Innate Immunity最新文献

{"title":"1105 Response Gene to Complement-32 expression is upregulated in the kidney and promotes renal fibrosis in lupus nephritis","authors":"Vinh Phu Nguyen, A. Tatomir, C. Drachenberg, H. Rus, V. Rus","doi":"10.1136/lupus-2022-lupus21century.70","DOIUrl":"https://doi.org/10.1136/lupus-2022-lupus21century.70","url":null,"abstract":"","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42259334","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":"Surfactant proteins and innate immunity of otitis media.","authors":"Osama Abdel-Razek,&nbsp;Jason Audlin,&nbsp;Dennis S Poe,&nbsp;Guirong Wang","doi":"10.1177/17534259221123309","DOIUrl":"https://doi.org/10.1177/17534259221123309","url":null,"abstract":"<p><p>Otitis media (OM) is the most common disease among young children and one of the most frequent reasons to visit the pediatrician. Development of OM requires nasopharyngeal colonization by a pathogen which must gain access to the tympanic cavity through the eustachian tube (ET) along with being able to overcome the defense mechanisms of the immune system and middle ear mucosa. OM can be caused by viral or bacterial infection. The three main bacterial pathogens are <i>Streptococcus pneumoniae</i>, <i>nontypeable Haemophilus influenzae</i> (NTHi), and <i>Moraxella catarrhalis.</i> Innate immunity is important in OM resolution as the disease occurs in very young children before the development of specific immunity. Elements of innate immunity include natural barriers and pattern recognition receptors such as Toll like receptors (TLRs), and Nod like receptors (NLRs). Surfactant proteins A (SP-A) and D (SP-D) act as pattern recognition receptors and are found in the lung and many other tissues including the ET and the middle ear where they probably function in host defense. Surfactant has a potential for use in the treatment of OM due to surface tension lowering function in the ET, and the possible immune functions of SP-D and SP-A in the middle ear and ET.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 7-8","pages":"213-223"},"PeriodicalIF":3.2,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/23/6a/10.1177_17534259221123309.PMC9900255.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9218295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intravenous anti-<i>P. aeruginosa</i> IgY-antibodies do not decrease pulmonary bacterial concentrations in a porcine model of ventilator-associated pneumonia.","authors":"A Otterbeck,&nbsp;P Skorup,&nbsp;K Hanslin,&nbsp;A Larsson,&nbsp;J Stålberg,&nbsp;H Hjelmqvist,&nbsp;M Lipcsey","doi":"10.1177/17534259221114217","DOIUrl":"10.1177/17534259221114217","url":null,"abstract":"<p><p>Ventilator associated pneumonia (VAP) caused by <i>P. aeruginosa</i> is a cause of morbidity and mortality in critically ill patients. The spread of pathogens with anti-microbial resistance mandates the investigation of novel therapies. Specific polyclonal anti-<i>P. aeruginosa</i> IgY-antibodies (<i>Pa-</i>IgY) might be effective for VAP caused by <i>P. aeruginosa.</i> The objective of this study was to investigate if intravenous <i>Pa-</i>IgY decreases the lower airway concentration of <i>P. aeruginosa</i> in VAP. We used a double blind randomized placebo controlled porcine model of VAP caused by <i>P. aeruginosa</i>. Eighteen pigs were randomized to either receive intravenous <i>Pa-</i>IgY or placebo. Repeated registration of physiological parameters and sampling was performed for 27 h. Concentration of <i>P. aeruginosa</i> in BAL-cultures was similar in both groups with 10^4.97 ± 10^2.09 CFU/mL in the intervention group vs 10^4.37 ± 10^2.62 CFU/mL in the control group at the end of the experiment. The intervention group had higher heart rate, cardiac index, oxygen delivery and arterial oxygen tension/fraction of inspired oxygen-ratio, but lower plasma lactate and blood hemoglobin levels than the control group. In summary, in an anesthetized and mechanically ventilated porcine model of VAP, <i>Pa-</i>IgY at the dose used did not decrease concentrations of <i>P. aeruginosa</i> in the lower airways.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 7-8","pages":"224-234"},"PeriodicalIF":3.2,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9900256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9234861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Natural killer cell exhaustion in SARS-CoV-2 infection.","authors":"Janet Gallardo-Zapata,&nbsp;Carmen Maldonado-Bernal","doi":"10.1177/17534259221077750","DOIUrl":"https://doi.org/10.1177/17534259221077750","url":null,"abstract":"<p><p>At the end of 2019, an outbreak of a severe respiratory disease occurred in Wuhan China, and an increase in cases of unknown pneumonia was alerted. In January 2020, a new coronavirus named SARS-CoV-2 was identified as the cause. The virus spreads primarily through the respiratory tract, and lymphopenia and cytokine storms have been observed in severely ill patients. This suggests the existence of an immune dysregulation as an accompanying event during a serious illness caused by this virus. Natural killer (NK) cells are innate immune responders, critical for virus shedding and immunomodulation. Despite its importance in viral infections, the contribution of NK cells in the fight against SARS-CoV-2 has yet to be deciphered. Different studies in patients with COVID-19 suggest a significant reduction in the number and function of NK cells due to their exhaustion. In this review, we summarize the current understanding of how NK cells respond to SARS-CoV-2 infection.