Muhammad Adil Malik, Quan Zhuang, Junjie Huang, Xu Cao
{"title":"A comprehensive review on the role of PM2.5 in modulating transplant immunity and graft survival.","authors":"Muhammad Adil Malik, Quan Zhuang, Junjie Huang, Xu Cao","doi":"10.1186/s12989-026-00660-1","DOIUrl":"10.1186/s12989-026-00660-1","url":null,"abstract":"<p><p>Organ transplantation is an indispensable therapeutic approach for patients experiencing end-stage organ failure. Despite ongoing advancements and refinements in immunosuppressive therapies aimed at mitigating graft rejection and enhancing graft longevity, environmental influences including particulate matter 2.5 (PM2.5) have emerged as significant determinants of post-transplant health. PM2.5, a prevalent environmental contaminant, is particularly concerning due to its widespread presence and detrimental biological effects. Notably, the living environment of transplant recipients further exacerbates the complexity of post-transplant outcomes. Evaluating findings from recent investigations, this review delves into the influence of PM2.5 exposure on the immune system. The findings identify its capacity to provoke systemic inflammation, disrupt cytokine profiles, and compromise immune tolerance mechanisms. Such immune dysfunction poses direct risks to graft integrity, with potential implications for both graft health and the prospects of achieving long-term graft survival in affected patients.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":"23 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13036968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147593828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Small particles, large questions: unravelling the toxicity and potential health risks of PET micro-/nanoplastics.","authors":"Michaela Hanzlova, Drahomira Holmannova, Tereza Svadlakova, Zdenek Fiala","doi":"10.1186/s12989-026-00673-w","DOIUrl":"10.1186/s12989-026-00673-w","url":null,"abstract":"<p><p>Despite the extensive use of polyethylene terephthalate (PET), the public health implications of its micro- and nanoparticles (MNPs) remain poorly understood, raising credible concerns about human exposure and health risks. We conducted a comprehensive literature search to synthesise evidence on human exposure to PET MNPs, their detection in human tissues and biological fluids, and the human-relevant toxicity of PET particles in vitro and in vivo. Studies consistently identify PET MNPs across consumer and environmental sources, and several investigations have detected PET in human matrices, supporting the plausibility of systemic translocation across biological barriers. Toxicological findings consistently indicate size- and shape-dependent uptake and effects: smaller particles exhibit greater cellular internalisation, reactivity, and biodistribution, with predominant oxidative, inflammatory, metabolic, and genotoxic responses, whereas larger microplastics more often provoke mechanical irritation. Key gaps include limited protocol harmonisation, unrealistic exposure levels, scarce long-term/kinetic data, and insufficiently standardised, well-characterised PET MNPs preparations. While evidence for exposure, detection in human matrices, and biological activity is growing, these deficits still hinder robust cross-study comparisons and clinically meaningful quantitative risk assessment.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13064395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147530749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dirk Broßell, Asmus Meyer-Plath, Oliver Gräb, Elisabeth Heunisch, Kerstin Kämpf, Andrea Haase, Martin Wiemann
{"title":"Macrophages bend long fibres with flexural rigidity lower than 3 mN·nm<sup>2</sup> to avoid frustrated phagocytosis.","authors":"Dirk Broßell, Asmus Meyer-Plath, Oliver Gräb, Elisabeth Heunisch, Kerstin Kämpf, Andrea Haase, Martin Wiemann","doi":"10.1186/s12989-026-00666-9","DOIUrl":"10.1186/s12989-026-00666-9","url":null,"abstract":"<p><strong>Background: </strong>It is an established toxicological principle that the inhalation pathogenicity of respirable and biodurable fibres is caused by excessive fibre length as alveolar macrophages fail to uptake and remove such fibres. However, studies on carbon nanotubes showed that this principle needs revision, as thin, flexible variants showed reduced fibre-specific toxicity. One potential explanation is that the low flexural rigidity of thin fibres enables macrophages to bend and internalize even those that are long relative to the cell size. To evaluate this proposed \"rigidity hypothesis,\" the mechanisms governing the uptake of flexible long fibres that determine a critical threshold value for flexural rigidity require clarification.