Table of Content

05 May 2026, Volume 46 Issue 5

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Original Articles

Proteomic characteristic analysis of adult H3K27-altered diffuse midline glioma

NI Yanying, ZHAI Chunyan, SHEN Ping, ZHANG Fanshuang, JIANG Zhongcai

2026, 46(5):  607-613.  doi:10.16352/j.issn.1001-6325.2026.05.0607

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Objective To investigate pathological characteristics of adult H3K27-altered diffuse midline glioma (DMG) and differential protein expression in tumor brain tissue, for providing more comprehensive diagnostic clues. Methods Clinical and pathological data from eight adult patients with H3K27-altered DMG were collected. Proteomics analysis of tumor tissue was performed using laser microdissection combined with mass spectrometry. Differentially expressed proteins were screened for functional analysis, and four key proteins among these proteins were selected for immuno-histochemical validation. Results A total of 6 171 proteins were identified in these tissue samples. Compared with the non-tumor control group, 867 proteins were significantly expressed in the tumor group; compared with the para-neoplastic group, 277 proteins were significantly expressed tumor group. It was mainly related to mRNA synthesis and protein synthesis. CTBP2, YBX1, SRSF1, and SRSF2, which were significantly up-regulated in tumor tissues, were verified by immuno-histochemistry(P＜0.05). Conclusions The tumor tissue exhibits significant proteomic characteristic differences. Differential protein expression analysis can provide more comprehensive information to support diagnosis.

Proteomic and metabolomic analysis of urine in sleep-deprived mouse models

ZHANG Yuxue, LIU Tingting, HE Mengzhen, HU Siqi, LI Jun, SUN Wei

2026, 46(5):  614-620.  doi:10.16352/j.issn.1001-6325.2026.05.0614

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Objective To explore the patho-physiological changes of sleep deprivation (SD) by analyzing the urinary proteome and metabolome of sleep-deprived mouse models. Methods Twelve male mice were randomly divided into a control group and a model group with six in each. Urine samples were collected daily from metabolic cages for 8 consecutive days and subjected to liquid chromatography-mass spectrometry (LC-MS)-based proteomic and metabolomic analyses. Results A total of 855 differential proteins were identified in the urine of sleep-deprived mouse models. Function annotation analysis showed an enrichment in the complement and coagulation cascades and glutathione metabolism pathways. Additionally, 158 differential metabolites were identified, which were primarily enriched in metabolic pathways such as pigment metabolic processes, signal transduction/ regulation and immune response activation. Integrated proteomic and metabolomic analysis revealed that the core function pathways were glutathione metabolism and complement and coagulation cascades. Conclusions Changes in SD-related protein and metabolite metabolic pathways provide novel insights into the mechanisms underlying sleep deprivation.

EXOSC5 inhibits ferroptosis in diffuse large B-cell lymphoma cell lines of SU-DHL-4 and OCI-LY3

WANG Yanhe, WANG Tian, YANG Qingzhu, LIU Aichun

2026, 46(5):  621-628.  doi:10.16352/j.issn.1001-6325.2026.05.0621

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Objective To investigate the expression of exosome component 5 (EXOSC5) in diffuse large B-cell lymphoma (DLBCL) tissue and its impact on the ferroptosis of DLBCL cells. Methods Immunohistochemistry, RT-qPCR and Western blot were used to detect the expression of EXOSC5 in DLBCL tissues, cell lines (SUDHL4 and OCILY3) and human peripheral blood B lymphocyte cell lines (IM9), the expression of keyferrop- tosisrelated genes including nuclear factor erythroid 2-related factor 2(NRF2), ferritin heavy chain 1 (FTH1) and glutathione peroxidase 4(GPX4). Malondialdehyde (MDA) and Fe²⁺ assay kits were used to measure MDA and Fe²⁺ levels in cells. Flow cytometry was used to determine lipid reactive oxygen species (ROS) in cells. CCK8 assay was used to assess cell proliferation and viability. Results Expression of EXOSC5 significantly increased in DLBCL tissues. The expression level of EXOSC5 was higher in SUDHL4 and OCILY3 cells as compared to IM9 cells (P＜0.01). Inhibition of EXOSC5 in SUDHL4 and OCILY3 cells led to a decreased cell proliferation(P＜0.01), down-regulated expression of the key ferroptosis-related genes NRF2, FTH1, and GPX4(P＜0.05)and elevated intracellular levels of MDA, Fe²⁺, and lipid ROS (P＜0.01). These effects could be partially reversed by the ferroptosis inhibitor ferrostatin-1. Knockdown of EXOSC5enhanced cell sensitivity to the ferroptosis inducer RSL3(P＜0.01). Conclusions EXOSC5 is highly expressed in DLBCL and acts as an oncogene. EXOSC5 down regulation might be a target strategy to inhibit malignant proliferation in DLBCL.

