Cardiovascular Committee, Pediatrician Association, Chinese Medical Doctor Association, Cardiovascular Council, Chinese Pediatric Society of the Chinese Medical Association, Editorial Board of Chinese Journal of Pediatrics
Chinese Medical JournalVol.139,No.172026
DOI: 10.1097/CM9.0000000000003747
Abstract
Congenital heart disease (CHD) is the most prevalent cardiac anomaly in children and a leading cause of birth defect-related morbidity and mortality in China. Since the 1980s, minimally invasive interventional techniques have become a cornerstone of CHD management. Over the past decade, advances in materials and methodologies have led to significant updates in clinical indications, contraindications, and technical protocols. Therefore, the guideline was developed to standardize and promote interventional treatment for CHD in children.
Xiaoxia Zhu, Yingqian Mo, Lihua Duan, Yufeng Qing, Lie Dai, Zhuoli Zhang, Yan Zhao, Hejian Zou
Chinese Medical JournalVol.139,No.172026
DOI: 10.1097/CM9.0000000000004167
Abstract
Hyperuricemia (HUA) is a common chronic condition diagnosed when serum uric acid (SUA) exceeds 420 µmol/L (7.0 mg/dL) on two separate occasions. The prevalence of HUA in China has shown a marked upward trend, increasing from 11.1% in 2015–2016 to 14.0% in 2018–2019.[1,2]Although established recommendations are available for urate-lowering therapy (ULT) in gout, substantial controversy remains regarding ULT strategies for high-risk hyperuricemia (HrHUA), especially HrHUA with nephrolithiasis, chronic kidney disease, cardiovascular disorders, and metabolic comorbidities.[3,4,5]To address these challenges, the Chinese Rheumatology Association and the Committee for Rheumatologists and Immunologists of Chinese Primary Health Care Foundation convened national experts to develop this consensus. The consensus aimed to define HrHUA, optimize ULT strategies for this population, and provide evidence-based guidance for comorbidity-specific management.
Musculoskeletal disorders (MSDs) represent a diverse group of conditions affecting bones, cartilage, intervertebral discs, tendons, muscles, and related structures, and continue to be a leading cause of global disability. Despite advancements in surgery and pharmacotherapy, issues such as incomplete regeneration, limited longevity, and procedure-related complications remain unresolved. As a result, hydrogel technologies have garnered increasing attention due to their hydrated three-dimensional networks, customizable mechanical properties, and extracellular matrix (ECM)-mimicking features. Hydrogels have been developed in various forms, including injectable systems, scaffolds, and patches, to facilitate tissue regeneration, deliver bioactive molecules, modulate inflammation, and provide mechanical or interfacial support. This review comprehensively examines recent advancements in hydrogel technologies for MSD treatment, focusing on bone and cartilage repair, osteoarthritis management, intervertebral disc regeneration, tendon and muscle healing, and spinal dural repair. It covers laboratory studies, preclinical animal trials, and clinically approved or translational products. By critically evaluating representative materials, design strategies, and disease-specific requirements, this review highlights the therapeutic potential and translational barriers of current hydrogel systems. Challenges such as mechanical durability, spatiotemporal control of bioactivity, scalable manufacturing, and clinically relevant evaluation are addressed, providing insights into the development of next-generation hydrogels for MSDs.
