Life Science Alliance最新文献_第2页

Wnt10b signaling regulates replication stress-induced chromosomal instability in human cancer. Wnt10b信号调节人类癌症中复制应激诱导的染色体不稳定性。

IF 2.9 2区生物学

Life Science Alliance Pub Date : 2025-08-22 Print Date: 2025-11-01 DOI: 10.26508/lsa.202503295

Alexander Haas, Friederike Wenz, Janina Hattemer, Janine Wesslowski, Gary Davidson, Oksana Voloshanenko, Michael Boutros, Sergio P Acebron, Holger Bastians

引用次数: 0

Dysregulated SASS6 expression promotes increased ciliogenesis and cell invasion phenotypes. 失调的SASS6表达促进纤毛发生和细胞侵袭表型的增加。

IF 2.9 2区生物学

Life Science Alliance Pub Date : 2025-08-18 Print Date: 2025-10-01 DOI: 10.26508/lsa.202402820

Eleanor Hargreaves, Rebecca Collinson, Andrew D Jenks, Adina Staszewski, Athanasios Tsalikis, Raquel Bodoque, Mar Arias-Garcia, Yasmin Abdi, Abdulaziz Al-Malki, Yinyin Yuan, Rachael Natrajan, Syed Haider, Thomas Iskratsch, Won-Jing Wang, Susana Godinho, Nicolaos J Palaskas, Fernando Calvo, Igor Vivanco, Tobias Zech, Barbara E Tanos

{"title":"Dysregulated SASS6 expression promotes increased ciliogenesis and cell invasion phenotypes.","authors":"Eleanor Hargreaves, Rebecca Collinson, Andrew D Jenks, Adina Staszewski, Athanasios Tsalikis, Raquel Bodoque, Mar Arias-Garcia, Yasmin Abdi, Abdulaziz Al-Malki, Yinyin Yuan, Rachael Natrajan, Syed Haider, Thomas Iskratsch, Won-Jing Wang, Susana Godinho, Nicolaos J Palaskas, Fernando Calvo, Igor Vivanco, Tobias Zech, Barbara E Tanos","doi":"10.26508/lsa.202402820","DOIUrl":"10.26508/lsa.202402820","url":null,"abstract":"Centriole and/or cilium defects are characteristic of cancer cells and have been linked to cancer cell invasion. However, the mechanistic bases of this regulation remain incompletely understood. Spindle assembly abnormal protein 6 homolog (SAS-6) is essential for centriole biogenesis and cilium formation. SAS-6 levels decrease at the end of mitosis and G1, resulting from APCCdh1-targeted degradation. To examine the biological consequences of unrestrained SAS-6 expression, we used a nondegradable SAS-6 mutant (SAS-6ND). This led to an increase in ciliation and cell invasion and caused an up-regulation of the YAP/TAZ pathway. SAS-6ND expression resulted in cell morphology changes, nuclear deformation, and YAP translocation to the nucleus, resulting in increased TEAD-dependent transcription. SAS-6-mediated invasion was prevented by YAP down-regulation or by blocking ciliogenesis. Similarly, down-regulation of SAS-6 in DMS273, a highly invasive and highly ciliated lung cancer cell line that overexpresses SAS-6, completely blocked cell invasion and depleted YAP protein levels. Thus, our data provide evidence for a defined role of SAS-6 in cell invasion through the activation of the YAP/TAZ pathway.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"8 10","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12361644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144873889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

In vivo detection of antisense HIV-1 transcripts in untreated and ART-treated individuals. 在未治疗和抗逆转录病毒治疗的个体中检测反义HIV-1转录物。

IF 2.9 2区生物学

Life Science Alliance Pub Date : 2025-07-14 Print Date: 2025-09-01 DOI: 10.26508/lsa.202503204

Adam A Capoferri, Rachel Sklutuis, Toluleke O Famuyiwa, Sachi Pathak, Rui Li, Jason W Rausch, Brian T Luke, Rebecca Hoh, Steven G Deeks, John W Mellors, John M Coffin, Jennifer L Groebner, Fabio Romerio, Mary F Kearney

