Microbes and Infection最新文献

{"title":"Porphyromonas gingivalis inhibits ferroptosis and promotes malignant phenotype in oral squamous cell carcinoma cells via upregulation of SIRT5.","authors":"Yiqun Jia, Jing Ou, Hongxia You, Weixuan Chen, Yuyan Zheng","doi":"10.1016/j.micinf.2025.105564","DOIUrl":"10.1016/j.micinf.2025.105564","url":null,"abstract":"<p><strong>Introduction: </strong>Oral squamous cell carcinoma (OSCC) exhibits aggressive behavior and poor prognosis. Porphyromonas gingivalis (P. gingivalis) affects the tumor microenvironment, but its role in ferroptosis inhibition in OSCC remains unclear. This study explores the impact of P. gingivalis on ferroptosis through SIRT5 upregulation.</p><p><strong>Materials and methods: </strong>OSCC cell lines (Cal27, SCC9) were treated with the ferroptosis inducer RSL3, with or without P. gingivalis infection. Cell viability, ferroptosis markers (MDA, ROS, GPX4), and cell behavior (proliferation, migration, invasion) were assessed. SIRT5 and downstream targets (IDH2, GCLC) were analyzed using Western blot, qRT-PCR, and immunofluorescence. A SIRT5 knockdown model was used to evaluate its role in ferroptosis resistance.</p><p><strong>Results: </strong>P. gingivalis infection increased OSCC cell survival, reduced ROS and MDA levels, enhanced GPX4 expression, and promoted proliferation, migration, and invasion. Elevated SIRT5 and its targets IDH2 and GCLC were observed. SIRT5 knockdown reversed ferroptosis resistance.</p><p><strong>Conclusion: </strong>The findings suggest that P. gingivalis plays a critical role in promoting OSCC malignancy by inhibiting ferroptosis through the upregulation of SIRT5. This highlights the potential of targeting SIRT5 as a therapeutic strategy to counteract the effects of P. gingivalis in OSCC.</p>","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105564"},"PeriodicalIF":2.7,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145251958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Haemophilus spp. in acute exacerbations of COPD and co-occurrence of selected microbiota components.","authors":"Weronika Gawor, Katarzyna Góralska, Sandra Wysocka, Sebastian Majewski, Wojciech Piotrowski, Joanna Miłkowska-Dymanowska, Ewa Brzeziańska-Lasota","doi":"10.1016/j.micinf.2025.105568","DOIUrl":"10.1016/j.micinf.2025.105568","url":null,"abstract":"<p><p>Most studies on Haemophilus influenzae in the course of COPD focus on occurrence of this species in the respiratory tract. However, the relationship between the intestinal microbiota and the respiratory tract, may play a role in the course of COPD. Our study examined the presence of Haemophilus spp. in the oral cavity, respiratory tract and large intestine, and the level of anti-H. influenzae antibodies in patients during acute exacerbations of COPD (AECOPD). An additional goal was to identify the potential microbiota components co-occurring with Haemophilus spp. The study included 35 patients with AECOPD and the control group (23 people). Haemophilus spp. were isolated from 20 % patients in the AECOPD and 17.39 % from the control group, the difference was not statistically significant (p = 0.74). Mean levels of anti-H. influenzae antibodies were 0.491 ± 0.871 μg/ml in the AECOPD group and 1.021 ± 1.421 μg/ml in the control group, the difference was not statistically significant (p = 0.332). Greater diversity within Streptococci and Gram-negative bacilli was found in biological materials from AECOPD. We noted a more common frequency of isolation of Haemophilus spp. from the large intestine of AECOPD, which may indicate the occurrence of gut dysbiosis during exacerbations. The analysis of selected associated species showed that the bacteriological status of a COPD patient may influence the frequency and course of exacerbations.</p>","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105568"},"PeriodicalIF":2.7,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145318565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exopolysaccharides from lactic acid bacteria: Structure, biosynthesis, and health benefits.","authors":"Lylia Ouarabi, Liza Ouarabi, Samia Hamma-Faradji, Mari Luz Mohedano, Paloma López, Djamel Drider","doi":"10.1016/j.micinf.2025.105581","DOIUrl":"10.1016/j.micinf.2025.105581","url":null,"abstract":"<p><p>Exopolysaccharides (EPS) are extracellular metabolites secreted by various bacteria, including lactic acid bacteria (LAB). EPS vary in structure and their composition depends on a number of production factors. In particular, they are used as thickeners to improve the organoleptic properties of foods. In any case, they can also have beneficial effects on human well-being, such as prebiotic effects, antioxidant effects, antimicrobial effects, and modulation of the immune system. This review aims to summarize the results of recent research on EPS produced by LAB in the regulation of intestinal health by acting as prebiotic and antimicrobial agents, as well as their antioxidant, hypocholesterolemic and immunomodulatory effects.