PAIN®最新文献

{"title":"Rejuvenation alleviates prolonged postsurgical pain in aging mice by mitigating inflammaging.","authors":"Basma Abdelkader, Xiang Qun Shi, Wen Bo Sam Zhou, Jesus D Castaño, Audrey V Grant, Francis Beaudry, Ji Zhang","doi":"10.1097/j.pain.0000000000003684","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003684","url":null,"abstract":"<p><strong>Abstract: </strong>As individuals age, they often experience persistent, unresolved pain, impacting their quality of life. Aging as a process is accompanied by \"inflammaging,\" a state of chronic, low-grade systemic inflammation contributing to various diseases. Understanding the functional link between inflammaging and age-related development of pain is crucial for identifying novel therapeutic targets. We hypothesized that the circulatory milieu plays a role in regulating pain and that inflammaging contributes to changes in pain behavior with age. To test these hypotheses, we monitored nociception and postsurgical pain in male and female mice aged 3 and 24 months and analyzed their serum proteome, including cytokine/chemokine profiles. Our results demonstrated that compared with young mice, aging mice were hyposensitive to mechanical stimulation, yet their pain response to incision was aggravated and prolonged. Serum proteomic analysis revealed sex-specific inflammaging patterns. To explore the link between inflammaging and age-related alteration in pain behavior, we applied a rejuvenation strategy by transferring serum from 3-month-old mice to 19- to 21-month-old mice. Young serum normalized mechanical sensitivity in aged mice, alleviated postsurgical mechanical pain, and promoted recovery. Alongside the improvements in pain behavior phenotype, young serum recalibrated the aging serum profile. It reduced age-associated increases of cytokine/chemokine levels in male mice and rescued age-related, female-selective downregulation of inflammatory pathways such as liver X receptor/retinoid X receptor activation, D24-dehydrocholesterol reductase, and complement signaling. Our findings suggest that the circulatory environment, notably inflammaging, plays a significant role in altered pain behavior of aging mice. The sex-specific signature of age-dependent systemic inflammation highlights the importance of investigating inflammaging through the lens of sexual dimorphism.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144369130","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}

{"title":"Factors influencing the recruitment of diverse populations into pain research: findings from a qualitative study with underrepresented participants.","authors":"Kendrick V Kennedy,Anna Tupetz,Wanda Boone,Stephanie Eucker,Carson Herman,Jaran White,Nadine Barrett,Alexander T Limkakeng,Rosa Gonzalez-Guarda","doi":"10.1097/j.pain.0000000000003641","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003641","url":null,"abstract":"The inclusion of diverse populations in pain research is crucial to obtaining a complete understanding of how the biopsychosocial experience of pain is seen through the lens of different populations. Traditionally, individuals who identify as Black/African American or Hispanic/Latino have not participated in early phase clinical trials, and as a result, their unique perspectives of the management of pain have not been included in study results. In this qualitative research study, we sought to uncover barriers that prevent diverse populations from participating in pain treatment clinical trials. Partnering with a community organization, we used a semistructured interview to conduct nine focus groups among underrepresented populations to obtain these perspectives. A total of 54 patients with ages ranging from 23 to 77 years old were recruited for this study. Of the patients recruited for the study, 74% identified as non-Hispanic Black, and 24% identified as Hispanic/Latino. Results were recorded, transcribed, and analyzed for thematic saturation using inductive qualitative content analysis. Results uncovered an array of different perspectives including the recognition of historical wrongs that lead to mistrust of the research and healthcare systems. However, other perspectives include recognition that the location of study sites, time required for participation, and overall accessibility of the study play a significant role in an individual's willingness to participate.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"70 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144328962","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}