{"title":"In vivo detection of antisense HIV-1 transcripts in untreated and ART-treated individuals.","authors":"Adam A Capoferri, Rachel Sklutuis, Toluleke O Famuyiwa, Sachi Pathak, Rui Li, Jason W Rausch, Brian T Luke, Rebecca Hoh, Steven G Deeks, John W Mellors, John M Coffin, Jennifer L Groebner, Fabio Romerio, Mary F Kearney","doi":"10.26508/lsa.202503204","DOIUrl":"10.26508/lsa.202503204","url":null,"abstract":"Natural antisense transcripts (AST) are expressed in eukaryotes, prokaryotes, and viruses and can possess regulatory functions at the transcriptional and/or post-transcriptional levels. In vitro studies have shown that HIV-1 AST promote viral latency through epigenetic silencing of the proviral 5' long terminal repeat. However, expression of AST in vivo has not been convincingly demonstrated. Here, we used single RNA template amplification and sequencing to demonstrate expression of AST in unstimulated PBMC collected from people with HIV-1 (PWH). Our results show that expression levels of AST could be higher during ART compared with untreated individuals and that clones of infected cells persisting under ART continue to express HIV AST. This study is the first to verify HIV-1 AST expression in vivo with sequencing, documenting AST presence without cellular activation and suggest its natural occurrence in PWH. These findings advance our understanding of HIV-1 persistence and underscore the need for larger studies to determine if targeting AST in viral reservoirs could lead to new approaches for the design of strategies towards achieving HIV remission without ART.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"8 9","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12260654/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

DEK promotes mammary hyperplasia and is associated with H3K27me3 epigenetic modifications. DEK促进乳腺增生，并与H3K27me3表观遗传修饰相关。

IF 2.9 2区生物学

Life Science Alliance Pub Date : 2025-06-25 Print Date: 2025-09-01 DOI: 10.26508/lsa.202503230

Megan E Johnstone, Ashley L Leck, Taylor E Lange, Katherine E Wilcher, Miranda S Shephard, Aditi Paranjpe, Sophia Schutte, Susanne I Wells, Ferdinand Kappes, Nathan Salomonis, Lisa M Privette Vinnedge

{"title":"DEK promotes mammary hyperplasia and is associated with H3K27me3 epigenetic modifications.","authors":"Megan E Johnstone, Ashley L Leck, Taylor E Lange, Katherine E Wilcher, Miranda S Shephard, Aditi Paranjpe, Sophia Schutte, Susanne I Wells, Ferdinand Kappes, Nathan Salomonis, Lisa M Privette Vinnedge","doi":"10.26508/lsa.202503230","DOIUrl":"10.26508/lsa.202503230","url":null,"abstract":"The DEK chromatin remodeling protein has oncogenic functions in breast cancers, but its functional role in normal mammary gland epithelium has remained unexplored. We developed two novel genetically engineered mouse models to study the role of Dek in normal mammary gland biology in vivo. Mammary gland-specific Dek transgenic mice developed hyperplasia and had a transcriptional profile that revealed increased expression of cell cycle, mammary stem/progenitor, and lactation-associated genes. Conversely, Dek knockout mice exhibited mammary gland functional defects resulting in dramatically reduced pup survival. Analysis of previously published scRNA-sequencing of mouse mammary glands revealed that Dek is most highly expressed in mammary stem cells and alveolar progenitor cells, supporting the observed phenotypes. Mechanistically, we discovered that Dek is a modifier of Ezh2 methyltransferase activity, up-regulating the levels of histone H3K27me3 to control gene transcription. Combined, this is the first report to show that Dek promotes proliferation of mammary epithelial cells via transcriptional deregulation of cell cycle genes, potentially via epigenetic mechanisms, in vivo.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"8 9","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144497427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

AURKA controls oocyte spindle assembly checkpoint and chromosome alignment by HEC1 phosphorylation. AURKA通过HEC1磷酸化控制卵母细胞纺锤体组装检查点和染色体排列。

IF 2.9 2区生物学

Life Science Alliance Pub Date : 2025-05-06 Print Date: 2025-07-01 DOI: 10.26508/lsa.202403146

Cecilia S Blengini, Shuang Tang, Robert J Mendola, G John Garrisi, Jason E Swain, Karen Schindler

{"title":"AURKA controls oocyte spindle assembly checkpoint and chromosome alignment by HEC1 phosphorylation.","authors":"Cecilia S Blengini, Shuang Tang, Robert J Mendola, G John Garrisi, Jason E Swain, Karen Schindler","doi":"10.26508/lsa.202403146","DOIUrl":"10.26508/lsa.202403146","url":null,"abstract":"In human oocytes, meiosis I is error-prone, causing early miscarriages and developmental disorders. The Aurora protein kinases are key regulators of chromosome segregation in mitosis and meiosis, and their dysfunction is associated with aneuploidy. Oocytes express three Aurora kinase (AURK) proteins, but only AURKA is necessary and sufficient to support oocyte meiosis in mice. However, the unique molecular contributions to ensuring high egg quality of AURKA remain unclear. Here, using a combination of genetic and pharmacological approaches, we evaluated how AURKA phosphorylation regulates outer kinetochore function during oocyte meiosis. We found that the outer kinetochore protein Ndc80/HEC1 is constitutively phosphorylated at multiple residues by Aurora kinases during meiosis I, but that serine 69 is specifically phosphorylated by AURKA in mouse and human oocytes. We further show that serine 69 phosphorylation contributes to spindle assembly checkpoint activation and chromosome alignment during meiosis I. These results provide a fundamental mechanistic understanding of how AURKA regulates meiosis and kinetochore function to ensure meiosis I fidelity.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"8 7","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12056248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

