Molecular Pain最新文献

{"title":"miRNA-let7b5p alleviates visceral hypersensitivity by inhibiting the activation of spinal microglial in male IBS-like rats.","authors":"Xianhe Wu, Ying Tang, Zhengqing He, Fan Yang, Yiqian Liu, Qianli Zhang, Aiqin Chen, Yu Chen, Chun Lin","doi":"10.1177/17448069261430202","DOIUrl":"10.1177/17448069261430202","url":null,"abstract":"<p><p>Visceral hypersensitivity is a hallmark feature of irritable bowel syndrome (IBS), yet its underlying mechanisms remain incompletely understood. In the present study, we found that miRNA-let7b5p was downregulated in the spinal cord of IBS model rats induced by neonatal colorectal distension. Concurrently, microglia exhibited a shift toward a pro-inflammatory M1 phenotype and selectively engulfed inhibitory synapses, resulting in impaired GABAergic neuronal function and disruption of the excitatory/inhibitory balance. Intrathecal administration of a miRNA-let7b5p agomir suppressed M1-type microglial activation in the spinal cord, reduced pro-inflammatory cytokine levels, and alleviated visceral hypersensitivity, whereas antagomir treatment induced visceral hypersensitivity in control rats. Mechanistically, MAP3K3 was identified as a direct target of miRNA-let7b5p, and its knockdown recapitulated the protective effects conferred by miRNA upregulation. Collectively, these findings demonstrate that miRNA-let7b5p attenuates IBS-associated visceral hypersensitivity by downregulating MAP3K3, thereby inhibiting spinal microglial activation and restoring GABAergic neuronal function. This study provides novel insights into the pathogenesis of IBS-related visceral hypersensitivity and highlights a potential therapeutic target for drug development.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261430202"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The enhanced analgesic effects of electroacupuncture and repetitive transcranial magnetic stimulation on visceral pain via ventral lateral septal nucleus.","authors":"Rui-Xia Weng, Yuan Gao, Chen-Hao Zhang, Ru-Yu Yan, Qi Liu, Zhen-Hua Xu, Hua-Zheng Wang, Rui Li, Rong Gao, Yong-Chang Li, Guang-Yin Xu","doi":"10.1177/17448069261428970","DOIUrl":"10.1177/17448069261428970","url":null,"abstract":"<p><p>Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder characterized primarily by chronic visceral pain, with a complex pathogenesis and limited efficacy of current therapeutic interventions. Growing evidence indicates that electroacupuncture (EA) and repetitive transcranial magnetic stimulation (rTMS) exert significant analgesic effects on visceral pain. However, the underlying neural circuit mechanisms remain poorly understood. In this study, the ventral part of the lateral septal nucleus (LSV) was identified as a critical brain region mediating the analgesic effects of EA and rTMS in a mouse model of visceral pain. Visceral nociceptive stimulation significantly increased c-Fos expression in the LSV, predominantly within glutamatergic (Glu⁺) neurons. Optogenetic inhibition of LSV Glu⁺ neurons attenuated visceral pain, whereas their activation exacerbated pain-related behaviors. Both EA and rTMS individually reduced visceral pain-induced c-Fos expression and alleviated pain behaviors, with the combined EA + rTMS treatment producing a more pronounced analgesic effect than either treatment alone. Moreover, fiber photometry recordings demonstrated that EA and rTMS decreased glutamate release and concurrently increased cannabinoid signaling in the LSV, suggesting that these interventions modulate neurotransmitter dynamics to regulate neuronal excitability. In summary, our findings highlight the pivotal role of LSV Glu⁺ neurons in the modulation of visceral pain. EA and rTMS exert their therapeutic effects by regulating glutamate and cannabinoid release within this circuit. These insights provide a foundation for developing targeted neuromodulatory strategies for the treatment of chronic visceral pain.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261428970"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13087329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147513828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterisation of neurotensin-expressing interneurons in the mouse spinal dorsal horn.","authors":"Erika Polgár, Allen C Dickie, Maria Gutierrez-Mecinas, Masahiko Watanabe, Andrew M Bell, Andrew J Todd","doi":"10.1177/17448069261468203","DOIUrl":"10.1177/17448069261468203","url":null,"abstract":"<p><p>The spinal dorsal horn contains numerous excitatory interneurons, which can be assigned to functional classes based on morphological, electrophysiological and neurochemical criteria. One population consists of neurons that express neurotensin, and these belong to a larger group defined by the presence of protein kinase Cγ (PKCγ). It has been proposed that PKCγ neurons form part of a circuit that can convey low-threshold mechanoreceptive information to nociceptive projection neurons in lamina I, forming a pathway that could underlie mechanical allodynia in