PLoS Pathogens最新文献

{"title":"Systemic infection by Candida albicans requires FASN-α subunit induced cell wall remodeling to perturb immune response.","authors":"Yajing Zhao, Zhishan Zhou, Guiyue Cai, Dandan Zhang, Xiaoting Yu, Dongmei Li, Shuixiu Li, Zhanpeng Zhang, Dongli Zhang, Jiyao Luo, Yunfeng Hu, Aili Gao, Hong Zhang","doi":"10.1371/journal.ppat.1012865","DOIUrl":"10.1371/journal.ppat.1012865","url":null,"abstract":"<p><p>Invasive fungal infections are a leading cause of mortality and morbidity in patients with severely impaired host defenses, while treatment options remain limited. Fatty acid synthase (FASN), the key enzyme regulating de novo biosynthesis of fatty acids, is crucial for the lethal infection of fungi; however, its pathogenic mechanism is still far from clear. Here, we identified the α subunit of FASN as a potential immunotherapeutic target against systemic Candida albicans infection. The avirulence of the encoded gene (FAS2) -deleted mutant in a mouse model of systemic candidiasis is not due to its fitness defects, because sufficient exogenous fatty acids in serum can overcome FASN inhibition. However, the FAS2-deleted mutant displays increased circulating innate immune responses and enhances activated neutrophil fungicidal activity through the unmasking of immunogenic cell wall epitopes via the Rho-1 dependent Mkc1-MAPK signaling pathway, which facilitates fungal clearance, reduces renal tissue damage and inflammatory cell infiltration, ultimately lowers fungal pathogenicity. Priming with the FAS2-deleted mutant provided significant protection against subsequent lethal infection with wild-type C. albicans in mice as early as one week, and it was well-tolerated with limited toxicity. Our findings indicate that the FASN-α subunit plays key roles in the regulation of neutrophil-associated antifungal immunity and could be a potential target for immunotherapeutic intervention.</p>","PeriodicalId":48999,"journal":{"name":"PLoS Pathogens","volume":"21 3","pages":"e1012865"},"PeriodicalIF":5.5,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11940687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143732711","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":"Dissecting transmission to understand parasite evolution.","authors":"Luís M Silva, Kayla C King, Jacob C Koella","doi":"10.1371/journal.ppat.1012964","DOIUrl":"10.1371/journal.ppat.1012964","url":null,"abstract":"<p><p>Parasite transmission is a complex, multi-stage process that significantly impacts host-parasite dynamics. Transmission plays a key role in epidemiology and virulence evolution, where it is expected to trade off with virulence. However, the extent to which classical models on virulence-transmission relationships apply in the real world is unclear. This insight piece proposes a novel framework that breaks transmission into three distinct stages: within-host infectiousness, an intermediate between-host stage (biotic or abiotic), and new host infection. Each stage is influenced by intrinsic and extrinsic factors to the parasite, which together will determine its transmission success. Analyzing the transmission stages separately and how they affect each other might enhance our understanding of which host-, parasite- or environmental-driven factors might shape parasite evolution and inform us about new effectors to act on when designing disease control strategies.</p>","PeriodicalId":48999,"journal":{"name":"PLoS Pathogens","volume":"21 3","pages":"e1012964"},"PeriodicalIF":5.5,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11936216/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711827","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":"Gene deletion as a possible strategy adopted by New World Leishmania infantum to maximize geographic dispersion.","authors":"Monique Florêncio, Marne Coimbra Batalha Chagas, Anderson Guimarães-Costa, Jullyanna Oliveira, Ingrid Waclawiak, Thamara K F Oliveira, Elvira Maria Saraiva, Anita Leocadio Freitas-Mesquita, José Roberto Meyer-Fernandes, Laura Aragão-Farias, Camilly Enes