Biochemical and biophysical research communications最新文献

{"title":"Localization of Asgard archaeal ESCRT proteins to eukaryotic cellular structures","authors":"Kishore Babu Naripogu ,&nbsp;Yee Han Tee ,&nbsp;Yosuke Senju ,&nbsp;Alexander Bershadsky ,&nbsp;Robert C. Robinson","doi":"10.1016/j.bbrc.2026.153301","DOIUrl":"10.1016/j.bbrc.2026.153301","url":null,"abstract":"<div><div>The emergence of internal membrane systems was a defining step in eukaryogenesis, but how pre-eukaryotic proteins were adapted to these novel compartments and structures remains unclear. Asgard archaea, the closest known prokaryotic relatives of eukaryotes, encode homologs of ESCRT (Endosomal Sorting Complex Required for Transport) proteins, which mediate membrane remodeling in eukaryotic cells, processes ranging from endosomal sorting to cytokinetic abscission. Here, we show that ESCRT-II and ESCRT-III homologs, VSP4 and ubiquitin from the Asgard achaeon <em>Promethearchaeum syntrophicum</em> (MK-D1) are recruited to discrete structures when expressed in human cells. These archaeal proteins localize to canonical eukaryotic ESCRT recruitment sites, midbodies and centrosomes, structures which are absent from MK-D1. This localization reflects conserved molecular interactions that predate the emergence of eukaryotic internal membranes and other eukaryotic cellular structures. These findings support a model in which protein machines were repurposed to support cellular complexity during eukaryogenesis, allowing the integration of ancestral ESCRT molecular functions and networks in to novel cellular architectures.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153301"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146025591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Opposing effects of Gα12 and Gα13 loss on myotube size regulation via mTORC1 signaling","authors":"Mai Kubota ,&nbsp;Shuhei Fujita ,&nbsp;Ryohei Kamata ,&nbsp;Kazuma Tamura ,&nbsp;Keiichiro Sugimoto ,&nbsp;Tomoya Kitakaze ,&nbsp;Naoki Harada ,&nbsp;Ryoichi Yamaji","doi":"10.1016/j.bbrc.2026.153326","DOIUrl":"10.1016/j.bbrc.2026.153326","url":null,"abstract":"<div><div>To reduce the risk of diseases caused by a reduction in skeletal muscle mass and quality, it is important to understand the molecular mechanisms underlying the maintenance and improvement of skeletal muscle mass and quality. Gα12 and/or Gα13 have been implicated in the regulation of myotube size through the mechanistic target of rapamycin complex 1 (mTORC1) signaling; however, their specific and potentially distinct molecular mechanisms remain unknown. Knockdown and rescue experiments revealed that the loss of Gα12 decreased myotube size, whereas the loss of Gα13 increased it. Gα12 knockdown reduced the phosphorylation levels of mTORC1 signaling components (Akt, mTOR, and p70S6K) and the levels of puromycin-labeled proteins, whereas Gα13 knockdown increased these levels. Loss of Gα12 or Gα13 suppressed SRF-RE-dependent transcriptional activity. While expression of a constitutively active form of RhoA (RhoA-CA) activated SRF-RE activity, notably, RhoA-CA expression did not affect myotube size, nor did it alter myotube atrophy induced by Gα12 knockdown or hypertrophy induced by Gα13 knockdown. Depletion of Gα12 increased the mRNA expression of oxidative myosin heavy chain (MyHC) isoforms <em>Myh7</em> and <em>Myh2</em> and decreased the mRNA expression of <em>Myh1</em> and <em>Myh4</em>, whereas depletion of Gα13 increased the mRNA expression of <em>Myh7</em>, <em>Myh2</em>, <em>Myh1</em>, and <em>Myh4</em>. These results indicate that loss of Gα12 induces myotube atrophy by suppressing mTORC1 signaling and protein synthesis, whereas loss of Gα13 induces myotube hypertrophy by enhancing these processes, likely independent of SRF-RE-mediated transcription. Notably, Gα12 and Gα13 oppositely regulated the mRNA expression of MyHC isoforms, particularly <em>Myh1</em> and <em>Myh4</em>.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153326"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146025602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural characterization of a glucose-activated β-glucosidase from Bacillus thermoamylovorans","authors":"Wendi Yang ,&nbsp;Panpan Dong ,&nbsp;Guosi Li ,&nbsp;Hanyu Wu ,&nbsp;Lanlan Li ,&nbsp;Min Gao ,&nbsp;Lin Li ,&nbsp;Yunkun Wu","doi":"10.1016/j.bbrc.2026.153261","DOIUrl":"10.1016/j.bbrc.2026.153261","url":null,"abstract":"<div><div>β-glucosidases play crucial roles in lignocellulosic biomass conversion, but their applications were limited by thermostability and glucose sensitivity. In this study, the high-resolution crystal structure of a thermostable glucose-activated β-glucosidase Bgl52 from <em>Bacillus