</p><p><strong>Methods: </strong>We exposed NR8383 rat alveolar macrophages to three silver nanowire variants differing in diameter and length. Time-lapse microscopy captured fibre uptake processes. Successful internalization of long fibres was found to require fibre bending during uptake. A mechanical model was developed by combining established cytoskeletal biophysics with the observed fibre deformation dynamics. As flexural rigidity describes fibre behaviour under load, our model estimated rigidity by reproducing the observed bent fibre shape. By defining limit cases for physically 'weak' and 'strong' NR8383 macrophages, i.e., assuming upper bounds on the forces generated by their cytoskeletal nanomachinery, our model enabled us to derive a range for the critical fibre rigidity threshold.</p><p><strong>Results and conclusion: </strong>A macrophage was observed bending an exceptionally long fibre (~ 140 μm) first into an arc and then a spiral for full internalization, initiated by a pseudopod extending along the fibre and buckling the internalized segment. Our model can reproduce such behaviour. It yielded a flexural rigidity of 20 mN·nm² for this fibre. Predicted critical rigidity limits for fibres that just fit into NR8383 macrophages range from 3 to 62 mN·nm². Using the conservative lower bound, long and biodurable fibres with a rigidity lower than 3 mN·nm² are expected to be readily phagocytized by this cell line. Although this rigidity scale may not be directly translatable to human alveolar macrophages, our experimental findings and their modeling emphasize the key role of rigidity in fibre-cell interactions. Fibre rigidity is therefore central for material safety aspects and sustainable product design.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":"23 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12998087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147474873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lan Ma-Hock, Heidi Stratmann, Matthias Hufnagel, Anthony M Bowden, Blanca Serrano Ramón, David Warheit, Rüdiger Battersby, Shannon M Krieger, Marco Kellert, Nils Krueger, Bennard van Ravenzwaay, Robert Landsiedel, Helmut Greim
{"title":"A quantitative definition for poorly soluble particles.","authors":"Lan Ma-Hock, Heidi Stratmann, Matthias Hufnagel, Anthony M Bowden, Blanca Serrano Ramón, David Warheit, Rüdiger Battersby, Shannon M Krieger, Marco Kellert, Nils Krueger, Bennard van Ravenzwaay, Robert Landsiedel, Helmut Greim","doi":"10.1186/s12989-026-00670-z","DOIUrl":"10.1186/s12989-026-00670-z","url":null,"abstract":"<p><p>Poorly soluble low toxicity particles (PSLT) have long been a concept in particle toxicology and regulatory frameworks addressing inhalation hazards. The term PSLT refers to particles that exhibit low toxicity and minimal solubility in biological fluids, leading to prolonged retention in the lungs and potential overload effects. Historically, PSLT has been used to distinguish materials whose adverse effects are primarily driven by particle burden rather than intrinsic chemical toxicity. While the \"low toxicity\" (LT) component of the definition has been examined to a certain degree (Driscoll and Borm in Inhal Toxicol 32(2):53-62, 2020), the poorly soluble (PS)-criterion does not yet have a precise definition although it is critically influencing the interpretation of toxicological inhalation repeated dose studies and hazard classifications. An ECETOC Task Force (TF) was formed to define criteria for \"poorly soluble\" particles (PSPs). This paper presents a quantitative non-animal approach for defining PSP using a model particle, with a focus on its potential to cause volumetric lung overload and affect macrophage clearance mechanisms. The analysis allows to calculate a dissolution rate that would lead to a lung burden of about 1 µL/g of lung tissue (lung overload threshold according to Morrow (Morrow in Fundam Appl Toxicol 10(3):369, 1988)). Below this threshold dissolution rate, this specific model particle would qualify as PSP. In addition, a formula was presented to translate abiotic dissolution rates into biotic (rat) dissolution rates to allow a PS-assessment in an animal-free system. As proof of concept, the TF collected existing in vivo data from member companies, publicly available literature of presumed PS-substances, and reference materials. The collected data revealed that most substances exhibited dissolution rates below the critical threshold and that the lung burden at no observed adverse effect concentrations (NOAECs) remained below the lung overload limit. Importantly, this threshold dissolution rate can differ from particle to particle, depending on factors such as agglomerate density, particle size distribution, and expected concentration. Thus, it should be evaluated on a case-by-case basis.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":"23 1","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12983584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nádia Vital, Célia Ventura, Camila Fernandes, Luís Vieira, Ana Valente, Michel Kranendonk, Maria João Silva, Henriqueta Louro
