Neuroendocrinology最新文献

{"title":"The Clinician's Role in Diagnostic Pathways and the Impact of Clinicopathological Collaboration on Outcomes in Patients with Neuroendocrine Neoplasms: Current Perspectives.","authors":"Alice Laffi, Andrea Lania, Alessandro Zerbi, Elisabetta Lavezzi, Silvia Carrara, Silvia Uccella","doi":"10.1159/000548924","DOIUrl":"10.1159/000548924","url":null,"abstract":"<p><strong>Introduction: </strong>Neuroendocrine neoplasms (NENs) classification and diagnosis have substantially advanced, prompting specialization of pathologists and clinicians in NEN fields and fostering close interdisciplinary collaboration. In these rare diseases, misdiagnosis may undermine therapeutic strategies, highlighting the importance of a strong clinician-pathologist partnership. While the NEN-dedicated pathologist's role is well acknowledged, in clinical practice, accurate histological review depends on the clinician's ability to pose focused diagnostic questions within a well-defined clinical context.</p><p><strong>Methods: </strong>We retrospectively analyzed all NEN histological second opinions performed by a dedicated pathologist at our ENETS Center of Excellence in 01/2023-12/2024. Second opinions were requested by referring clinicians in cases of diagnostic uncertainty or clinical-pathological discordance. Discrepancies between initial and final diagnoses were categorized as \"major\" (with a substantial impact on patients' management) or \"minor.\"</p><p><strong>Results: </strong>Of 63 reviewed cases, we identified 36 not concordant cases. Among them, we reported 29/36 (81%) cases with significant discrepancies between the initial and the final diagnosis, with a following change in therapeutic strategy in 28 (e.g., shift from surveillance to surgery or modification of systemic therapy). Clinical requests for a histological review were prompted by inconsistency between clinical history and pathological diagnosis, incomplete or incoherent initial pathology report, or need for diagnostic confirmation to support specific clinical indications (e.g., surgery or chemotherapy).</p><p><strong>Conclusion: </strong>Our findings underscore the critical role of clinician's expertise in the multidisciplinary management of NEN patients. Underestimating clinician's role in coordinating the diagnostic process can lead to suboptimal care. Additionally, there is an urgent need to redesign the NEN care pathway, ensuring early access to specialized evaluation since the early diagnostic phase.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"55-61"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145280920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Systematic Review of the Effects of N-Methyl-D-Aspartate Receptor Antagonists on Pancreatic Islets.","authors":"Sabrina Wong, Gia Han Le, John Uhlig, Ellen Yang, Christine E Dri, Joshua D Rosenblat, Rodrigo B Mansur, Roger S McIntyre","doi":"10.1159/000549276","DOIUrl":"10.1159/000549276","url":null,"abstract":"<p><p><p>Background: N-methyl-D-aspartate receptors (NMDARs) are widely distributed in the brain and pancreas. Preliminary evidence indicates that aberrant NMDAR-mediated glutamatergic signaling may disrupt pancreatic islet function and glucose-insulin homeostasis. The frequent comorbidity of depression and diabetes underscores the potential role of NMDAR signaling in pancreatic function as a shared pathophysiological mechanism. Herein, this systematic review aims to evaluate the effects of NMDAR antagonism on pancreatic cells (i.e., alpha, beta, delta) viability and function (i.e., activation, hormone production, and release).</p><p><strong>Methods: </strong>We performed a systematic search on PubMed and Ovid databases from inception to September 11, 2024. A manual search was also conducted on Google Scholar and Scopus databases. Eligible studies were primary, controlled in vitro or in vivo studies investigating the effects of NMDAR antagonism on pancreatic islet function and viability. Results were synthesized and presented descriptively. Risk of bias was assessed independently by two reviewers using a modified SYRCLE risk of bias tool.</p><p><strong>Results: </strong>We reviewed 14 studies evaluating NMDA receptor antagonism in whole islets, beta and alpha cells; however, no studies evaluated delta cells. Within beta cells, NMDAR antagonism improved glucose-stimulated insulin secretion and increased cell proliferation and viability. Similarly, alpha cells were protected against stress-induced apoptosis.</p><p><strong>Conclusion: </strong>Our results suggest that NMDAR antagonism improves alpha and beta cell function and viability, which may have translational relevance to comorbid metabolic dysfunction in depression. These mechanisms may subserve the antidepressant effects of select NMDA antagonists (e.g., ketamine/esketamine, dextromethorphan). Further research should aim to investigate the effects of subanesthetic doses of ketamine/esketamine on pancreatic function and on delta cells. </p>.