British Journal of Pharmacology最新文献

{"title":"Biodiversity2Drugs-Renaissance of exploring nature-derived peptides for GPCR ligand discovery.","authors":"Christian W Gruber, Isabel Beets, Pierre-Luc Boudreault, Vanderlan da S Bolzani, Jens Carlsson, Pedro A Fernandes, Michael Freissmuth, Nicolas Gilles, Ulf Göransson, Alexander S Hauser, Christian Heinis, Jeroen Kool, William D Lubell, Maria Vittoria Modica, Jana Selent, Jan Tytgat, Eivind A B Undheim","doi":"10.1111/bph.70072","DOIUrl":"https://doi.org/10.1111/bph.70072","url":null,"abstract":"","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181174","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":"Klebsiella pneumoniae contributes to altered cytotoxicity of thiopurines in vitro: Possible implications of biotransformation and bacterial metabolism.","authors":"Martina Franzin, Cristina Lagatolla, Sofia Sindici Forgiarini, Mathias Haag, Sylvia Karin Neef, Manola Comar, Elke Schaeffeler, Barbara Bellich, Matteo Bramuzzo, Giuliana Decorti, Marianna Lucafò, Ute Hofmann, Matthias Schwab, Gabriele Stocco","doi":"10.1111/bph.70089","DOIUrl":"https://doi.org/10.1111/bph.70089","url":null,"abstract":"<p><strong>Background and purpose: </strong>Thiopurines are used in paediatric inflammatory bowel disease (IBD), but some patients do not respond. Because the gut microbiota influences drug efficacy and IBD-patient microbiota presents increased bacterial abundance, we investigated the impact of candidate Enterobacteriaceae on drug cytotoxicity, metabolism and efficacy.</p><p><strong>Experimental approach: </strong>Thiopurines were exposed in vitro to bacteria for 4 h at 37°C and drug concentrations measured by UV spectrophotometry. Cytotoxic effects and drug metabolite concentrations on NALM6 and JURKAT cells were determined after treatment with thiopurines exposed or not to bacteria. Drugs were measured in Klebsiella pneumoniae lysates and bacterial conditioned media were used for metabolomic analyses. Shotgun metagenomic sequencing was performed on eight IBD-patient faecal stools.</p><p><strong>Key results: </strong>Incubation of thiopurines with K. pneumoniae, but not Escherichia coli and Salmonella enterica, reduced thiopurine concentrations and cytotoxicity on NALM6 and JURKAT cells. Thiopurine metabolites were lower in cells treated with drugs previously exposed to K. pneumoniae. Internalisation of drugs was demonstrated by their detection in lysates after bacterial incubation. Untargeted metabolomics revealed biotransformation of thiopurines by K. pneumoniae, as reactions of deconjugation, reduction, glycosylation, acetylation or conjugation with propionic acid. Incubation with thiopurines led to changes in the secretion of endogenous bacterial metabolites. K. pneumoniae faecal abundance was associated with lower thiopurine metabolite concentrations in erythrocytes of paediatric IBD-patients.</p><p><strong>Conclusions and implications: </strong>K. pneumoniae decreases the cytotoxicity of thiopurines through internalisation of MP and TG. We revealed potential bacterial drug biotransformation, as well as negative correlations between bacterial abundance and drug metabolites.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172701","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":"The use of different types of networks, alone and in combination, for drug target identification.","authors":"Paolo Parini","doi":"10.1111/bph.70091","DOIUrl":"https://doi.org/10.1111/bph.70091","url":null,"abstract":"<p><p>Current therapeutic approaches often focus on targeting clinical symptoms or peripheral phenotypes rather than the underlying molecular mechanisms, or endophenotypes, that drive diseases. While symptom-based drugs can alleviate discomfort, they do not necessarily alter disease progression and may overlook opportunities for prevention or early intervention in asymptomatic patients. This approach can lead to overtreatment of certain disease traits while neglecting others that are critical for long-term outcomes. In contrast, mechanism-based therapies offer advantages such as specificity and reduced side effects, allowing for the management of previously untreatable conditions or complementing established treatments. These therapies enable monitoring of drug effects on the endophenotype driving the disease, facilitating personalised treatment regimens and improving patient compliance. Mechanism-based drugs are essential for precision prevention and therapy. Network Medicine plays a vital role in understanding diseases by identifying key endophenotypes and determinants influencing disease expression. Unlike reductionist methods, it provides insights into disease mechanisms and potential therapeutic targets by examining interactions among genetic, molecular and environmental factors. As part of Network Medicine, Network Pharmacology bridges the gap between symptom-based and mechanism-based strategies, guiding drug development while considering symptomatic relief. This short review focus on creating heterogeneous networks to integrate various drug, target and disease-related information. These approaches can create comprehensive representations of drugs and targets by incorporating diverse profiles, enhancing the prediction performance of drug target interactions.