IF 5.5 1区医学

PAIN® Pub Date : 2025-07-18 DOI: 10.1097/j.pain.0000000000003738

Laura Schillebeeckx, Ashlee Caldwell, Katrien Luyten, Malgorzata Sliwinska, Thomas Gevaert, Wouter Everaerts, Thomas Voets

{"title":"A catheter-associated urinary tract infection mouse model to study bladder dysfunction and pain.","authors":"Laura Schillebeeckx, Ashlee Caldwell, Katrien Luyten, Malgorzata Sliwinska, Thomas Gevaert, Wouter Everaerts, Thomas Voets","doi":"10.1097/j.pain.0000000000003738","DOIUrl":"10.1097/j.pain.0000000000003738","url":null,"abstract":"Abstract: Bladder pain and dysfunction are common symptoms in patients with urinary tract infections (UTIs), including catheter-associated UTIs (CAUTIs). Underlying mechanisms of chronic bladder pain and recurrent UTIs remain poorly understood, and good translational mice models are sparse. Here, we developed a female mouse suprapubic CAUTI model, and combined in vivo and ex vivo imaging techniques and behavioral assays to longitudinally evaluate the consequences for bladder function, inflammation, abdominal pain, bacterial colonization, and biofilm. Catheter-associated urinary tract infection animals, with an implanted suprapubic bladder catheter infected with the bioluminescent uropathogenic Escherichia coli (UPEC) UTI89-Lux strain, were compared with sham-operated mice (SHAM), mice with a sterile catheter (CACON), and mice infected via transurethral instillation (UTI). Compared to transient infections in UTI mice, CAUTI mice exhibited sustained bacterial infection during >2 weeks, which was associated with bacterial biofilm formation on the catheter inner surface. Compared to CACON mice, CAUTI mice showed a more pronounced increase in suprapubic sensitivity, which was sensitive to antibiotic treatment. Void spot assays and fluoroscopic volumetry further revealed a smaller bladder capacity in both CAUTI and CACON mice, but only in CAUTI mice this was associated with reduced voiding efficiency. This model successfully recapitulates clinically relevant symptoms of CAUTI in patients and demonstrates that sustained bacterial colonization of the catheter directly contributes to bladder hypersensitivity and voiding dysfunction. This novel in vivo research model may be instrumental in the search for new therapies aimed at disrupting biofilms and treatments of bladder-related pain, infections, and dysfunction.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":""},"PeriodicalIF":5.5,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144732696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Autoreactive immunoglobulin G levels and Fc receptor γ subunit upregulation drive mechanical allodynia after nerve constriction or crush injury. 自身反应性免疫球蛋白G水平和Fc受体γ亚基上调驱动神经收缩或挤压损伤后的机械性异常性痛。

IF 5.5 1区医学

PAIN® Pub Date : 2025-07-18 DOI: 10.1097/j.pain.0000000000003734

Nathan T Fiore, Kendal F Willcox, Anamaria R Grieco, Dorsa Dayani, Younus A Zuberi, Cobi J Heijnen, Peter M Grace