pathological pain states. However, despite their potential importance, relatively little is known about the properties of the neurotensin-expressing cells. Here we have used a neurotensin-Cre line, together with intraspinal injection of AAVs coding for Cre-dependent constructs, to characterise the morphological and electrophysiological properties of these cells. Reconstruction of their dendritic trees revealed that they were morphologically diverse, although many could be assigned to a class known as central cells. All cells examined received synaptic contacts from putative A- and C-low-threshold mechanoreceptors (identified by expression of VGLUT1 and VGLUT3, respectively). However, these only accounted for a minority of their excitatory synapses. Around 40% of their synapses were from VGLUT2-immunoreactive boutons, which are likely to have originated mainly from local excitatory interneurons. Electrophysiological analysis revealed similarities to, and differences, from other neurochemically-defined excitatory interneuron populations. Our findings are compatible with the proposed role of neurotensin cells in mechanical allodynia, but suggest additional functions for these cells.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261468203"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148448224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A life in pain research: The scientific legacy of Howard L. Fields.","authors":"Min Zhuo, Jianguo Gu","doi":"10.1177/17448069261455315","DOIUrl":"10.1177/17448069261455315","url":null,"abstract":"","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":"22 ","pages":"17448069261455315"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13247283/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148199579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of cooling on the excitability of trigeminal Aβ-afferent nociceptors in mice: Involvement of temperature-sensitive K2P channels.","authors":"Amit Raj Sharma, Jennifer Ling, Saurav Gupta, Jianguo Gu","doi":"10.1177/17448069261463365","DOIUrl":"10.1177/17448069261463365","url":null,"abstract":"<p><p>Aβ-afferents are traditionally believed to be low-threshold mechanoreceptors (LTMRs) involved in sensing innocuous mechanical stimuli such as gentle touch; however, emerging evidence indicates that a subset of Aβ-afferents functions as high-threshold mechanoreceptors (HTMRs) involved in mechanical pain and termed Aβ-afferent nociceptors. While cooling is known to usually suppress neuronal excitability, its effects on the excitability of Aβ-afferent nociceptors remain unclear. Here, we used Nav1.8^ChR2/eYFP mice and patch-clamp recordings to examine how cooling affects intrinsic membrane properties, excitability, and ionic currents in Aβ-afferent nociceptors in the trigeminal ganglia (TG). Aβ-afferent nociceptors were identified as Nav1.8-positive (eYFP-positive) large-diameter (34-43 μm) TG neurons with their axon conduction velocities >13 m/s at 33°C. Cooling from 33 to 10°C progressively reduced axon conduction velocity and increased their stimulation threshold. However, at the soma of Aβ-afferent nociceptors, cooling decreased the action potential (AP) rheobase, increased AP amplitude and input resistance, and depolarized the resting membrane potential, although it increased the AP threshold and width. Voltage-clamp recordings showed that cooling suppressed both inward Na⁺ and outward K⁺ currents at the soma. Interestingly, the cooling-induced reduction in outward K⁺ currents was largely mediated by temperature-sensitive two-pore-domain potassium (K2P) channels at the soma, suggesting a role in shifting intrinsic membrane properties toward increased excitability. Enhancing intrinsic membrane excitability at the soma of Aβ-afferent nociceptors raises the possibility that cooling may similarly affect excitability at their endings.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261463365"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13329007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148278223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cortical mechanism of emotional pain.","authors":"Min Zhuo","doi":"10.1177/17448069251414261","DOIUrl":"10.1177/17448069251414261","url":null,"abstract":"<p><p>Most basic and clinical research on chronic pain has traditionally focused on the mechanisms and treatment of physical pain resulting from peripheral injuries in individual animals or humans. However, growing evidence highlights the importance of emotional pain, a form of distress that extends beyond the individual to include family members, partners, and friends affected by another's suffering. In this review, I summarize recent advances in animal models of empathic pain and explore cortical synaptic mechanisms underlying this form of social or emotional pain. I compare the cortical processes mediating physical pain and emotional pain, drawing on evidence from both human brain imaging and animal studies. Converging findings suggest that the anterior cingulate cortex (ACC) and insular cortex (IC) play central roles in the perception and persistence of emotional pain. Cortical potentiation appears to be a key synaptic mechanism driving long-term emotional pain, and cortical top-down modulation of spinal nociceptive transmission may help explain how emotional distress leads to abnormal somatosensory perception. Finally, the calcium-stimulated adenylyl cyclase subtype 1 (AC1) is discussed as a potential therapeutic target for the treatment of chronic pain and its associated emotional disorders.