Wei Fu, Yang Zheng, Hao Chen, Xiang Dong, Wei Li, Huiling Liang, Shiwei Chen, Cezmi A Akdis, Yadong Gao
Chinese Medical JournalVol.139,No.172026
DOI: 10.1097/CM9.0000000000004189
Abstract
Allergen immunotherapy (AIT) remains the only disease-modifying treatment for immunoglobulin (Ig) E-mediated allergic diseases, including allergic rhinitis (AR), asthma, food allergy, and atopic dermatitis (AD). This review provides a comprehensive update on recent advances in AIT, focusing on immunological mechanisms, novel vaccines, biomarkers, clinical outcomes across different diseases, and emerging combination strategies with biologics. We discussed the pivotal roles of regulatory T and B cells, innate lymphoid cells (ILCs), and blocking antibodies (immunoglobulin G4 [IgG4], immunoglobulin A [IgA]) in establishing long-term tolerance. Novel allergen vaccines—including recombinant and hypoallergenic derivatives, virus-like particle (VLP) conjugates, and transgenic peptide vaccines—aim to improve safety and efficacy. We critically evaluate current biomarkers for predicting and monitoring AIT response, such as the allergen-specific IgE (sIgE)/total immunoglobulin E (tIgE) ratio, basophil activation test, and cellular markers. Clinical evidence supports AIT efficacy in asthma, AR, and AD, with emerging applications in food allergies. Furthermore, combining AIT with biologics (e.g., anti-IgE and anti-interleukin [IL]-4/IL-4 receptor [IL-4R]) shows promise in enhancing safety and efficacy, particularly in severe asthma. Despite these advances, challenges remain in patient selection, treatment duration, and extract standardization. Future research should prioritize predictive biomarkers, short-course regimens, and synergistic biologic-AIT approaches.
Hematopoietic stem cell transplantation (HSCT) is a foundational treatment for hematological disorders. While its efficacy is established, the conditioning regimens required for HSCT (high-dose chemotherapy and radiotherapy), along with transplant-related immunological and metabolic changes, can induce significant neurological complications. These treatment-related effects necessitate a comprehensive evaluation of their impact on brain structure and function. A synthesis of current evidence on these neurological outcomes is essential to guide clinical practice and future research. This review synthesizes literature on the effects of HSCT-associated treatments on neuroanatomy, cognitive performance, and long-term neurological sequelae. Evidence indicates consistent reductions in gray-matter volume, particularly within frontal, temporal, and parietal cortices, alongside diffuse white-matter alterations affecting major commissural and association tracts. These structural changes correlate with clinically meaningful deficits in attention, executive function, and memory. The underlying pathogenic mechanisms are multifactorial, involving direct neurotoxicity from conditioning regimens, systemic and neuroinflammatory responses, and oxidative stress. The findings underscore the importance of integrating thorough neurological evaluation and longitudinal monitoring into routine care for HSCT recipients. Future research should elucidate detailed mechanisms and develop personalized, evidence-based neuroprotective and rehabilitative strategies. A deeper understanding of these neurological consequences is paramount for improving outcomes and long-term quality of life.
Kun Huang, Songmei Geng, Xiaohua Tao, Liangdan Sun, Chao Ji, Bin Yang, Yan Lu, Rong Xiao, Chunlei Zhang, Furen Zhang, et al.
Chinese Medical JournalVol.139,No.172026
DOI: 10.1097/CM9.0000000000003771
Abstract
Background:
Guselkumab is effective in treating moderate-to-severe plaque psoriasis; however, data from randomized controlled trials in the Chinese population are limited. This study evaluated and verified the efficacy and safety profile of guselkumab in Chinese patients with moderate-to-severe plaque psoriasis.
Methods:
This was a randomized, double-blind, placebo-controlled, phase 4 study. Patients with moderate-to-severe plaque psoriasis were randomized 2:1 to the guselkumab group (guselkumab 100 mg by subcutaneous injection at weeks 0 and 4, then every 8 weeks thereafter through week 44) or the placebo-to-guselkumab group (placebo at weeks 0, 4, and 12, then guselkumab at weeks 16, 20, 28, 36, and 44). Coprimary efficacy endpoints were the proportion of patients achieving Psoriasis Area and Severity Index (PASI) 90 response and the proportion of patients achieving Investigator’s Global Assessment (IGA) 0/1 response at week 16.