DNA methylation predicts infection risk in kidney transplant recipients. DNA甲基化预测肾移植受者感染风险。

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2025-05-05 Print Date: 2025-07-01 DOI: 10.26508/lsa.202403124

Fei-Man Hsu, Harry Pickering, Liudmilla Rubbi, Michael Thompson, Elaine F Reed, Matteo Pellegrini, Joanna M Schaenman

{"title":"DNA methylation predicts infection risk in kidney transplant recipients.","authors":"Fei-Man Hsu, Harry Pickering, Liudmilla Rubbi, Michael Thompson, Elaine F Reed, Matteo Pellegrini, Joanna M Schaenman","doi":"10.26508/lsa.202403124","DOIUrl":"10.26508/lsa.202403124","url":null,"abstract":"Kidney transplantation (KTx) is the method of choice for treating kidney failure. Identifying biomarkers predictive of transplant (Tx) outcomes is critical to optimize KTx; however, the immunosuppressive therapies required after KTx must also be considered. We applied targeted bisulfite sequencing (TBS-seq) to PBMCs isolated from 90 patients, with samples collected pre- and post-Tx (day 90), to measure DNA methylation changes. Our findings indicate that the PBMC DNA methylome is significantly affected by induction immunosuppression with anti-thymocyte globulin (ATG). We discovered that the risk of infection can be predicted using DNA methylation profiles, but not gene expression profiles. Specifically, 515 CpG loci associated with 275 genes were significantly impacted by ATG induction, even after accounting for age, sex, and cell-type composition. Notably, ATG-associated hyper-methylation down-regulates genes critical for immune response. In conclusion, this clinical omics study reveals that the immunosuppressant ATG profoundly impacts the DNA methylome of KTx recipients and identifies biomarkers that could be used in pre-Tx screening of patients vulnerable to infection, thereby informing immunosuppression strategies post-Tx.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"8 7","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12053434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144000750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Message from the new Executive Editor. 来自新任执行编辑的信息。

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2025-04-22 Print Date: 2025-05-01 DOI: 10.26508/lsa.202503362

Tim Fessenden

引用次数: 0

STAT5B leukemic mutations, altering SH2 tyrosine 665, have opposing impacts on immune gene programs. STAT5B白血病突变，改变SH2酪氨酸665，对免疫基因程序有相反的影响。

IF 2.9 2区生物学

Life Science Alliance Pub Date : 2025-04-14 Print Date: 2025-07-01 DOI: 10.26508/lsa.202503222

Hye Kyung Lee, Jichun Chen, Rachael L Philips, Sung-Gwon Lee, Xingmin Feng, Zhijie Wu, Chengyu Liu, Aaron B Schultz, Molly Dalzell, Manja Meggendorfer, Claudia Haferlach, Foster Birnbaum, Joel A Sexton, Amy E Keating, John J O'Shea, Neal S Young, Alejandro V Villarino, Priscilla A Furth, Lothar Hennighausen

{"title":"STAT5B leukemic mutations, altering SH2 tyrosine 665, have opposing impacts on immune gene programs.","authors":"Hye Kyung Lee, Jichun Chen, Rachael L Philips, Sung-Gwon Lee, Xingmin Feng, Zhijie Wu, Chengyu Liu, Aaron B Schultz, Molly Dalzell, Manja Meggendorfer, Claudia Haferlach, Foster Birnbaum, Joel A Sexton, Amy E Keating, John J O'Shea, Neal S Young, Alejandro V Villarino, Priscilla A Furth, Lothar Hennighausen","doi":"10.26508/lsa.202503222","DOIUrl":"10.26508/lsa.202503222","url":null,"abstract":"STAT5B is a vital transcription factor for lymphocytes. Here, the function of two STAT5B mutations from human T-cell leukemias: one substituting tyrosine 665 with phenylalanine (STAT5BY665F) and the other with histidine (STAT5BY665H), was interrogated. In silico modeling predicted divergent energetic effects on homodimerization with a range of pathogenicity. In primary T cells in vitro, STAT5BY665F showed gain-of-function, whereas STAT5BY665H demonstrated loss-of-function. Introducing the mutation into the mouse genome illustrated that the gain-of-function Stat5b Y665F mutation resulted in accumulation of CD8+ effector and memory and CD4+ regulatory T cells, altering CD8+/CD4+ ratios. In contrast, STAT5BY665H \"knock-in\" mice showed diminished CD8+ effector and memory and CD4+ regulatory T cells. In contrast to WT STAT5B, the STAT5BY665F variant displayed greater STAT5 phosphorylation, DNA binding, and transcriptional activity after cytokine activation, whereas the STAT5BY665H variant resembled a null. The work exemplifies how joining in silico and in vivo studies of single nucleotides deepens our understanding of disease-associated variants, revealing structural determinants of altered function, defining mechanistic roles, and, specifically here, identifying a gain-of-function variant that does not directly induce hematopoietic malignancy.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"8 7","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11999048/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Predicting cell cycle stage from 3D single-cell nuclear-stained images. 从三维单细胞核染色图像预测细胞周期阶段。