{"title":"The effects of ingested cellulose nanomaterials on DNA methylation in intestinal cells.","authors":"Nádia Vital, Célia Ventura, Camila Fernandes, Luís Vieira, Ana Valente, Michel Kranendonk, Maria João Silva, Henriqueta Louro","doi":"10.1186/s12989-026-00672-x","DOIUrl":"https://doi.org/10.1186/s12989-026-00672-x","url":null,"abstract":"<p><strong>Background: </strong>Cellulose nanomaterials (CNMs) are emerging materials under development for various applications in biomedicine and the food industry. Consequently, their potential human health effects warrant evaluation, particularly after oral exposure. Previous studies on two innovative CNMs, CNF-TEMPO and CMF-ENZ, indicated that genotoxicity could not be ruled out, as DNA damage was observed in Caco-2 cells. Whether these CNMs may affect gene expression regulation and induce downstream effects not assessed through genotoxicity testing, is still an open question. This work presents a new approach methodology coupling in vitro simulated digestion with epigenomics, to investigate changes in DNA methylation upon exposure of intestinal cells to these CNMs.</p><p><strong>Results: </strong>DNA methylation patterns differed upon cell exposure to undigested or digested samples, showing a trend towards hypermethylation for undigested and hypomethylation for digested samples. Using Reduced Representation Bisulfite Sequencing, significant differentially methylated regions (DMR) and genes were identified in undigested and digested CNMs-exposed cells. Pathway analysis revealed that CNMs influenced multiple signal transduction pathways. CMF-ENZ and CNF-TEMPO impacted glycosaminoglycan metabolism and glycosylation pathways, possibly involved in cell proliferation. CMF-ENZ affected a DNA repair pathway, while CNF-TEMPO impacted pathways associated with glucose metabolism, independently of the digestion process. Both CNMs seemed to affect pathways implicated in overall cytoskeletal and extracellular matrix dynamics. For digested CNMs, particularly digested CNF-TEMPO, this impact suggests a possible deleterious disturbance given the involvement of ERBB2/PIK3 signaling.</p><p><strong>Conclusions: </strong>This study shows that CNMs may have a biological effect on Caco-2 cells, affecting DNA methylation, and highlights the importance of epigenetic analysis in pointing out the way for unraveling the mechanisms underlying their toxicity.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Inhibition of PADI2-mediated vimentin citrullination alleviates silica-induced pulmonary fibrosis in mice.","authors":"Fuyu Jin, Yaqian Li, Tian Li, Shupeng Liu, Dingjie Xu, Heliang Liu, Zhongqiu Wei, Xuemin Gao, Na Mao, Wenchen Cai, Yiwei Shi, Haibo Zhang, Hong Xu","doi":"10.1186/s12989-026-00671-y","DOIUrl":"10.1186/s12989-026-00671-y","url":null,"abstract":"<p><p>Silicosis remains a critical occupational health concern worldwide, lacking effective treatments due to unclear mechanisms. In this study, we investigated the citrullinated proteomic profile and its effects in mice exposed to silica. Our findings demonstrated elevated levels of citrullinated peptides and citrullinated vimentin (Cit-Vim) in silicotic mice and silica-treated macrophages, regulated by peptidylarginine deiminase (PADI2). Unlike vimentin, Cit-Vim amplified the production of tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6), and IL-1β in silica-treated macrophages through interaction with Toll-like receptor 4 (TLR4) signaling. RNA sequencing revealed that early growth response protein 1 (EGR1) is a target of PADI2, with Cit-Vim inducing lung inflammation via EGR1 signaling. Pharmacological inhibition or genetic knockout of Padi2 attenuated silica-induced lung inflammation and fibrosis. These findings suggest that targeting PADI2 may represent a novel therapeutic strategy of silicosis.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13019754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147373062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Haonan Li, Elizabeth A Holzhausen, Devendra Paudel, Nathan D Young, Jonatan Ottino-González, Frederick W Lurmann, Douglas I Walker, Howard H Chang, Donghai Liang, Ravi Bansal, Michael I Goran, Bradley S Peterson, Tanya L Alderete
{"title":"Associations of prenatal fine particulate matter mixtures with neurodevelopmental outcomes in early childhood: component- and source-specific insights.","authors":"Haonan Li, Elizabeth A Holzhausen, Devendra Paudel, Nathan D Young, Jonatan Ottino-González, Frederick W Lurmann, Douglas I Walker, Howard H Chang, Donghai Liang, Ravi Bansal, Michael I Goran, Bradley S Peterson, Tanya L Alderete","doi":"10.1186/s12989-025-00657-2","DOIUrl":"10.1186/s12989-025-00657-2","url":null,"abstract":"","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12990619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147326835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gang Liu, Qiuya Cai, Tingchen Qin, Xiatian Yu, Binbin Pan, Lin Ye, Lisha Jia, Xianwei Wang