Trindade, Patricia Cuervo Escobar, Renata Azevedo do Nascimento, Otacilio C Moreira, Flávia Lima Ribeiro-Gomes, Yara M Traub-Csekö, Erich Loza Telleria, Slavica Vaselek, Tereza Leštinová, Petr Volf, Gerald F Späth, Elisa Cupolillo, Mariana Côrtes Boité","doi":"10.1371/journal.ppat.1012938","DOIUrl":"https://doi.org/10.1371/journal.ppat.1012938","url":null,"abstract":"<p><strong>Background: </strong>The present study investigates implications of a sub-chromosomal deletion in Leishmania infantum strains, the causative agent of American Visceral Leishmaniasis (AVL). Primarily found in New World strains, the deletion leads to the absence of the ecto-3'-nucleotidase/nuclease enzyme, impacting parasite virulence, pathogenicity, and drug susceptibility. The factors favoring prevalence and the widespread geographic distribution of these deleted mutant parasites (DEL) in the NW (NW) are discussed under the generated data.</p><p><strong>Methods: </strong>We conducted phenotypic assessments of the sub-chromosomal deletion through in vitro assays with axenic parasites and experimental infections in both in vitro and in vivo models of vertebrate and invertebrate hosts using geographically diverse mutant field isolates.</p><p><strong>Results: </strong>Despite reduced pathogenicity, the DEL strains efficiently infect vertebrate hosts and exhibit relevant differences, including enhanced metacyclogenesis and colonization rates in sand flies, potentially facilitating transmission. This combination may represent a more effective way to maintain and disperse the transmission cycle of DEL strains.</p><p><strong>Conclusions: </strong>Phenotypic assessments reveal altered parasite fitness, with potential enhanced transmissibility at the population level. Reduced susceptibility of DEL strains to miltefosine, a key drug in VL treatment, further complicates control efforts. The study underscores the importance of typing parasite genomes for surveillance and control, advocating for the sub-chromosomal deletion as a molecular marker in AVL management.</p>","PeriodicalId":48999,"journal":{"name":"PLoS Pathogens","volume":"21 3","pages":"e1012938"},"PeriodicalIF":5.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143671636","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":"Discovery of a novel Betacoronavirus 1, cpCoV, in goats in China: The new risk of cross-species transmission.","authors":"Li Mao, Xuhang Cai, Jizong Li, Xia Li, Siyuan Li, Wenliang Li, Honghui Lu, Yichun Dong, Junjun Zhai, Xingang Xu, Bin Li","doi":"10.1371/journal.ppat.1012974","DOIUrl":"10.1371/journal.ppat.1012974","url":null,"abstract":"<p><p>Betacoronavirus is a causative agent of respiratory and enteric diseases in humans and animals. Several ruminants are recognized to be intermediate hosts in the transmission of emerging coronaviruses from reservoir hosts to humans. Here, we first report a novel Betacoronavirus isolated from goats suffering from diarrhea in China, putatively named caprine coronavirus (cpCoV). Full-genome characterization and nuclear acid comparisons demonstrated that this virus is an evolutionarily distinct Betacoronavirus belonging to the subgenus Embecovirus and is a Betacoronavirus 1 species. Notably, on phylogenetic trees based on complete genomes and RdRp, S, and N genes, the cpCoVs were grouped into a clade distinct from other Betacoronavirus strains and were closely related to the HKU23- and HKU23-associated coronaviruses. CpCoV possessed a unique genome organization with a truncated NS4a protein and an elongated NS4b protein that showed no significant matches in the GenBank database. The homology of the S and NS4a-4b genes between cpCoV and Embecovirus was less than 95%. Analysis revealed possible recombination events occurred during the evolution of cpCoV and HKU23, and there are striking similarities between the two viruses in evolutionary terms. In addition, cpCoV showed a narrow cell tropism, replicating in human- and bovine-origin cells in vitro, and caused diarrhea and enteric pathologic changes in goats and calves in vivo. We have provided epidemiological, virological, evolutionary, and experimental evidence that cpCoV is a novel etiological agent for enteric disease in goats. Evidently, a spilling-over event might have occurred between ruminants, including goats, camels, cattle, and wild animals. This study highlights the importance of identifying coronavirus diversity and inter-species transmission in ruminants worldwide, broadens our understanding of the ecology of coronaviruses, and aids in the prevention of animal-to-human transmission and outbreaks.