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 6","pages":"189-198"},"PeriodicalIF":3.2,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/04/1f/10.1177_17534259221077750.PMC9389049.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40209946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-classical monocytes contribute to innate immune training in cattle.","authors":"Lisa-Marie Schünemann,&nbsp;Hans-Joachim Schuberth","doi":"10.1177/17534259221114219","DOIUrl":"https://doi.org/10.1177/17534259221114219","url":null,"abstract":"<p><p>Innate immune training is defined as a property of innate immune cells to react stronger to a secondary contact with pathogens. Induction of innate immune training has been reported for a variety of pathogens and selected pattern recognition receptor-ligands, such as β-glucans (βG). We examined whether <i>Saccharomyces cerevisiae</i> cell wall component βG induces training in bovine monocytes <i>in vitro</i> based on a heightened TNF secretion after stimulation by trained monocyte-derived macrophages with <i>Escherichia coli</i> LPS. Sorted CD14-expressing monocytes (classical and intermediate monocytes), as well as single populations of sorted classical, intermediate and non-classical monocytes could not be trained by βG, whereas macrophages derived from plastic-adherent mononuclear cell preparations displayed features of a trained function. The hypothesis, that non-classical monocytes need to be present in a mixed monocyte population in order to be trained by βG could be verified by a successful training of positively sorted whole monocyte populations (CD14CD16/M) containing all three monocyte subpopulations. The trainability depended on conditions favoring M1 polarization of macrophages. Altogether, innate immune training of bovine monocytes seems to depend on the presence of non-classical monocytes. This adds new information to the role of this monocyte subpopulation in the bovine immune system.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 6","pages":"199-210"},"PeriodicalIF":3.2,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7d/05/10.1177_17534259221114219.PMC9389050.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40623438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ObituaryLouis Selim Chedid, MD PhDIEIIS honorary life member","authors":"J. Cavaillon","doi":"10.1177/17534259221116799","DOIUrl":"https://doi.org/10.1177/17534259221116799","url":null,"abstract":"Louis Selim Chedid was born in Cairo (Egypt) in June 1922 anddied inParis inMarch2021at the ageof98.After obtaining his bachelor’s degree in Cairo, he started hismedical studies in Beirut and completed them in Paris, defending his medical thesis on artificial estrogen in 1947. After being trained in Egypt and the United States, he joined the laboratory of Robert Courrier at the College de France (1946). In 1952, he was recruited by the CNRS (National Center for Scientific Research, France). In 1955, he defended his PhD on hormones and infection and started working at the Institut Pasteur (Paris) in the laboratory of Therapeutic Chemistry under André Lamensans.He joined the Institut Pasteur in 1961 andwas promoted to Professor in 1972. In 1973, he became the head of the Experimental Immunotherapy laboratory. In 1986, he moved to the H. Lee Moffit Cancer Center and Research Institute at the Universiy of South Florida, Tampa where he founded a startup working on vaccine adjuvants (VacSyn). Louis Chedid was the co-author of 26 patents. He investigated immune mechanisms with the goal of boosting the defense against infections. Among his main contributions is the identification with Edgar Lederer (1908–1988) of the muramyl dipeptide (MDP), the smallest active part of the peptidoglycan of mycobacteria present in complete Freund adjuvant. He then devoted part of his career to study homologs of MDP and their bioactivities, synthetic vaccines, and adjuvants. He also performed numerous investigations on endotoxins including investigations on enhanced resistance to infection by endotoxins, LPS-induced abortion, production of interleukin-1 and tumor necrosis factor in response to endotoxins, the synergy between MDP and LPS, prevention of endotoxin-induced lethality, the influence of endotoxin on bone marrow cells, endotoxin