生理学报 Pub Date : 2026-02-25

Liu Tang, Ying-Qi Cheng, Wei Gui, Yan Zhang

{"title":"A glutamatergic Sp5C-STN circuit mediates chronic migraine in mice.","authors":"Liu Tang, Ying-Qi Cheng, Wei Gui, Yan Zhang","doi":"","DOIUrl":"","url":null,"abstract":"Chronic migraine (CM) is a prevalent and highly debilitating neurological disorder. Functional magnetic resonance imaging (fMRI) studies have demonstrated associations between abnormal brain region activation and CM, yet the underlying complex neural circuitry mechanisms remain unclear. The spinal trigeminal nucleus caudalis (Sp5C) serves as the primary central hub for orofacial nociceptive input, receiving trigeminal pain signals and projecting to higher-order centers such as the thalamus. Therefore, we sought to investigate whether the Sp5C region and its associated circuits were involved in CM pathogenesis. In this study, we established a CM mouse model through repeated intraperitoneal injections of nitroglycerin (NTG). Using a combination of in vivo fiber photometry and in vitro c-Fos immunohistochemistry, we found a marked periorbital and plantar mechanical allodynia in CM mice, accompanied by increased glutamatergic neuronal activity in Sp5C. Chemogenetic manipulation of Sp5C glutamatergic neurons (Sp5CVglut2) bidirectionally modulated migraine-like behaviors and induced pain-related affective states, as evidenced by conditioned place preference/aversion (CPP/CPA) paradigms. Anterograde viral tracing revealed dense projections from Sp5CVglut2 to the subthalamic nucleus (STN), which was activated in CM mice. Optogenetic activation of the Sp5C-STN pathway similarly produced migraine-like behaviors and pain-related aversive memory in mice. Altogether, we revealed a critical role of the Sp5CVglut2-STN circuit in the development and modulation of CM. Our findings provide novel mechanistic insights into the central mechanisms underlying CM, establishing potential theoretical foundations for clinical diagnosis and therapeutic development.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"159-172"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346985","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}

引用次数: 0

Oxytocin relieves visceral hypersensitivity through GABAB1-TRPV1 in rats with irritable bowel syndrome. 催产素通过GABAB1-TRPV1缓解肠易激综合征大鼠内脏超敏反应。

生理学报 Pub Date : 2026-02-25

Fei Fan, Yang Cao, Zheng-Qing He, Fan Yang, Yu Chen, Ai-Qin Chen, Chun Lin

{"title":"Oxytocin relieves visceral hypersensitivity through GABAB1-TRPV1 in rats with irritable bowel syndrome.","authors":"Fei Fan, Yang Cao, Zheng-Qing He, Fan Yang, Yu Chen, Ai-Qin Chen, Chun Lin","doi":"","DOIUrl":"","url":null,"abstract":"Oxytocin has been found to modulate and improve pain in humans, but the mechanisms underlying these antinociceptive properties, especially in visceral hypersensitivity, are still unclear. Irritable bowel syndrome (IBS) models were established by colorectal distention in newborn rats aged 8 to 14 days, and visceral hypersensitivity was assessed using electromyogram (EMG). Oxytocin or saclofen was administered intrathecally to evaluate visceral hypersensitivity in the rats. The protein expressions of oxytocin receptor (OTR), γ-aminobutyric acid type B1 receptor (GABAB1), and transient receptor potential vanilloid 1 (TRPV1) in the lumbosacral spinal cord regions were measured. IBS rats exhibited a unique spinal cord molecular signature comprising decreased OTR/GABAB1 and increased TRPV1 expression. Intrathecal oxytocin treatment not only normalized these molecular alterations (increasing GABAB1 while decreasing TRPV1) but also ameliorated visceral pain behaviors. Crucially, this therapeutic effect was fully reversed by GABAB1 inhibition, establishing the necessity of intact GABAergic signaling for oxytocin-mediated analgesia. Collectively, these findings indicate that oxytocin relieves visceral hypersensitivity through the regulation of GABAB1 and TRPV1 in the spinal cord of IBS rats.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"173-181"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346976","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}