</p>","PeriodicalId":48999,"journal":{"name":"PLoS Pathogens","volume":"21 3","pages":"e1012974"},"PeriodicalIF":5.5,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11918373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143659379","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":"The efflux pump SugE2 involved in protection of Salmonella 4,[5],12:i:- against quaternary ammonium salts and inhibition of virulence.","authors":"Yuqi Tian, Yaya Wen, Xueying Wang, Youkun Zhang, Xilong Kang, Chuang Meng, Zhiming Pan, Xinan Jiao, Dan Gu","doi":"10.1371/journal.ppat.1012951","DOIUrl":"10.1371/journal.ppat.1012951","url":null,"abstract":"<p><p>Salmonella enterica serovar 4,[5],12:i:-, a monophasic variant of Salmonella Typhimurium, has emerged as a common nontyphoidal Salmonella serotype to cause human foodborne disease, exhibiting antibiotic and multidrug resistance. In this study, we identified the isolates of S. 4,[5],12:i:- resistant to quaternary ammonium compounds (QACs) disinfectants, displaying elevated minimum inhibitory concentration (MIC) values (200 μg/mL) in Mueller-Hinton (MH) broth. The efflux pump SugE1 and SugE2 could be induced by didecyldimethylammonium bromide (DDAB) and found to be indispensable for S. 4,[5],12:i:- resistance to DDAB. The Hoechst 33342 dye accumulation and reduced ethidium bromide efflux in ΔsugE1, ΔsugE2 and ΔsugE1ΔsugE2 further confirmed the efflux function of SugE1 and SugE2. Moreover, DDAB inhibited the expression of Salmonella pathogenicity island 1 (SPI-1) to decrease the adhesion and invasion ability of S. 4,[5],12:i:- in IPEC-J2 cells, whereas the deletion of sugE2 increased the adhesion and invasion ability. In an in vivo mice model, the virulence of ΔsugE2 and ΔsugE1ΔsugE2 mutant strains were enhanced and showed significantly increased bacterial loads in the liver, spleen, and cecum. The ΔsugE2 and ΔsugE1ΔsugE2 mutant strains exhibited an enhanced ability to disrupt the intestinal barrier, leading to systemic infection. Finally, we discovered that intestinal extracts could induce sugE1 and sugE2 expression, subsequently suppressing SPI-1 expression through SugE2, mediating the Salmonella intestinal infection process. In conclusion, our findings provide the pivotal role of the SugE2 efflux pump in conferring resistance to DDAB disinfectants and influencing bacterial virulence in S. 4,[5],12:i:-.</p>","PeriodicalId":48999,"journal":{"name":"PLoS Pathogens","volume":"21 3","pages":"e1012951"},"PeriodicalIF":5.5,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11918376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143659387","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":"Virolithopanspermia: Might viruses be transported in rocks through space?","authors":"Frederic D Bushman","doi":"10.1371/journal.ppat.1012955","DOIUrl":"10.1371/journal.ppat.1012955","url":null,"abstract":"","PeriodicalId":48999,"journal":{"name":"PLoS Pathogens","volume":"21 3","pages":"e1012955"},"PeriodicalIF":5.5,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11918348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143659391","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":"NLRP3 and AIM2 inflammasomes exacerbate the pathogenic Th17 cell response to eggs of the helminth Schistosoma mansoni.","authors":"Madhusoodhanan Suresh Kumar Meena Kumari, Pengyu Liu, Megan S Nitchman, Santoshi Chaudhary, Kaile Jump, Yoelkys Morales, Emily A Miller, Ilana Shecter, Miguel J Stadecker, Parisa Kalantari","doi":"10.1371/journal.ppat.1012108","DOIUrl":"10.1371/journal.ppat.1012108","url":null,"abstract":"<p><p>Infection