outstanding report is a must read for physiologists interested in the physiological mechanisms that contribute to endurance exercise performance.&lt;/p&gt;&lt;p&gt;The second report in this special issue addresses the important topic of ‘sex differences in human performance’. Drs Sandra Hunter and Jonathon Senefeld coauthored this thought-provoking review (Hunter &amp; Senefeld, &lt;span&gt;2024&lt;/span&gt;) and, like the Jones review, this paper highlights Dr Hunters’ keynote lecture presented at the Integrative Physiology of Exercise meeting held in Baltimore, MD in 2022. This well-written review carefully chronicles our current understanding of the physiological mechanisms responsible for the sex differences in human physical performance. The report concludes that males outperform females in many exercise events because they are faster, stronger and more powerful. The review highlights the key physiological differences that contribute to these sex differences in human performance and the physiological mechanisms responsible for these differences. Specifically, the role that sex-steroid hormones, sex hormones and epigenetics play in sex differences in physical performance is discussed. Importantly, this review also provides a scientific rationale for policy decisions on sex-based categories in sports participati","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1113/JP287382","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141972208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Presynaptic H₃ receptor: A modulator for CeL excitatory-inhibitory homeostasis.","authors":"Qian-Yi Ma, Wei-Wei Hu","doi":"10.1113/JP287082","DOIUrl":"https://doi.org/10.1113/JP287082","url":null,"abstract":"","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141972209","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}

{"title":"Using mechanistic knowledge to appraise contemporary approaches to the rehabilitation of upper limb function following stroke.","authors":"Richard G Carson, Kathryn S Hayward","doi":"10.1113/JP285559","DOIUrl":"https://doi.org/10.1113/JP285559","url":null,"abstract":"<p><p>It is a paradox of neurological rehabilitation that, in an era in which preclinical models have produced significant advances in our mechanistic understanding of neural plasticity, there is inadequate support for many therapies recommended for use in clinical practice. When the goal is to estimate the probability that a specific form of therapy will have a positive clinical effect, the integration of mechanistic knowledge (concerning 'the structure or way of working of the parts in a natural system') may improve the quality of inference. This is illustrated by analysis of three contemporary approaches to the rehabilitation of lateralized dysfunction affecting people living with stroke: constraint-induced movement therapy; mental practice; and mirror therapy. Damage to 'cross-road' regions of the structural (white matter) brain connectome generates deficits that span multiple domains (motor, language, attention and verbal/spatial memory). The structural integrity of these regions determines not only the initial functional status, but also the response to therapy. As structural disconnection constrains the recovery of functional capability, 'disconnectome' modelling provides a basis for personalized prognosis and precision rehabilitation. It is now feasible to refer a lesion delineated using a standard clinical scan to a (dis)connectivity atlas derived from the brains of other stroke survivors. As the individual disconnection pattern thus obtained suggests the functional domains most likely be compromised, a therapeutic regimen can be tailored accordingly. Stroke is a complex disorder that burdens individuals with distinct constellations of brain damage. Mechanistic knowledge is indispensable when seeking to ameliorate the behavioural impairments to which such damage gives rise.</p>","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141917920","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}

{"title":"Hypoxic training as a doping method - the final whistle from Norway and Italy.","authors":"Grégoire P Millet, Franck Brocherie","doi":"10.1113/JP287323","DOIUrl":"https://doi.org/10.1113/JP287323","url":null,"abstract":"","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141914459","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}

{"title":"Exploring neuronal mechanisms of osteosarcopenia in older adults.","authors":"Ilhan Karacan, Kemal Sıtkı Türker","doi":"10.1113/JP285666","DOIUrl":"https://doi.org/10.1113/JP285666","url":null,"abstract":"<p><p>Until recently, research on the pathogenesis and treatment of osteoporosis and sarcopenia has primarily focused on local and systemic humoral mechanisms, often overlooking neuronal mechanisms. However, there is a growing body of literature on the neuronal regulation of bone and skeletal muscle structure and function, which may provide insights into the pathogenesis of osteosarcopenia. This review aims to integrate these neuronal regulatory mechanisms to form a comprehensive understanding and inspire future research that could uncover novel strategies for preventing and treating osteosarcopenia. Specifically, the review explores the functional adaptation of weight-bearing bone to mechanical loading throughout evolutionary development, from Wolff's law and Frost's mechanostat theory to the mosaic hypothesis, which emphasizes neuronal regulation. The recently introduced bone osteoregulation reflex points to the importance of the osteocytic mechanoreceptive network as a receptor in this neuronal regulation mechanism. Finally, the review focuses on the bone myoregulation reflex, which is known as a mechanism by which bone loading regulates muscle functions neuronally. Considering the ageing-related regressive changes in the nerve fibres that provide both structural and functional regulation in bone and skeletal muscle tissue and the bone and muscle tissues they innervate, it is suggested that neuronal mechanisms might play a central role in explaining osteosarcopenia in older adults.</p>","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":null,"pages":null},"PeriodicalIF":4.7,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141908175","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}