生理学报最新文献

{"title":"[Exercise improves osteoporosis through bone-fat crosstalk].","authors":"Yi-Lin Ou, Rui Peng, Shao-Jie Xu, Xi-Quan Weng, Yu Yuan","doi":"10.13294/j.aps.2025.0073","DOIUrl":"10.13294/j.aps.2025.0073","url":null,"abstract":"<p><p>Osteoporosis (OP) is a prevalent systemic metabolic bone disease characterized by reduced bone mass and compromised bone microstructure. Recent studies have demonstrated that the occurrence of OP is closely related to the imbalance of bone and lipid metabolism. Bone and lipid can communicate and influence each other by secreting bone-derived factors or adipokines. This kind of crosstalk is crucial for maintaining the equilibrium between bone and fat. Meanwhile, multiple signaling pathways such as Wnt/β-catenin, bone morphogenetic protein (BMP), mitogen-activated protein kinase (MAPK), peroxisome proliferator-activated receptor γ (PPARγ), Notch, Hedgehog, and PI3K/Akt pathways can also regulate bone-fat crosstalk. In addition, in the bone marrow microenvironment, bone marrow mesenchymal stem cells (BMSCs), osteoblasts, osteoclasts, osteocytes, and adipocytes also have close interactions, jointly maintaining bone-lipid metabolic balance. Exercise, as a non-invasive intervention method, can regulate bone tissue, adipose tissue, and bone marrow adipose tissue in multiple aspects and shows great potential in improving OP. Although the effect of exercise on bone-lipid metabolism has been widely confirmed, its specific molecular mechanism and its role in bone-fat crosstalk still need further exploration. In light of this, based on the review of research progress related to bone-fat crosstalk, this article summarizes the effects of exercise on this crosstalk and its underlying mechanism in improving OP, providing theoretical basis for the prevention and treatment of OP through exercise.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"395-412"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[The role of mesenchymal stem cells in cancer therapy: friend or foe?]","authors":"Shu-Ting Zhou, Jian-Ping Jiang","doi":"10.13294/j.aps.2025.0092","DOIUrl":"10.13294/j.aps.2025.0092","url":null,"abstract":"<p><p>Mesenchymal stem cells (MSCs) can adhere to plastic surfaces and express specific differentiation markers such as CD73, CD90, and CD105. They can differentiate into osteoblasts, chondrocytes, or adipocytes <i>in vitro</i> and do not express markers like CD14, CD34, CD45, CD11b, CD19, and HLA-DR. MSCs play a complex role in cancer therapy, acting as both a potential ally and an adversary. On one hand, MSCs can inhibit tumor growth and metastasis by modulating signaling pathways and immune responses, exerting anti-tumor effects. On the other hand, they may enhance the invasiveness, metastatic ability, and angiogenesis of tumor cells, thereby promoting tumor progression. The impact of MSCs on tumors depends on their intrinsic properties, the tumor microenvironment, and the activation or inhibition of signaling pathways. Therefore, in cancer treatment, it is necessary to consider these factors comprehensively and optimize the application strategies of MSCs. This article reviews the characteristics of MSCs, their dual roles and mechanisms in cancer therapy, and proposes the idea and strategy of \"turning enemies into friends\" to achieve breakthroughs in MSC-based cancer treatments and to safely and effectively apply them in clinical practice.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"306-314"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Inhibition of cathepsin K improves the learning and memory function of the vascular dementia model rats through blocking pyroptosis pathway].","authors":"Jia-Yao Qiu, Li Chen, Xin-Yi Wang, Pei-Yan Xi, Wei-Jian Li, Hao-Nan Zhang, Zhi He, Hai-Ying Jiang","doi":"10.13294/j.aps.2026.0033","DOIUrl":"10.13294/j.aps.2026.0033","url":null,"abstract":"<p><p>The study aimed to investigate the mechanism of cathepsin K (CatK) on hippocampal learning and memory dysfunction in rats with vascular dementia (VD). Sprague-Dawley (SD) male rats were randomly divided into control group (Control), control+ CatK blocker group (Control+CatKⅡ), VD model group (VD), and VD model + CatK blocker group (VD+CatKⅡ). Four weeks after the establishment of the VD model by permanent ligation of bilateral common carotid arteries, CatK inhibitor Ⅱ (CatKⅡ) or equivalent artificial cerebrospinal fluid was injected into the dentate gyrus of hippocampus. Oxygen glucose deprivation (OGD) cell model was established using the HT22 cells. Morris water maze (MWM) experiment was used to observe the spatial learning and memory abilities of rats, and the expression levels of CatK, NLRP3, GSDMD, Caspase-1 and other pyroptosis-related proteins were detected by Western blot assay. The MWM place navigation test