{"title":"Autoreactive immunoglobulin G levels and Fc receptor γ subunit upregulation drive mechanical allodynia after nerve constriction or crush injury.","authors":"Nathan T Fiore, Kendal F Willcox, Anamaria R Grieco, Dorsa Dayani, Younus A Zuberi, Cobi J Heijnen, Peter M Grace","doi":"10.1097/j.pain.0000000000003734","DOIUrl":"10.1097/j.pain.0000000000003734","url":null,"abstract":"Abstract: B cells contribute to the development of pain after sciatic nerve chronic constriction injury (CCI) through binding of immunoglobulin G (IgG) to Fc gamma receptors (FcγRs) in the lumbar dorsal root ganglia (DRG) and spinal cord. Yet the contribution of B cells to pain after different types of peripheral nerve injury is uncertain. Using male and female mice, we demonstrate a divergent role for B cell-IgG-FcγR signaling underlying mechanical allodynia between CCI, nerve crush (NC), spared nerve injury (SNI), and spinal nerve ligation (SNL). Depletion (monoclonal anti-CD20) or genetic deletion (muMT mice) of B cells prevented development of allodynia after NC and CCI, but not SNI or SNL. In apparent contradiction, circulating levels of autoreactive IgG and circulating immune complexes were increased in all models, although more prominent after NC and CCI. Passive transfer of IgG from SNI donor mice induced allodynia in CCI muMT recipient mice, demonstrating that IgG secreted after SNI is pronociceptive. To investigate why pronociceptive IgG did not contribute to mechanical allodynia after SNI, we evaluated the levels of the Fc receptor γ subunit. Spared nerve injury or spinal nerve ligation did not increase γ subunit levels in the DRG and spinal cord, whereas CCI and NC did, in agreement with B cell-dependent allodynia in these models. Together, the results suggest that traumatic peripheral nerve injury drives secretion of autoreactive IgG from B cells. However, levels of cognate FcγRs are increased after sciatic nerve constriction and crush, but not transection, nerve injury.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":""},"PeriodicalIF":5.5,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12313113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144732697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Androgen receptors expressed in the primary sensory neurons regulate mechanical pain sensitivity. 在初级感觉神经元中表达的雄激素受体调节机械疼痛敏感性。

IF 7.4 1区医学

PAIN® Pub Date : 2025-07-16 DOI: 10.1097/j.pain.0000000000003736

Fumihiro Saika,Daisuke Uta,Yohji Fukazawa,Yuko Hino,Yu Hatano,Shiroh Kishioka,Hiroyuki Nawa,Shinjiro Hino,Kentaro Suzuki,Norikazu Kiguchi

{"title":"Androgen receptors expressed in the primary sensory neurons regulate mechanical pain sensitivity.","authors":"Fumihiro Saika,Daisuke Uta,Yohji Fukazawa,Yuko Hino,Yu Hatano,Shiroh Kishioka,Hiroyuki Nawa,Shinjiro Hino,Kentaro Suzuki,Norikazu Kiguchi","doi":"10.1097/j.pain.0000000000003736","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003736","url":null,"abstract":"The expression of hormonal receptors in pain-processing regions complicates understanding the hormonal effects on pain mechanisms. This study investigates androgen receptor (AR) involvement in pain sensitivity and sex differences in pain perception. Mechanical pain thresholds were higher in normal male mice compared to gonadectomized (GDX) male and normal female mice, correlating with serum testosterone levels. In the dorsal root ganglia (DRG), AR was expressed in normal males but undetectable in GDX males and normal females. Androgen receptor overlapped with NeuN, a neuronal nuclei marker, indicating androgen signaling activation in sensory neurons. In male sensory neuron-selective AR conditional knockout (AR-cKO) mice, mechanical pain thresholds were significantly lower than in wild-type males, with the greatest AR depletion in calcitonin gene-related peptide (CGRP)+ neurons. Electrophysiological analyses revealed increased excitability of spinal dorsal horn neurons in both GDX males and AR-cKO males. In female mice, administration of testosterone propionate or dihydrotestosterone significantly raised mechanical pain thresholds, accompanied by increased AR expression in the DRG. This effect was abolished in AR-cKO females, where AR depletion was most prominent in CGRP+ neurons, consistent with male findings. These results indicate that primary sensory neurons, particularly CGRP+ neurons, are critical targets of androgen in regulating mechanical pain sensitivity. Therefore, manipulating androgen signaling in sensory neurons may offer a promising approach to managing mechanical pain.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"84 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144639739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neurophysiological encoding of aversive prediction errors. 厌恶预测误差的神经生理编码。

IF 7.4 1区医学

PAIN® Pub Date : 2025-07-16 DOI: 10.1097/j.pain.0000000000003712

Raghavan Gopalakrishnan,Claire Sonneborn,Sylvain Baillet,Andre G Machado,Tor D Wager,Mathieu Roy

