Open Life Sciences最新文献

{"title":"High-temperature requirement serine protease A2 inhibitor UCF-101 ameliorates damaged neurons in traumatic brain-injured rats by the AMPK/NF-κB pathway.","authors":"Tian-Wen Qiu, Zhan Jin, Zhi-Zhan Fu, Xin-Jiang Yan, Cheng-Peng Zhan, Hui-Wen Zheng, Mei-Ying Li, Guo-Feng Yu","doi":"10.1515/biol-2022-0971","DOIUrl":"10.1515/biol-2022-0971","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) leads to permanent damage, including neurological deficits, cognitive deficits, and cerebral edema. The specific inhibitor of serine protease Omi/high-temperature requirement A2 (Omi/HtrA2), UCF-101, exerts neuroprotective effects, but its role in TBI remains unclear. Eighty-four male Sprague Dawley rats were randomized to control, TBI, UCF-101 of low dose (1.5 μmol/kg), middle dose (3.0 μmol/kg), and high dose (6.0 μmol/kg), Compound C (AMPK inhibitor, 20 mg/kg), and high dose + Compound C groups. TBI rat modeling was operated by the controlled cortical impact method. Modified neurological severity score (mNSS) cognitive function, cerebral edema index, hematoxylin-eosin staining, TUNEL staining for apoptosis, ethidium bromide staining for blood-brain barrier (BBB) permeability, enzyme-linked immunosorbent assay for inflammation response, and Western blot analysis were performed. In TBI rats, UCF-101 caused decreased mNSS score, brain edema, neuronal apoptosis, as well as P-NF-κBp65/NF-κBp65, tumor necrosis factor-α, interleukin (IL)-1β, and IL-8 expression, while P-AMPK/AMPK, zonula occludens protein, Occludin, and Claudin-5 expression increased, accompanied with up-regulated cognitive function. Moreover, Compound C further exacerbated brain tissue lesions, neuronal damage, inflammation response, and neuronal apoptosis, while high-dose UCF-101 offset its effect. UCF-101 may inhibit apoptosis and BBB permeability to exert neuroprotective effects in TBI rats by regulating the AMPK/NF-κB pathway, advancing UCF-101 clinical applications for TBI treatment.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"20 1","pages":"20220971"},"PeriodicalIF":1.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of Aurora kinase B alleviates high glucose-triggered trophoblast cells damage and inflammation during gestational diabetes.","authors":"Yuzhuo Ma, Yongyun Shi, Yujie Liu","doi":"10.1515/biol-2022-1031","DOIUrl":"10.1515/biol-2022-1031","url":null,"abstract":"<p><p>This research investigates how Aurora kinase B (AURKB) functions in trophoblast cells when they are exposed to high levels of glucose during gestational diabetes. The findings from RT-qPCR and western blotting show that when in a high-glucose environment, AURKB expression increases in both the placenta and trophoblast cells of patients with gestational diabetes mellitus. Additionally, when AURKB is silenced in high-glucose conditions, it leads to boosted proliferation of trophoblast cells and reduced inflammation. Knockdown of AURKB inhibits the expression of phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway in high glucose (HG) environment. Knockdown of AURKB may ameliorate injury and inflammatory responses in HG-exposed trophoblast cell lines in part by regulating the PI3K/AKT signaling pathway.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"20 1","pages":"20221031"},"PeriodicalIF":1.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889497/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimization and comparative study of <i>Bacillus</i> consortia for cellulolytic potential and cellulase enzyme activity.","authors":"Ogechukwu Bose Chukwuma, Mohd Rafatullah, Riti Thapar Kapoor, Husnul Azan Tajarudin, Norli Ismail, Mahboob Alam, Masoom Raza Siddiqui","doi":"10.1515/biol-2025-1066","DOIUrl":"10.1515/biol-2025-1066","url":null,"abstract":"<p><p>Lignocellulosic biomass, owing to its recalcitrant nature, requires a consortium of enzymes for its breakdown. The present study deals with the isolation of cellulolytic bacterial strains from landfill leachate collected from the Pulau Burung landfill site of Penang, Malaysia, and consortia were constructed to test their cellulolytic efficiency. The dinitro salicylate method was used for the estimation of enzyme activity, and consortia were compared with promising bacterial strains. The combined potential of promising bacterial strains was optimized at varying experimental conditions to detect their maximum cellulolytic activity. The results showed that eight bacterial strains reflected hydrolytic activities, and these were identified by 16S rDNA sequence as <i>Bacillus subtilis, Bacillus pumilus, Bacillus proteolyticus, Bacillus paramycoides, Bacillus cereus, Bacillus altitudinis, Bacillus niacin,</i> and <i>Bacillus thuringiensis.