Clinical application of RASi and risk of all-cause mortality in patients with steatotic liver disease and hypertension

HAO Yifei, CHEN Shuohua, YANG Chenlu, ZHOU Di, YE Qingfeng, WU Shouling, WANG Li

2026, 46(5):  629-636.  doi:10.16352/j.issn.1001-6325.2026.05.0629

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Objective To investigate the association between renin-angiotensin system inhibitor(RASi) use and the risk of all-cause mortality among patients with steatotic liver disease(SLD) and hypertension. Methods Using an emulated target clinical trial design, that included new users of either RASi or calcium channel blocker(CCB) for at least 60 days among patients with SLD and hypertension who participated in chronic disease manage- ment in the Kailuan cohort from 2006 to 2020. Baseline characteristic differences between the groups were balanced by multivariable adjustment and propensity score(PS) matching. Cox proportional hazards regression models were used to evaluate the association between RASi use and all-cause mortality risk. Furthermore, the landmark analysis was applied to explore the dose-response relationship between the cumulative duration of RASi use and all-cause mortality risk. Results A total of 2 085 patients with SLD and hypertension were included. During a median follow-up of 7.01 years, 510 patients died. The mortality rate was lower in the RASi group than that in the CCB group(8-year mortality: 19.53% vs. 22.78%, P＜0.01). After multivariable adjustment for baseline factors, the risk of all-cause mortality in the RASi group was reduced by 28% when compared to that in the CCB group(HR=0.72, 95% CI: 0.60-0.87). Stratified analyses found no heterogeneity in the negative association between RASi use and all-cause mortality risk across the subgroups. The results were consistent in the PS-matched population(HR=0.77, 95% CI: 0.62-0.96). Dose-response analysis indicated a decreasing trend in all-cause mortality risk with increasing cumulative duration of RASi use(P for trend ＜0.05). Conclusions RASi use is associated with a reduced risk of all-cause mortality among patients with SLD and hypertension, and this benefit increases with longer cumulative duration of RASi use. These results provide strong evidence to guide medication selection and to long-term management in this population.

IDH1 functions as a noncanonical RNA-binding protein to maintain differentiation blockade in acute myeloid leukemia cell line HL-60

ZOU Binbin, CHEN Zhongyang, MA Yanni, YANG Jiabin, YU Jia

2026, 46(5):  637-642.  doi:10.16352/j.issn.1001-6325.2026.05.0637

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Objective To investigate the novel mechanism by which isocitrate dehydrogenase 1(IDH1) suppresses differentiation in acute myeloid leukemia(AML) HL-60 cells. Methods Potential RNA-binding proteins were initially screened through literature review and database analyses, leading to the selection of IDH1 as the candidate of interest. RNA immunoprecipitation followed by sequencing(RIP-seq) was performed to identify RNAs bound by IDH1 in HL-60 cells. In parallel, IDH1 was knocked down via lentiviral transduction, and transcriptome profiling was conducted by RNA sequencing(RNA-seq) to assess global gene expression changes induced by IDH1 depletion. Integrated analysis of RIP-seq and RNA-seq data was further carried out to systematically characterize the expression patterns of IDH1-bound transcripts following IDH1 knockdown. Results IDH1 was found to bind a broad spectrum of RNA molecules in HL-60 cells, with mRNAs representing the predominant class. Knockdown of IDH1 resulted in marked alterations in the cellular gene expression profile. Integrated analysis revealed that IDH1-bound transcripts exhibited an overall downregulation upon IDH1 depletion and were significantly enriched in genes associated with differentiation blockade in leukemic cells. Conclusions IDH1 functions as a non-canonical RNA-binding protein that participates in the regulation of differentiation-associated genes in AML, thereby contributing to the maintenance of the undifferentiated state of leukemia cells.