thermoamylovorans</em> was determined at 2.00 Å. Bgl52 belongs to the GH1 family, and exhibited a canonical (β/α)₈ TIM barrel architecture typical to GH1 enzymes. Comparison analysis and site-directed mutagenesis revealed that its catalytic sites were Glu166 and Glu353 and its gatekeeper residues were Trp169 and Leu173, which involved in the glucose tolerance. Features contributing to its thermostability were also explored, including the composition of amino acids, number of mobile loops, total area of major hydrophobic clusters and number of salt bridges. Our study shed light on the molecular basis for glucose tolerance and thermostability of GH1 β-glucosidases and provide possibility of improving the characteristics for potential industrial applications by structure-guided engineering.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153261"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146006638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical advances in CD47-SIRPα axis-targeted cancer immunotherapy: Mechanisms, strategies, challenges, and future perspectives","authors":"Yuanyuan Li ,&nbsp;Xiaomei He ,&nbsp;Hongli Zhou,&nbsp;Yu Tian,&nbsp;Qingqing Zhang,&nbsp;Yiguo Zhou,&nbsp;Jianyun Zhou","doi":"10.1016/j.bbrc.2026.153330","DOIUrl":"10.1016/j.bbrc.2026.153330","url":null,"abstract":"<div><div>The CD47-SIRPα signaling axis has emerged as a promising target in cancer immunotherapy by disrupting the “don't eat me” signal, thereby promoting macrophage-mediated phagocytosis. However, its clinical translation confronts a significant challenge due to the “on-target off-tumor” effect, primarily leading to hematological toxicity, notably anemia. This challenge was underscored by a pivotal setback in the field: the Phase III trial of Magrolimab, the first anti-CD47 therapy to reach this stage, which failed to meet its primary endpoint and ultimately led to the discontinuation of its development program. This comprehensive review systematically traces the evolution of therapeutic strategies targeting the CD47-SIRPα axis, from first-generation monoclonal antibodies to advanced fusion proteins, bispecific antibodies, and cutting-edge approaches such as oncolytic viruses and CAR-macrophages. It also provides a detailed summary of the clinical trial landscape, analyzing the differential efficacy observed between hematological malignancies and solid tumors. Furthermore, we summarize the major clinical challenges, including safety concerns, resistance mechanisms, and diagnostic complexities. By synthesizing these key findings, this review provides valuable insights for optimizing future drug design, refining combination regimens, and guiding patient selection strategies, thereby offering a crucial reference for overcoming current limitations and fully realizing the therapeutic potential of this promising axis.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153330"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146026172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of CDC25C attenuates IL-17A-driven keratinocyte hyperproliferation and psoriasis progression","authors":"Xuejiao Liang ,&nbsp;Ningxin Wang ,&nbsp;Quanyao Yang ,&nbsp;Xuecheng Shen ,&nbsp;Wenxuan Qiao ,&nbsp;Qiang Xu ,&nbsp;Qiong Luo","doi":"10.1016/j.bbrc.2026.153342","DOIUrl":"10.1016/j.bbrc.2026.153342","url":null,"abstract":"<div><div>Psoriasis is an IL-17-driven chronic inflammatory skin disease characterized by excessive keratinocyte proliferation. Although anti-IL-17 biologics have shown substantial clinical benefit, incomplete efficacy and disease recurrence remain common, underscoring the need to identify additional downstream targets. We previously identified CDC25C as a key effector in a non-canonical IL-17A pathway that promotes epidermal hyperplasia. Here, we explored its therapeutic potential. Analysis of single-cell RNA-seq datasets from psoriatic patients revealed that CDC25C was significantly upregulated in lesional skin and selectively enriched in proliferative and inflammatory epidermal keratinocyte subsets. <em>In vitro</em>, IL-17A increased CDC25C expression and promoted keratinocytes proliferation. CDC25C inhibition with NSC95397 induced G2-phase arrest and significantly suppressed keratinocyte hyperproliferation and migration. Notably, it did not impair classical IL-17-induced proinflammatory factors expression, such as <em>IL6</em> and <em>CSF1</em>. In an IMQ-induced psoriasis-like mouse model, CDC25C inhibition markedly alleviated epidermal hyperplasia, splenomegaly, and keratinocyte proliferation without affecting upstream cytokines such as <em>I</em>l<em>-6</em> or <em>T</em>nf. This selective inhibition profile is consistent with the operation of CDC25C within a non-canonical IL-17 signaling pathway. In addition, prophylactic administration of NSC95397 prior to disease induction provided stronger protection than therapeutic treatment, suggesting the role of CDC25C during early disease initiation. Together, these findings identify CDC25C as a key mediator of IL-17-driven keratinocyte hyperproliferation and validate it as a promising therapeutic strategy.