Results:
Among the 419 patients screened for eligibility between August 25, 2021, and July 21, 2022, 327 patients were enrolled. All 327 randomized patients (mean age, 41.5 [standard deviation, 12.7] years; 259 [79.2%] men) were treated and included in the analyses. At week 16, 103/110 patients assigned to the placebo group at baseline started guselkumab treatment. Most patients completed the study (210 in guselkumab group and 101 in placebo-to-guselkumab group). Significantly higher proportions of patients with guselkumab achieved PASI 90 (82.4% vs. 2.0%; P <0.001) and IGA score 0/1 (88.8% vs. 7.1%; P <0.001) compared with placebo at week 16. At week 48, response rates were maintained in the guselkumab group (PASI 90: 79.2%; IGA 0/1: 82.4%) and increased in the placebo-to-guselkumab group (PASI 90: 80.2%; IGA 0/1: 86.3%). During the first 16 weeks, the incidence of adverse events was comparable between groups (41.9% guselkumab vs. 39.1% placebo) and the incidence of serious adverse events was low (0.9% vs. 5.5%), respectively.
Conclusion:
Guselkumab was highly effective and displayed a favorable safety profile for the treatment of moderate-to-severe plaque psoriasis in Chinese patients.
Xiaoshan Ji, Zhongmeng Xiong, Ting Peng, Liyuan Hu, Guoqiang Cheng, Liling Qian, Peng Zhang, Xiaofen Zhao, Henry C. Lee, Wenhao Zhou, et al.
Chinese Medical JournalVol.139,No.172026
DOI: 10.1097/CM9.0000000000003642
Abstract
Background:
Neonatal encephalopathy (NE) due to birth asphyxia and trauma has become the second leading cause of global neonatal and under-5 deaths. However, comprehensive data on the global NE burden are scarce. This study aimed to determine the global, regional, and national trends in NE burden from 1990 to 2019, utilizing the 2019 Global Burden of Disease (GBD) study data.
Methods:
Annual incident cases, deaths, disability-adjusted life years (DALYs), and age-standardized rates (incidence [ASIR], mortality [ASMR], DALYs) of NE were collected from the 2019 GBD study. The percentage of relative changes and estimated annual percentage changes (EAPCs) were calculated to assess temporal trends.
Results:
NE global incident cases increased from 1.33 million in 1990 to 1.38 million in 2019, with a 4.87% rise in ASIR. Global NE deaths remained at 0.57 million in 2019, despite a 29.88% reduction from 1990. Significant annual reductions in ASMR and DALYs were observed post-2005. South Asia and sub-Saharan Africa accounted for 80.00% of global NE cases, with South Asia, Eastern and Western sub-Saharan Africa contributing to 81.42% of global deaths and 79.50% of DALYs. NE-related deaths comprised 22.76% and 11.24% of neonatal and under-5 mortality. There were 3.91 million epilepsy, 4.23 million developmental intellectual disability, and 0.57 million blindness cases caused by NE globally in 2019.
Conclusions:
Despite a significant reduction in NE mortality from 1990 to 2019, the ongoing rise in incidence, particularly in South Asia and sub-Saharan Africa, is alarming. Targeted initiatives to prevent NE are needed, especially tailored to high-burden regions.
Background:
Refractory epilepsy remains a global clinical challenge. This first-in-human cohort study aimed to evaluate the efficacy and safety of washed microbiota transplantation (WMT) in the treatment of epilepsy.
Methods:
A prospective, single-center, open-label study of WMT in patients with epilepsy was conducted at the Second Affiliated Hospital of Nanjing Medical University from November 2016 to November 2023. The primary outcome was the clinical response rate (≥50% reduction in seizure frequency) at one month post-WMT. Parallel experiments using a pentylenetetrazole-induced epileptic mouse model were performed to validate clinical findings and investigate the role of specific core bacterial species.
