Toxicology and applied pharmacology最新文献

{"title":"Corrigendum to “the different impacts of ambient air pollution exposure on the risks of gestational hypertension and preeclampsia in twin pregnancies” [toxicology and applied pharmacology volume 503, October 2025, 117505]","authors":"Wei-Zhen Tang , Hong-Yu Xu , Qin-Yu Cai , Yun-Ren Pan , Hao-Wen Chen , Ya-Ting Jia , Tai-Hang Liu , Yong Heng Wang , Fei Han , Niya Zhou","doi":"10.1016/j.taap.2025.117511","DOIUrl":"10.1016/j.taap.2025.117511","url":null,"abstract":"","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"504 ","pages":"Article 117511"},"PeriodicalIF":3.4,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paracetamol exposure induces rapid alterations in the human plasma proteome","authors":"Mohammed A. Assiri ,&nbsp;Faris Almutairi ,&nbsp;Abdullah Alsulais ,&nbsp;Mohammed F. Alhamdan ,&nbsp;Omar A. Almohammed ,&nbsp;Fawaz Alasmari ,&nbsp;Nouf Albishi ,&nbsp;Ali Aghamdi ,&nbsp;Lamia AlMuhareb ,&nbsp;Rana AlMotawa ,&nbsp;Sara Alrasheed ,&nbsp;Feras S. Aldawsari ,&nbsp;Saud T. Aloyayd ,&nbsp;Abdullah A. Alhejji ,&nbsp;Abdulrazaq Albilali ,&nbsp;Riham A.ElToukhy ,&nbsp;Ghada A. Aldrees ,&nbsp;Doaa A. Bintaleb ,&nbsp;Hicham Benabdelkamel ,&nbsp;Assim A. Alfadda ,&nbsp;Sary Alsanea","doi":"10.1016/j.taap.2025.117501","DOIUrl":"10.1016/j.taap.2025.117501","url":null,"abstract":"<div><h3>Background</h3><div>Paracetamol is a widely used analgesic and antipyretic, yet its effect on human plasma proteome remains poorly characterized. This study aims to evaluate the impact of a single therapeutic dose of paracetamol on the plasma proteome, potentially providing insights into its pharmacological and toxicological pathways.</div></div><div><h3>Methods</h3><div>We conducted a cross-sectional study with 28 age-matched fasting subjects (14 controls and 14 treated with paracetamol). Anthropometric measurements and laboratory parameters were assessed, and blood samples were collected. An untargeted label-free LC-MS/MS approach, bioinformatics, and network pathway analysis were employed to examine changes in the proteomic profile.</div></div><div><h3>Results</h3><div>Proteomic analyses revealed significant differences in plasma protein abundance between the groups. A total of 78 dysregulated proteins were identified, with 23 upregulated and 55 downregulated in the paracetamol group. Transthyretin and vascular cell adhesion protein 1 were upregulated, while doublecortin domain-containing protein 1 and alpha-1-acid glycoprotein 1 were downregulated. These proteins were associated with key pathways, including ligand binding, Fc gamma receptor-dependent phagocytosis, and IL-12 signaling.</div></div><div><h3>Conclusion</h3><div>This proteomic analysis lays the groundwork for further studies to elucidate the mechanisms underlying paracetamol's therapeutic and toxicological effects by highlighting significant dysregulated proteins and related pathways.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"504 ","pages":"Article 117501"},"PeriodicalIF":3.4,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144813379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of hepatic and renal effects of acute and subacute oral exposure to bromochloromethane in rats","authors":"Jane Ellen Simmons ,&nbsp;TaCriasha L. Willoughby ,&nbsp;Mikayla D. Armstrong ,&nbsp;Maura J. Donohue ,&nbsp;A. McDonald ,&nbsp;Yusupha Mahtarr Sey","doi":"10.1016/j.taap.2025.117509","DOIUrl":"10.1016/j.taap.2025.117509","url":null,"abstract":"<div><div>Bromochloromethane (BCM) is a disinfection byproduct (DBP) formed in drinking water when oxidizing disinfectants (i.e., chlorine) react with natural organic matter. BCM is structurally analogous to other DBPs, such as chloroform and bromodichloromethane, that have human health effects, specifically hepatic or renal toxicity. Given the lack of robust studies in rodents and the structural similarity of BCM to known liver and kidney toxicants, the current study was designed to examine the potential for hepatotoxicity or nephrotoxicity from either acute or subacute oral exposure to BCM in male and female Fischer 344 rats. Biomarkers of liver and kidney injury were evaluated in serum and urine samples. In the acute exposure study to 1000 mg/kg body weight BCM, there was little evidence of liver or kidney toxicity. In the subacute exposure studies to 1000 mg/kg body weight BCM, lethality occurred in both male and female rats following multiple oral doses. In the subacute exposure to 750 mg/kg/day BCM, there were only temporary changes to hepatic biomarkers in females, and there were no histological changes observed. These oral gavage studies indicate that BCM is less toxic to the liver and the kidney relative to their structural analogs.