</p>","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105581"},"PeriodicalIF":2.7,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145329610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The unfolded protein response is a critical mediator in Campylobacter jejuni pathogenesis and host defence.","authors":"Geunhye Hong, Zahra Omole, Cadi Davies, Janie Liaw, Anna D Grabowska, Barbara Canonico, Nicolae Corcionivoschi, Brendan W Wren, Ezra Aksoy, Nick Dorrell, Abdi Elmi, Ozan Gundogdu","doi":"10.1016/j.micinf.2025.105582","DOIUrl":"10.1016/j.micinf.2025.105582","url":null,"abstract":"<p><p>Campylobacter jejuni is the major bacterial cause of foodborne gastroenteritis worldwide. How this pathogen interacts with the host defence machinery of human intestinal epithelial cells (IECs) and is involved in pathogenesis remains elusive. Bacterial pathogens utilise strategies to gain access to the eukaryotic cell machinery that can involve subversion of biological processes in host. Unfolded protein response (UPR) is a highly conserved host cell stress response to the accumulation of misfolded proteins in the endoplasmic reticulum (ER) and is a conserved evolutionary response against invading pathogens. Several bacterial pathogens can induce the UPR for their own survival and thus design a dual scenario where UPR can both protect and facilitate pathogen evasion. Herein, we investigated whether UPR represents a virulence mechanism exploited by C. jejuni during bacterial invasion in human IECs. Our data show that following C. jejuni infection, we observe consistent upregulation of protein kinase R-like ER kinase (PERK), inositol-requiring enzyme 1α and (IRE1α), with activating transcription factor 6 (ATF6) activation occurring in a strain- and cell line-dependent manner. Chemical induction of UPR by thapsigargin in host cells reduced intracellular survival of C. jejuni while conversely pretreatment with UPR inhibitors increased intracellular survival of C. jejuni and attenuated IL-8 release. Finally, we show using C. jejuni mutants that the capsular polysaccharide and flagella contribute to UPR activation in IECs. Collectively, these findings provide observational insights into UPR activation during infections and how C. jejuni infection leads to UPR activation and inflammation, potentially contributing to downstream C. jejuni-mediated damage.</p>","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105582"},"PeriodicalIF":2.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145409437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the link between genetically predicted plasma cathepsins and COVID-19: A mendelian randomization study of susceptibility and severity.","authors":"Zhenyu Yang, Da Liu, Huiqing Qiu, Yajuan Yin, Xiangbin Meng, Jiadong Xue, Li Zhang, Chao Chang, Jing Li, Chunli Shao, Shuanli Xin, Mengdan Miao","doi":"10.1016/j.micinf.2025.105590","DOIUrl":"10.1016/j.micinf.2025.105590","url":null,"abstract":"<p><strong>Background: </strong>Cathepsin play a crucial role in the progression of various diseases, including cancer, neurodegenerative disorders, and processes involving inflammation and immune modulation. The global pandemic of COVID-19 has heightened the need for further exploration into the interactions between cathepsin and the virus, and their impact on disease progression.</p><p><strong>Methods: </strong>This study employed Mendelian randomization to analyze the causal relationships between specific genetically predicted plasma cathepsin and COVID-19 outcomes, both severe and non-severe. Using data from genome-wide association studies, we evaluated the associations of genetically predicted plasma levels of cathepsin B, D, F, and S with susceptibility to and severity of COVID-19.</p><p><strong>Results: </strong>An increase in genetically predicted circulating cathepsin S levels might be associated with a reduced susceptibility risk to COVID-19 (P < 0.05). Furthermore, while there appears to be a correlation where increased susceptibility to COVID-19 leads to elevated levels of genetically predicted circulating cathepsin F and a reduction in genetically predicted cathepsin S levels (P < 0.05), these associations should be interpreted with caution. There is also suggestive evidence of a causal association between the progression of COVID-19 severity and increased levels of genetically predicted circulating cathepsin F (P < 0.05). However, due to the inherent limitations of the Mendelian randomization approach, further studies are warranted to substantiate these initial findings.</p><p><strong>Conclusion: </strong>This study highlights the potential role of cathepsin in the pathophysiology of COVID-19 and suggests that modulating the expression or activity of these enzymes could influence susceptibility and disease severity. These findings provide a new perspective on the interaction between genetically predicted plasma cathepsin and COVID-19, suggesting further research is needed to explore the mechanisms behind these findings and the potential efficacy of interventions targeting specific cathepsin in the prevention or treatment of COVID-19.</p>","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105590"},"PeriodicalIF":2.