showed that the daily escape latency of the VD group was significantly longer than that of the Control group. The escape latency of the VD+CatKⅡ group was significantly shorter than that of the VD group on days 3 and 4 (<i>P</i> < 0.05). The space exploration test showed that the frequency of crossing the original platform area and the percentage of residence time in the target quadrant in the VD group were significantly less than those in the Control group (<i>P</i> < 0.05), while those in the VD+CatKⅡ group were significantly increased compared with the VD group (<i>P</i> < 0.05). Western blot analysis showed that the expression of NLRP3, GSDMD, Caspase-1, IL-18 and IL-1β in the VD+CatKⅡ group was significantly decreased compared with those in the VD group (<i>P</i> < 0.05). It was also observed in the OGD HT22 cell experiment that the levels of Caspase-1 and other pyroptosis-related proteins were significantly decreased when CatK was inhibited by pharmacological or gene interference methods. In conclusion, CatK can affect the learning and memory function of VD model rats. Inhibition of CatK can attenuate cell pyroptosis pathway to improve the learning and memory impairment of the VD model rats.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"425-432"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Recent advances in non-coding RNA-mediated PI3K/AKT/mTOR signaling pathway regulation involved in triple-negative breast cancer pathogenesis and progression].","authors":"Zhu Huang, Wen-Jing Li, Zi-Juan Song, Si-Yi Huang, Zi-Qing Yang, Ya-Ya Chu, Fu-Sheng Ding, Cong-Hu Li","doi":"10.13294/j.aps.2025.0109","DOIUrl":"10.13294/j.aps.2025.0109","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is characterized by high invasion and metastasis, poor prognosis, and high mortality, making it the most aggressive form of breast cancer. Currently, there is still a lack of effective therapeutic targets for TNBC. Aberrant activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway is prevalent in TNBC, leading to increased resistance to chemotherapeutic agents and poor prognosis. Non-coding RNA (ncRNA), including microRNA (miRNA), long non-coding RNA (lncRNA) and circular RNA (circRNA), are involved in a variety of biological processes and can be used as oncogenes or tumor suppressor genes to regulate the PI3K/AKT/mTOR pathway to promote or inhibit the occurrence and development of TNBC. This article reviews some important miRNA, lncRNA, circRNA, and their targets and molecular mechanisms that regulate the PI3K/AKT/mTOR pathway in TNBC, hoping to open up new avenues for the research of TNBC and ultimately promote the development of precise and effective treatments for TNBC.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"315-330"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Mechanism of the unstable proteins generated by P346H-BEST1 and P233L-BEST1 mutations and their role in causing RP50 and BVMD].","authors":"Qing-Xiang Lu, Jing-Ye Yang, Hong-Xia Tian, Zhong-Xue Zhou, Ding-An Zhou","doi":"10.13294/j.aps.2026.0034","DOIUrl":"10.13294/j.aps.2026.0034","url":null,"abstract":"<p><p><i>BEST1</i> mutations are associated with a spectrum of ocular disorders collectively termed Bestrophinopathies, including autosomal dominant Best vitelliform macular dystrophy (BVMD), adult-onset vitelliform macular dystrophy (AVMD), autosomal dominant vitreoretinochoroidopathy (ADVIRC), retinitis pigmentosa type 50 (RP50), and autosomal recessive bestrophinopathy (ARB). The molecular mechanisms underlying their distinct retinal phenotypes remain largely unknown. In this study, we characterized disease subtypes, causative genes, and mutation sites through comprehensive ophthalmic evaluations, whole-genome sequencing, and Sanger sequencing validation. Cellular immunofluorescence assays were performed to assess the impact of <i>BEST1</i> mutations on the subcellular localization of Bestrophin-1. Protein stability of wild-type and mutant Bestrophin-1 was investigated in transiently transfected MDCK II cells treated with proteasome or lysosome inhibitors. We identified <i>BEST1</i> c.1037C>A (p.P346H) and <i>BEST1</i> c.698C>T (p.P233L) mutations in two families diagnosed with RP50 and BVMD, respectively. These mutations induced protein destabilization and subsequent degradation via the ubiquitin-proteasome-dependent pathway. Additionally, both p.P346H and p.P233L caused cytoplasmic mislocalization of the mutant Bestrophin-1 protein. Our findings suggest that the pathogenic mechanisms associated with p.P233L and p.P346H likely involve mislocalization of the mutant protein, protein instability and its targeted degradation via ubiquitin-proteasome-dependent pathway.