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153342"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Plasmodium falciparum Raf kinase inhibitor is a lipid binding protein that interacts with and regulates the activity of PfCDPK1, an essential plant-like kinase required for red blood cell invasion” [Biochem. Biophys. Res. Commun. 749 (2025) 151350]","authors":"Manish Sharma ,&nbsp;Deepak Krishnan ,&nbsp;Ayushi Singh ,&nbsp;Pooja Negi ,&nbsp;Komal Rani ,&nbsp;Amjesh Revikumar ,&nbsp;Manoj Munde ,&nbsp;Abhisheka Bansal","doi":"10.1016/j.bbrc.2026.153375","DOIUrl":"10.1016/j.bbrc.2026.153375","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153375"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcription factor PITX2 protects intestinal epithelial cells against inflammatory stress: Implications for ulcerative colitis rectal predilection and therapeutic resistance","authors":"Hirosumi Suzuki ,&nbsp;Xiangning Guo ,&nbsp;Taku Sawafuji ,&nbsp;Satoshi Fukuda ,&nbsp;Mikiya Fujiwara ,&nbsp;Kazunori Sasaki ,&nbsp;Takeshi Yamada ,&nbsp;Yoshiyuki Yamamoto ,&nbsp;Mariko Kobayashi ,&nbsp;Toshiaki Narasaka ,&nbsp;Hiroko Isoda ,&nbsp;Kiichiro Tsuchiya","doi":"10.1016/j.bbrc.2026.153312","DOIUrl":"10.1016/j.bbrc.2026.153312","url":null,"abstract":"<div><div>Ulcerative Colitis (UC) is an inflammatory bowel disease (IBD) primarily characterized by inflammation of the colonic mucosa. Although the disease frequently demonstrates a predilection for the rectum, the underlying mechanism for this specific localization and the reasons for the therapeutic resistance observed in the rectum remain unknown. This study hypothesized that differences in intestinal epithelial cells (IECs) between the lesional rectum and the non-lesional ascending colon contribute to UC pathogenesis. We analyzed gene expression in patient-matched colon organoids to control for individual variables. We identified the transcription factor PITX2 as being elevated in organoids derived from non-lesional ascending colon tissue. Under inflammatory stimulation, PITX2 knockdown significantly reduced the proliferative and sphere-formation capacity of IECs, driven by a marked increase in apoptosis. This heightened vulnerability was independent of enhanced inflammatory signaling (NF-κB) or reactive oxygen species (ROS) production. In conclusion, PITX2 exerts a protective function by promoting IEC survival and inhibiting apoptosis under inflammatory stress. Its relative absence in the rectum may explain why this segment is the primary site of UC onset and therapeutic resistance. PITX2 is a novel candidate molecule regulating the colonic epithelial defense response in IBD.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153312"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146025592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GALNT3-mediated AKT1 glycosylation activates the AKT1/CREB signaling pathway to inhibit high glucose-induced spermatogenic cell apoptosis and mitochondrial dysfunction","authors":"Yong Zhao,&nbsp;Jia Luo,&nbsp;Lu Wu","doi":"10.1016/j.bbrc.2026.153329","DOIUrl":"10.1016/j.bbrc.2026.153329","url":null,"abstract":"<div><div>Diabetes-induced testicular damage (DITD) is a common complication of diabetes mellitus (DM), impairing spermatogenesis and contributing to male infertility, a condition associated with polypeptide N-acetylgalactoacyltransferase 3 (GALNT3), a critical enzyme for protein glycosylation. However, the role of GALNT3 in DITD progression remains elusive. This study elucidated the action of GALNT3 on DITD pathogenesis and investigated the potential underlying mechanism. Mouse spermatogenic GC-1 spg cells were stimulated by high glucose (HG) to establish <em>the in vitro</em> model of DITD. Cell viability and apoptosis were evaluated utilizing the CCK-8 method and flow cytometry, respectively. Reactive oxygen species (ROS) production and mitochondrial membrane potential (MMP) levels were measured utilizing flow cytometry. Coimmunoprecipitation was performed to measure the binding of GALNT3 to AKT1. The GalNAc-type O-glycosylation of AKT1 was defined utilizing the lectin pull-down assay. The ChIP-PCR and dual-luciferase reporter assays were performed to determine the binding of cAMP response element-binding (CREB) to the GLANT3 promoter. GLANT3 expression was reduced in HG-induced GC-1 spg cells. Overexpressed <em>Glant3</em> restrained HG-stimulated apoptosis and ROS production and elevated the HG-induced decrease of the MMP levels of GC-1 spg cells. Besides, AKT1 signaling pathway inactivation mediated the induction of silenced <em>Glant3</em> on apoptosis and mitochondrial dysfunction. Further investigation found that GLANT3 induced AKT1 glycosylation to suppress HG-induced apoptosis and mitochondrial dysfunction. Moreover, transcription factor CREB could bind to the <em>Glant3</em> promoter and regulate promoter activity. GALNT3-mediated AKT1 glycosylation activated the AKT1/CREB signaling pathway to inhibit HG-induced spermatogenic cell apoptosis and mitochondrial dysfunction. Therefore, GLANT3 might be a valuable target for DITD management.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153329"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146059198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Live-cell atomic force microscopy nanoprofiling reveals protease-responsive membrane protein dynamics and cell-type-specific surface codes","authors":"Xueyan Liu ,&nbsp;Lin Liu","doi":"10.1016/j.bbrc.2026.153338","DOIUrl":"10.1016/j.bbrc.2026.153338","url":null,"abstract":"<div><div>Cell membranes, as phospholipid-protein interfaces, regulate cellular recognition and communication. However, real-time nanoscale observation of native membrane proteins in live cells remains challenging. Here, we employed atomic force microscopy (AFM) to characterize the surface properties of live HeLa cells, and found that mild trypsin digestion reduced significantly surface roughness (Rq: ∼150 → 120 nm) and adhesion force (∼27 → 20 pN), whereas chemical fixation obscured these dynamic changes. Comparative AFM imaging across four cell lines revealed distinct topographies: MCF-7 cancer cells exhibited the highest surface roughness (Rq = 212 nm), versus smoother morphology of NIH-3T3 fibroblasts (Rq = 172 nm). These findings demonstrate that nanoscale surface morphology encodes cell identity, functional state, and malignancy, with increased roughness reflecting complex membrane protein organization. Live-cell AFM thus decodes membrane protein dynamics and cell-type-specific surface codes, offering a powerful platform for physiological studies and translational applications in biology, cancer research, neuroscience, and drug development.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153338"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146026171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporal changes in Krüppel-like factor 2 and thrombomodulin correlate with coagulation, endothelial, and liver damage in exertional heat stroke rats","authors":"Yuqi Shen ,&nbsp;Chunyang Liu ,&nbsp;Zewei Wang ,&nbsp;Hongxu Jin ,&nbsp;Ying Liu","doi":"10.1016/j.bbrc.2026.153327","DOIUrl":"10.1016/j.bbrc.2026.153327","url":null,"abstract":"<div><div>The Krüppel-like Factor 2 (KLF2) -Thrombomodulin (TM) axis is crucial for maintaining vascular homeostasis and coagulation balance. This study investigated its dynamic role and temporal characteristics in the development of coagulopathy following exertional heat stroke (EHS). Using a well-established rat model of EHS induced by strenuous exercise under high-temperature and high-humidity conditions, we conducted a detailed time-course analysis. Our findings revealed that plasma levels of KLF2 and TM underwent significant dynamic fluctuations following EHS induction. These alterations showed a clear correlation with progressive prolongations in standard coagulation parameters, specifically activated partial thromboplastin time (APTT) and prothrombin time (PT). The most profound disturbances in both the KLF2-TM axis and coagulation function were consistently observed at 4 h post-EHS. Notably, this critical time point was also associated with the peak severity of hepatic injury, as comprehensively assessed through histopathological examination and confirmatory liver function tests. Further analysis demonstrated that the aberrant expression of the KLF2-TM pathway within the liver tissue exhibited a distinct temporal consistency with the observed progression of hepatic pathological damage. Collectively, these results indicated that the KLF2-TM axis was actively involved in the pathogenic mechanisms underlying EHS-associated coagulopathy. Monitoring the dynamic changes of this axis may provide valuable predictive insights into the dysregulation of coagulation during EHS, suggesting its potential as a biomarker for disease severity.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"802 ","pages":"Article 153327"},"PeriodicalIF":2.2,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146025593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}