Frontiers in Pediatrics最新文献

{"title":"Case Report: Bladder perforation in an extremely preterm neonate secondary to multifactorial etiology.","authors":"Ismail Alwadani, Tahseen Elwahsh, Batool Albahrani","doi":"10.3389/fped.2026.1912735","DOIUrl":"10.3389/fped.2026.1912735","url":null,"abstract":"<p><strong>Background: </strong>Neonatal bladder perforation is a rare but life-threatening condition associated with significant morbidity if not promptly recognized.</p><p><strong>Case presentation: </strong>We report the case of an extremely preterm male infant born at 26 weeks of gestation who developed bladder perforation on day 15 of life, presenting with abdominal distension, decreased urine output, and respiratory distress. The diagnosis was confirmed by fluoroscopic voiding cystourethrogram demonstrating contrast extravasation into the peritoneal cavity. The etiology was multifactorial, involving extreme prematurity, umbilical arterial catheterization, repeated urinary catheter insertions, and heavy sedation. Initial conservative management with urinary catheterization and broad-spectrum antibiotics was followed by successful surgical repair via exploratory laparotomy on day 23 of life.</p><p><strong>Conclusion: </strong>This case highlights the importance of maintaining a high index of suspicion for bladder perforation in extremely preterm neonates presenting with ascites and sepsis-like features, particularly in the presence of multiple iatrogenic risk factors. Early diagnosis and timely intervention are critical for optimizing outcomes.</p>","PeriodicalId":12637,"journal":{"name":"Frontiers in Pediatrics","volume":"14 ","pages":"1912735"},"PeriodicalIF":2.2,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672595/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Case Report: Chemical gastropathy associated with Scotch mint candy ingestion.","authors":"Melody Petty, David A Gremse","doi":"10.3389/fped.2026.1969803","DOIUrl":"10.3389/fped.2026.1969803","url":null,"abstract":"<p><p>Erosive lesions may occur in the gastric mucosa after exposure to toxic substances such as alcohol, non-steroidal anti-inflammatory drugs, or iron. Candies rarely contain compounds that cause mucosal erosions. However, Scotch mints in combination with carbonated sodas are known to cause vigorous effervescence. The microporous surface of Scotch mint candy allows for rapid release of dissolved carbon dioxide from carbonated soda that produces carbon dioxide bubbles. We report a case of a 3-year-old child who presented with abdominal pain and feeding refusal and was found to have erosive chemical gastropathy. Dietary history revealed ingestion of Scotch mint candies and lemon-lime soda for 2 days prior to the onset of symptoms. This case demonstrates the potential for mucosal injury when ingesting excessive amounts of Scotch mint candy and carbonated soda and the importance of a careful dietary history in children with gastrointestinal mucosal injury.</p>","PeriodicalId":12637,"journal":{"name":"Frontiers in Pediatrics","volume":"14 ","pages":"1969803"},"PeriodicalIF":2.2,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vacuole histomorphology characteristics and their same immunophenotype with the gut wall: A histological study using human fetuses.","authors":"Xuelai Liu, Zhe-Wu Jin, Yuqiang Chen, Mao Ye, Feng He, Xiaoyun Cui, Huan Wang, Chaosheng He","doi":"10.3389/fped.2026.1915639","DOIUrl":"10.3389/fped.2026.1915639","url":null,"abstract":"<p><strong>Background: </strong>Intestinal atresia (IA) has been associated with abnormal embryonic intestinal recanalization, a developmental process in which transient vacuoles form and merge with the developing mucosa. This study aimed to investigate the histomorphological characteristics of developing vacuoles and the immunophenotypic similarities between developing vacuoles and the gut wall.</p><p><strong>Methods: </strong>Serial sagittal sections from human fetuses of estimated gestational age (GA) of 8-12 weeks were examined by hematoxylin and eosin (H&E) staining and immunohistochemistry for CK19, CK5/6, and vimentin.</p><p><strong>Results: </strong>A total of eight human fetuses were included in this study. In fetuses at GA 8 weeks, HE staining showed that vacuoles were divided into two components: a peripheral basal compartment and a central luminal compartment, which were separated by a basal membrane. The basal compartment contained a single layer of columnar epithelial cells located on the basal membrane, whereas the luminal compartment contained scattered cells. Few histological changes were observed in fetuses at GA 10 weeks. Immunohistochemical staining showed cytokeratin 19- and cytokeratin 5/6-positive cells in both vacuolar epithelia and gut mucosal epithelium, and they were present continuously, whereas the vimentin-positive cells were present in the luminal compartment of vacuoles, as well as the lamina propria and submucosa of the gut wall.