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172703","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":"Dexrazoxane protects against doxorubicin-induced cardiotoxicity in susceptible human living myocardial slices: A proof-of-concept study.","authors":"Jort S A van der Geest, Ilse R Kelters, Bauke Arends, Willem B van Ham, Ernest Diez Benavente, Thirza A Lapré, Petra van der Kraak, Pim van der Harst, Arco J Teske, Andreas Dendorfer, M Mostafa Mokhles, Pieter A Doevendans, Teun P de Boer, Linda W van Laake, Joost P G Sluijter, Vasco Sampaio-Pinto","doi":"10.1111/bph.70085","DOIUrl":"https://doi.org/10.1111/bph.70085","url":null,"abstract":"<p><strong>Background and purpose: </strong>The increasing number of cancer survivors has caused growing concern over chemotherapy-induced cardiotoxicity. This study aimed to investigate a novel human model of cardiotoxicity and explore cardioprotection.</p><p><strong>Experimental approach: </strong>Living myocardial slices (LMS) were obtained from explanted end-stage heart failure hearts, then exposed to doxorubicin (Dox) to investigate cardiotoxic effects and to dexrazoxane (Dex) to explore cardioprotection. We assessed contractile function and glucose consumption, followed by evaluation of calcium transients, structural integrity and transcriptomic changes. Additionally, electrocardiogram (ECG) alterations were analysed in patients treated with anthracyclines to corroborate the cardiotoxicity findings from LMS.</p><p><strong>Key results: </strong>We observed distinct functional responses to Dox, with LMS derived from some patients exhibiting high susceptibility to Dox-induced cardiotoxicity. LMS from susceptible patients displayed reduced contractile function and excitability, myofibre dyssynchrony, structural damage and decreased metabolic activity. Dex pretreatment partially mitigated these effects, preserving contractile function and preventing structural damage. Consistent with ex vivo findings, patients treated with anthracyclines exhibited acute and chronic alterations in T-, P- and R-wave morphology of the ECG, confirming variable susceptibility at the clinical level.</p><p><strong>Conclusions and implications: </strong>We highlight the value of human LMS in studying Dox-induced cardiotoxicity and the cardioprotective potential of Dex, even when sourced from end-stage heart failure patients. Susceptible patients harboured cardiomyopathy-associated genetic mutations, suggesting that genetic screening including cardiomyopathy-associated genes, prior to anthracycline treatment, could enable improved patient risk stratification. We demonstrate the potential utility of ECG changes for early detection of subclinical cardiotoxicity.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172699","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":"RETRACTION: L6H21 protects against cognitive impairment and brain pathologies via toll-like receptor 4-myeloid differentiation factor 2 Signalling in Prediabetic rats.","authors":"","doi":"10.1111/bph.70104","DOIUrl":"https://doi.org/10.1111/bph.70104","url":null,"abstract":"","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149427","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":"Cannabidiol dose dependently reduces alcohol intake in mice via a non-5-HT_1A receptor mechanism: Exploration of other potential receptor targets.","authors":"Connie J Badolato, Erin A Lynch, Jonathon C Arnold, Iain S McGregor, Michael T Bowen","doi":"10.1111/bph.70070","DOIUrl":"https://doi.org/10.1111/bph.70070","url":null,"abstract":"<p><strong>Background and purpose: </strong>Binge drinking is a risky pattern of alcohol intake and a major predictor of alcohol use disorder (AUD). Current AUD medications have limited efficacy and poor patient compliance, calling for more effective therapeutics. Cannabidiol (CBD), a non-intoxicating component of cannabis, has emerged as a potential novel therapeutic. However, receptor mechanisms in CBD's alcohol-related effects have not been investigated comprehensively.</p><p><strong>Experimental approach: </strong>Using the murine drinking-in-the-dark model of binge drinking, our research aimed to confirm a reduction of alcohol consumption with CBD (7.5, 15, 30, 60, 120 mg kg^-1) in male and female mice. Behavioural pharmacological approaches were used to explore CBD interactions with identified target mechanisms: serotonin-1A receptor (5-HT_1AR) and peroxisome proliferator-activated receptor-gamma (PPARɣ), and the novel targets, chemokine receptor type-4 (CXCR4) and neuropeptide S receptor (NPSR).