{"title":"Neurophysiological encoding of aversive prediction errors.","authors":"Raghavan Gopalakrishnan,Claire Sonneborn,Sylvain Baillet,Andre G Machado,Tor D Wager,Mathieu Roy","doi":"10.1097/j.pain.0000000000003712","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003712","url":null,"abstract":"Aversive prediction error (PE) brain signals generated by unexpected pain or pain absence are crucial for learning to avoid future pain. Yet, the detailed neurophysiological origins of PE signaling remain unclear. In this study, we combined an instrumental pain avoidance task with computational modeling and magnetoencephalography to detect time-resolved activations underlying pain expectations and aversive PE signals in the human brain. The task entailed learning probabilistically changing cue-pain associations to avoid receiving a pain stimulus. We used an axiomatic approach to identify general aversive PE signals that encode the degree to which the outcome deviated from expectations. Our findings indicate that aversive PE signals are generated in the alpha band (8-12 Hz) by the midbrain/diencephalon, lateral orbitofrontal cortex, and ventrolateral prefrontal cortex approximately 150 milliseconds after outcome delivery. Moreover, alpha oscillations in these regions also encoded pain expectations before the outcome. We speculate that this may facilitate the rapid generation of PEs by allowing outcome-related nociceptive activity to be integrated with ongoing predictive signals. Finally, decisions to avoid pain recruited alpha oscillations in the anterior cingulate and dorsomedial prefrontal cortices, suggesting their active engagement in comparing predicted action values. Overall, our data reveal the rapid neurophysiological mechanisms underlying the generation of aversive PEs and subsequent decision-making.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"104 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144639737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

STIM1 functionally couples to transient receptor potential ankyrin 1 contributing to nociception. STIM1在功能上与瞬时受体电位锚蛋白1偶联，参与伤害感受。

IF 7.4 1区医学

PAIN® Pub Date : 2025-07-16 DOI: 10.1097/j.pain.0000000000003729

Yixiao Mei,Hareram Birla,Bo Hyun Lee,Zhixiao Li,Vipin Rai,Isis Zhang,Xiaodong Huo,Anni Yi,Qiao Zhang,Daling Li,Yu Zhong,Fengying Wang,Bushra Yasin,Carol Apai,Tibor Rohacs,Yuan-Xiang Tao,Alex Bekker,Huijuan Hu

{"title":"STIM1 functionally couples to transient receptor potential ankyrin 1 contributing to nociception.","authors":"Yixiao Mei,Hareram Birla,Bo Hyun Lee,Zhixiao Li,Vipin Rai,Isis Zhang,Xiaodong Huo,Anni Yi,Qiao Zhang,Daling Li,Yu Zhong,Fengying Wang,Bushra Yasin,Carol Apai,Tibor Rohacs,Yuan-Xiang Tao,Alex Bekker,Huijuan Hu","doi":"10.1097/j.pain.0000000000003729","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003729","url":null,"abstract":"STIM1 is a calcium sensor that can sense calcium level changes in the endoplasmic reticulum (ER) and respond to extracellular stimuli. We have reported that STIM1 is expressed in nociceptors. However, its functional significance remains unclear. Here, we show that STIM1 plays an important role in sensing cold, chemical, and noxious mechanical stimuli in both male and female mice. We found that activation of transient receptor potential ankyrin 1 (TRPA1) triggers ER Ca2+ release, STIM1 translocation, and store-operated Ca2+ entry (SOCE). Immunostaining and western blot results reveal that TRPA1 is expressed in the ER. In addition, STIM1 deficiency in the primary sensory neurons reduces cold-, allyl isothiocyanate (TRPA1 agonist)-, and bradykinin-induced Ca2+ entry and nociception. Moreover, intraplantar injection of thapsigargin, an ER Ca2+-ATPase inhibitor, evokes nociception and increases pain hypersensitivity, which is significantly attenuated in STIM1 conditional knockout or L3/L4 dorsal root ganglia STIM1 knockdown mice. Mechanistic studies demonstrate that STIM1-mediated SOCE increases neuronal excitability and decreases potassium channel Kv4-mediated outward currents in small to medium-sized dorsal root ganglion neurons, which is abolished by inhibiting the mitogen-activated protein kinase/extracellular receptor kinase pathway. Our findings demonstrate that STIM1 acts as a transducer of nociception and uncover a novel link between STIM1 and TRPA1ER. Our study also provides new insights into TRPA1-mediated nociception.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"24 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144639738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Evaluating the efficacy of neurokinin-1 (substance P) receptor antagonist CP-99994 on facial grimacing and allodynia in mice postsurgery: a comparative study with known analgesics. 评估神经激肽-1 （P物质）受体拮抗剂CP-99994对术后小鼠面部鬼脸和异常性疼痛的疗效：与已知镇痛药的比较研究