tolerance, polyclonal activation, LPS-induced radioresistance, localization of injected Cr-labeled LPS, and studies on alkalyl detoxified endotoxins. He offered the basis for an universal anti-endotoxin antibody: “Thereafter, the presence of a few types of “R’ (rough) antibodies or of serum factors reacting with rough antigens have the capability of coping, like masterkeys, with a wide range of infection due to serologically unrelated organisms”. He collaborated with eminent US scientists including JJ Oppenheim, HS Warren, CA Dinarello, SM Wolff, and JM Krueger. With the latter three, he investigated the links between slow wave sleep and IL-1, his most cited paper (462 citations), and addressed the links between sleep and MDP. A Romanian scientist, Constantin Bona (1934–2015) worked for a while in his laboratory on so-called nonspecific immunity before joining the Mount Sinaï Hospital in New York, working on idiotypes and neonatal immunity. They are co-authors of 17 papers including reports on a Nocardia water soluble mitogen. Claude Leclerc started her bright career on vaccines and cancer at Institut Pasteur in his laboratory. Based on an","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 1","pages":"187 - 188"},"PeriodicalIF":3.2,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42603474","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":"Ursolic acid inhibits Th17 cell differentiation via STAT3/RORγt pathway and suppresses Schwann cell-mediated Th17 cell migration by reducing CXCL9/10 expression.","authors":"Hua Xu, Ai-Ling Yu, Da-Peng Zhao, Guang-Yuan Meng, Ling Wang, Min Shan, Nai-Xia Hu, Yun-Lin Liu","doi":"10.1177/17534259221094559","DOIUrl":"10.1177/17534259221094559","url":null,"abstract":"<p><p>Th17 cells represent important immune cells. Ursolic acid (UA) can regulate immune cell activities. This study was aimed to explore the effects of UA on Th17 cell differentiation and Schwann cell(SCs)-mediated migration and the potential mechanism. Naïve CD4⁺ T cells were isolated from rat peripheral blood, induced for Th17 cell differentiation, and treated with UA. The proportion of Th17 cells was detected by flow cytometry assay. SCs were co-cultured with Th17 cells. Th17 cell migration was detected by Transwell assay. The molecule expression was determined by Western blot and qRT-PCR. UA inhibited the Th17 cell differentiation and suppressed the STAT3/RORγt pathway. STAT3 overexpression up-regulated p-STAT3 and RORγt expression and promoted Th17 cell differentiation under the UA treatment. In LPS- and IFN-γ-stimulated-SCs, UA suppressed the expression of chemokines CXCL9/10, but had no significant effect of CCL20 expression. The expression CXCL9/10 receptor CXCR3 was higher in Th17 cells than that in Treg cells, while the expression CCL20 receptor CCR6 was lower in Th17 cells than that in Treg cells. UA, anti-CXCR3, and anti-CCR6 treatment inhibited SCs-mediated Th17 cell migration, and anti-CXCR3 exerted stronger inhibitory effect than Anti-CCR6. UA inhibited Th17 cell differentiation through STAT3/RORγt pathway and suppressed Th17 cell migration through down-regulating CXCL9/10 expression in SCs.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 1","pages":"155-163"},"PeriodicalIF":3.2,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9189552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45669541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ_0062491 alleviates LPS-induced apoptosis and inflammation in periodontitis by regulating miR-498/SOCS6 axis","authors":"Lie Wang, Yanli Li, Feifei Hong, Haiyan Ning","doi":"10.1177/17534259211072302","DOIUrl":"https://doi.org/10.1177/17534259211072302","url":null,"abstract":"Periodontitis is a prevalent chronic inflammatory disease. Circular RNAs (circRNAs) have been revealed to play roles in the inflammatory response. Hence, this work aimed to explore the role and mechanism of circ_0062491 in periodontitis progression. Human periodontal ligament cells (PDLCs) were isolated from the periodontal ligament (PDL) of the healthy teeth with orthodontic requirement after tooth extraction. In vitro experiments were conducted by cell counting Kit-8 (CCK-8) assay, flow cytometry, Western blot, and ELISA to determine cell viability, apoptosis, and inflammatory response. The binding between miR-498 and circ_0062491 or SOCS6 was confirmed using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Circ_0062491 expression was decreased in periodontitis and LPS-induced PDLCs. Restoration of circ_0062491 attenuated LPS-induced apoptosis and inflammation in PDLCs in vitro. Mechanistically, circ_0062491 functioned as a sponge for miR-498, and miR-498 directly targeted SOCS6. Rescue experiments showed that miR-498 up-regulation reversed the protective action of circ_0062491 on PDLCs under LPS treatment. Moreover, silencing of miR-498 protected PDLCs from LPS-induced apoptosis and inflammation, which were abolished by SOCS6 knockdown. Circ_0062491 protected PDLCs from LPS-induced apoptosis and inflammation, suggesting a new target for the amelioration of periodontitis patients.