</i> Consortia A included <i>Bacillus proteolyticus, Bacillus subtilis, Bacillus pumilus,</i> and <i>Bacillus paramycoides</i> and reflected high thermophilic inclination as the optimal temperature was 45°C at pH 6 with the highest cellulase activity of 0.90 U/ml. Consortia B included <i>Bacillus cereus, Bacillus altitudinis, Bacillus niacin,</i> and <i>Bacillus thuringiensis</i> and showed a cellulase activity of 0.78 U/ml at 38°C and pH 6. The results reflected the significant potential of these <i>Bacillus</i> strains and consortia in the breakdown of cellulose into useful end products. The consortia further proved that a synergistic relationship was more favourable for bioconversion processes.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"20 1","pages":"20251066"},"PeriodicalIF":1.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIK1 inhibits IL-1β-stimulated cartilage apoptosis and inflammation <i>in vitro</i> through the CRTC2/CREB1 signaling.","authors":"Mangmang Chen, Luyou Ye, Shenglei Lin","doi":"10.1515/biol-2022-1016","DOIUrl":"10.1515/biol-2022-1016","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a chronic degenerative joint disease that affects 70-90% of individuals over the age of 75 and over 100 million people globally. Current treatments primarily offer symptomatic relief and do not effectively halt disease progression, highlighting the need for improved therapeutic strategies. Salt-inducible kinase 1 (SIK1) plays a role in regulating key physiological processes, including gluconeogenesis, glycolysis, and bone metabolism. Despite these insights, the specific role and underlying mechanisms of SIK1 in OA pathogenesis remain inadequately understood. This study aims to elucidate the function of SIK1 in OA cells. We observed that SIK1 was downregulated in a cell model of OA. The overexpression of SIK1 was found to inhibit IL-1β-induced chondrocyte apoptosis and inflammation. Additionally, SIK1 overexpression enhanced the activation of the CRTC2/CREB1 axis, suggesting a protective role for SIK1 in cartilage cells. In summary, SIK1 exerts a protective effect against IL-1β-induced cartilage apoptosis and inflammation <i>in vitro</i> through the CRTC2/CREB1 signaling axis.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"20 1","pages":"20221016"},"PeriodicalIF":1.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889496/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rutin-chitooligosaccharide complex: Comprehensive evaluation of its anti-inflammatory and analgesic properties <i>in vitro</i> and <i>in vivo</i>.","authors":"Chuanyun Wen, Mei Zhu, Yin Wang, Jinyu Man, Ramesh Priyanka","doi":"10.1515/biol-2022-1021","DOIUrl":"10.1515/biol-2022-1021","url":null,"abstract":"<p><p>This study investigated the potential anti-inflammatory and analgesic effects of the rutin-chitooligosaccharide (R-COS) complex both <i>in vitro</i> and <i>in vivo</i>. Initially, the cytotoxicity of R-COS was assessed in RAW 264.7 cells using an MTT assay. Subsequently, an inflammatory study was conducted where R-COS demonstrated a significant reduction in various pro-inflammatory factors (nitric oxide [NO], prostaglandin E2, tumor necrosis factor-α, interleukin-6, interleukin-1, inducible nitric oxide synthase [iNOS], and cyclooxygenase [COX-2]) in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells without compromising cell viability. Furthermore, <i>in vivo</i> analysis showcased the protective effect of R-COS on zebrafish embryos exposed to inflammatory stress induced by LPS. R-COS exhibited inhibition against pro-inflammatory factors, specifically COX-2 and iNOS. Notably, R-COS played a modulatory role in calcitonin gene-related peptide and NO levels in zebrafish, reducing the expression of pro-inflammatory factors. Additionally, the study observed analgesic activity in zebrafish treated with R-COS, which mitigated pain-like behavior triggered by acetic acid. Overall, these findings highlight the potential of R-COS, derived from chitosan, as a promising anti-inflammatory agent with broad applications in healthcare and tissue engineering.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"20 1","pages":"20221021"},"PeriodicalIF":1.