IF 5.5 1区医学

PAIN® Pub Date : 2025-07-15 DOI: 10.1097/j.pain.0000000000003720

Eric S McCoy, Dan F Ryan, Sang Kyoon Park, Mark J Zylka

{"title":"Evaluating the efficacy of neurokinin-1 (substance P) receptor antagonist CP-99994 on facial grimacing and allodynia in mice postsurgery: a comparative study with known analgesics.","authors":"Eric S McCoy, Dan F Ryan, Sang Kyoon Park, Mark J Zylka","doi":"10.1097/j.pain.0000000000003720","DOIUrl":"10.1097/j.pain.0000000000003720","url":null,"abstract":"Abstract: Neurokinin-1 (substance P) receptor (NK1R) antagonists failed to effectively treat pain in humans despite having antinociceptive properties in animals. Here, we sought to evaluate the efficacy of NK1R antagonist CP-99994 at reducing facial grimacing in white-coated CD-1 mice after laparotomy surgery when compared to the analgesics carprofen and buprenorphine. To enable this investigation, we developed a machine learning algorithm to automatically score facial grimacing in white-coated mice using the PainFace software platform. This algorithm detects 5 facial action units of the mouse grimace scale (MGS; orbitals, nose, ears, whiskers, cheeks) and assigns a facial grimace score (0-10) for each video frame analyzed. Carprofen and buprenorphine significantly reduced mean MGS scores and percentage of high grimace (MGS scores ≥5) frames for up to 4 hours postsurgery across multiple doses. In contrast, CP-99994 showed limited efficacy, with only the highest 30 mg/kg dose reducing grimacing at 2 hours. Likewise, principal component analysis of grimace data over time indicated that carprofen and buprenorphine were effective at reducing facial grimacing, whereas CP-99994 was not. However, both buprenorphine and CP-99994 reduced mechanical allodynia at the incision site. These findings reveal a dissociation between the effects of CP-99994 on a spontaneous pain measure (grimacing) and an evoked nociceptive response, whereas a known analgesic reduced both measures. Our study suggests that using facial grimacing to assess spontaneous pain alongside traditional nociceptive assays may better predict analgesic potential and possibly reduce risk of translational failures when selecting drug candidates for clinical advancement.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":""},"PeriodicalIF":5.5,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12313106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Quantitative sensory testing for detecting small fiber impairment-the same old story or finally evidence-based decision making? 定量感官测试用于检测小纤维损伤——还是老故事还是最终基于证据的决策？

IF 7.4 1区医学

PAIN® Pub Date : 2025-07-14 DOI: 10.1097/j.pain.0000000000003686

Elena K Enax-Krumova

引用次数: 0

Androgen levels and experimental pain sensitivity in healthy young adolescent girls. 健康青春期少女的雄激素水平与实验性疼痛敏感性

IF 7.4 1区医学

PAIN® Pub Date : 2025-07-11 DOI: 10.1097/j.pain.0000000000003704

Gourav Banerjee,Joel Brown,Alana McMichael,Arbi Ben Abdallah,Sarah Buday,Thomas J Baranski,Simon Haroutounian,Deanna Barch,Jacob AuBuchon,Hadas Nahman-Averbuch