引用次数: 0

[Research progress on the neural mechanisms of alcohol use disorder-induced hyperalgesia]. 酒精使用障碍致痛觉过敏的神经机制研究进展

生理学报 Pub Date : 2026-02-25

Ling-Jie Ma, Xiao-Hong Chen, Yong-Jing Gao

{"title":"[Research progress on the neural mechanisms of alcohol use disorder-induced hyperalgesia].","authors":"Ling-Jie Ma, Xiao-Hong Chen, Yong-Jing Gao","doi":"","DOIUrl":"","url":null,"abstract":"Alcohol use disorder (AUD) is a complex chronic relapsing brain disease that poses significant threats to individual health and public healthcare systems. Hyperalgesia, an increased sensitivity to pain, has been recognized as a critical factor leading to treatment failure in AUD management. Existing pharmacotherapies inadequately alleviate pain symptoms in AUD patients, highlighting an urgent need for novel therapeutic strategies. This review systematically summarizes the multi-system neurobiological mechanisms underlying AUD-induced hyperalgesia, spanning from molecular to circuit levels, and from the central to the peripheral nervous systems. It elucidates classic pathways including neurotransmitter imbalances (e.g., enhanced glutamatergic excitation and weakened GABAergic inhibition) and glial cell-mediated neuroinflammation. This article conducts an in-depth analysis of emerging mechanisms including epigenetic regulation (DNA methylation, histone modifications, and microRNA-mediated expression control of key genes) and the gut-brain axis (where gut microbiota influence the central nervous system via metabolites), while emphasizing sex hormone mediated gender differences. Based on these insights, we propose novel intervention strategies targeting neural circuits, epigenetic modifying enzymes, and gut microbiota, offering new perspectives for clinical treatment of AUD-induced hyperalgesia, which holds significant promise for reducing relapse rates and improving patient prognosis.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"109-122"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346924","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}

引用次数: 0

New insights into the pain of knee osteoarthritis: the characteristics of deep pain and abnormal central processing. 膝关节骨关节炎疼痛的新认识：深度疼痛和中枢加工异常的特征。

生理学报 Pub Date : 2026-02-25

Mu-Lan Chen, Yu-Qing DU, Bo-Yang Xu, Feng Zhao, Xiao-Qing Hu, Yun Wang, Ying Zhang

引用次数: 0

Mechanisms of cancer pain and the multitarget therapeutic potential of Traditional Chinese Medicine. 癌性疼痛的机制及中医多靶点治疗潜力。

生理学报 Pub Date : 2026-02-25

Guo-Qun Xu, Ying-Xin Tian, Guang-Yi Si, Xiao-Na Bu, Min Zhang, Hui-Feng Jiao, Hai-Li Pan

{"title":"Mechanisms of cancer pain and the multitarget therapeutic potential of Traditional Chinese Medicine.","authors":"Guo-Qun Xu, Ying-Xin Tian, Guang-Yi Si, Xiao-Na Bu, Min Zhang, Hui-Feng Jiao, Hai-Li Pan","doi":"","DOIUrl":"","url":null,"abstract":"Cancer pain is one of the most prevalent and debilitating symptoms in patients with advanced malignancies, arising from multifactorial mechanisms involving peripheral, central, and systemic pathways. Conventional analgesics, including opioids and nonsteroidal anti-inflammatory drugs, are often limited by their insufficient efficacy, tolerance, and risk of dependence. Traditional Chinese Medicine (TCM), characterized by its multi-component, multi-target, and systemic regulatory properties, has shown promising potential in cancer pain management. This review provides a comprehensive overview of the clinical classification and underlying mechanisms of cancer pain (including nerve infiltration, dysregulation of inflammatory mediators and ion channels, central sensitization, neuro-immune crosstalk, metabolic reprogramming, and gut-brain axis impairment), as well as the analgesic effects of representative TCM agents in cancer pain management. For example, bioactive components such as tetrahydroberberine, levo-tetrahydropalmatine, and piperine exert analgesic effects, thereby improving the quality of life of patients by inhibiting inflammatory cascades, regulating neurotransmitter systems, and preserving neural integrity. Commonly used preclinical models, including bone cancer pain, pancreatic cancer pain, and chemotherapy-induced peripheral neuropathy models, are summarized for their utility in mechanistic studies and efficacy evaluations. This review also discusses the current limitations of clinical evidence, such as small sample sizes, short follow-up periods, and limited translation from animal models, alongside major challenges in standardization, mechanistic elucidation, and clinical trial design. Future directions should focus on precise pain phenotyping, integrated multi-target interventions, rigorous efficacy-safety validation, and innovations in drug delivery to facilitate the standardization and global adoption of TCM in cancer pain management.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"16-46"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346941","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}