</p><p><strong>Key results: </strong>Acute CBD dose dependently suppressed binge-like drinking and blood ethanol concentration. The effect was not driven by locomotor impairments and was maintained across sub-chronic treatment. Blockade of 5-HT_1AR and PPARɣ had no impact on CBD's reduction of alcohol consumption. Co-administration of subthreshold CBD doses and a NPSR antagonist implicated NPSR blockade as a potential mechanism contributing to CBD's effect, whereas co-administration of CBD and a CXCR4 antagonist suggested CXCR4 was not involved. However, the potent and selective CXCR4 antagonist AMD3100 reduced ethanol consumption.</p><p><strong>Conclusions and implications: </strong>CBD represents a promising candidate to reduce voluntary alcohol consumption. Mechanisms driving CBD's alcohol-related effects remain unclear and may involve polypharmacology, including actions at the NPSR identified in the present study.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144156962","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":"Neuropsychopharmacology of hallucinogenic and non-hallucinogenic 5-HT_2A receptor agonists.","authors":"Trevor Sharp, Aurelija Ippolito","doi":"10.1111/bph.70050","DOIUrl":"https://doi.org/10.1111/bph.70050","url":null,"abstract":"<p><p>Psychedelic drugs such as LSD and psilocin were once relegated to the fringes of medical research because of their association with counterculture movements and a perceived concern about harm through recreational use, and their consequent legal prohibition in the early 1970s. However, these drugs are now experiencing a renaissance in the field of psychiatry based on increasing evidence that they can produce long-lasting improvements in health across a wide variety of mental illnesses, including major depression, addictions and anxiety disorders. These drugs interact with many different 5-HT receptor subtypes but the powerful psychedelic experience, which (depending on set and setting) includes profound alterations in perception, mood and cognition, accompanied by vivid hallucinations, is now widely considered mediated by an agonist action at 5-HT_2A receptors. However, the link between the psychedelic experience, 5-HT_2A receptor agonism and therapeutic effects is currently uncertain. Indeed, recent research has revealed a new class of 5-HT_2A receptor agonists which appear to retain the therapeutic potential of psychedelics drugs without inducing disorienting hallucinatory experiences. Biased signalling, partial agonism and non-selectivity at the 5-HT_2A receptor are amongst the possible explanations for the differential properties of these drugs, whereas increased neuroplasticity offers a likely account of their common therapeutic effects. This article explores the neuropsychopharmacological properties of hallucinogenic and non-hallucinogenic 5-HT_2A receptor agonists in the context of their promise as novel drug treatments in psychiatry.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126820","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":"Nervonic acid, a long chain monounsaturated fatty acid, improves mitochondrial function in adrenomyeloneuropathy fibroblasts.","authors":"Chenxu Li, Marcia R Terluk, Reena V Kartha","doi":"10.1111/bph.70044","DOIUrl":"https://doi.org/10.1111/bph.70044","url":null,"abstract":"<p><strong>Background and purpose: </strong>Nervonic acid plays a vital role in maintaining normal brain and neuronal function. Nervonic acid has gained increasing attention because of its potential neuroprotective and anti-inflammatory properties. Nonetheless, the beneficial effects of nervonic acid are yet to be fully investigated. Adrenomyeloneuropathy (AMN), a type of X-linked adrenoleukodystrophy (ALD), is a progressive inherited metabolic disease characterised by accumulation of saturated very long-chain fatty acids (VLCFAs) in plasma and tissues, leading to increasing oxidative stress, mitochondrial dysfunction, neuroinflammation, cognitive dysfunction and disability. We previously found that nervonic acid can biochemically reverse the accumulation of saturated VLCFAs and increase cellular ATP production in ALD. Here, we investigated nervonic acid as a potential therapy for ALD by assessing its impact on mitochondrial function.</p><p><strong>Experimental approach: </strong>We assessed the effect of nervonic acid on cellular bioenergetics and oxidative stress in AMN patient-derived fibroblasts. We employed Seahorse real-time cell metabolic analysis and imaging of cells treated with increasing concentrations of nervonic acid. Normal dermal fibroblasts served as the healthy control.</p><p><strong>Key results: </strong>AMN cells demonstrate significantly impaired basal respiration, ATP production, maximal respiration and spare respiratory capacity compared to healthy fibroblasts. These mitochondrial respiration parameters significantly improved on treatment with nervonic acid in a concentration-dependent manner. Nervonic acid treatment also significantly reduced mitochondria-derived and total cellular reactive oxygen species, indicating mitigation of total oxidative stress.</p><p><strong>Conclusion and implications: </strong>Our findings indicate a new mechanism of action for nervonic acid in ALD and other mitochondrial dysfunction-associated diseases. This can also indirectly prevent downstream inflammation, thus altering disease progression.