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"443-451"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Mechanism of mitochondrial transcellular transfer in cerebral ischemia-reperfusion injury].","authors":"Rui-Shu An, Wen-Xiu Qin, Jian Yang, Jun-Feng Xu","doi":"10.13294/j.aps.2026.0030","DOIUrl":"10.13294/j.aps.2026.0030","url":null,"abstract":"<p><p>Ischemic stroke (IS) is an acute cerebrovascular disease in which blood circulation to brain tissue and neurological function are impaired due to obstruction of cerebral blood vessels, and it is one of the most common causes of death worldwide. Therapies such as intravenous thrombolysis and endovascular thrombectomy can open occluded cerebral vessels and restore blood flow through reperfusion, but ischemia/reperfusion (I/R) may trigger pathological processes such as oxidative stress, electrolyte disorders, and inflammatory responses, leading to secondary tissue damage such as cerebral edema and intracranial hemorrhage. Therefore, it is crucial to mitigate cerebral ischemia-reperfusion injury (CIRI). Mitochondria, as organelles, usually exist inside cells. However, under the stimulation of CIRI, mitochondria and their components can affect brain tissue cells by transcellular transfer through tunneling nanotubes (TNTs), gap junctions (GJs), and releasing and capturing of extracellular vesicles (EVs), <i>etc</i>. The mitochondrial transcellular transfer therapy for CIRI can reduce oxidative stress damage, improve neuronal energy metabolism, regulate neuroinflammation, and promote neural repair and regeneration. Mitochondrial transcellular transfer is regarded as a promising therapeutic approach for the treatment of CIRI, and in-depth investigation of the mechanism of mitochondrial transcellular transfer is expected to open up a new clinical pathway for the treatment of CIRI. This paper explores the molecular mechanism of mitochondrial transcellular transfer and its effects in the treatment of CIRI, which is expected to broaden clinical therapeutic approaches and provide a new direction for the treatment of CIRI.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"295-305"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Knockout of <i>LCN2</i> attenuates lung injury and ferroptosis in septic mice likely through inhibiting the TLR4/NF-κB signaling pathway].","authors":"Yi-Ren Wang, Meng-Jie Yu, Ruo-Li DU, Yu-Ying He, Yi-Xin Zhang, Jia-Hui Wang, Hong-Wei Ye, Qin Gao","doi":"10.13294/j.aps.2025.0070","DOIUrl":"10.13294/j.aps.2025.0070","url":null,"abstract":"<p><p>This study aimed to investigate the effects of lipocalin-2 (LCN2) gene knockout (LCN2KO) on cecal ligation and perforation (CLP)-induced lung injury and ferroptosis in septic mice, and further to clarify the potential role of the Toll-like receptor 4 (TLR4)/nuclear factor κB (NF-κB) pathway. A CLP model was established using LCN2KO mice. The levels of serum interleukin-6 (IL-6) and IL-1β were measured by ELISA. The contents of malondialdehyde (MDA) and glutathione (GSH) in lung tissue were determined using the corresponding assay kits. Reactive oxygen species (ROS) levels in lung tissue were detected using dihydroethidium (DHE) fluorescent probe. The expression levels of ferroptosis-related proteins in lung tissue were assessed by Western blot. The results showed that, compared to wild-type (WT)-Sham group, WT-CLP group exhibited significant lung tissue damage, elevated serum IL-6 and IL-1β levels, increased MDA content and ROS level, decreased GSH content, up-regulated protein expression levels of LCN2 and TLR4, increased p-P65/P65 ratio, and significantly down-regulated protein expression levels of ferroptosis suppressor protein 1 (FSP1) and glutathione peroxidase 4 (GPX4). LCN2KO reversed these changes induced by CLP. Both TLR4 inhibitor TAK-242 and NF-κB inhibitor PDTC down-regulated lung LCN2 protein expression, reversed sepsis-induced ferroptosis and lung injury, which is similar to the role of LCN2KO. These results suggest that LCN2KO may ameliorate lung injury in sepsis-induced mouse model by attenuating ferroptosis through modulating the TLR4/NF-κB signaling pathway.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"452-462"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Advances in assessment methods of lymphatic drainage function].","authors":"Jia-Hui Zhao, Ye Wu, Tai-Wei Wang, Ke Zhen, Hui-Rong Liu, Yi-Si Liu","doi":"10.13294/j.aps.2025.0113","DOIUrl":"10.13294/j.aps.2025.0113","url":null,"abstract":"<p><p>The assessment of lymphatic drainage function is essential for understanding the role of the lymphatic system in fluid homeostasis, immunosurveillance and disease processes. Conventional methods of evaluation rely on dynamic visualization with tracers, such as X-ray lymphangiography, lymphoscintigraphy and magnetic resonance lymphangiography. However, these methods have limitations in terms of invasiveness and