with the helminth Schistosoma mansoni can cause exacerbated morbidity and mortality via a pathogenic host CD4 T cell-mediated immune response directed against parasite egg antigens, with T helper (Th) 17 cells playing a major role in the development of severe granulomatous hepatic immunopathology. The role of inflammasomes in intensifying disease has been reported; however, neither the types of caspases and inflammasomes involved, nor their impact on the Th17 response are known. Here we show that enhanced egg-induced IL-1β secretion and pyroptotic cell death required both caspase-1 and caspase-8 as well as NLRP3 and AIM2 inflammasome activation. Schistosome genomic DNA activated AIM2, whereas reactive oxygen species, potassium efflux and cathepsin B, were the major activators of NLRP3. NLRP3 and AIM2 deficiency led to a significant reduction in pathogenic Th17 responses, suggesting their crucial and non-redundant role in promoting inflammation. Additionally, we show that NLRP3- and AIM2-induced IL-1β suppressed IL-4 and protective Type I IFN (IFN-I) production, which further enhanced inflammation. IFN-I signaling also curbed inflammasome- mediated IL-1β production suggesting that these two antagonistic pathways shape the severity of disease. Lastly, Gasdermin D (Gsdmd) deficiency resulted in a marked decrease in egg-induced granulomatous inflammation. Our findings establish NLRP3/AIM2-Gsdmd axis as a central inducer of pathogenic Th17 responses which is counteracted by IFN-I pathway in schistosomiasis.</p>","PeriodicalId":48999,"journal":{"name":"PLoS Pathogens","volume":"21 3","pages":"e1012108"},"PeriodicalIF":5.5,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11918320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143659384","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":"Modeling natural coinfection in a bat reservoir shows modulation of Marburg virus shedding and spillover potential.","authors":"Amy J Schuh, Brian R Amman, Jonathan C Guito, James C Graziano, Tara K Sealy, Jonathan S Towner","doi":"10.1371/journal.ppat.1012901","DOIUrl":"https://doi.org/10.1371/journal.ppat.1012901","url":null,"abstract":"<p><p>The Egyptian rousette bat (ERB) is a natural reservoir for Marburg virus (MARV; family Filoviridae), a putative reservoir for Sosuga virus (SOSV; family Paramyxoviridae), and a vertebrate reservoir for Kasokero virus (KASV; family Orthonairoviridae); however, the effect of naturally occurring coinfection by those viruses on MARV shedding and spillover potential is unknown. To answer this question, we experimentally infected one cohort of captive-bred ERBs with SOSV+MARV (n=12 bats) or MARV only (n=12 bats) and a second cohort with KASV+MARV (n=12 bats) or MARV only (n=12 bats), and then collected blood, oral swab, and rectal swab specimens throughout the course of infection to monitor viral shedding. Compared to the MARV-monoinfected bat group, the SOSV+MARV-coinfected bat group exhibited a significantly shortened duration of MARV oral shedding and a significantly decreased anti-MARV IgG response, which may increase the capacity for MARV reinfection. In contrast, relative to the MARV-monoinfected bat group, the KASV+MARV-coinfected bat group exhibited significantly increased peak magnitudes and durations of MARV viremia and oral shedding, as well as a significantly increased anti-MARV IgG response. Correspondingly, cumulative MARV shedding loads, a measure of infectiousness, were significantly higher in the KASV+MARV-coinfected bat group than the MARV-monoinfected bat group. Four of the KASV+MARV-coinfected bats were classified as MARV supershedders, together accounting for 72.5% of the KASV-MARV experimental cohort's total shedding. Our results demonstrate that SOSV+MARV and KASV+MARV coinfection of ERBs differentially modulates MARV shedding and anti-MARV IgG responses, thereby implicating MARV coinfection as playing a critical role in bat-to-bat MARV transmission dynamics and spillover potential.