</p><p><strong>Conclusion: </strong>Vacuoles comprise both mesenchymal cells morphologically in the central luminal compartment and epithelial cells in the peripheral basal compartment. The basal compartment of vacuoles and gut mucosal epithelium have the same epithelial immunophenotype; the luminal compartment of vacuoles and the lamina propria and submucosa of the gut wall have the same mesenchymal immunophenotype.</p>","PeriodicalId":12637,"journal":{"name":"Frontiers in Pediatrics","volume":"14 ","pages":"1915639"},"PeriodicalIF":2.2,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672508/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and validation of a nomogram for stratifying severe <i>Mycoplasma pneumoniae</i> pneumonia risk in children early.","authors":"Zhongying Chen, Wugao Ding, Zhengyan Gao","doi":"10.3389/fped.2026.1927137","DOIUrl":"10.3389/fped.2026.1927137","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to develop and validate a clinically applicable diagnostic predictive model to facilitate early identification of severe <i>Mycoplasma pneumoniae</i> pneumonia (SMPP) within 24 h of admission.</p><p><strong>Methods: </strong>Clinical data from children with MPP hospitalized from January 2023 to December 2023, were retrospectively collected as the training set. Patients were classified into general MPP (GMPP) or SMPP groups based on whether SMPP occurred within 24 h of admission. After comparing the differences in clinical data between the two groups at admission, multivariate logistic regression was used to identify risk indicators for SMPP and construct a diagnostic predictive model. A nomogram was developed to visualize the model. Subsequently, data from children with MPP hospitalized between January 2024 and December 2024 were collected to conduct temporal external validation of the model. The predictive performance of the model was evaluated using receiver operating characteristic (ROC) curves, Hosmer-Lemeshow goodness-of-fit test, calibration curves, decision curve analysis (DCA), and clinical impact curves (CIC).</p><p><strong>Results: </strong>In total, 412 children with MPP were included, with 222 cases within the training set (119 SMPP, 53.60%) and 190 within the temporal external validation set (129 SMPP, 67.89%). Independent risk indicators for the occurrence of SMPP included the duration of fever before admission (OR = 2.019, 95% CI: 1.387-2.938), shortness of breath (OR = 111.599, 95% CI: 11.512-1,081.834), unresponsive to macrolide before admission (OR = 3.687, 95% CI: 1.529-8.892), interleukin-6 (IL-6) (OR = 1.052, 95% CI: 1.010-1.095), and pulmonary consolidation (OR = 31.634, 95% CI: 11.643-85.948) (all <i>P</i> < 0.05). The nomogram based on the five aforementioned variables demonstrated favorable discriminative performance, with areas under the ROC curve (AUC) of 0.916 (95% CI: 0.880-0.951) within the training set, 0.907 (95% CI: 0.873-0.946) within the internal validation, and 0.817 (95% CI: 0.758-0.876) within the temporal external validation set. The calibration curve and Hosmer-Lemeshow goodness-of-fit test showed that the model had good calibration. Both the DCA and CIC demonstrated favorable clinical utility of the model.</p><p><strong>Conclusion: </strong>The model developed in this study provides valuable reference for early risk stratification of pediatric SMPP and timely, individualized clinical decision-making in children with MPP. However, extensive external validation is required.</p>","PeriodicalId":12637,"journal":{"name":"Frontiers in Pediatrics","volume":"14 ","pages":"1927137"},"PeriodicalIF":2.2,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporal trends in surfactant replacement therapy among U.S. infants, 2016-2024.","authors":"Xuezheng Sun, Wenhao Wang, Daniel Fuentes","doi":"10.3389/fped.2026.1907867","DOIUrl":"10.3389/fped.2026.1907867","url":null,"abstract":"<p><strong>Objective: </strong>Surfactant replacement therapy (SRT) remains a cornerstone of neonatal respiratory management, but contemporary national data on temporal trends in SRT use across gestational age groups in the United States remain limited. We aimed to characterize gestational age-specific SRT rates among U.S. live-born infants and assess temporal trends over time.</p><p><strong>Study design: </strong>We conducted a serial cross-sectional analysis using the U.S. Centers for Disease Control and Prevention WONDER Natality Expanded database from 2016 to 2024. Findings were examined in parallel using a cohort of preterm infants from the Premier Healthcare Database from 2020 to 2024. In CDC WONDER, SRT was defined using the birth certificate item for surfactant replacement therapy. In the Premier Healthcare Database, SRT was defined as receipt of exogenous surfactant during the birth hospitalization identified from billing records. Annual percentages of infants receiving SRT were estimated by gestational age group. Temporal trends were summarized as annual percent change (APC) using Poisson regression.