Results:
Among 21 patients (mean age, 18.9 years), including 18 with refractory epilepsy, the clinical response rates were 43% (9/21), 57% (12/21), and 38% (8/21) at one, three, and six months post-WMT, respectively. A second maintenance WMT course at three months was associated with a higher response rate at six months compared to no maintenance therapy (odds ratio [OR] >999, 95% confidence interval [CI]: [1.12, +infinity], P = 0.080). WMT significantly increased Akkermansia muciniphila (A. muciniphila) levels in responders (P = 0.038). A higher baseline A. muciniphila abundance was associated with improved clinical outcomes (Z = 3.28, P = 0.001). The preclinical study confirmed that A. muciniphila augmented the effects of WMT against seizures, significantly reducing seizure severity and duration, and prolonging seizure latency.
Conclusions:
Integrating clinical and preclinical findings, this study demonstrates that A. muciniphila synergistically enhances the effects of WMT against epileptic seizures. This study provides evidence for a new concept of microbiome-based therapeutics in epilepsy treatment.
Jinrong Wang, Jianfu Yang, Kun Yao, Jing Tan, Jun Gao, Lei Zhou
Chinese Medical JournalVol.139,No.172026
DOI: 10.1097/CM9.0000000000003744
Abstract
Background:
Bladder cancer (BCa) is the most common genitourinary malignancy and causes substantial economic losses worldwide. Recent studies suggest overexpression of circCD2AP in BCa, but its mechanistic contributions to carcinogenesis and ferroptosis regulation remain unclear.
Methods:
From August 2021 to January 2024, 98 pairs of BCa and adjacent normal tissue samples were collected from the Third Xiangya Hospital, Central South University. Gene/protein expression, lipid reactive oxygen species (ROS) levels, and cell viability were analyzed. Interactions among circCD2AP/YTH domain-containing protein 1 (YTHDC1), circCD2AP, insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3), and IGF2BP3/forkhead box C1 (FOXC1) were validated, along with circCD2AP-IGF2BP3 colocalization. FOXC1 binding sites in the Parkinson’s disease protein 7 (PARK7) promoter were mapped. N6-methyladenosine (m6A) modifications on circCD2AP were quantified via methylated RNA immunoprecipitation polymerase chain reaction.
Results:
circCD2AP was significantly upregulated in BCa and positively correlated with PARK7 expression (R2 = 0.1357, P = 0.0002). Patients with high circCD2AP expression showed poorer survival rates. CircCD2AP knockdown sensitized BCa cells to ferroptosis inducers (erastin and Ras-selective lethal small molecule 3). Methyltransferase-like 3 (METTL3) knockdown inhibited circCD2AP m6A modification and relative expression. YTHDC1 mediated m6A-dependent cytoplasmic export of circCD2AP (2.8-fold increase). Besides, circCD2AP stabilized FOXC1 messenger RNA (mRNA), and FOXC1 bound the PARK7 promoter to enhance its expression. Knockdown of FOXC1 or PARK7 blocked the antiferroptotic effect of circCD2AP overexpression in BCa cells. Knockdown of METTL3 or circCD2AP reduced tumor burden in mice, decreasing both volume (approximately 48.3% or 56.4%) and weight (approximately 65.3% or 58.7%) through FOXC1/PARK7-mediated ferroptosis.
Conclusions:
METTL3-mediated m6A modification drives circCD2AP overexpression, which is subsequently exported to the cytoplasm with enhanced efficiency mediated by YTHDC1. Cytoplasmic circCD2AP stabilizes FOXC1 mRNA, enabling FOXC1-dependent transcriptional activation of PARK7. This axis suppresses ferroptosis and promotes BCa progression, revealing a novel therapeutic target.
Background:
Sensorineural hearing loss is characterized by irreversible hair cell (HC) degeneration. Ferroptosis, which is marked by the accumulation of reactive oxygen species and elevated levels of lipid peroxidation products, has been shown to contribute to drug-mediated auditory impairment. This study aimed to elucidate the role of mixed-lineage leukemia 1 (MLL1) in HC survival in the auditory system.