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251414261"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13167270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145892751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redox-associated gene and microRNA signatures in degenerative intervertebral disc disease.","authors":"Damian Strojny, Karol Szwej, Rafał Staszkiewicz, Dawid Sobański, Paweł Gogol, Mária Lehotská, Bozena Majchrowicz, Beniamin Oskar Grabarek","doi":"10.1177/17448069261444495","DOIUrl":"10.1177/17448069261444495","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IVDD) is a major cause of chronic low back pain and disability worldwide. Growing evidence highlights oxidative stress as a key driver of disc degeneration; however, the integrated relationships between gene expression, regulatory microRNAs (miRNAs), and protein-level changes across disease stages remain insufficiently understood. This study aimed to identify oxidative stress-related molecular signatures in IVDD and to explore their miRNA-mediated regulation across degeneration grades. The study included 200 patients with lumbosacral IVDD undergoing microdiscectomy and 100 postmortem control samples without spinal pathology. Degeneration severity was classified using the Pfirrmann scale, and pain intensity was assessed with the Visual Analog Scale (VAS). Gene expression of oxidative stress markers was evaluated using RT-qPCR, while protein levels were quantified by ELISA. Additionally, bioinformatic prediction and RT-qPCR validation were used to analyze mRNA-miRNA interactions. Gene expression analysis revealed progressive downregulation of antioxidant genes <i>CAT</i> (FC ≈ -6.40) and <i>GPX1</i> (FC ≈ -9.56), alongside upregulation of <i>MAPK8</i> (FC ≈ 8.18) and <i>IL6</i> (FC ≈ 8.18), with a moderate increase in <i>NRF1</i> expression. These values reflect comparisons between advanced degeneration (G5) and controls. In contrast, protein analysis showed an inverse trend, with increasing levels of CAT, GPX1, and NRF1 and decreasing levels of MAPK8 and IL6 as degeneration progressed. miRNA profiling demonstrated significant dysregulation, including downregulation of miR-3163 and miR-196a-1-3p and upregulation of miR-665-3p and miR-4686. Correlation analysis indicated that molecular alterations were more strongly associated with structural degeneration than with pain intensity, as VAS-related differences were generally weak and non-significant. Overall, the results reveal a complex regulatory network in IVDD, characterized by discordant mRNA-protein expression and significant miRNA involvement. Oxidative stress and inflammatory pathways appear tightly regulated at transcriptional and post-transcriptional levels and are more closely linked to structural degeneration than clinical pain.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261444495"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13180124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain networking pain and anxiety: From basic mechanism to future treatment.","authors":"Min Zhuo","doi":"10.1177/17448069251411647","DOIUrl":"10.1177/17448069251411647","url":null,"abstract":"<p><p>It is well known that pain and anxiety can enhance each other in both animals and humans. In case of chronic pain, patients often suffer anxiety and depression. Animal experiments provide important basic mechanisms for the interaction between chronic pain and anxiety. At cortical level, recent studies have consistently indicated that anterior cingulate cortex (ACC) and insular cortex (IC), two critical cortical regions for pain-related unpleasantness and suffering, are also involved in the process of emotional anxiety. At synaptic level, long-term potentiation (LTP), a key cellular mechanism for memory and chronic pain, has also been found to contribute to emotional anxiety in animal models of chronic pain. In a recent study published in <i>Neuron</i> by the group of Prof. Xu, it has been found that at subcortical level, anterior and posterior paraventricular nucleus of the thalamus (PVT) contribute to pain and anxiety through distinct projections to the basolateral amygdala (BLA) and central amygdala (CeA). In this review, I will first introduce the recent work by Prof Xu, and then discuss possible mechanisms at different levels for pain and anxiety in the condition of chronic pain, including chronic visceral pain. Some of medicines used in the current treatment will be analyzed, and potential future treatment for pain and anxiety in chronic pain conditions will be discussed.