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COLEC10: A potential tumor suppressor and prognostic biomarker in hepatocellular carcinoma through modulation of EMT and PI3K-AKT pathways.","authors":"Rui-Sheng Ke, Yun Dai, Yan-Ling Tu, Zhao-Hui Liu, Kun-Zhai Huang, Fu-Xing Zhang","doi":"10.1515/biol-2022-0988","DOIUrl":"https://doi.org/10.1515/biol-2022-0988","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a cancer with poor prognosis, underscoring the urgent need for enhanced detection and management. This study aimed to investigate the role of Collectin Subfamily Member 10 (COLEC10) in HCC, which was revealed to be associated with various diseases. Bioinformatics tools, including GEO, cBioPortal, and TCGA, were used to identify differentially expressed genes. The prognostic significance of COLEC10 was assessed in two patient cohorts, and its functional impact on Hep3B and SMMC7721 cells was evaluated through CCK-8 and Transwell assays. The underlying mechanisms of COLEC10 in HCC progression were explored using flow cytometry and western blot. COLEC10 was downregulated in HCC and associated with poorer overall survival and disease progression. The potential interaction of COLEC10, CCBE1, and FCN3 was predicted. COLEC10, CCBE1, and FCN3 were identified as prognostic indicators for HCC. Overexpression of COLEC10 inhibited the proliferation, migration, and invasion of HCC cells. COLEC10 overexpression induced G0/G1 cell cycle arrest and suppressed epithelial-mesenchymal transition (EMT), COLEC10 regulated protein expression in the Hedgehog pathway and phosphorylation of key proteins in the PI3K-AKT pathway. COLEC10 is an independent prognostic factor of HCC. COLEC10 regulates EMT, Hedgehog, and PI3K-AKT pathways, providing new ideas for targeted therapy of HCC.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"20 1","pages":"20220988"},"PeriodicalIF":1.7,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11868708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Battling COVID-19 leveraging nanobiotechnology: Gold and silver nanoparticle-B-escin conjugates as SARS-CoV-2 inhibitors.","authors":"Ilyes Zatla, Lamia Boublenza","doi":"10.1515/biol-2022-1047","DOIUrl":"https://doi.org/10.1515/biol-2022-1047","url":null,"abstract":"<p><p>The COVID-19 pandemic, an unprecedented global health crisis, has thrust humanity into a relentless battle with a variety of treatments and vaccines against the SARS-CoV-2 virus. Recent developments in nanotechnology have garnered significant interest in the application of metallic nanoparticles (NPs); specifically, silver nanoparticles (AgNPs) and gold nanoparticles (AuNPs) have demonstrated antimicrobial and antiviral properties. This study investigates the molecular interactions between the receptor binding domains of five SARS-CoV-2 spike protein variants (Alpha, Beta, Delta, Omicron, and Gamma) and the angiotensin-converting enzyme 2 (ACE2) receptor, followed by the docking of AuNPs and AgNPs and the natural compound Beta-escin onto these complexes. As well as the inspection of both NPs against the virus main protease (Mpro) and RNA-dependent RNA polymerase (RdRp). Comprehensive computational simulations utilizing Autodock 4.2 and HDOCK server were employed to evaluate the binding affinities of these NPs toward key viral targets, SARS-CoV-2 Mpro, RdRp, and the spike glycoprotein. The results revealed that both AgNPs and AuNPs exhibited successful binding to the active pockets of SARS-CoV-2 Mpro, with slightly varying binding energies. In contrast, for RdRp, AgNPs demonstrated superior binding affinity compared to AuNPs, with differences in the residues involved in the binding pocket. AuNPs exhibited stronger binding affinities in the spike protein pocket. We also determined robust binding affinities between ACE2 and the spike variants, with the Omicron variant exhibiting the highest affinity. Subsequent docking of AuNPs and AgNPs revealed strong interactions with all ACE2-spike complexes, with AuNPs showing slightly higher affinities. The findings contribute to a deeper understanding of the interactions between NPs and viral proteins, shedding light on their mechanisms of action and their potential to offer innovative solutions for combating infectious diseases, particularly those caused by SARS-CoV-2.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"20 1","pages":"20221047"},"PeriodicalIF":1.7,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11868714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of fracture fixation surgery on cognitive function and the gut microbiota in mice with a history of stroke.","authors":"Yu Lu, Zixuan Li, Rukun Xu, Yajie Xu, Wenwen Zhang, Yong Zhang, Zhaojing Fang, Cailong Pan, Xiaoliang Wang","doi":"10.1515/biol-2022-1061","DOIUrl":"https://doi.org/10.1515/biol-2022-1061","url":null,"abstract":"<p><p>Perioperative cognitive dysfunction is a common complication in stroke patients undergoing secondary surgeries. This study investigated the effects of tibial fracture internal fixation (TFIF) surgery on cognitive function and the gut microbiota in mice with a history of stroke. Using the middle cerebral