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"504 ","pages":"Article 117509"},"PeriodicalIF":3.4,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gestational exposure to micro and nanoplastics differentially impactscardiac development and function in male and female rats throughout the lifespan","authors":"Chelsea M. Cary ,&nbsp;Samantha Adams ,&nbsp;Gina M. Moreno ,&nbsp;Talia N. Seymore ,&nbsp;Marianne Polunas ,&nbsp;Michael J. Goedken ,&nbsp;Xiang Wang ,&nbsp;Edward J. Yurkow ,&nbsp;Phoebe A. Stapleton","doi":"10.1016/j.taap.2025.117507","DOIUrl":"10.1016/j.taap.2025.117507","url":null,"abstract":"<div><div>Micro- and nanoplastics (MNPs) are a ubiquitous contaminant. Identification of MNPs in the human placenta suggests this toxicant poses a danger to developing offspring. Previously, we demonstrated that maternal pulmonary MNP exposure restricts fetal growth and disrupts fetoplacental cardiovascular function in rats. Herein, we investigated how repeated maternal inhalation of polyamide-12 MNP from gestational day 4–19 during pregnancy (10 mg/m³, geometric mean 175.8 ± 1.9 nm, mode particle size 19 nm, size range 6 nm-8 μm) in Sprague Dawley rats influences cardiovascular development and function in male and female offspring at gestational day 20, 2 weeks, 1 month and 3 months of age. Exposed neonates demonstrated decreased relative left ventricle wall thickness while dilation of the left ventricle was identified in MNP-exposed adolescents and adults. Analyses of offspring myocardial mRNA suggest that maternal MNP exposure disrupted mitochondrial function, calcium handling, and defense against oxidative species. MNP exposure increased blood flow velocity within the left ventricle, decreased fractional shortening, and increased relative cardiac output at the fetal, adolescent and adult stages, respectively. Although variable, select experimental outcomes were changed in a sexually dimorphic manner after gestational MNP.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"504 ","pages":"Article 117507"},"PeriodicalIF":3.4,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144813855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The hepatic and developmental toxicity of chronic morphine and disulfiram co-treatment for pain relief - a comprehensive in vitro and in vivo assessment","authors":"Zuzanna Zelazewska ,&nbsp;Marzena Lazarczyk ,&nbsp;Justyna Paszkiewicz ,&nbsp;Marta Marszalek-Grabska ,&nbsp;Kinga Gawel ,&nbsp;Agata Nawrocka ,&nbsp;Patrycja Andrzejuk ,&nbsp;Mariusz Sacharczuk ,&nbsp;Anna Lesniak","doi":"10.1016/j.taap.2025.117499","DOIUrl":"10.1016/j.taap.2025.117499","url":null,"abstract":"<div><div>Tolerance and opioid-induced hyperalgesia are clinically relevant side effects that may hinder prolonged opioid use. Recent studies report that disulfiram – a drug registered for alcohol use disorder, fully suppresses their onset. Unfortunately, morphine exacerbating the risk of disulfiram-induced acute liver injury has recently been reported. However, the single dose of disulfiram used, vastly exceeded that effective for pain relief. Hence, this study aimed to comprehensively reevaluate the interaction of disulfiram and morphine in terms of liver and developmental toxicity in various models. The antiproliferative effect was studied in the MTS test in human HepG2 cells, following a 5–day exposure to disulfiram and morphine. Cytotoxicity was determined in the lactate dehydrogenase (LDH) assay. Developmental toxicity was assessed in zebrafish larvae by studying hatching rate, morphology, and locomotor activity, following 24 h and 5–day exposure. Liver function markers were tested in rat serum following 19 days of morphine and disulfiram co-treatment. We determined that the combination of morphine and low-dose disulfiram exerted a synergistic antiproliferative effect in HepG2 cells, but was not cytotoxic. However, it delayed the zebrafish hatching rate by 21 % and impaired swim bladder inflation in a concentration-dependent manner. In clinically relevant doses, disulfiram decreased serum alkaline phosphatase levels in morphine-treated rats, but not outside the physiological range. The potential use of disulfiram as a co-analgesic in morphine therapy is not associated with significant liver toxicity, but could potentially be limited in subjects with impaired liver function. Morphine and disulfiram co-treatment may also have a potentially negative impact on lung organogenesis.