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"70-87"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12734414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145409791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crosstalk between Circadian Rhythm and Neuroinflammation.","authors":"Guocheng Mei, Huiqiong Pan, Jinyu Zheng, Kepei Chen, Weihong Zheng, Hang Xu, Zhiming Liu, Wei Lin, Zhenlang Lin, Min Zhang","doi":"10.1159/000551312","DOIUrl":"10.1159/000551312","url":null,"abstract":"<p><strong>Background: </strong>The circadian rhythm is an intrinsic, approximately 24-h cycle of physiological, behavioral, and psychological changes formed through organisms' long-term evolutionary adaptation to the 24-h light-dark cycle on Earth. It regulates the body's homeostatic processes according to a daily schedule, ensuring the proper execution of physiological processes and the stability of the internal environment. In recent years, numerous studies have indicated crosstalk between the circadian rhythm and neuroinflammation. Disruption of the circadian rhythm can influence the onset and progression of various acute and chronic central nervous system diseases.</p><p><strong>Summary: </strong>This review outlines the basic components and mechanisms of the circadian timing system and divides the development of neuroinflammation into several parts: initiation of neuroinflammation, glial cell activation, disruption of the neurovascular unit, oxidative stress response, and cellular energy metabolism. By revealing the role of circadian mechanisms in each part, the relationship between the biological clock and neuroinflammation is analyzed from a molecular biology perspective, aiming to provide a new theoretical basis for the clinical intervention of neuroinflammation and the treatment of related diseases.</p><p><strong>Key messages: </strong>Disrupted circadian rhythms participate in various stages of neuroinflammation through \"crosstalk,\" making them a factor that cannot be ignored in the treatment of neurological disorders.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"229-243"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147344792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anxiety, Depression and Quality of Life in Neuroendocrine Neoplasm Patients: Insights from Regression and Network Analysis.","authors":"Kuan Zhao, Yun Liang, Jie Chen, Wei Feng","doi":"10.1159/000551891","DOIUrl":"10.1159/000551891","url":null,"abstract":"<p><strong>Background: </strong>Neuroendocrine neoplasms (NENs) are rare, heterogeneous malignancies with increasing incidence and poor survival in China. Beyond physical symptoms, patients frequently experience psychological distress and impaired quality of life (QOL), yet comprehensive evidence remains limited.</p><p><strong>Methods: </strong>Patients with NENs were recruited from the oncology outpatient clinic at Fudan University Shanghai Cancer Center. Psychological status and QOL were assessed using the Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder Questionnaire-7 (GAD-7), and the Quality-of-Life Questionnaire-Gastrointestinal Neuroendocrine Tumors-21 (QLQ-GI.NET21). Multivariable regression and network analysis were performed.</p><p><strong>Results: </strong>Among 327 patients, 34.3% exhibited significant depressive symptoms and 34.9% anxiety. Nonmetastatic NEN patients showed higher anxiety, although this finding should be interpreted with caution. Survival time, gender, tumor site, and disease phase significantly influenced anxiety and depression scores. In the gastrointestinal subgroup, G3-grade patients experienced greater distress and poorer QOL. Network analysis revealed a complex interrelationship among anxiety, depression, and QOL dimensions. High-centrality nodes included GAD2 (\"uncontrollable worry\"), the QLQ-GI.NET21 social function domain, GAD5 (\"restlessness\"), PHQ9 (\"suicide\"), and PHQ4 (\"fatigue\"). Key bridge symptoms were identified as PHQ2 (\"sad mood\"), GAD5 (\"restlessness\"), the QLQ-GI.NET21 sexual function domain, PHQ1 (\"anhedonia\"), and GAD7 (\"feeling afraid\"). Gender and metastatic status did not significantly affect network structure.</p><p><strong>Conclusion: </strong>These findings underscore the need for integrated psychological assessments and tailored interventions throughout treatment, particularly for high-risk subgroups. The core symptoms and bridge nodes identified may serve as potential targets for reducing psychological distress in NEN patients.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"261-274"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum.","authors":"","doi":"10.1159/000549428","DOIUrl":"10.1159/000549428","url":null,"abstract":"<p><p>In the article \"Epidemiology of Neuroendocrine Neoplasia Worldwide: A Review of the Literature (2012-2022)\" [Neuroendocrinology. 2025; https://doi.org/10.1159/000548790] by Nwoguh et al., the third author's name should correctly read Ayanna Gadsden-Jeffers.The original online article has been updated to reflect this.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"173"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13143258/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145781492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gastrointestinal Neuroendocrine Neoplasms in Children and Adolescents: Data from the German MET Studies (1997-2024).","authors":"Katharina Karges, Marina Kunstreich, Michael Abele, Jörg Fuchs, Christian Vokuhl, Ines B Brecht, Dominik T Schneider, Michael C Frühwald, Peter Vorwerk, Constantin Lapa, Antje Redlich, Michaela Kuhlen","doi":"10.1159/000548618","DOIUrl":"10.1159/000548618","url":null,"abstract":"<p><p><p>Introduction: Gastrointestinal neuroendocrine neoplasms (GI-NENs) outside the appendix and pancreas are exceptionally rare in children and adolescents. Limited data on presentation, treatment, and outcomes hinder clinical decision-making.