</p><p><strong>Results: </strong>From 2016 to 2024, the observed SRT rate increased from 0.48% (95% CI, 0.48%-0.49%) to 0.51% (95% CI, 0.50%-0.51%), an absolute difference of approximately 0.03 percentage points, corresponding to a model-estimated cumulative relative increase of 7.60% [95% CI, 6.00%-9.22%; APC, 0.92% (95% CI, 0.73%-1.11%)], with a transient deviation in 2021. The increase was most pronounced among late preterm infants born at 34-36 weeks (APC, 0.90% [95% CI, 0.45%-1.36%]) and term infants born at 37 weeks or later (APC, 3.31% [95% CI, 2.82%-3.79%]). Similar upward patterns were observed in the Premier Healthcare Database among preterm infants. The calibrated SRT rate among preterm births in 2024 was 11.39% (95% CI, 11.23%-11.54%).</p><p><strong>Conclusion: </strong>Across 2 national data sources, SRT rates increased among infants born at 34 weeks' gestation or later. These findings suggest evolving patterns of neonatal respiratory care and inform surveillance and interpretation of national birth data.</p>","PeriodicalId":12637,"journal":{"name":"Frontiers in Pediatrics","volume":"14 ","pages":"1907867"},"PeriodicalIF":2.2,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Case Report: Contezolid-containing regimens for disseminated Bacillus Calmette-Guérin disease in three children with primary immunodeficiency.","authors":"Zhen Zhang, Junchi Xu, Li Gao, Junjia Liu, Zhijian Ye, Yong Xu, Jianping Zhang, Xin Yu","doi":"10.3389/fped.2026.1928342","DOIUrl":"10.3389/fped.2026.1928342","url":null,"abstract":"<p><strong>Introduction: </strong>Disseminated Bacillus Calmette-Guérin (BCG) disease is a rare but life-threatening complication in children with primary immunodeficiency (PID). Linezolid (LZD) is effective but limited by myelosuppression. Contezolid (CZD), a novel oxazolidinone, has shown better hematological safety in adults, but pediatric data are scarce. This retrospective case series aims to provide real-world experience on CZD use in this challenging population.</p><p><strong>Case description: </strong>We report three children (aged 3-9.5 months) with PID (Wiskott-Aldrich syndrome, X-linked severe combined immunodeficiency, and IL-12 receptor β1 deficiency) who developed clinically presumed or confirmed disseminated BCG disease after routine vaccination. All received CZD-containing regimens (12-20 mg/kg/dose, q12 h) alongside other antimycobacterial agents and hematopoietic stem cell transplantation (HSCT).</p><p><strong>Outcomes: </strong>Over 11-12 months of CZD-containing multidrug therapy followed by 1 year of post-treatment telephone follow-up, all patients achieved satisfactory clinical resolution of infectious lesions and no clinical relapse was observed. No CZD-attributable hematological, hepatic, renal, or neurological adverse events occurred. However, because all patients received concurrent HSCT and multiple antimycobacterial agents, the independent contribution of CZD cannot be determined.</p><p><strong>Conclusion: </strong>CZD-containing regimens were well tolerated and associated with clinical improvement in these complex cases. CZD may serve as a valuable alternative when LZD is poorly tolerated. However, definitive attribution of efficacy to CZD alone is precluded by concurrent HSCT and multi-drug therapy.</p>","PeriodicalId":12637,"journal":{"name":"Frontiers in Pediatrics","volume":"14 ","pages":"1928342"},"PeriodicalIF":2.2,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672542/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ketogenic diet in treating NADH accumulation caused by complex I dysfunction: the metabolic wisdom of \"dredging, not repairing\".","authors":"Xiaoying Qiao, Jianxiang Liao","doi":"10.3389/fped.2026.1939961","DOIUrl":"10.3389/fped.2026.1939961","url":null,"abstract":"<p><p>Genetic mutations causing Complex I (CI) dysfunction lead to the accumulation of NADH in the mitochondrial matrix due to impaired oxidation. An elevated NADH/NAD⁺ ratio feedback-inhibits key enzymes of the tricarboxylic acid (TCA) cycle, reducing metabolic flux, while concurrent electron transport chain (ETC) blockade exacerbates reactive oxygen species (ROS) generation and oxidative stress. Conventional views propose that the ketogenic diet (KD) bypasses the defective CI to restore downstream ETC electron transfer. However, this perspective harbors an inherent contradiction: CI is the primary entry point for NADH oxidation; bypassing it may sustain some electron flow but fails to consume the accumulated NADH in the matrix, leaving the fate of this critical reducing equivalent inadequately explained. This article proposes the metabolic wisdom of \"dredging, not repairing\", positing that KD, through metabolic reprogramming, diverts the accumulated NADH into multiple utilizable pathways. These include intra-matrix conversion and consumption (generating NADPH and ketone bodies), pumping malate from the matrix into the cytosol via the reverse malate-aspartate shuttle (rMAS), and further cytosolic malate utilization (gluconeogenesis, NADPH generation, glycerol-3-phosphate shuttle, etc.). This multi-pathway synergy achieves \"dredging\"rather than \"repair\". This paper aims to elucidate how KD, via metabolic reprogramming, alleviates the inhibition of the TCA cycle caused by NADH accumulation and restores its flux, thereby offering new insights into metabolic therapeutic strategies for CI-deficient mitochondrial diseases.