{"title":"Deficits in temporal pain inhibition are associated with greater pain and functional impairment in osteoarthritis.","authors":"Benedict J Alter,Maya Maurer,Brian O'Connell,Andrea Gomez Sanchez,A Murat Kaynar,Anthony M DiGioia,Theodore Huppert,Ajay D Wasan","doi":"10.1097/j.pain.0000000000003648","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003648","url":null,"abstract":"Offset analgesia reflects time-dependent, central nervous system pain inhibition and refers to a dramatic drop in pain intensity after an offset of noxious stimulus intensity. Neuropathic and nociplastic pain conditions with strong central nervous system pathophysiologic mechanisms show deficits in offset analgesia. Whether offset analgesia is altered in more peripherally driven chronic nociceptive pain was unknown. Therefore, the primary goal of the current study was to determine whether chronic nociceptive pain is associated with changes in offset analgesia. We measured offset analgesia and sensory function using quantitative sensory tests, patient-reported pain and function, and walking and stair climbing performance using standardized tasks in knee osteoarthritis patients with equivalent joint degeneration but Moderate-to-Severe (n = 36) or Mild pain intensity (n = 36) and Pain-free controls without knee osteoarthritis (n = 30) matching for age, gender, and body mass index. Offset analgesia was significantly reduced in knee osteoarthritis groups compared with the Pain-free controls, with deficits occurring at both the nonpainful forearm and painful knee and in both genders. Greater deficits in offset analgesia were associated with more impairment in walking and stair climbing. Onset hyperalgesia, a novel measure of time-dependent pain facilitation, was reduced in women with Mild knee pain but not in men. These results suggest that deficits in temporal pain inhibition and gender-specific changes in temporal pain facilitation may contribute to pain and functional impairment in knee osteoarthritis, supporting further study of central pain modulation as a clinically relevant mechanism of chronic nociceptive pain.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"44 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144328963","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}

{"title":"Diagnostic accuracy of quantitative sensory testing for detecting small fiber impairment in polyneuropathy and diagnosing small fiber neuropathy.","authors":"Eleonora Galosi,Daniel Litewczuk,Gianfranco De Stefano,Giuseppe Di Pietro,Giulia Di Stefano,Nicoletta Esposito,Enrico Evangelisti,Pietro Falco,Caterina Leone,Juliane Sachau,Ralf Baron,Nanna Brix Finnerup,Andrea Truini","doi":"10.1097/j.pain.0000000000003685","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003685","url":null,"abstract":"This cross-sectional retrospective study evaluated the diagnostic accuracy of cold detection thresholds (CDT) and warm detection thresholds (WDT), measured by quantitative sensory testing, for detecting small fiber impairment in polyneuropathy and diagnosing small fiber neuropathy (SFN). A total of 384 individuals with distally distributed sensory disturbances were included. Using ACTTION criteria, 138 patients with polyneuropathy were identified. Among them, 36 were diagnosed with SFN, 91 with mixed fiber polyneuropathy, and 11 with pure large fiber polyneuropathy. First, we assessed CDT and WDT accuracy, both individually and combined (ie, an abnormal value in either CDT or WDT), in detecting small fiber impairment in polyneuropathy. Next, we calculated CDT and WDT diagnostic accuracy for SFN, both alone and combined, and evaluated their accuracy when integrated with small fiber-related clinical abnormalities. Isolated abnormalities in CDT or WDT showed relatively low diagnostic accuracy. However, combined abnormalities achieved a sensitivity of 69% and specificity of 70% for detecting small fiber impairment in distal symmetric polyneuropathy. For SFN diagnosis, combining CDT and WDT yielded 78% sensitivity, 70% specificity, and a 94% negative predictive value. These metrics improved to 78% sensitivity and 100% specificity when CDT or WDT were integrated with small-fiber-related clinical abnormalities. Although individual CDT and WDT assessments offer limited diagnostic accuracy, their combination provides a practical, noninvasive approach for screening small fiber impairment in distal symmetric polyneuropathy and diagnosing SFN. This strategy may reduce the need for more invasive and less cost-effective procedures, like skin biopsy.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"34 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144328965","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}