Methods:
The HEI-OC1 auditory cell line and postnatal cochlear explants were evaluated using MM-102, a specific MLL1 histone methyltransferase inhibitor. Western blotting, quantitative polymerase chain reaction, electron microscopy, and immunofluorescence were used to elucidate the role of MLL1 in regulating ferroptosis in HC injury. RNA sequencing (RNA-seq) was used to analyze the molecular mechanisms of MLL1 intervention in HC injury from an epigenetic perspective.
Results:
Our findings demonstrated that immunofluorescence staining revealed a crucial role of MM-102 in promoting intracellular accumulation of lipid peroxides and ferrous ions. Subsequent analysis showed MLL1 downregulation-induced mitochondrial dysfunction and endoplasmic reticulum (ER) stress, with transmission electron microscopy imaging confirming ultrastructural alterations in mitochondria and ER. Mechanistic investigations identified the PERK–eIF2α–ATF4–Chop signaling axis as the regulatory pathway, evidenced by Western blotting quantification of phosphorylated PERK (p-PERK), ATF4, and Chop levels. RNA-seq analysis revealed 741 differentially expressed genes (335 upregulated and 406 downregulated). Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis specifically highlighted significant enrichment of the PI3K/Akt-Lrp1 pathway, with corresponding activation patterns of phospho (p)-Akt and Lrp1 confirmed through Western blotting analysis.
Conclusions:
MLL1 downregulation initiates ferroptosis in cochlear HCs. This process is intrinsically associated with the activation of mitochondrial dysfunction and ER stress. The study highlights the importance of MLL1 in HC survival, suggesting its potential as a therapeutic target for treating hearing loss.
Background:
Endometriosis (EMs) is one of the most common gynecologic diseases, and the roles of ferroptosis in EMs have not been fully clarified. The induction of ferroptosis has been demonstrated to inhibit the growth of ectopic lesions in EMs. Although acetyl-CoA carboxylase 1 (ACC1), the rate-limiting enzyme for fatty acid biosynthesis, has been shown to regulate ferroptosis, the detailed mechanism involved has not been fully elucidated. In addition, the role of ACC1, encoded by ACACA, in EMs remains unclear. Thus, the present study aimed to explore the role of ACC1 in ferroptosis and the potential therapeutic effect of the ferroptosis inducer the ferroptosis inducer 56 (FIN56) in EMs.
Methods:
The effects of ACACA, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4), and p38 mitogen-activated protein kinase (MAPK) on FIN56-induced ferroptosis were analyzed in ectopic endometrial stromal cells (ecESCs) through Cell Counting Kit-8 (CCK-8) assays, lipid reactive oxygen species (ROS) assays using flow cytometry, lipid peroxidation malondialdehyde (MDA) assays, and transmission electron microscopy (TEM). RNA sequencing (RNA-seq) and Venn diagram analysis were used to explore the possible ACACA-related genes. Drug inhibitor administration, plasmid overexpression, and small interfering RNA (siRNA) knockdown were used to investigate the role of ACACA and NOX4 in ferroptosis. Immunofluorescence analysis and chromatin immunoprecipitation (ChIP) analysis were subsequently conducted to assess the interaction between AT-rich interaction domain 5A (ARID5A) and NOX4. The effects of ACACA and NOX4 on mitochondrial function were assessed via mitochondrial membrane potential (MMP) analysis, mitochondrial ROS (mtROS) production analysis, and adenosine triphosphate (ATP) assays. Ferro orange staining was used to determine the intracellular levels of iron. An EMs mouse model was generated to evaluate the therapeutic effect of FIN56 in vivo.