Dynamic transcriptomic characteristics of CHO cells during temperature downshift culture

BAO Yongli, XIA Wanping, WANG Xiaoyue, WU Rucheng, LI Shuxiang, LI Xueyuan, CHEN Yang

2026, 46(5):  643-650.  doi:10.16352/j.issn.1001-6325.2026.05.0643

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Objective To investigate the dynamic transcriptomic changes of Chinese hamster ovary (CHO) cells during reduced-temperature culture and to characterize the temporal patterns and potential regulatory features of gene expression under low-temperature conditions. Methods CHO cells were cultured under standard conditions (37 ℃) and reduced temperature (30 ℃) separately. Cells were harvested at 0 h, 24 h, and 48 h for RNA sequencing (RNA-seq). Both preprocessing and downstream analyses of the sequencing data were performed, including differential gene expression analysis, temporal expression clustering, functional enrichment. Protein-protein interaction (PPI) network analysis was performed to evaluate alterations in key signaling pathways during temperature reduction. Results Temperature reduction markedly altered the transcriptomic profile of CHO cells. Temporal clustering identified six distinct gene expression patterns, mainly associated with protein translation and ribosome biogenesis, cell cycle regulation, and vesicle transport. Biomolecular interaction network analysis revealed that translation-related molecules and membrane structure/signaling-related nodes formed relatively concentrated interaction modules, exhibiting differential temporal dynamics. Conclusions CHO cells undergo pronounced time-dependent transcriptomic remodeling during reduced-temperature culture characterized by stage-specific adjustments in translation-related and membrane structure-related processes. These findings provide transcriptome-level evidence for cellular state transitions and production-related regulation in low-temperature.

Long non-coding RNA SNHG1 interacting with splicing factors influences erythroid differentiation

SHEN Xinyan, GUO Jia, MA Yanni, YU Jia, LIU Siqi

2026, 46(5):  651-657.  doi:10.16352/j.issn.1001-6325.2026.05.0651

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Objective To investigate the function and molecular mechanism of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1(SNHG1) in erythroid differentiation. Methods During erythroid differentiation of CD34⁺ hematopoietic stem/progenitor cells derived from human umbilical cord blood, expression of SNHG1 was suppressed. Erythroid differentiation was assessed by flow cytometry with surface markers CD71 and CD235a, while the mRNA expression of globin genes was measured by reverse transcription quantitative PCR (RT-qPCR). Nuclear-cytoplasm fractionation and RNA fluorescence in situ hybridization (RNA-FISH) were applied to determine the sub-cellular localization of SNHG1. RNA pull-down and RNA immunoprecipitation (RIP) assays were applied to identify SNHG1-interacting proteins. Results Suppression of SNHG1 significantly decreased the proportion of CD71⁺/CD235a⁺ erythroid progenitor cells(P＜0.001) and reduced the expression of globingene (P＜0.01).SNHG1 was found to be predominantly localized in the nucleus and interacted with multiple splicing regulators, including SFPQ and NONO. Conclusions SNHG1 may affect erythroid differentiation by recruiting splicing-related proteins such as SFPQ and NONO and thereby regulating RNA splicing and processing.

KRT15 regulates the immune microenvironment and suppresses malignant phenotypes in gastric cancer