引用次数: 0

The dorsal root ganglion T-junction: a critical node in somatosensory processing and pain pathogenesis. 背根神经节t结：躯体感觉加工和疼痛发病的关键节点。

生理学报 Pub Date : 2026-02-25

Zhi-He Zhang, Yun-Jie Fu, Yun Wang

{"title":"The dorsal root ganglion T-junction: a critical node in somatosensory processing and pain pathogenesis.","authors":"Zhi-He Zhang, Yun-Jie Fu, Yun Wang","doi":"","DOIUrl":"","url":null,"abstract":"Pseudounipolar neurons in the dorsal root ganglia (DRG), as the central nodes of primary sensory afferents, possess a distinctive T-junction that is not merely a morphological peculiarity but also performs complex roles in rapid, multiplexed shunting and regulation of sensory signals. This specialized geometry enables separation, filtering, and feedback regulation of neuronal signals, thereby coordinating peripheral and central responses at multiple levels. Recent advances, including spatial transcriptomics, single-cell sequencing, super-resolution microscopy, organoid models, and novel electrophysiological methods, have permitted more precise dissection of the T-junction's molecular composition, ion-channel distribution, and electrophysiological properties. Here, we review current knowledge of the T-junction's developmental regulation and multilayered molecular networks, and we detail its functional alterations in both physiological signaling and pathological pain states, with particular emphasis on ion-channel modulation, signal attenuation, and selective transmission mechanisms. Finally, we discuss contemporary pain-intervention approaches and prospects for precision-targeted therapies, aiming to provide a theoretical foundation for future studies in pain physiology and clinical translation.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"5-15"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346968","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}

引用次数: 0

[Research progress on neurobiological mechanisms of chronic postoperative pain]. [术后慢性疼痛神经生物学机制研究进展]。

生理学报 Pub Date : 2026-02-25

Yi-Qin Wang, Wen-Jing Zhang, Wu-Jun Geng, Ming-Gang Liu

{"title":"[Research progress on neurobiological mechanisms of chronic postoperative pain].","authors":"Yi-Qin Wang, Wen-Jing Zhang, Wu-Jun Geng, Ming-Gang Liu","doi":"","DOIUrl":"","url":null,"abstract":"Postoperative pain is a common complication caused by surgical trauma. Epidemiological studies indicate that the incidence of moderate to severe acute postoperative pain ranges from 41% to 85%, with approximately 10% to 50% of patients potentially progressing to chronic pain. This progression not only significantly impairs patients' quality of life, but also imposes substantial medical and socioeconomic burdens. The mechanisms underlying chronic postoperative pain are highly complex, involving the activation and sensitization of peripheral nociceptors, central sensitization of spinal dorsal horn neurons, and maladaptive alterations in higher-order cortical neural circuits. Additionally, local and systemic inflammatory responses induced by surgical injury, and psychosocial factors, such as anxiety, depression, and sleep disturbances, have all been shown to play critical roles in the transition from acute to chronic postoperative pain. This article systematically reviews the latest advances in risk factors, animal models, pathophysiological mechanisms, and therapeutic strategies of postoperative pain, with particular emphasis on key processes and potential intervention targets involved in the transition from acute to chronic pain, aiming to offer a more solid theoretical foundation and evidence-based guidance for clinical practice.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"83-100"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346964","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}