Results:
FIN56 increased intracellular iron levels, lipid peroxidation, and mitochondrial damage, which further triggered ferroptosis in ecESCs. ACACA expression was significantly decreased in ecESCs and ectopic endometrial tissues. Treatment with 5-(tetradecyloxy)-2-furoic acid (TOFA), an allosteric inhibitor of ACC1, alleviated ferroptosis induced by FIN56 in ecESCs. Mechanistically, FIN56 treatment resulted in upregulation of NOX4 expression in ecESCs via activation of the p38 MAPK/ARID5A signaling pathway, which was alleviated by ACACA inhibition. Additionally, ACACA and NOX4 increase ferroptosis-dependent cytotoxicity by impairing mitochondrial function and oxidative stress-induced lipid peroxidation in ecESCs. Finally, the regression of ectopic lesions after FIN56 administration was verified in an EMs mouse model.
Conclusions:
The findings reveal that ACACA deficiency protected ecESCs from ferroptosis-dependent cytotoxicity through the p38 MAPK/ARID5A/NOX4 pathway. Moreover, ferroptosis induction by FIN56 in the EMs model mice alleviated the disease. Thus, the ferroptosis inducer FIN56 may be a new therapeutic for EMs.
Dongyan Zhao, Geyujia Zhou, Zifan Shen, Yin Hong, Rui Li
Chinese Medical JournalVol.139,No.172026
DOI: 10.1097/CM9.0000000000003750
Abstract
Irritable bowel syndrome (IBS) is a common gastrointestinal disorder characterized by recurrent abdominal pain and altered stool patterns, with diarrhea-predominant IBS (IBS-D) having the highest morbidity and increasing prevalence. The pathophysiological mechanisms of IBS-D remain unclear, hindering the development of effective treatments.[1]Capsaicin, the active compound in chili peppers, acts as a transient receptor potential vanilloid 1 (TRPV1) agonist. Although capsaicin has shown various beneficial effects, its potential for treating IBS remains understudied. A recent study published inCellindicated that the absence of TRPV1 led to weight loss, colon shortening, and disruption of the gut barrier.[2]This study suggests that capsaicin, a TRPV1 agonist, may have the potential to treat IBS. Therefore, we aimed to investigate the therapeutic effects of capsaicin on IBS mice.
Xiaomei Leng, Yi Liu, Lin Tang, Lingyun Sun, Jingyang Li, Jiankang Hu, Hongbin Li, Shanhui Ye, Lijun Wu, Xinwang Duan, et al.
Chinese Medical JournalVol.139,No.172026
DOI: 10.1097/CM9.0000000000003924
Abstract
To the Editor: In China, about 10.4% of patients with psoriasis (PsO) have concomitant psoriatic arthritis (PsA).[1]In this population with PsA, polyarticular involvement is the most common feature, along with substantial disease severity and comorbidities,[2]suggesting a significant unmet need in the optimal management of PsA in China.[3]Biologics have considerably changed the treatment landscape for PsA by targeting multiple signaling pathways. Interleukin (IL)-17A antagonism is one such therapeutic approach that selectively targets the predominant pro-inflammatory cytokine of the T-helper 17 (Th17) cell subset.[4]Secukinumab (AIN457) is a high-affinity fully human monoclonal antibody that neutralizes IL-17A activity and an approved therapeutic agent for PsO, PsA, and axial spondyloarthritis (axSpA) in more than 100 countries.[5,6]Secukinumab has demonstrated a sustained long-term efficacy and a consistent safety profile in patients with PsA.[7]In this work, we aimed to report the efficacy and safety of secukinumab versus placebo in Chinese participants with active PsA, intending to compare whether the clinical benefits in these participants are consistent with those observed in global studies (FUTURE 2, FUTURE 3, FUTURE 4, and FUTURE 5).[8,9,10,11]
To the Editor: Clinical trials have confirmed the efficacy and safety of ustekinumab for treating Crohn’s disease (CD). The international guidelines of the European Crohn’s Colitis Organization also strongly recommend ustekinumab as a first-line biologic agent for treating moderate-to-severe CD.[1]Ustekinumab was approved for treating moderate-to-severe CD in March 2020 in China.