ZHANG Shuai, WANG Tengqi, TIAN Yongjing, PANG Jian, SUN Haibin, LEI Xinwen

2026, 46(5):  658-665.  doi:10.16352/j.issn.1001-6325.2026.05.0658

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Objective To investigate the expression pattern, function, potential clinical use of prognosis and regulatory mechanisms of keratin 15 (KRT15) in gastric cancer. Methods Transcriptomic and clinical data from the The Cancer Genome Atlas Stomach Adenocarcinoma(TCGA-STAD)cohort were analyzed to evaluate the expression level and prognostic value of KRT15 in gastric cancer. Bio-informatic analyse was performed to assess the biological significance of KRT15. KRT15 expression in gastric cancer tissues and cell lines was examined by RT-qPCR and Western blot. Stable KRT15-knockdown and KRT15-over-expression cell models were established to evaluate the effects of KRT15 on gastric cancer cell proliferation, colony formation, migration, invasion,membrane permeability and xenograft tumor growth in nude mice. Changes in PI3K/AKT signaling activity were also examined. Results KRT15 was down-regulated in gastric cancer tissues (P＜0.05) and low KRT15 expression was associated with poor prognosis. KRT15 knockdown promoted the proliferation, migration, invasion, and tumorigenic capacity of gastric cancer cells, whereas KRT15 over-expression exerted the opposite effects (P＜0.05). Bio-informatics analyses showed that KRT15-related genes were mainly enriched in pathways related to cell proliferation, adhesion, and PI3K/AKT signaling and were closely associated with alterations in the tumor immune microenvironment(P＜0.001). In addition, reduced KRT15 expression was accompanied by increased phosphorylation of PI3K and AKT (P＜0.001). Conclusions KRT15 is down-regulated in gastric cancer, which is associated with poor prognosis and aggressive tumor phenotypes. KRT15 may suppress malignant phenotypes of gastric cancer by regulating the PI3K/AKT signaling pathway and the tumor immune microenvironment.

Elucidating the transcription-translation uncoupling mechanism in somatotroph adenomas via single-cell multi-omics

WU Jiamin, WU Yinzi, WANG Fang, YU Jia, MA Yanni, WANG Xiaoshuang

2026, 46(5):  666-672.  doi:10.16352/j.issn.1001-6325.2026.05.0666

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Objective To investigate the transcriptomic and translatomic heterogeneity of sparsely granulated somatotroph tumor (SGST) and to elucidate the synergistic mechanisms of gene expression at the transcriptional and translational level. Methods Single-cell RNA sequencing (scRNA-seq) and single-cell ribosome sequencing(scRibo-seq) were performed on tumor tissue samples from one patient with SGST. Dimensionality reduction and clustering were utilized to identify cell subpopulations. The CytoTRACE algorithm was applied to assess cell differ- entiation states. By comparing gene expression at both RNA and translational level, the transcriptional-translational association characteristics of invasion-related genes were explored. Results Three distinct cell subpopulations were identified, including tumor cells, pericytes, and endothelial cells, with tumor cells accounting for 94.9%. The tumor cells exhibited high heterogeneity and could be further subdivided into distinct functional states, including “proliferative” “oxidative phosphorylation(OXPHOS)” and “pituitary-like” subtypes. CytoTRACE analysis indicated that low different ion state of some tumor subpopulations significantly down-regulated ribosome biogenesis and translation pathways while up-regulated OXPHOS and autophagy-related pathways, suggesting that the inhibition of translational activity might be closely related to the maintenance of a poorly differentiated tumor state. Integrated analysis revealed a significant transcriptional-translational uncoupling: Key invasion genes such as MMP1 and SNAI2 showed low transcriptional levels but significantly elevated translation efficiency. Conversely, ribosome-related genes exhibited low translation efficiency. Conclusions SGST possesses significant transcriptomic heterogeneity, where subpopulations of low differention maintain a hypometabolic and undifferentiated state by suppressing ribosome biogenesis. Rather than relying on transcriptional abundance, tumor cells drive a rapid synthesis of invasion-related proteins by specifically enhancing translation efficiency. This reveals a key post-transcriptional regulatory mechanism underlying the invasive growth of SGST.

Adiponectin/APPL1 axis alleviates diabetic vascular endothelial injury by regulating tight junctions