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251411647"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12764751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145768712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CGRP expression and signaling sensitization in a mouse model of chronic oxaliplatin-induced peripheral neuropathy.","authors":"Junwei Du, Leland C Sudlow, Margaret H Johnson, Kanishk Satish, Abraham Villagomez, Hongzhen Hu, Mikhail Y Berezin","doi":"10.1177/17448069261432028","DOIUrl":"10.1177/17448069261432028","url":null,"abstract":"<p><p>Chemotherapy-induced peripheral neuropathy (CIPN) is a frequent and dose-limiting side effect of oxaliplatin treatment, yet its molecular mechanisms remain incompletely understood. Calcitonin gene-related peptide alpha (CGRPα, encoded by <i>Calca</i>) is a neuropeptide implicated in several chronic pain conditions and has been proposed to mediate CIPN-related hypersensitivity. Here, we investigated the role of CGRPα in a mouse model of chronic oxaliplatin-induced neuropathy. Mice treated with oxaliplatin over 8 weeks developed cold allodynia and reduced sensory nerve conduction velocity, recapitulating hallmark clinical symptoms of chronic CIPN. However, contrary to expectations, we observed no increase in <i>Calca</i> mRNA expression or protein levels in the dorsal root ganglia (DRG) of male mice and a significant decrease in female mice. The proportion of CGRP-expressing neurons remained unchanged. RNA-seq revealed a two-fold upregulation of <i>Ramp1</i>, a subunit of the CGRP receptor complex. These results suggest that CGRPα signaling may be enhanced not by increased peptide expression, but rather by increased calcium-dependent release from existing neurons and increased CGRP receptor sensitization. This is consistent with known effects of oxaliplatin-induced oxidative stress, which can activate TRPA1 channels and promote calcium-dependent vesicular release of neuropeptides. Although additional validation of this model is needed, our data support a revised rationale of CGRP involvement in CIPN based on sensitization and neuropeptide release, rather than upregulation, and point to TRPA1-CGRP interactions as a potential therapeutic target in oxaliplatin-induced neuropathic pain.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069261432028"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13018710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147308099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture at Zusanli (ST36) alleviates paclitaxel-induced neuropathic pain in rats via regulating TLR4 signaling pathway in the spinal cord.","authors":"Man-Ni Wang, Yuan-Xi Zhou, Yu-Xue Zhao, Jing-Wei Tan, Xiao Sang","doi":"10.1177/17448069251413879","DOIUrl":"10.1177/17448069251413879","url":null,"abstract":"<p><p>Paclitaxel (PTX) treatment induces a pathological pain state that is often associated with neuroinflammation in the central nervous system. The available interventions for PTX-induced pathological pain encounter adverse effects and limited efficacies. Recent studies have shown the significant effectiveness of Electroacupuncture (EA) in pain management as a simple and safe alternative medical treatment. Here, we evaluated the analgesic effect of EA on pain behaviors in PTX-treated rats and investigated its potential analgesic mechanisms. In this study, a pathological pain model was established in SD rats via intraperitoneal (<i>i.p</i>.) injection of PTX. EA or Sham EA treatments were applied every other day for PTX-treated rats. Pain behaviors of mechanical allodynia and thermal hyperalgesia in rats were measured, followed by analysis of the spinal cord tissue via using molecular biology methods. Here, we show that EA treatment is capable to alleviate PTX-induced mechanical allodynia and thermal hyperalgesia in rats. In addition, EA regulated the abnormal protein expression of astrocytes, microglia, neurons, TLR4-MyD88/TRIF signaling pathway and cytokines in the lumbar spinal cord of PTX-treated rats. Furthermore, we investigated the spinal co-expressions of TLR4 in astrocytes, microglia, and neurons respectively in rats and the regulatory effect of EA on TLR4 and cells mentioned above. In summary, EA shows analgesic properties as it ameliorates PTX-induced mechanical allodynia and thermal hyperalgesia probably by reducing central neuroinflammation. Therefore, we consider EA as a potential therapeutic candidate for the treatment of PTX-induced pathologic pain. Notably, this study provides the first morphological evidence that EA may concurrently influence TLR4-mediated neuroimmune interactions across multiple spinal cell types, suggesting a potential central mechanism distinct from previously reported peripheral actions.</p>","PeriodicalId":19010,"journal":{"name":"Molecular Pain","volume":" ","pages":"17448069251413879"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145892773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}