Ning Ji, Qingqing Xu, Xinying Zeng, Fulin Huang, Yamin Bai, Shiwei Liu
Chinese Medical JournalVol.139,No.172026
DOI: 10.1097/CM9.0000000000003872
Abstract
To the Editor: Alcohol consumption is a critical public health challenge in China, impeding progress toward achieving both the Sustainable Development Goals and the Healthy China 2030 initiative.[1]The Global Burden of Disease Study 2021 identifies alcohol as China’s 10th leading risk factor (6th for males) in terms of disability-adjusted life years and the primary cause of death among adolescents.[2]Given that a substantial proportion of Chinese adolescents engage in alcohol consumption, investigating the risk factors underlying this behavior is essential. Using nationally representative data, this study examines how parental and peer behavior and perspectives influence adolescent drinking behaviors.
An Song, Yingyu Chen, Rong Chen, Jiajia Wang, Shuzhong Liu, Surong Hua, Yan Jiang, Mei Li, Ya Hu, Weibo Xia, et al.
Chinese Medical JournalVol.139,No.172026
DOI: 10.1097/CM9.0000000000004206
Abstract
To the Editor: Primary hyperparathyroidism (PHPT), the third most frequent endocrine disorder in Western countries, is a metabolic bone disease caused by autonomous excessive parathyroid hormone (PTH). Classic symptoms include bone resorption, nephrolithiasis, and symptoms associated with hypercalcemia.
To the Editor: Tooth eruption is a physiological process essential for establishing proper occlusion. The gubernacular canal (GC), a bony tract connecting the dental follicle to the gingiva, has been recognized as a crucial anatomical pathway guiding eruptive movement. Previous studies have suggested that GC absence or structural disruption may be associated with eruption disturbances or tooth impaction, highlighting their potential importance.[1]Despite this theoretical significance, the distribution and developmental characteristics of GCs under physiological conditions remain poorly understood. To address these, the present study analyzed erupting permanent premolars using cone-beam computed tomography (CBCT), described the dynamic detection patterns of GCs, and identified differences of detection rate between the maxilla and mandible, providing evidence for their facilitating role in tooth eruption.
Xianli Li, Zijin Huang, Zhe Zhang, Juanjuan Li, Jinchi Xie, Oscar H Franco, Gang Liu, Yunfei Liao, An Pan, Tingting Geng
Chinese Medical JournalVol.139,No.172026
DOI: 10.1097/CM9.0000000000004182
Abstract
To the Editor: Major depressive disorder (MDD) is a pervasive global public health challenge, affecting approximately 300 million people worldwide and representing the leading cause of disability globally.[1]In addition to genetic factors, various lifestyle and environmental factors are strongly associated with MDD, including sleep status and physical activity (PA). Previous studies have reported a U-shaped association between sleep duration and depressive symptoms,[2]whereas increasing evidence indicates that adequate PA is associated with a lower risk of MDD. However, despite their individual benefits, the interdependence between sleep duration and PA and their potential joint effects on MDD have been largely overlooked, limiting the translation of existing findings into clinical practice.
The article entitled "Impact of Taurine on the proliferation and apoptosis of human cervical carcinoma cells and its mechanism" (Chin Med J 2019;132:948–956. doi: 10.1097/CM9.0000000000000162) by Li Hua, Ruan Wen-Jing, Liu Li-Qiao, Wan Hui-Fang, Yang Xiao-Hong, Zhu Wei-Feng, Yu Le-Han, Zhang Xia-Li, Wan Fu-Sheng[1]has been retracted by the Publisher and the Editor on behalf of the authors. Following receipt of a notification letter from a reader, alerting the Editorial Office to the similarities between the results presented in Figure 6A in this article and the results in a previously published article by the authors,[2]the Editors contacted the authors and their institution. The corresponding author requested to retract this article. After communication with the institution, the Editor decided to retract this article.