DUAN Yanru, RUAN Yanping, CHEN Jie, XING Yuanyuan

2026, 46(5):  673-680.  doi:10.16352/j.issn.1001-6325.2026.05.0673

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Objective To investigate the downstream molecular mechanisms by which the adiponectin(APN)/APPL1 signaling axis alleviates diabetic vascular endothelial injury. Methods APPL1-knockout diabetic mice were treated with APN. Hindlimb ischemia models were established to evaluate vascular regeneration. Endothelial injury and apoptosis were assessed by Western blot and caspase-3 activity. Human umbilical vein endothelial cells (HUVECs) were transfected with APPL1 siRNA to examine the effects of APN on apoptosis and permeability. Transcriptomic profiling was performed followed by GO and KEGG enrichment analyses. Selected targets were validated by RT-qPCR. Results APN markedly improved hindlimb blood flow recovery, increased CD31 expression and suppressed caspase-3 activity in diabetic mice, whereas these protective effects were completely abrogated in the absence of APPL1(P＜0.01). Consistently, in HUVECs, APN reduced high glucose/high lipid-induced apoptosis and permeability, but APPL1 silencing abolished these injury-suppressive effects (P＜0.01). Transcriptomic analysis identified 1 559 genes regulated by the APN/APPL1 signaling axis, predominantly enriched in tight junctions, cell adhesion and Hippo signaling pathways. Validation studies highlighted Occludin, a central tight junction protein, whose expression was strictly dependent on APPL1. Conclusions APN alleviates diabetic vascular endothelial injury through an APPL1-dependent signaling mechanism, with Occludin emerging as a pivotal downstream molecular target.

Single-point mutations non-additively regulate the conformational thermal stability of keratin 14-derived peptides

LI Zhenyan, LI Shuyuan, WANG Chenxuan, ZHANG Wenbo

2026, 46(5):  681-686.  doi:10.16352/j.issn.1001-6325.2026.05.0681

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Objective To elucidate the regulatory principles of how single-point amino acid mutations modulate polypeptide thermal stability, and reveal the holistic regulatory effects mediated by the local properties of side chains. Methods The keratin 14-derived peptide QNL system, comprising the wild-type QNL-R and three mutants (QNL-H, QNL-G, and QNL-S), was synthesized. AlphaFold3 was employed to predict the structural impacts of the single-point mutations. Conformational change of the polypeptide during the heating process was monitored by temperature-dependent intrinsic fluorescence spectroscopy. Based on a two-state transition model, Gibbs free energy (ΔG)and crossover temperature were calculated to quantitatively assess the effect of mutations on thermal stability. Results AlphaFold3 predictions showed a high structural similarity with the wild-type and mutant peptides(backbone RMSD=0.22 Å). However, variable-temperature fluorescence experiments revealed significant physicochemical discrepancies: at 25 ℃, the single-point mutations significantly altered the intrinsic fluorescence emission intensity by remodeling the local chemical microenvironment(P＜0.05). During the heating process, although all four peptides exhibited similar conformational evolution trends(decreased fluorescence intensity at 303 nm indicating unfolding, and increased fluorescence intensity at 391 nm indicating thermal aggregation), thermodynamic analysis demonstrated that the mutations significantly altered the thermal stability of the peptides which lead to systematic shift in the crossing-point temperatures as follows: QNL-G(55.9 ℃)＞QNL-H(54.7 ℃)＞QNL-S(54.2 ℃)＞QNL-R(52.2 ℃). Conclusions Single-point amino acid mutations alter the physicochemical properties of residue side chains and have significant impact on the overall conformational thermal stability of the peptides in a non-additive manner. This finding shows the limitation of theoretical predictions of protein structure on static conformations and the principle of energy minimization.

Effects of growth hormone therapy on serum resistin, leptin, and FGF-23 levels in children with growth hormone deficiency