</p><p><strong>Methods: </strong>We retrospectively analyzed 16 patients under 18 years with histologically confirmed NENs of gastrointestinal origin, enrolled in the German Malignant Endocrine Tumor (MET) Registry from 1997 to 2024. Neuroendocrine carcinomas were eligible for inclusion but were not observed. Findings were compared with a cohort (age 0-20 years) from the SEER database.</p><p><strong>Results: </strong>Median age at diagnosis was 15.4 years; 62.5% were male. Primary tumor sites included the stomach (43.8%), colorectum (18.8%), duodenum and Meckel's diverticulum (12.5% each), and jejunum and omentum majus (6.3% each). Distant metastases were present in 31.3%, with no isolated lymph node involvement. All tumors were well-differentiated NETs: G1 (43.8%), G2 (37.5%), and G3 (6.3%). Hereditary syndromes were confirmed in 18.8% and suspected in 12.5%. Somatostatin receptor 2 (SSTR2) expression was seen in most tested tumors. At 30.1-month median follow-up, 3-year overall survival (OS) and event-free survival were 93.3% and 73.3%, respectively, both associated with tumor grade, stage, and resection. The SEER cohort (n = 83) primarily had rectal primaries, localized disease, and the 3-year OS was 95.2%.</p><p><strong>Conclusion: </strong>Pediatric GI-NENs may present with advanced disease but have favorable outcomes following resection. Given the rarity and complexity, close evaluation by multidisciplinary tumor boards at each treatment step is strongly recommended to support individualized care. </p>.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"43-54"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12795540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Many Faces of Acromegaly: Understanding Its Clinical and Biological Heterogeneity.","authors":"Miriam da Costa Oliveira, Diego Paixão Côrtes Aguiar, Matheus Nejar Coan","doi":"10.1159/000552031","DOIUrl":"10.1159/000552031","url":null,"abstract":"<p><strong>Background: </strong>Acromegaly, in 95% of cases resulting from a PitNET that hypersecretes growth hormone (GH), is constantly revisited in the literature due to the repercussions on morbidity and mortality and difficulties that persist in early diagnosis.</p><p><strong>Summary: </strong>To shorten the interval between the onset of acromegaly manifestations and the diagnosis, our goal was to summarize the main situations that deviate from the typical presentation of the disease, highlighting the variability in phenotypic features, biochemical findings, and GH tumor expression. These non-classic findings contribute to the difficulties in managing the disease. The narrative literature review emphasized the diversity of presentations and recent and relevant publications.</p><p><strong>Key messages: </strong>The diagnosis of acromegaly can be challenging due to atypical clinical and biochemical presentations. Clinically, difficulties arise from the continuum of facial feature changes, which depend on several factors, including varying tissue sensitivity to excess GH. Biochemically, challenges include discordant GH and IGF-1 values, GH suppressibility in response to glucose, and borderline IGF-1 levels. There is also a wide range of immunohistochemical GH expressions in acromegaly, from complete absence of GH to rare multihormonal combinations. Awareness of these atypical forms of acromegaly presentation can improve early recognition and lead to timely diagnosis and management.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"321-331"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147699288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stress-Induced Activation of Orexin-A Neurons in the Lateral Hypothalamus Is Similar in Prepubertal and Adult Male and Female Rats despite Age-Dependent Differences in Hormonal Stress Reactivity.","authors":"Chelsea A Seidel, Sofia Cruz, Juliet Ortiz, Russell D Romeo","doi":"10.1159/000552033","DOIUrl":"10.1159/000552033","url":null,"abstract":"<p><strong>Introduction: </strong>Pubertal development is associated with changes in hypothalamic-pituitary-adrenal (HPA) axis reactivity, which may contribute to the increase in stress-related vulnerabilities observed during adolescence. In particular, prepubertal rats show significantly protracted stress-induced HPA responses compared to adults. However, the neuroendocrine mechanisms responsible for this developmental change are unclear. In adults, the orexigenic neuropeptide orexin-A has been shown to be a potent modulator of HPA reactivity, and activation of orexin-A neurons aligns with the magnitude of the hormonal stress response. However, it is currently unknown whether pubertal differences in HPA reactivity are associated with changes in orexin-A neurons.