引用次数: 0

[The involvement of claustrum/insular cortex-locus coeruleus neural pathway in modulating neuropathic pain in mice]. [关闭体/岛叶皮质-蓝斑神经通路参与小鼠神经性疼痛的调节]。

生理学报 Pub Date : 2026-02-25

Lyu-La Pan, Tao Gong, Zi-Ang Li, Xin-Tong Qiu, Ming-Ming Zhang, Yun-Qing Li

{"title":"[The involvement of claustrum/insular cortex-locus coeruleus neural pathway in modulating neuropathic pain in mice].","authors":"Lyu-La Pan, Tao Gong, Zi-Ang Li, Xin-Tong Qiu, Ming-Ming Zhang, Yun-Qing Li","doi":"","DOIUrl":"","url":null,"abstract":"To investigate the fiber connections between the claustrum (CLA)/insular cortex (IC) and the locus coeruleus (LC), as well as the role of this neural pathway in neuropathic pain, morphological techniques, patch-clamp recording, and chemogenetics were used in this study, to observe the CLA/IC-LC neural pathway in mice, the effects of neuropathic pain stimuli on the electrophysiological properties of CLA/IC neurons, and the impact of regulating the pathway on pain behaviors, respectively. The results showed that: (1) After injecting anterograde tracing virus into the CLA/IC, anterogradely labeled fibers and terminals were observed in the ipsilateral LC. When retrograde tracers were injected into the LC, retrogradely labeled neurons were observed in both the ipsilateral CLA/IC, whereas fewer labeled neurons were observed in the contralateral side; (2) In the neuropathic pain state, the presynaptic release of neurotransmitters from CLA/IC-LC projection neurons was increased, postsynaptic receptor responses were enhanced, and the number of action potential discharges was elevated; (3) Specific inhibition of the CLA/IC-LC neural pathway induced pain responses in sham-operated mice; specific activation of this pathway alleviated pain-related behaviors in neuropathic pain mice. The present results indicate the existence of functional projection from the CLA/IC to the LC. Under neuropathic pain condition, the CLA/IC-LC pathway exhibits enhanced neuronal activity, and selective activation of this pathway produces significant analgesic effects against neuropathic pain.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"148-158"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346956","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}

引用次数: 0

[Spinal lncRNA_RT1-CE10 attenuates chronic visceral hypersensitivity in rats with irritable bowel syndrome via inhibiting microglial activation]. [脊髓lncRNA_RT1-CE10通过抑制小胶质细胞激活减轻肠易激综合征大鼠的慢性内脏超敏反应]。