{"title":"Androgen levels and experimental pain sensitivity in healthy young adolescent girls.","authors":"Gourav Banerjee,Joel Brown,Alana McMichael,Arbi Ben Abdallah,Sarah Buday,Thomas J Baranski,Simon Haroutounian,Deanna Barch,Jacob AuBuchon,Hadas Nahman-Averbuch","doi":"10.1097/j.pain.0000000000003704","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003704","url":null,"abstract":"Androgens, such as testosterone, have an antinociceptive effect based on animal and adult studies. However, because androgens may exert different physiological effects during puberty, it is not clear whether the antinociceptive effect would also be found in adolescents. Thus, this study examined the relationships between testosterone levels and experimental pain sensitivity in healthy young adolescent girls. In addition, the relationships between experimental pain sensitivity and other androgens, including dehydroepiandrosterone (DHEA), dehydroepiandrosterone-sulfate (DHEA-S), dihydrotestosterone, and androstenedione, were explored, and the role of puberty in moderating these relationships was tested. Forty-five healthy girls (11.91 ± 1.35 years) completed comprehensive psychophysical assessments of heat, cold, and pressure pain thresholds, heat and cold pain intensity ratings, temporal summation, heat- and pressure-conditioned pain modulation, offset analgesia, and cold pain tolerance. Blood samples were collected to analyze sex hormone levels. Participants also completed the Pubertal Developmental Scale. Correlations and regression models examined the associations between androgens and experimental pain sensitivity, and whether pubertal stage moderated these relationships. Overall, no significant associations were found between levels of testosterone, DHEA, DHEA-S, dihydrotestosterone, or androstenedione and experimental pain sensitivity, nor were these associations moderated by pubertal stage. Only DHEA-S levels were related to cold pain threshold and tolerance, and pubertal stage moderated the relationship between DHEA-S and cold pain tolerance, which was significant only in the late (r = 0.453, P = 0.027) but not early-mid puberty group. The results of this study suggest that androgens may have a minimal effect on experimental pain sensitivity in healthy young adolescent girls.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"8 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144639837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Peripheral contributions to offset analgesia: effects of stimulus duration, intensity, and location. 外周对抵消性镇痛的贡献：刺激持续时间、强度和位置的影响。

IF 7.4 1区医学

PAIN® Pub Date : 2025-07-11 DOI: 10.1097/j.pain.0000000000003745

Pengyuan Sun,Alvin P H Wong,Christopher L Asplund,Stuart W G Derbyshire

{"title":"Peripheral contributions to offset analgesia: effects of stimulus duration, intensity, and location.","authors":"Pengyuan Sun,Alvin P H Wong,Christopher L Asplund,Stuart W G Derbyshire","doi":"10.1097/j.pain.0000000000003745","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003745","url":null,"abstract":"Offset analgesia (OA) is a substantial decrease in pain perception after a minor reduction in noxious stimulus intensity. The peripheral mechano- and heat-sensitive A-fibre nociceptors (AMH-I and AMH-II) and the C-fibre nociceptors (CMH) are hypothesised to contribute to OA. These nociceptors differ in initial response latency, peak response latency, and heat threshold, and the AMH-II fibres may be absent from the palm. Stimuli targeting those different nociceptive properties were used to decide which nociceptors critically contribute to OA. Healthy volunteers (N = 64) underwent 16 unique trials with continuous noxious heat (45-47°C). These trials included 3-second (short) or 12-second (long) periods of increased noxious heat (46-48°C), or an intense 0.2 seconds pulse of heat (51°C). Stimuli were delivered to the dorsum (back) and palm of the hands. Notable OA effects were observed for long-duration trials on both the dorsum and palm of the hand. Offset analgesia was inconsistently present and much smaller for the short-duration trials and for the pulse trials. Pain ratings generally increased more slowly during palm stimulation compared with dorsum stimulation. The demonstration of OA on the palm suggests that AMH-II nociceptors are either not critical for OA or that the AMH-II nociceptors are present in the palm. The small OA after the intense pulse and the substantial reduction in OA during the short trials suggests that AMH-I nociceptors are not necessary for OA and that the faster response of the AMH-II or CMH nociceptors is not sufficient to generate OA.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"8 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144639842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Autoantibody-driven pain-Challenges and opportunities. 自身抗体驱动的疼痛——挑战和机遇。

IF 5.9 1区医学

PAIN® Pub Date : 2025-07-11 DOI: 10.1097/j.pain.0000000000003735

John David Clark, Wade S Kingery

引用次数: 0

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