</p>","PeriodicalId":48999,"journal":{"name":"PLoS Pathogens","volume":"21 3","pages":"e1012901"},"PeriodicalIF":5.5,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651618","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":"Eating the brain - A multidisciplinary study provides new insights into the mechanisms underlying the cytopathogenicity of Naegleria fowleri.","authors":"Ronald Malych, Filipe Folgosa, Jana Pilátová, Libor Mikeš, Vít Dohnálek, Jan Mach, Magdaléna Matějková, Vladimír Kopecký, Pavel Doležal, Robert Sutak","doi":"10.1371/journal.ppat.1012995","DOIUrl":"10.1371/journal.ppat.1012995","url":null,"abstract":"<p><p>Naegleria fowleri, the causative agent of primary amoebic meningoencephalitis (PAM), requires increased research attention due to its high lethality and the potential for increased incidence as a result of global warming. The aim of this study was to investigate the interactions between N. fowleri and host cells in order to elucidate the mechanisms underlying the pathogenicity of this amoeba. A co-culture system comprising human fibrosarcoma cells was established to study both contact-dependent and contact-independent cytopathogenicity. Proteomic analyses of the amoebas exposed to human cell cultures or passaged through mouse brain were used to identify novel virulence factors. Our results indicate that actin dynamics, regulated by Arp2/3 and Src kinase, play a considerable role in ingestion of host cells by amoebae. We have identified three promising candidate virulence factors, namely lysozyme, cystatin and hemerythrin, which may be critical in facilitating N. fowleri evasion of host defenses, migration to the brain and induction of a lethal infection. Long-term co-culture secretome analysis revealed an increase in protease secretion, which enhances N. fowleri cytopathogenicity. Raman microspectroscopy revealed significant metabolic differences between axenic and brain-isolated amoebae, particularly in lipid storage and utilization. Taken together, our findings provide important new insights into the pathogenic mechanisms of N. fowleri and highlight potential targets for therapeutic intervention against PAM.</p>","PeriodicalId":48999,"journal":{"name":"PLoS Pathogens","volume":"21 3","pages":"e1012995"},"PeriodicalIF":5.5,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651601","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":"Adiponectin pathway activation dampens inflammation and enhances alveolar macrophage fungal killing via LC3-associated phagocytosis.","authors":"Sri Harshini Goli, Joo-Yeon Lim, Nese Basaran-Akgul, Steven P Templeton","doi":"10.1371/journal.ppat.1012363","DOIUrl":"10.1371/journal.ppat.1012363","url":null,"abstract":"<p><p>Although innate immunity is critical for antifungal host defense against the human opportunistic fungal pathogen Aspergillus fumigatus, potentially damaging inflammation must be controlled. Adiponectin (APN) is an adipokine produced mainly in adipose tissue that exerts anti-inflammatory effects in adipose-distal tissues such as the lung. We observed increased mortality and increased fungal burden and inflammation in neutropenic mice with invasive aspergillosis (IA) that lack APN or the APN receptors AdipoR1 or AdipoR2. Alveolar macrophages (AMs), early immune sentinels that detect and respond to lung infection, express both receptors, and APN-deficient AMs exhibited an inflammatory phenotype that was associated with decreased fungal killing. Pharmacological stimulation of AMs with AdipoR agonist AdipoRon rescued deficient killing in APN-/- AMs and was dependent on the presence of either receptor. Finally, APN-enhanced fungal killing was associated with increased activation of the non-canonical LC3 pathway of autophagy. Thus, our study identifies a novel role for APN in LC3-mediated killing of A.fumigatus.</p>","PeriodicalId":48999,"journal":{"name":"PLoS Pathogens","volume":"21 3","pages":"e1012363"},"PeriodicalIF":5.5,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11949351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651543","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}