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145687597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ESCMID workshop: Artificial intelligence and machine learning in medical microbiology diagnostics.","authors":"Mariella Greutmann, Karsten Borgwardt, Sarah Brüningk, Fabian Franzeck, Christian G Giske, Anna G Green, Alejandro Guerrero-López, Margaret Ip, Catherine Jutzeler, Andre Kahles, Michael Krauthammer, Nenad Macesic, Benjamin McFadden, Eline Meijer, Nathan Moore, Jacob Moran-Gilad, Imane Lboukili, Oliver Nolte, Robin Patel, Gerold Schneider, Markus A Seeger, Tavpritesh Sethi, Robert L Skov, Chang Ho Yoon, Belén Rodríguez-Sánchez, Adrian Egli","doi":"10.1016/j.micinf.2025.105562","DOIUrl":"10.1016/j.micinf.2025.105562","url":null,"abstract":"<p><p>Rapid advancements in artificial intelligence (AI) and machine learning (ML) offer significant potential to transform medical microbiology diagnostics, improving pathogen identification, antimicrobial susceptibility prediction and outbreak detection. To address these opportunities and challenges, the ESCMID workshop, \"Artificial Intelligence and Machine Learning in Medical Microbiology Diagnostics\", was held in Zurich, Switzerland, from June 2-5, 2025. The course featured expert lectures, practical sessions and panel discussions covering foundational ML concepts and deep learning architectures, data interoperability, quality control processes, model development and validation strategies. Key applications discussed included whole-genome sequencing for antimicrobial resistance detection, AI-enhanced digital microscopy automation and MALDI-TOF mass spectrometry-based diagnostics. Participants gained hands-on experience with essential AI tools and platforms. Special emphasis was placed on standardised laboratory protocols, regulatory compliance and ethical considerations, including data governance and patient privacy. Panel sessions further highlighted critical issues of equity, global disparities in AI access, sustainability and environmental impacts related to AI infrastructure. The workshop concluded by underscoring a necessity for ongoing interdisciplinary collaboration, continued education, and substantial investment in equitable AI infrastructure to realise the full potential of AI in clinical diagnostics.</p>","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105562"},"PeriodicalIF":2.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Lactococcus lactis and Bifidobacterium longum attenuate Clostridioides difficile- or Clostridium symbiosum-induced colitis and depression/anxiety-like behavior in male mice\" [Microb Infect 27(7) (2025) 105560].","authors":"Min-Kyung Joo, Dong-Hyun Kim","doi":"10.1016/j.micinf.2025.105587","DOIUrl":"10.1016/j.micinf.2025.105587","url":null,"abstract":"","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105587"},"PeriodicalIF":2.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145513317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Caffeic acid reduces Toxoplasma gondii proliferation in human extravillous trophoblast cells (HTR8/SVneo) through induction of pro-inflammatory cytokines and a death process suggestive of apoptosis.","authors":"Yasmin Munhoz Dos Santos-Destro, Angélica Paulina Nunes, Raquel Arruda da Silva Sanfelice, Virgínia Marcia Concato, Taylon Felipe Silva, Mariana Barbosa Detoni, Danielle Lazarin-Bidoia, Sara Mayumi Suzuki, Guilherme de Souza, João Luís Garcia, Ivete Conchon-Costa, Wander Rogério Pavanelli, Bellisa de Freitas Barbosa, Eloisa Amália Vieira Ferro, Idessania Nazareth Costa","doi":"10.1016/j.micinf.2025.105584","DOIUrl":"10.1016/j.micinf.2025.105584","url":null,"abstract":"<p><strong>Background: </strong>Toxoplasmosis, caused by the protozoan Toxoplasma gondii, is a public health problem, especially in congenital infections. Current treatments, with spiramycin or pyrimethamine and sulfadiazine, are highly toxic, prompting the search for effective and safe natural alternatives.</p><p><strong>Objective: </strong>This study evaluated the in vitro effect of caffeic acid (CA) on human extravillous trophoblast cells (HTR8/SVneo) infected by T. gondii.</p><p><strong>Methods: </strong>The microbicidal and metabolic activity of CA against free tachyzoites was analyzed, in addition to its immunological and anti-Toxoplasma action in infected trophoblast cells.</p><p><strong>Results: </strong>The compound was able to reduce the viability of tachyzoites (IC₅₀ 5 μg/mL) without any toxicity to the trophoblast cells (CC₅₀ 1950 μg/mL); in addition, it reduced the proliferation and infection by tachyzoites at all concentrations tested (5-50 μg/mL). CA also induced changes to the parasite's morphology, including mitochondrial integrity loss, increased production of reactive oxygen species, nitric oxide, exposure to phosphatidylserine and loss of plasmatic membrane integrity, characterizing an apoptosis-like process. Furthermore, there was an increase in interleukins interleukin-1 beta (IL-1β), macrophage migration inhibitory factor (MIF) and transforming growth factor beta (TGF-β) in the T. gondii infected HTR8/SVneo cells.