</p><p><strong>Methods: </strong>We examined the hormonal stress response and the number of activated orexin-A neurons in the lateral hypothalamus by co-labeling with c-Fos, a marker of cellular activation, before, during, or after stress exposure in prepubertal (30 days of age, 30 d) and adult (70 d) male and female rats. The number of immunoreactive orexin-A neurons was also quantified in prepubertal (30 d), mid-pubertal (45 d) and adult (70 d) males and females.</p><p><strong>Results: </strong>We found significantly prolonged stress-induced hormonal responses in prepubertal males and females compared to their adult counterparts. However, we found no developmental differences in either the number of orexin-A cells or their stress-induced activation in either sex.</p><p><strong>Conclusions: </strong>These data suggest minimal association between stress-induced activity of orexin-A neurons and pubertal-related differences in hormonal stress reactivity. However, these data indicate that the number of orexin-A cells is relatively stable throughout adolescent development and that orexin-A neurons are sensitive to stressors prior to pubertal maturation.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"288-298"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147699265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is Hypothalamic Dysfunction a Cause of Type II Diabetes Mellitus?","authors":"John Karl Young","doi":"10.1159/000550699","DOIUrl":"10.1159/000550699","url":null,"abstract":"<p><p><p>Background: A number of factors contribute to the development of diabetes mellitus (DM), but until recently, the role of hypothalamic dysfunction in the development of this disorder has not received sufficient attention. Hypothalamic neurons that project to the autonomic nervous system control overall glucose metabolism and insulin sensitivity. These neurons, in turn, are controlled by specialized astrocytes possessing proteins that enable them to function as nutrient sensors for glucose and fatty acids. An aging-related pathological process (that of mitochondrial degeneration) is present in these specific hypothalamic astrocytes. This mitochondrial degeneration can be accelerated by access to a high-fat diet, which also induces hypothalamic resistance to leptin, generalized insulin resistance, and an abnormal glucose homeostasis. An impaired astrocyte-neuron signaling, caused by this pathological mitochondrial degeneration, may underlie an abnormal hypothalamic function that leads to the development of type II diabetes. Pharmacological agents that protect astrocytes from mitochondrial degeneration may have a place in the treatment of type II diabetes. Summary: This article reviews evidence that hypothalamic pathology may make an important contribution to the etiology of type II DM. Key Messages: Abnormalities in hypothalamic astrocytes provoke a disturbed hypothalamic function that contributes to the development of DM. </p>.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"151-156"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931931/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146053260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Medial Preoptic Nucleus to Periaqueductal Gray GABAergic Pathway Underlies Individual Differences in Consolation-Like Behavior in Mice.","authors":"Jiao-Wen Wu, Jia Tian, Wei-Chi Li, Lu-Yi Zhang, Qing-He Zhao, Ming-Hao Zheng, Ying-Juan Liu, Lai-Fu Li","doi":"10.1159/000553129","DOIUrl":"10.1159/000553129","url":null,"abstract":"<p><strong>Introduction: </strong>Consolation is a complex empathic behavior that varies considerably across individuals, yet the neural basis of this heterogeneity remains poorly understood. The medial preoptic area is a key hub for instinctive social behaviors, but it remains unclear which of its subregions - the medial preoptic nucleus (MPN) versus the surrounding area (MPA) - or which neuronal subtypes (GABAergic, glutamatergic, or galanin-expressing) contribute to individual differences in consolation.</p><p><strong>Methods: </strong>We used a social defeat-induced consolation paradigm in male mice and categorized them into low- and high-consolation groups based on allogrooming duration toward distressed partners. We performed c-Fos immunofluorescence to compare neuronal activation in the MPN versus MPA, and to identify the specific neuronal subtypes activated in each group. We then used chemogenetic approaches to manipulate MPN GABAergic neurons, as well as their projection to the periaqueductal gray (PAG), and examined the effects on consolation behavior, sociability, and anxiety.</p><p><strong>Results: </strong>High-consolation mice showed selective c-Fos activation in the MPN, but not in the MPA, and this activation was specific to GABAergic neurons. Chemogenetic inhibition of MPN GABAergic neurons or the MPNGABA-PAG pathway selectively reduced allogrooming in high-consolation mice without affecting sociability or anxiety.</p><p><strong>Conclusion: </strong>The MPNGABA-PAG pathway is a critical modulator of individual variation in consolation-like behavior in mice, revealing a subregion- and cell-type-specific circuit mechanism underlying empathic heterogeneity.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"392-406"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148679242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}