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"504 ","pages":"Article 117499"},"PeriodicalIF":3.4,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Scorpion venom peptide S6540 induces caspase-independent apoptosis in non-small cell lung cancer A549 cells","authors":"Xilong Wang ,&nbsp;Yihan Gao ,&nbsp;Tienthanh Nguyen ,&nbsp;Jinwei Chai ,&nbsp;Xin Chen ,&nbsp;Xueqing Xu","doi":"10.1016/j.taap.2025.117498","DOIUrl":"10.1016/j.taap.2025.117498","url":null,"abstract":"<div><div>Lung cancer remains the leading cause of cancer death. Despite being effective in cancer treatment, the limitation of conventional chemotherapies that involve non-selective cytotoxicity and drug resistance leads to the urgent need for alternatives. Herein, we present the antitumor activity of S6540, a non-disulfide-bridge peptide identified from the venom gland of <em>Superstitionia donensis</em>. S6540 was found to enter the cell, target its mitochondria, induce caspase-independent apoptosis, and finally suppress the cell viability of A549 cells. Furthermore, S6540 could reduce the presence of Bcl-2 in mitochondrial membranes, induce apoptosis-inducing factor nuclear translocation, and suppress PI3K/Akt signaling pathway activation. <em>In vivo</em>, S6540 suppressed tumor growth in the A549 tumor xenograft model with a lower negative effect than Cisplatin. Accordingly, this study shed light on the antitumor mechanism of S6540, which may contribute to its further development as a potential agent in treating lung cancer cells.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"504 ","pages":"Article 117498"},"PeriodicalIF":3.4,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"S100A11 mediates the protective effects of edaravone dexborneol on docetaxel-induced cognitive impairment in rats by inhibiting the MAPK signaling pathway","authors":"Ping Liu ,&nbsp;Jiantao Jia ,&nbsp;Yinliang Lu ,&nbsp;Hanmin Tang ,&nbsp;Chengyi Gao ,&nbsp;Suxia Han","doi":"10.1016/j.taap.2025.117504","DOIUrl":"10.1016/j.taap.2025.117504","url":null,"abstract":"<div><div>Cognitive impairment is a common side effect of docetaxel (DTX)-based chemotherapy. The novel neuroprotective agent edaravone dexborneol (ED) was found to alleviate the adverse phenotype caused by DTX. However, the underlying mechanism remains unexplored. By analyzing mRNA-sequencing data, we noticed that the expression of S100 calcium-binding protein A11 (S100A11), a protector of the nervous system, was decreased in DTX-treated rats with cognitive damage, but ED administration reversed the trend. Therefore, we speculated that S100A11 might be involved in the protective effects of ED on DTX-induced cognitive impairment. Sprague-Dawley rats were intraperitoneally injected with DTX to induce cognitive impairment, followed by intraperitoneal injection of ED after DTX induction. The results showed that ED treatment mitigated cognitive impairment caused by DTX. Next, adenoviruses carrying sequences encoding S100A11 were given to rats receiving DTX treatment. S100A11 overexpression alleviated cognitive dysfunction of DTX-treated rats, as evidenced by the decreased escape latency and swimming distance, and the increased number of platform crossings. Mechanically, S100A11 overexpression inhibited neuronal apoptosis by inactivating the MAPK signaling pathway. Further rescue experiments showed that S100A11 knockdown reversed the defensive role of ED in DTX-induced neuronal damage. In conclusion, ED ameliorates cognitive dysfunction caused by DTX by upregulating the S100A11 expression and subsequently inactivating the MAPK signaling pathway.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"504 ","pages":"Article 117504"},"PeriodicalIF":3.4,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144804919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Carcinogenicity of some metals evaluated by the IARC Monographs: A synopsis of the evaluations of arsenic, cadmium, cobalt, and antimony","authors":"Aline de Conti ,&nbsp;Federica Madia,&nbsp;Mary K. Schubauer-Berigan,&nbsp;Lamia Benbrahim-Tallaa","doi":"10.1016/j.taap.2025.117506","DOIUrl":"10.1016/j.taap.2025.117506","url":null,"abstract":"<div><div>Metals represent a major area of concern due to their extensive industrial applications, environmental persistence, and well-documented adverse health effects. Notably, metals (and metalloids) such as arsenic, cadmium, beryllium, chromium, cobalt, lead, and nickel are known for their toxicity and carcinogenic potential, raising significant public health concerns. Human exposure to these metals occurs through different routes, posing both environmental and workplace hazards. The <em>Monographs</em> programme of the International Agency for Research on Cancer (IARC) plays a critical role in identifying carcinogenic hazards to humans, providing a robust scientific foundation for global actions to prevent cancer. This review focuses on selected metals and metalloids: arsenic, cadmium, cobalt, and antimony, emphasizing how the IARC evaluation process considers the biological properties of the metals and their compounds, and the evidence from experimental animal studies and mechanistic data, including the application of the key characteristics of carcinogens (KCs) framework, in determining carcinogenic potential. The <em>IARC Monographs</em> contribute to a comprehensive understanding of metal-induced carcinogenicity and reinforce the importance of systematic, evidence-based approaches to inform public health interventions and regulatory decision-making.