{"title":"Early life adversity increases risk for chronic post-traumatic pain, data from humans and rodents.","authors":"Lauren A McKibben, Alice Woolard, Samuel A McLean, Ying Zhao, Taanvii Verma, Jacqueline Mickelson, Hongxia Lu, Jarred Lobo, Stacey L House, Francesca L Beaudoin, Xinming An, Jennifer S Stevens, Thomas C Neylan, Tanja Jovanovic, Laura T Germine, Scott L Rauch, John P Haran, Alan B Storrow, Christopher Lewandowski, Phyllis L Hendry, Sophia Sheikh, Christopher W Jones, Brittany E Punches, Lauren A Hudak, Jose L Pascual, Mark J Seamon, Claire Pearson, David A Peak, Roland C Merchant, Robert M Domeier, Niels K Rathlev, Brian J O'Neil, Leon D Sanchez, Steven E Bruce, John F Sheridan, Ronald C Kessler, Karestan C Koenen, Kerry J Ressler, Sarah D Linnstaedt","doi":"10.1097/j.pain.0000000000003555","DOIUrl":"10.1097/j.pain.0000000000003555","url":null,"abstract":"<p><strong>Abstract: </strong>Traumatic stress exposures (TSEs) are common in life. Although most individuals recover after a TSE, a substantial subset develop adverse post-traumatic neuropsychiatric sequelae such as chronic post-traumatic musculoskeletal pain (CPMP). Vulnerability factors for CPMP are poorly understood, which hinders identification of high-risk individuals for targeted interventions. One known vulnerability factor for many pain types is exposure to early life adversity (ELA), but few studies have assessed whether ELA increases risk for CPMP. This study used data from the Advancing Understanding of RecOvery afteR traumA study, a prospective human cohort study of TSE survivors, to test the hypothesis that ELA increases risk for CPMP. In addition, in secondary analyses, we assessed which subtypes of ELA (including childhood bullying) were most predictive of CPMP and whether a rat ELA model consisting of neonatal limited bedding, combined with single prolonged stress (SPS) in adulthood, would accurately model human findings. In Advancing Understanding of RecOvery afteR traumA study participants (n = 2480), using multinomial logistic regression modeling of 4 identified latent pain classes, we found that ELA increased vulnerability to the high unremitting pain class (odds ratio [OR] = 1.047, P < 0.001), the moderate pain class (OR = 1.031, P < 0.001), and the moderate recovery pain class (OR = 1.018, P = 0.004), with physical abuse, emotional abuse, and bullying being the strongest predictors of high pain class assignment. Similarly, in male and female Sprague Dawley rats, in comparison with SPS alone, neonatal limited bedding combined with SPS caused increased baseline sensitivity and prolonged mechanical hypersensitivity (F(11,197) = 3.22, P < 0.001). Further studies in animals and humans are needed to understand mechanisms by which ELA confers vulnerability to CPMP.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333667","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}

{"title":"Differential maturation of the brain networks required for the sensory, emotional, and cognitive aspects of pain in human newborns.","authors":"Laura Jones,Dafnis Batalle,Judith Meek,A David Edwards,Maria Fitzgerald,Tomoki Arichi,Lorenzo Fabrizi","doi":"10.1097/j.pain.0000000000003619","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003619","url":null,"abstract":"Pain is multidimensional, including sensory-discriminative, affective-motivational, and cognitive-evaluative components. Although the concept of pain is learned through life, it is not known when and how the brain networks that are required to encode these different dimensions of pain develop. Using the 2 largest available databases of brain magnetic resonance images-the developing Human Connectome Project and the Human Connectome Project-we have mapped the development of the pain connectome-the neural network required for pain perception-in infants from 26 to 42 weeks of postmenstrual age (PMA, n = 372), compared with adults (n = 98). Partial correlation analysis of resting BOLD signal between pairwise combinations of 12 pain-related brain regions showed that overall functional connectivity is significantly weaker before 32 weeks PMA compared with adults. However, over the following weeks, significantly different developmental trajectories emerge across pain connectome subnetworks. The first subnetwork to reach adult levels in strength and proportion of connections is the sensory-discriminative subnetwork (34-36 weeks PMA), followed by the affective-motivational subnetwork (36-38 weeks PMA), while the cognitive-evaluative subnetwork has still not reached adult levels at term. This study reveals a previously unknown pattern of early development of the infrastructure necessary to encode different components of pain experience. Newborn neural pathways required for mature pain processing in the brain are incomplete in newborns compared with adults, particularly regarding the emotional and evaluative aspects of pain. The rapid age-related changes suggest that pain processing, and consequently pain experience, changes rapidly over this developmental period and unlikely to be the same as in adults, even at term.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"600 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144319818","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}

{"title":"The influence of genetic and epigenetic variations on dynamic experimental pain measures in adults with and without chronic musculoskeletal pain: a systematic review.","authors":"Amber Billens,Amber De Groote,Delfien Syx,Mira Meeus,Jessica Van Oosterwijck","doi":"10.1097/j.pain.0000000000003608","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003608","url":null,"abstract":"Chronic musculoskeletal pain (CMP) is the most prevalent form of chronic pain. A subgroup of patients with CMP shows altered pain processing, including impaired endogenous pain modulation, as evaluated by experimental pain measures. One hypothesis is that genetic and/or epigenetic variants may contribute to individual differences in outcomes of dynamic experimental pain assessment. Therefore, a systematic review was performed to comprehensively summarize the current evidence regarding genetic and epigenetic influences on dynamic experimental pain measures in adults with and without CMP. The review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Four electronic databases were searched to identify relevant studies. Risk of bias and quality of evidence were assessed using the Newcastle Ottawa Scale and the Grading of Recommendations, Assessment, Development, and Evaluation approach, respectively. A total of 24 articles were included, accounting for 34 different regions of interest. Low-quality evidence indicated no association between the rs4680 single-nucleotide polymorphism (SNP) of the COMT gene or the serotonin-transporter-linked polymorphic region SNP of the SLC6A gene and conditioned pain modulation in healthy volunteers or in patients with CMP. In addition, low-quality evidence was found for the lack of an association between the rs1799971 SNP of the OPRM1 gene and conditioned pain modulation in healthy volunteers. Other genetic and epigenetic variants provided limited or conflicting evidence. For now, it seems that dynamic experimental pain measurements are robust to genetic and epigenetic variations. However, more reproducible research is warranted to better understand whether or not and how genetic and epigenetic variations influence (altered) pain processing, which is crucial for advancing both preventive and therapeutic strategies in CMP populations.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"24 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144328966","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}