artery occlusion method to induce stroke, we assessed cognitive function via the fear conditioning test and analyzed the gut microbiota through 16S rRNA sequencing. Compared with those in the normal and stroke groups, the cognitive function of the mice in the stroke group that underwent TFIF surgery was significantly impaired. Gut microbiota analysis revealed significant changes in beta diversity, but not in alpha diversity, in these mice. Additionally, TFIF surgery increased microglial activation and IL-1β and lipopolysaccharide (LPS) levels in the brain while reducing α-defensin levels and increasing IL-1β and LPS levels in the colon. These results suggest that TFIF surgery exacerbates cognitive impairment in stroke mice, possibly through alterations in the gut microbiota that impair intestinal defense and promote inflammation. This study highlights the critical role of the gut microbiome in cognitive function and perioperative outcomes, offering insights into potential therapeutic strategies for perioperative cognitive dysfunction in stroke patients.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"20 1","pages":"20221061"},"PeriodicalIF":1.7,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11868713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of alginate-coated gold nanoparticles against antibiotics-resistant <i>Staphylococcus</i> and <i>Streptococcus</i> pathogens of acne origins.","authors":"Hanan A Abbas, Ali A Taha, Ghassan M Sulaiman, Amer Al Ali, Humood Al Shmrany, Haralambos Stamatis, Hamdoon A Mohammed, Riaz A Khan","doi":"10.1515/biol-2022-1045","DOIUrl":"https://doi.org/10.1515/biol-2022-1045","url":null,"abstract":"<p><p>Acne is a serious multifactorial inflammatory disease that leads to significant and long-lasting changes. The widespread occurrence of bacterial acne and the excessive use of antibiotics to treat it have increased resistance to antibiotic treatment and led researchers to seek and develop newer antimicrobial agents suitable for various medical purposes. In this study, alginate-coated gold nanoparticles (GANPs), synthesized by the previously reported known method, using sodium alginate and gold salt, investigated the efficacy of the GANPs against various clinical isolates of <i>Staphylococcus</i>, i.e., <i>Staphylococcus aureus</i>, <i>Staphylococcus lentus</i>, <i>Staphylococcus haemolyticus</i>, and <i>Streptococcus</i> <i>thoraltensis</i>, which were all obtained from patients suffering from acne conditions. The results showed that the GANPs had antibacterial efficacy against all the acne-isolated bacteria. The GANP activity against bacterial resistance suggested that metal-based nanoparticulate materials are a promising alternative for treating multidrug-resistant microorganisms.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"20 1","pages":"20221045"},"PeriodicalIF":1.7,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11868717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurodegenerative diseases and neuroinflammation-induced apoptosis.","authors":"Shi Huang, Yaxin Lu, Wanzhen Fang, Yanjiao Huang, Qiang Li, Zhiliang Xu","doi":"10.1515/biol-2022-1051","DOIUrl":"https://doi.org/10.1515/biol-2022-1051","url":null,"abstract":"<p><p>Neuroinflammation represents a critical pathway in the brain for the clearance of foreign bodies and the maintenance of homeostasis. When the neuroinflammatory process is dysregulate, such as the over-activation of microglia, which results in the excessive accumulation of free oxygen and inflammatory factors in the brain, among other factors, it can lead to an imbalance in homeostasis and the development of various diseases. Recent research has indicated that the development of numerous neurodegenerative diseases is closely associated with neuroinflammation. The pathogenesis of neuroinflammation in the brain is intricate, involving alterations in numerous genes and proteins, as well as the activation and inhibition of signaling pathways. Furthermore, excessive inflammation can result in neuronal cell apoptosis, which can further exacerbate the extent of the disease. This article presents a summary of recent studies on the relationship between neuronal apoptosis caused by excessive neuroinflammation and neurodegenerative diseases. The aim is to identify the link between the two and to provide new ideas and targets for exploring the pathogenesis, as well as the prevention and treatment of neurodegenerative diseases.</p>","PeriodicalId":19605,"journal":{"name":"Open Life Sciences","volume":"20 1","pages":"20221051"},"PeriodicalIF":1.7,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11868719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}