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144118850","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":"Casdatifan (AB521) is a novel and potent allosteric small molecule inhibitor of protumourigenic HIF-2α dependent transcription.","authors":"Patrick G Schweickert, Dana Piovesan, Casey G Mitchell, Bryan Zepeda-Carranza, Wandi S Zhu, Alejandra Y Lopez Espinoza, Lauren Rocha, Jaskirat Singh, Martin Ian P Malgapo, Cesar Meleza, Kyle R Northington, Rebecca D Ray, Xiaoning Zhao, Kenneth V Lawson, Matthew J Walters, Kelsey E Sivick","doi":"10.1111/bph.70075","DOIUrl":"https://doi.org/10.1111/bph.70075","url":null,"abstract":"<p><strong>Background and purpose: </strong>Hypoxia-inducible factor 2α (HIF-2α) is a transcription factor that mediates the expression of genes critical for cell adaptation and survival in low oxygen (hypoxic) conditions. In cancer, hypoxic conditions or molecular alterations within cancer cells can lead to HIF-2α accumulation and promote tumour growth and progression. Inactivating mutations in the von Hippel-Lindau (VHL) gene disable the oxygen-dependent HIF-2α degradation pathway and cause constitutive HIF-2α activity. VHL mutations are prevalent in clear cell renal cell carcinoma (ccRCC) where HIF-2α is a known tumourigenic driver. HIF-2α inhibition was shown to improve ccRCC patient outcomes clinically, warranting development of next-generation inhibitors.</p><p><strong>Experimental approach: </strong>Pharmacological effects of a novel small molecule allosteric inhibitor of HIF-2α, AB521 (casdatifan), were evaluated using in vitro cell-based assays and in vivo mouse models.</p><p><strong>Key results: </strong>AB521 inhibited HIF-2α-mediated transcription in cancer cells, endothelial cells, and M2-polarised macrophages. AB521 was selective for HIF-2α, displaying no activity against HIF-1α, and did not exhibit off-target cytotoxicity. When delivered orally to mice, AB521 caused dose-dependent decreases in HIF-2α-associated pharmacodynamic markers and significant regression of human ccRCC xenograft tumours. AB521 combined favourably with cabozantinib, a standard of care tyrosine kinase inhibitor, or zimberelimab, a clinical-stage anti-PD-1 antibody, in ccRCC xenograft studies.</p><p><strong>Conclusions and implications: </strong>AB521 is a potent, selective and orally bioavailable HIF-2α inhibitor, with favourable pharmacological properties, that is being explored clinically for the treatment of ccRCC.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144118847","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":"Dopamine D₃ receptor blockade accelerates the extinction of opioid withdrawal-induced drug-seeking behaviours and alters microglia in dopaminoceptive nuclei.","authors":"Aurelio Franco-García, Victoria Gómez-Murcia, M Victoria Milanés, Cristina Núñez","doi":"10.1111/bph.70081","DOIUrl":"https://doi.org/10.1111/bph.70081","url":null,"abstract":"<p><strong>Background and purpose: </strong>Among all drugs of abuse, opioids cause most of the deaths and treatment seeking. Despite abundant research in multifaceted therapeutic strategies, a high rate of relapse still characterises this condition. Dopamine D₃ receptor antagonists combined with cue-exposure therapies have been proposed to ameliorate the abused drugs-induced cognitive deficits, which consequently would aid to prevent the maladaptive behaviours responsible for drug use.</p><p><strong>Experimental approach: </strong>We used the morphine withdrawal-induced conditioned place aversion (CPA) paradigm to assess, in male rats, the efficacy of D₃ receptor blockade to improve the extinction of drug-seeking behaviours associated with the aversive contextual stimuli of its withdrawal. Then, using immunohistochemical methods, we evaluated the participation of neuroimmune mechanisms in the striatum and infralimbic cortex in D₃ receptor modulation of CPA extinction.</p><p><strong>Key results: </strong>Whereas the selective D₃ antagonist PG01037 accelerated the extinction of the morphine withdrawal-induced CPA, our findings indicate that decreased motivation might be involved in this action. Increased D₃ receptor expression in glial cells and the modulation of microglia activation state in specific dopaminoceptive areas could intervene in the behavioural outcomes of D₃ receptor blockade.</p><p><strong>Conclusions and implications: </strong>Our findings reveal a facilitatory role of D₃ antagonists in the inhibition of morphine-seeking behaviours triggered by contextual stimuli associated with its withdrawal. Nonetheless, their potential ability to reduce motivation might influence their therapeutic use. Future investigations elucidating the precise function of D₃ receptors will facilitate the identification of this receptor as a valuable therapeutic target for mitigating the recurrence of opioid withdrawal-induced drug-seeking behaviour.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":6.8,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144118849","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}