resolution, and other aspects. Recent advances in optical technologies and nanomaterials technology have enabled the development of noninvasive, high-precision testing methods, such as photoacoustic imaging and optical coherence tomography, which have made it possible to visualize and analyze lymphatic flow rates, tracer clearance rates and functional abnormalities. In addition, the application of artificial intelligence-assisted analysis, multimodal imaging, and targeted nanoprobes has significantly improved the precision and clinical applicability of these methods. In this article, we systematically review the principles, characteristics, clinical applications and preclinical research progress of nine classical or novel lymphatic drainage function testing techniques. We also discuss the advantages and limitations of each technique and explore the future development trend, aiming to provide insights for basic research and clinical practice.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"342-352"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Research progress on protein succination modification in cancer].","authors":"Qian-Qian Ju, Cheng Sun","doi":"10.13294/j.aps.2026.0036","DOIUrl":"10.13294/j.aps.2026.0036","url":null,"abstract":"<p><p>Metabolic dysregulation is a hallmark of cancer. Mutations in genes encoding key enzymes of the tricarboxylic acid (TCA) cycle can result in the accumulation of \"oncometabolites\". These metabolites play essential roles in tumor initiation, progression, and immune evasion by inhibiting enzymatic activity or driving covalent protein modifications. Accumulation of fumarate due to TCA cycle disruptions or fumarate hydratase (FH) inactivation mutation affects mitochondrial function, DNA repair, protein function, and the tumor microenvironment. As an α,β-unsaturated electrophilic metabolite, fumarate reacts with cysteine residues on susceptible proteins via Michael addition, generating stable S-(2-succinyl)cysteine (2SC) modifications, a post-translational modification process known as protein succination modification. Research has shown that protein succination modification plays a critical role in tumor initiation, progression, and immune evasion, providing new insights for cancer diagnosis and therapy. Future metabolic interventions targeting succination modification could significantly improve cancer therapies. This review offers a comprehensive overview of the role of protein succination modification in tumor metabolism and immune evasion, along with its potential clinical applications.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"331-341"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of nociceptin receptor attenuates methamphetamine motivation and relapse in rats: Involvement of phosphorylated CREB and Akt in the nucleus accumbens.","authors":"Yu-Jia Cai, Fang-Min Wang, Miao-Jun Lai, Yi-Ying Zhou, Ding-Ding Zhuang, Man-Qing Wu, Hui-Zhen Liu, Wen-Wen Shen, Wen-Hua Zhou","doi":"10.13294/j.aps.2026.0027","DOIUrl":"10.13294/j.aps.2026.0027","url":null,"abstract":"<p><p>Accumulating evidence has highlighted the functional role of the endogenous nociceptin/orphanin FQ peptide (N/OFQ) and its nociceptin opioid receptor (NOP) in alcohol and cocaine reward. However, the effects of NOP agonists on methamphetamine (MAP) reinforcement, motivation, and relapse remain uncertain. In this study, we evaluated the effects of Ro 64-6198, a selective NOP agonist, on MAP reinforcement, motivation, and relapse in rats. Rats underwent a fixed-ratio 1 (FR1) training to establish stable MAP intravenous self-administration (0.05 mg/kg/infusion) for 12 days, and the motivation for MAP was quantified using a progressive-ratio (PR) schedule, while the relapse was assessed through cue- and MAP-primed reinstatement after abstinence. Western blot analysis was employed to measure the relative expression of phosphorylated CREB, ERK, and Akt in the nucleus accumbens (NAc) following drug priming. Acute treatment of Ro 64-6198 (1 mg/kg) significantly reduced the motivated behavior for MAP under PR testing (<i>P</i> < 0.05 <i>vs.</i> vehicle). Ro 64-6198 at doses of 0.3 and 1 mg/kg could suppress the drug-seeking behavior induced by extinction or cues, respectively (<i>P</i> < 0.05), whereas only the higher dose (1 mg/kg) could attenuate MAP primed drug-seeking (<i>P</i> < 0.05). These behavioral effects were related to the upregulated phosphorylation of CREB and Akt in the NAc. Our results provide preclinical evidence that NOP activation disrupts multiple addiction-relevant behaviors, positioning Ro 64-6198 as a potential therapeutic candidate for treating MAP use disorders.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 2","pages":"413-424"},"PeriodicalIF":0.0,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}