{"title":"Emerging cardiovascular risks of micro- and nanoplastics: toxic effects and mechanistic pathways.","authors":"Gang Liu, Qiuya Cai, Tingchen Qin, Xiatian Yu, Binbin Pan, Lin Ye, Lisha Jia, Xianwei Wang","doi":"10.1186/s12989-026-00669-6","DOIUrl":"10.1186/s12989-026-00669-6","url":null,"abstract":"<p><p>Micro- and nanoplastics (MNPs), due to their widespread distribution and chemical stability, have emerged as novel environmental contaminants threatening cardiovascular health. Evidence links MNPs to conditions such as atherosclerosis, cardiac fibrosis, myocardial infarction, and other cardiovascular diseases (CVDs). Recently, MNPs have been found within atherosclerotic plaques and in the myocardial tissues of surgery patients, highlighting their close association with cardiovascular pathology. Investigations have demonstrated that MNPs can enter the human body through oral ingestion, inhalation, dermal contact, and medical procedures, and subsequently accumulate in the blood, blood vessels, and cardiac tissues. Once deposited, these particles induce oxidative and endoplasmic reticulum stress, disrupt mitochondrial function, and activate inflammatory signaling pathways, ultimately triggering cell death. These processes contribute to endothelial dysfunction, cardiac damage and fibrosis, vascular smooth muscle cell phenotypic switching, and macrophage foam cell formation, thereby likely contributing to the onset and progression of CVDs. Despite these findings, the potential cardiovascular risks of MNPs and the underlying mechanisms remain largely unexplored. This review summarizes the basic properties of MNPs, their biodistribution within the cardiovascular system, toxic effects, and underlying molecular mechanisms, providing a foundation for future risk assessment and the development of preventive strategies.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13001288/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jialyu Huang, Yiwei Zhang, Penghui Nie, Qimei Luo, Rili Hu, Ruiying Zhang, Yan Zhao, Maolin Yu, Hengyi Xu
{"title":"Gut-ovary axis mediated synergistic reproductive toxicity of polystyrene nanoplastics and perfluorobutanoic acid co-exposure: pyroptotic signaling and probiotic mitigation.","authors":"Jialyu Huang, Yiwei Zhang, Penghui Nie, Qimei Luo, Rili Hu, Ruiying Zhang, Yan Zhao, Maolin Yu, Hengyi Xu","doi":"10.1186/s12989-026-00667-8","DOIUrl":"10.1186/s12989-026-00667-8","url":null,"abstract":"<p><p>Polystyrene nanoplastics (PS-NPLs) and perfluorobutanoic acid (PFBA) are pervasive contaminants of great concern and can enter human body primarily through gastrointestinal tract. However, their single and combined effects on female reproductive health remain poorly explored. In this study, PFBA was found to be adsorbed onto PS-NPLs through both chemical and physical interactions. Compared with single exposure, co-exposure to PS-NPLs (0.04 mg/d) and PFBA (0.28 mg/d) for 28 days caused more severe ovarian toxicity in rats, as evidenced by decreased primordial follicles, increased follicular atresia, and sex hormone abnormalities. Mechanistically, the co-exposure was associated with the gut barrier damage and elevated levels of lipopolysaccharide in the bloodstream, concomitant with altered redox homeostasis, inflammation and NLRP3/caspase-1-related pyroptosis of the ovary. Moreover, supplementation with probiotic Lactiplantibacillus plantarum P101 partially attenuated ovarian injury via modulating gut microbiota and mitigating the above process. Taken together, our study revealed a synergistic impact of PS-NPLs and PFBA on female reproduction, uncovered the underlying mechanisms from the perspective of gut-ovary axis, and provided valuable insights into potential preventive strategies.</p>","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12961878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146776549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wenting Zhang, Muhammad Daniyal Ghouri, Magda Blosi, Ying Liu, Chunying Chen, Flemming R Cassee, Rong Cai
{"title":"A comparative biodistribution and toxicity study of single and multi-component nanomaterials: NMs: TiO<sub>2</sub>, SiC, and SiC@TiO<sub>2</sub>.","authors":"Wenting Zhang, Muhammad Daniyal Ghouri, Magda Blosi, Ying Liu, Chunying Chen, Flemming R Cassee, Rong Cai","doi":"10.1186/s12989-026-00664-x","DOIUrl":"10.1186/s12989-026-00664-x","url":null,"abstract":"","PeriodicalId":19847,"journal":{"name":"Particle and Fibre Toxicology","volume":" ","pages":""},"PeriodicalIF":8.2,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146228069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}