</p>","PeriodicalId":12637,"journal":{"name":"Frontiers in Pediatrics","volume":"14 ","pages":"1939961"},"PeriodicalIF":2.2,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interactions between chronic kidney disease and hyperuricemia in children: mechanisms, clinical manifestations and management updates.","authors":"Huang Xiaoxia, Liu Yuhua","doi":"10.3389/fped.2026.1975951","DOIUrl":"10.3389/fped.2026.1975951","url":null,"abstract":"<p><p>A bidirectional pathogenic interplay exists between pediatric chronic kidney disease (CKD) and hyperuricemia (HUA). Hyperuricemia serves as an independent risk factor for the onset and progression of CKD, while also representing a common complication arising from impaired renal excretory function. Amid the rising global prevalence of pediatric CKD and growing evidence implicating metabolic disturbances in renal injury, the reciprocal pathological mechanisms underlying uric acid-mediated kidney damage have emerged as a critical research focus. Elevated serum uric acid induces renal tubulointerstitial injury through oxidative stress, systemic inflammatory cascades, and endothelial dysfunction. Conversely, diminished uric acid excretion resulting from CKD further aggravates hyperuricemia, establishing a self-perpetuating vicious cycle. However, epidemiological evidence specific to the pediatric population remains limited, and current clinical management strategies are largely extrapolated from adult studies, lacking evidence-based guidelines tailored to the unique growth and developmental characteristics of children. This review systematically summarizes the epidemiological features, molecular pathogenic mechanisms, clinical implications, and therapeutic approaches for HUA comorbid with pediatric CKD. We specifically highlight uric acid-driven renal injury pathways, the accelerating effect of HUA on CKD progression, and age-specific challenges in pediatric diagnosis and standardized intervention. By integrating recent advances in preclinical and clinical research, this review aims to provide a theoretical foundation for the early screening, timely diagnosis, and individualized standardized management of hyperuricemia in children with CKD.</p>","PeriodicalId":12637,"journal":{"name":"Frontiers in Pediatrics","volume":"14 ","pages":"1975951"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Indoor environmental quality in day-care centers, kindergartens, and primary schools.","authors":"Dadi Zhang, Hailin Zheng","doi":"10.3389/fped.2026.2005928","DOIUrl":"10.3389/fped.2026.2005928","url":null,"abstract":"","PeriodicalId":12637,"journal":{"name":"Frontiers in Pediatrics","volume":"14 ","pages":"2005928"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13668817/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Translating the 2024 ACR lupus nephritis guidelines to pediatric practice.","authors":"Minh Dien Duong, Quang Le, Siddharth Shah","doi":"10.3389/fped.2026.1970903","DOIUrl":"10.3389/fped.2026.1970903","url":null,"abstract":"<p><p>Lupus nephritis (LN) is more common and often more aggressive in children than in adults, yet most randomized trials informing current LN management have enrolled adults. The 2024 American College of Rheumatology (ACR) guideline is the first ACR guideline on lupus nephritis to explicitly state that its recommendations apply to both adults and children<b>,</b> although its evidence base remains largely adult-derived. This review uses the 2024 ACR guideline as an organizing framework, cross-referenced with the 2024 KDIGO and 2025 EULAR recommendations, to examine which aspects of LN management translate effectively to pediatric practice and which require caution. We review the diagnostic pathway, including screening, kidney biopsy, and ISN/RPS classification, as well as therapeutic strategies, including the shift from sequential dual therapy to upfront triple therapy, response targets, class-specific treatment, and selection between belimumab and calcineurin inhibitors. We then examine areas where pediatric evidence remains limited, particularly glucocorticoid dosing, long-term biologic safety, fertility and growth, and transition to adult care. While the fundamental principles of LN management are largely age-agnostic, many quantitative recommendations are not. Steroid dosing, long-term treatment exposure, and developmental consequences remain important pediatric-specific considerations that current guidelines cannot fully address. We conclude by highlighting the pediatric evidence available to date and the need for dedicated pediatric trials to replace adult-derived extrapolation with child-specific evidence.</p>","PeriodicalId":12637,"journal":{"name":"Frontiers in Pediatrics","volume":"14 ","pages":"1970903"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}