IF 2.9 2区生物学

Life Science Alliance Pub Date : 2025-04-03 Print Date: 2025-06-01 DOI: 10.26508/lsa.202403067

Gang Li, Eva K Nichols, Valentino E Browning, Nicolas J Longhi, Madison Sanchez-Forman, Conor K Camplisson, Brian J Beliveau, William Stafford Noble

{"title":"Predicting cell cycle stage from 3D single-cell nuclear-stained images.","authors":"Gang Li, Eva K Nichols, Valentino E Browning, Nicolas J Longhi, Madison Sanchez-Forman, Conor K Camplisson, Brian J Beliveau, William Stafford Noble","doi":"10.26508/lsa.202403067","DOIUrl":"10.26508/lsa.202403067","url":null,"abstract":"The cell cycle governs the proliferation of all eukaryotic cells. Profiling cell cycle dynamics is therefore central to basic and biomedical research. However, current approaches to cell cycle profiling involve complex interventions that may confound experimental interpretation. We developed CellCycleNet, a machine learning (ML) workflow, to simplify cell cycle staging from fluorescent microscopy data with minimal experimenter intervention and cost. CellCycleNet accurately predicts cell cycle phase using only a fluorescent nuclear stain (DAPI) in fixed interphase cells. Using the Fucci2a cell cycle reporter system as ground truth, we collected two benchmarking image datasets and trained 2D and 3D ML models-of support vector machine and deep neural network architecture-to classify nuclei in the G1 or S/G2 phases. Our results show that 3D CellCycleNet outperforms support vector machine models on each dataset. When trained on two image datasets simultaneously, CellCycleNet achieves the highest classification accuracy (AUROC of 0.94-0.95). Overall, we found that using 3D features, rather than 2D features alone, significantly improves classification performance for all model architectures. We released our image data, models, and software as a community resource.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"8 6","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11969383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The MFN2 Q367H variant reveals a novel pathomechanism connected to mtDNA-mediated inflammation. MFN2 Q367H变异揭示了与mtdna介导的炎症相关的一种新的病理机制。

IF 3.3 2区生物学

Life Science Alliance Pub Date : 2025-04-02 Print Date: 2025-06-01 DOI: 10.26508/lsa.202402921

Mashiat Zaman, Govinda Sharma, Walaa Almutawa, Tyler Gb Soule, Rasha Sabouny, Matt Joel, Armaan Mohan, Cole Chute, Jeffrey T Joseph, Gerald Pfeffer, Timothy E Shutt

{"title":"The MFN2 Q367H variant reveals a novel pathomechanism connected to mtDNA-mediated inflammation.","authors":"Mashiat Zaman, Govinda Sharma, Walaa Almutawa, Tyler Gb Soule, Rasha Sabouny, Matt Joel, Armaan Mohan, Cole Chute, Jeffrey T Joseph, Gerald Pfeffer, Timothy E Shutt","doi":"10.26508/lsa.202402921","DOIUrl":"10.26508/lsa.202402921","url":null,"abstract":"Pathogenic variants in the mitochondrial protein MFN2 are typically associated with a peripheral neuropathy phenotype, but can also cause a variety of additional pathologies including myopathy. Here, we identified an uncharacterized MFN2 variant, Q367H, in a patient diagnosed with late-onset distal myopathy, but without peripheral neuropathy. Supporting the hypothesis that this variant contributes to the patient's pathology, patient fibroblasts and transdifferentiated myoblasts showed changes consistent with impairment of several MFN2 functions. We also observed mtDNA outside of the mitochondrial network that colocalized with early endosomes, and measured activation of both TLR9 and cGAS-STING inflammation pathways that sense mtDNA. Re-expressing the Q367H variant in MFN2 KO cells also induced mtDNA release, demonstrating this phenotype is a direct result of the variant. As elevated inflammation can cause myopathy, our findings linking the Q367H MFN2 variant with elevated TLR9 and cGAS-STING signalling can explain the patient's myopathy. Thus, we characterize a novel MFN2 variant in a patient with an atypical presentation that separates peripheral neuropathy and myopathy phenotypes, and establish a potential pathomechanism connecting MFN2 dysfunction to mtDNA-mediated inflammation.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"8 6","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11966011/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0