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"504 ","pages":"Article 117506"},"PeriodicalIF":3.4,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144804917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of the teratogenic toxicity of disperse blue 79 on pregnant rats and their fetuses","authors":"Fang Tan ,&nbsp;Pingjing Wen ,&nbsp;Yixin Ye,&nbsp;Yafei Wang,&nbsp;Penghe Liu,&nbsp;Guangqiu Qin","doi":"10.1016/j.taap.2025.117500","DOIUrl":"10.1016/j.taap.2025.117500","url":null,"abstract":"<div><div>Disperse Blue 79 (DB79), an azo dye dispersant, is widely used across various industries, thereby increasing the likelihood of human exposure to this substance. However, research on the toxicological effects of DB79 remains limited, especially concerning its potential teratogenic toxicity. This study aims to assess the toxicological effects of DB79 on pregnant rats and their fetuses following exposure during pregnancy. A total of 60 pregnant Sprague-Dawley (SD) rats were randomly assigned to 5 groups, including 3 treatment groups, a negative control group, and a positive control group. The treatment groups were orally exposed to DB79 at doses of 100, 10, and 1 mg/kg, respectively, while the negative control group received distilled water, and the positive control group received 300 mg/kg of aspirin. The rats received daily oral gavage from the 6th to the 15th day of gestation, and were euthanized on the 20th day of gestation for maternal and fetal examinations. The results indicate that no significant changes in body weight or clinical symptoms were observed in pregnant rats exposed to DB79 at doses up to 100 mg/kg. Additionally, no adverse effects were noted on fetal weight, skeletal development, or internal organs. These findings indicated that DB79 demonstrates little teratogenic toxicity under the conditions of this study. Consequently, the no observed adverse effect level (NOAEL) for DB79 can be established at 100 mg/kg body weight in SD rats.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"503 ","pages":"Article 117500"},"PeriodicalIF":3.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144781279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network pharmacology and experimental validation reveal Thiamphenicol ameliorates dextran sulfate sodium-induced colitis in mice via inhibition of intestinal senescence and modulation of the NF-κB/AMPK signaling pathway","authors":"Bingxiang Zhao ,&nbsp;Zhenlin Liu ,&nbsp;Li Xiang ,&nbsp;Shujia Song ,&nbsp;Yaxing Xu ,&nbsp;Fuxing Li ,&nbsp;Zhengze Liu ,&nbsp;Zhenxiong Yang ,&nbsp;Mingzhu Li ,&nbsp;Lihua Li ,&nbsp;Xiaobo Wang","doi":"10.1016/j.taap.2025.117497","DOIUrl":"10.1016/j.taap.2025.117497","url":null,"abstract":"<div><h3>Background</h3><div>Ulcerative colitis (UC), as a prevalent subtype of inflammatory bowel disease (IBD), is a chronic, non-specific inflammatory bowel disease characterized by persistent inflammation of the colonic mucosa, impaired intestinal barrier function, and recurrent clinical manifestations such as diarrhea and hematochezia. Recent studies have revealed that cellular senescence plays a pivotal role in UC pathogenesis, wherein senescent cells exacerbate intestinal inflammation through the secretion of the senescence-associated secretory phenotype (SASP), which primarily consists of pro-inflammatory factors. Thiamphenicol (TP), a broad-spectrum antibiotic, has exhibited promising anti-inflammatory and senescence-modulating properties beyond its conventional antimicrobial effects.</div></div><div><h3>Methods</h3><div>This study aimed to investigate whether TP alleviates dextran sulfate sodium (DSS)-induced UC in mice by mitigating cellular senescence and modulating the NF-κB/AMPK signaling pathway. DSS-induced senescence models in NCM460 cells and DSS-induced murine UC models were established to systematically evaluate the effects of TP on cellular senescence, colonic inflammation, and intestinal barrier function; network pharmacology and in vivo/in vitro experiments were employed to validate its regulatory role in the NF-κB/AMPK pathway.</div></div><div><h3>Results</h3><div>TP significantly reduced senescent cell accumulation, downregulated pro-inflammatory cytokines (IL-1, IL-6, TNF-α) via NF-κB/AMPK modulation, attenuated DSS-induced colitis, and restored the expression of tight junction proteins (ZO-1, Occludin, Claudin-1), thereby improving intestinal barrier integrity.</div></div><div><h3>Conclusion</h3><div>TP ameliorates cellular senescence and inflammatory responses through modulation of the NF-κB/AMPK pathway, thereby providing novel insights into and potential therapeutic strategies for UC treatment.</div></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"503 ","pages":"Article 117497"},"PeriodicalIF":3.4,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144765579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}