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 1","pages":"174 - 184"},"PeriodicalIF":3.2,"publicationDate":"2022-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49668998","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":"Circ_0066881 targets miR-144-5p/RORA axis to alleviate LPS-induced apoptotic and inflammatory damages in human periodontal ligament cells","authors":"Qin Li, Zhaopeng Hu, Fang Yang, Yi Peng","doi":"10.1177/17534259221079812","DOIUrl":"https://doi.org/10.1177/17534259221079812","url":null,"abstract":"Circular RNAs (circRNAs) are involved in the regulation of various diseases, including periodontitis. The objective of this study was to analyze the biological role and regulatory mechanism of circ_0066881 in LPS-induced periodontal ligament cells (PDLCs). Circ_0066881, microRNA-144-5p (miR-144-5p) and retinoid acid-related orphan receptor A (RORA) levels were determined using reverse transcription-quantitative PCR (RT-qPCR) assay. Cell viability detection was performed by Cell Counting Kit-8 assay. Cell apoptosis was assessed through flow cytometry and caspase-3 activity assay. The protein analysis was completed via Western blot. Inflammatory cytokines were measured by ELISA. The target interaction was validated by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The level of circ_0066881 was down-regulated in periodontitis tissues. Overexpression of circ_0066881 relieved LPS-induced cell viability inhibition and apoptosis or inflammation promotion in PDLCs. Circ_0066881 could bind to miR-144-5p. The protective function of circ_0066881 was achieved by sponging miR-144-5p in PDLCs. Circ_0066881 acts as a miR-144-5p sponge to mediate the RORA level. Inhibition of miR-144-5p attenuated LPS-induced cell injury via targeting RORA. All these results demonstrated that circ_0066881 partly prevented LPS-evoked cell dysfunction in PDLCs through miR-144-5p-mediated up-regulation of RORA.","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 1","pages":"164 - 173"},"PeriodicalIF":3.2,"publicationDate":"2022-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48610270","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":"Soluble CD163 is produced by monocyte-derived and alveolar macrophages, and is not associated with the severity of idiopathic pulmonary fibrosis.","authors":"Pierre Chauvin,&nbsp;Claudie Morzadec,&nbsp;Bertrand de Latour,&nbsp;Francisco Llamas-Gutierrez,&nbsp;David Luque-Paz,&nbsp;Stéphane Jouneau,&nbsp;Laurent Vernhet","doi":"10.1177/17534259221097835","DOIUrl":"https://doi.org/10.1177/17534259221097835","url":null,"abstract":"<p><p>The soluble form of the membrane hemoglobin scavenger receptor CD163 (sCD163), released by shedding, is a strong marker for macrophage activation. Serum sCD163 levels rise in several acute inflammatory states and some fibrosing diseases. Monocyte-derived macrophages (MoDM) differentiated by macrophage colony-stimulating factor (M-MoDM) contribute to the pathophysiology of idiopathic pulmonary fibrosis (IPF), an irreversible and rapidly fatal interstitial lung disease. Since M-MoDM express high membrane CD163 levels, we thus postulated that sCD163 could be a relevant biomarker for macrophage activation in IPF. We found that M-MoDM constitutively released higher amounts of sCD163 (49.5 ± 24.5 ng/ml) than monocytes (0.45 ± 0.32 ng/ml) or MoDM differentiated with granulocyte macrophage-stimulating factor (2.24 ± 0.98 ng/ml). The basal production of sCD163 by M-MoDM was increased following stimulation with lipopolysaccharide (123.4 ± 54.9 ng/ml) or ATP (168.9 ± 41.8 ng/ml). The sCD163 release was controlled by metalloproteases but not through ADAM17 activation. Moreover, CD163-positive macrophages and sCD163 were detected in pulmonary tissues and alveolar fluids of Caucasian patients with IPF, respectively. IPF alveolar macrophages constitutively secreted sCD163 amounts (67.6 ± 44.6 ng/µg RNA) which were significantly higher than those released by alveolar macrophages isolated from controls (19.2 ± 7.6 ng/µg RNA) or patients with other interstitial lung disease (31.5 ± 16.6 ng/µg RNA). However, the concentrations of sCD163 in blood serum collected from 155 patients with IPF did not correlate with the severity of their disease. In conclusion, our results show that M-MoDM constituted a pertinent model to study the regulation of sCD163 production. Yet, serum sCD163 values could not provide a prognostic biomarker for IPF in our cohort.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 3-4","pages":"138-151"},"PeriodicalIF":3.2,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8f/8f/10.1177_17534259221097835.PMC9136464.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10304219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}