</p><p><strong>Conclusion: </strong>CA is a potential candidate for further research aimed at the development of novel therapies for congenital toxoplasmosis.</p>","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105584"},"PeriodicalIF":2.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145452396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SNPs at the IL-2, IL-12, TNF-α and TGF-β1 regulatory gene regions are probably important for Toxoplasma gondii congenital transmission and disease severity in humans.","authors":"Claudia P Rico-Torres, Adriana Reyes-León, Ricardo Figueroa-Damián, Marcela Vela-Amieva, Mercedes Macias-Parra, Matilde Ruiz-García, Vanessa Bosch-Canto, Fernando Gómez-Chávez, Luz Belinda Ortiz-Alegría, Irma Cañedo-Solares, Patricia Saltigeral-Simentel, Juan Carlos Ordaz-Favila, Mónica Patricia Escobedo-Torres, Carmen Sánchez-Pérez, Carlos López-Candiani, Ivan Rolando Rivera-González, Blanca Gloria Hernández-Antunez, Lorena Hernández-Delgado, Héctor Luna-Pastén, José A Vargas-Villavicencio, Dolores Correa","doi":"10.1016/j.micinf.2025.105565","DOIUrl":"10.1016/j.micinf.2025.105565","url":null,"abstract":"<p><p>Toxoplasma gondii infection in pregnant females can cause congenital toxoplasmosis. Although maternal and infant immune profiles appear to play a role, studies on this topic are scarce. We analyzed SNPs in the regulatory regions of cytokine genes in 30 mother-newborn pairs, five mothers and two infants with known status, with respect to vertical transmission and the clinical outcome of those infected. Polymorphisms in the IL-2, IL-10, IL-12, IL-17, TNF-α, and TGF-β1 gene promoter or regulatory regions were obtained by sequencing, and genotype and allele frequencies were related to transmission and clinical outcome of the offspring. In children, the polymorphic \"G\" TNF-α -308 allele, as well as the related low- and high-level homozygous GG or TT genotypes of the 3'UTR region of the IL-12reg gene, were associated with congenital infection. Both cytokines have been shown to be expressed in the cyto- and syncytiotrophoblast; therefore, the fetus might be able to regulate infection at the placental level. In mothers of infected children, the T allele of the IL-12reg 3'UTR gene was associated with more severe disease in their offspring, suggesting that a strong maternal response reduces parasite spread in the fetus. Furthermore, SNPs in the promoter region of IL-2 and TGF-β1 genes were associated with elevated levels and milder disease in children with congenital infection, which is congruent with a regulation of a strong, damaging, inflammatory response. Our results suggest that some up and down regulatory cytokine genes may predispose to vertical transmission or disease severity in congenital toxoplasmosis.</p>","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105565"},"PeriodicalIF":2.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncSSBP1/FOXO3 axis modulates autophagy: a novel insight into bronchial epithelial cells defense against Talaromyces marneffei infection.","authors":"Lu Lin, Shitong Pan, Mingpeng Xu, Huan Chen, Zhiyi He, Yinghua Li","doi":"10.1016/j.micinf.2025.105561","DOIUrl":"10.1016/j.micinf.2025.105561","url":null,"abstract":"<p><strong>Background: </strong>While autophagy is pivotal in antimicrobial defense, its regulatory role in Talaromyces marneffei (TM) infected bronchial epithelium remains elusive.</p><p><strong>Objective: </strong>To elucidate the impact of TM infection on autophagy in bronchial epithelial cells and to identify the key molecular regulators involved in this process.</p><p><strong>Methods: </strong>Primary computational screening identified core autophagy modulators. Autophagy flux was monitored through LC3B-II/P62 immunoblotting and transmission electron microscopy. Mechanistic validation was performed using siRNA-mediated FOXO3 silencing, lentivirus-mediated lncSSBP1 knockdown and overexpression cell models, combined with immunofluorescence staining for nuclear localization.</p><p><strong>Results: </strong>Bioinformatics analysis identified seven autophagy modulating effectors, with FOXO3 emerging as the central regulator. Quantitative proteomics revealed biphasic autophagic responses: initial LC3B-II accumulation with P62 degradation at 4h post-infection, followed by P62 rebound at 24h, indicating time-dependent flux impairment. FOXO3 was identified as a critical mediator of TM-induced autophagy. Furthermore, we identified a strong positive correlation between lncSSBP1 and FOXO3 expression, with lncSSBP1 overexpression enhancing FOXO3 levels and promoting autophagosome maturation.</p><p><strong>Conclusion: </strong>This study uncovers a previously unrecognized lncRNA-mediated regulatory axis wherein lncSSBP1 orchestrates FOXO3-driven autophagy during TM infection. These results provide new insights into the molecular mechanisms of host-pathogen interactions.</p>","PeriodicalId":18497,"journal":{"name":"Microbes and Infection","volume":" ","pages":"105561"},"PeriodicalIF":2.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}