生理学报 Pub Date : 2026-02-25

Zi-Han Liu, Yi-Qian Liu, Qian-Li Zhang, Chun Lin, Yang Huang

{"title":"[Spinal lncRNA_RT1-CE10 attenuates chronic visceral hypersensitivity in rats with irritable bowel syndrome via inhibiting microglial activation].","authors":"Zi-Han Liu, Yi-Qian Liu, Qian-Li Zhang, Chun Lin, Yang Huang","doi":"","DOIUrl":"","url":null,"abstract":"The purpose of the study was to investigate the role of the long non-coding RNA (lncRNA)_RT1-CE10 and its molecular mechanisms in chronic visceral pain of rats with irritable bowel syndrome (IBS). Sprague-Dawley (SD) rats were exposed to colorectal distention (CRD) stimulation at a pressure of 60 mmHg for 1 min from 8 to 14 days after birth. The visceral hypersensitivity was assessed by measuring electromyographic (EMG) responses of external oblique muscle to CRD at 40 mmHg and 60 mmHg when the rats were 6 weeks old. The expression of lncRNA_RT1-CE10, Iba-1 and MHCII in the spinal cord was detected by RT-qPCR or Western blot. After intrathecal injection of minocycline (an inhibitor of microglia), the expression of Iba-1, MHCII and the visceral hypersensitivity were determined by Western blot and EMG, respectively. After intrathecal injection of AAV-lncRT1-CE10 and AAV-shlncRT1-CE10, the expression of Iba-1 and MHCII was examined by Western blot, respectively. The results showed that the expression of lncRNA_RT1-CE10 was decreased in the spinal cord of IBS rats, while the expression of Iba-1 and MHCII was increased. Inhibition of microglial activation by minocycline attenuated visceral hypersensitivity in IBS rats. Over-expression of lncRNA_RT1-CE10 decreased the Iba-1 and MHCⅡ levels in IBS rats, while knockdown of lncRNA_RT1-CE10 increased the Iba-1 and MHCⅡ levels in control rats. Collectively, these results demonstrate that lncRNA_RT1-CE10 attenuates visceral hypersensitivity by inhibiting microglial activation in IBS rats.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"246-252"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346922","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}

引用次数: 0

[5-HT_1A receptors in the anterior cingulate cortex mediate electroacupuncture to alleviate the affective pain in rats]. [前扣带皮层5-HT1A受体介导电针减轻大鼠情感性疼痛]。

生理学报 Pub Date : 2026-02-25

Jie Shen, Kai-Ni Wang, Jie Gao, Yu Shi, Tao-Ran Bi, Xin Zhao, Yu Zhang

{"title":"[5-HT1A receptors in the anterior cingulate cortex mediate electroacupuncture to alleviate the affective pain in rats].","authors":"Jie Shen, Kai-Ni Wang, Jie Gao, Yu Shi, Tao-Ran Bi, Xin Zhao, Yu Zhang","doi":"","DOIUrl":"","url":null,"abstract":"This study aimed to investigate the role of 5-hydroxytryptamine 1A (5-HT1A) receptors in the anterior cingulate cortex (ACC) in regulating the affective pain in rats. In the ACC, normal saline (NS), the 5-HT1A receptor agonist 8-OH-DPAT or the 5-HT1A receptor antagonist WAY-100635 was pre-injected respectively. A persistent inflammatory pain model was established by subcutaneously injecting 0.08 mL of complete Freund's adjuvant (CFA) into the left hind paw of rats, which was then paired with a specific environment to induce a conditioned place avoidance (CPA) response. Then the electroacupuncture (EA, 10 Hz, 3 mA) was applied to stimulate the Huantiao acupoint (GB30). The CPA responses of rats in the pain-paired environment and the firing activities of ACC neurons were simultaneously observed. Subsequently, open-field behavior, paw withdrawal latency (PWL), and 50% paw withdrawal threshold (PWT) tests were conducted. The results showed that: (1) Rats injected with CFA showed significant reductions in PWL and 50% PWT, and spent less time in the \"pain-paired environment\" and the center of the open field, compared to the control group (P < 0.05). (2) Immunofluorescence double-labeling results showed a high co-expression of Fos protein and 5-HT1A receptors in the ACC of the EA-treated normal rats. (3) Pre-treatment with the 5-HT1A receptor agonist 8-OH-DPAT (8 μg) in the ACC alleviated CFA-induced affective pain (P < 0.05) and reversed the increase in firing frequency of pyramidal neurons in the ACC induced by CFA (P < 0.05). (4) Pre-treatment with the 5-HT1A receptor antagonist WAY-100635 (8 μg) in the ACC, combined with EA stimulation, reversed the CPA-like behavioral responses induced by CFA in rats and increased the firing frequency of pyramidal neurons in the ACC (P < 0.05). These results suggest that the 5-HT1A receptors in ACC mediate the alleviating effect of EA on the affective pain of CFA-induced rats.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"78 1","pages":"233-245"},"PeriodicalIF":0.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147347179","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}

引用次数: 0

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