{"title":"SARS-CoV-2 N protein interacts with Nav1.7 to promote pathological pain.","authors":"Jin-Kun Liu, Zi-Su Zhou, Shu-Hang Wang, Shi-Yu Zuo, Xiao-Fan Lu, Ying He, Hao Tang, Yan Xie, Man-Xiu Xie, Xiao-Long Zhang","doi":"10.1097/j.pain.0000000000003675","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003675","url":null,"abstract":"<p><strong>Abstract: </strong>Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to a global health crisis, with many patients experiencing not only acute neurological and sensory symptoms but also persistent sensory abnormalities, commonly referred to as long COVID sequelae. The mechanisms underlying somatosensory abnormalities induced by SARS-CoV-2 remain largely unclear. In this study, we investigate the role of the SARS-CoV-2 nucleocapsid (N) protein in pain regulation. Our data show that SARS-CoV-2 N protein exacerbates pathological pain in mouse models of bone cancer, chemotherapy, neuropathic, and inflammatory, and promotes the chronification of acute inflammatory pain. We also identify a potential interaction between the N protein and Nav1.7 in dorsal root ganglion neurons from mice, monkeys, and humans. Furthermore, the N protein significantly increases Nav1.7 currents in dorsal root ganglion neurons from both mice and monkeys by delaying Nav1.7 inactivation without altering its expression or membrane trafficking. This modulation of Nav1.7 function by the N protein not only intensifies pain hypersensitivity but also prolongs the duration of pain, potentially facilitating the transition from acute to chronic pain. Our findings underscore the importance of vigilant management of SARS-CoV-2 infection in patients with pathological pain and suggest potential therapeutic targets for mitigating COVID-19-related pain.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249140","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}

{"title":"From acute injury to chronic pain: key factors and future research directions.","authors":"Chengyu Wang, Jiaming Ji, Chaojin Chen","doi":"10.1097/j.pain.0000000000003538","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003538","url":null,"abstract":"","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"166 6","pages":"1459"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143987056","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}

{"title":"Radiation of pain: psychophysical evidence for a population coding mechanism in humans.","authors":"Wacław M Adamczyk, Vishwanath Ramu, Catherine Jackson, Geraldine Schulze, Kenneth R Goldschneider, Susmita Kashikar-Zuck, Christopher D King, Robert C Coghill","doi":"10.1097/j.pain.0000000000003474","DOIUrl":"10.1097/j.pain.0000000000003474","url":null,"abstract":"<p><strong>Abstract: </strong>The spread of pain across body locations remains poorly understood but may provide important insights into the encoding of sensory features of noxious stimuli by populations of neurons. In this psychophysical experiment, we hypothesized that more intense noxious stimuli would lead to spread of pain, but more intense light stimuli would not produce perceptual radiation. Fifty healthy volunteers (27 females, 23 males, ages 14-44 years) participated in this study wherein noxious stimuli (43, 45, 47, and 49°C) were applied to glabrous (hand) and hairy skin (forearm) skin with 5-second and 10-second durations. Also, visual stimuli displayed on the target bodily area were used as a control. Participants provided pain (and light) spatial extent ratings as well as pain (and light) intensity ratings. In the extent rating procedure, participants adjusted the extent of the square displayed on the screen with the extent of pain (or light) that they experienced. Pain extent ratings showed statistically significant radiation of pain indicated by 12.42× greater spatial spread of pain (pain extent) than the area of the stimulation with 49°C ( P < 0.001), in contrast to visual ratings, which closely approximated the size of the stimulus (1.22×). Pain radiation was more pronounced in hairy than glabrous skin ( P < 0.05) and was more pronounced with longer stimulus duration ( P < 0.001). Pain intensity explained only 14% of the pain radiation variability. The relative independence of the pain radiation from pain intensity indicates that distinct components of population coding mechanisms may be involved in the spatial representation of pain vs intensity coding.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":"1285-1295"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12067604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142771238","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}