ZHENG Zeyan, ZHOU Zhibo, SUN Yunxin, GUO Xiaoyuan, ZHU Huijuan, PAN Hui

2026, 46(5):  687-693.  doi:10.16352/j.issn.1001-6325.2026.05.0687

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Objective To compare serum level of resistin, leptin, and fibroblast growth factor 23(FGF-23)in children with growth hormone deficiency(GHD), children with idiopathic short stature(ISS), and healthy(children) control(HC) in order to evaluate the dynamic effects and clinical significance of one-year growth hormone(GH) therapy on these biomarkers. Methods This prospective cohort study enrolled 25 children with GHD, 25 children with ISS and 30 healthy children. Children with GHD received one-year growth hormone therapy. Fasting venous blood samples were collected before growth hormone therapy and at 6 and 12 months during treatment. Serum resistin, leptin, and FGF-23 levels were measured using ELISA. Clinical parameters including height, weight, growth velocity(GV),insulin-like growth factor 1(IGF-1), lipid profiles, fasting blood glucose(FBG), and homeostatic model assessment of insulin resistance(HOMA-IR) were collected at the same time. A linear mixed-effects model was used to adjust for confounders and evaluate indicator changes. Results The baseline level of serum resistin and FGF-23 in the GHD group was significantly higher than those in the healthy controls group(P＜0.05), leptin level was significantly higher than those in the ISS group(P＜0.05). After one-year GH therapy all three biomarkers significantly decreased in GHD children(P＜0.01) and was still significant after adjustment for age, gender, body mass index standard deviation score(BMI SDS), and IGF-1 standard deviation score(IGF-1 SDS). Concurrently, height standard deviation score(Ht SDS) improved from(-1.8±0.7) to(-1.5±2.2), annual growth velocity increased from(4.6±1.1)cm/year to(9.3±1.7)cm/year, and IGF-1 SDS significantly increased(P＜0.001). During treatment, FBG and triglyceride level mildly increased(P＜0.05,P＜0.01), but still kept within normal reference ranges; other metabolic parameters showed no significant changes. Conclusions GH therapy significantly improves linear growth and reduces resistin, leptin, and FGF-23 levels in children with GHD, demonstrating good short-term metabolic safety.

Clinical Sciences

Clinical and genetic characterization of children with SCN8A mutation-associated epilepsy

WANG Chu, XU Xiaoqing, TAO Yichen, LI Rui, DAI Yuanyuan, FAN Hongbin

2026, 46(5):  694-697.  doi:10.16352/j.issn.1001-6325.2026.05.0694

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Objective To analyze the clinical and genetic characteristics of children with epilepsy associated with SCN8A mutations. Methods High-throughput whole-exome genetic testing was performed in children with suspected gene mutation-related epilepsy and 15 children with seizures caused by SCN8A mutations were identified. Retrospective analysis was used to collect medical records and genetic results of children with the disease. Results Totally 12 cases were identified with de novo mutations and three cases were identified with genetic heterozygous mutations. The earliest age of onset was only 10 minutes after birth, and the maximum age of onset was 2 years old. Three patients were treated with a single drug, 5 patients were treated with two anti-seizure medicines (ASMs), 7 patients were treated with three or more ASMs and 2 patients were treated with a ketogenic diet, but the efficacy was not satisfactory. Ten patients responded to sodium-blocking agents, with doses ranging from higher than the standard pediatric dosage. Except for one case with normal electro-encephalogram, all others were abnormal, mainly with multifocal and widespread discharge mainly characterized by multifocal and widespread dischargess. Conclusions SCN8A mutation causes early-onset childhood epilepsy with early onset, mostly within 1 year of age or even in the neonatal period, with common manifestation of focal or focal secondary generalized seizures, and seizure types such as convulsions and myoclonus are uncommon.

Predictive value of serum RANTES and LTC4 for outcomes in patients with autoimmune encephalitis

PENG Fuzhi, FANG Fang, TU Ewen, CHEN Xi

2026, 46(5):  698-702.  doi:10.16352/j.issn.1001-6325.2026.05.0698

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Objective To explore the predictive value of expression and secretion of RANTES(regulated upon activation, normal T cell expressed, and secreted) and leukotriene C4 (LTC4) by peripheral T cells on disease outcomes in patients with autoimmune encephalitis (AE). Methods The patients with AE (144 cases) admitted from August 2020 to August 2024 were selected as the AE group and then were divided into the good prognosis group (98 cases) and the poor prognosis group (46 cases) based on the disease outcomes. Another 120 patients with viral encephalitis (VE) were selected as the VE group, and 150 healthy medical checkup participants were selected as the control group. ELISA was used to detect serum CRP, IL-6, TNF-α, RANTES, and LTC4. The data and serum level of RANTES and LTC4 were compared among different groups. The data and serum RANTES and LTC4 level were compared among patients with different prognoses. Pearson method was used to explore the correlation between RANTES,LTC4 with CRP, IL-6, and TNF-α. Multivariate logistic regression was used to explore the influencing factors of poor prognosis in AE patients. ROC curve was plotted to explore the predictive value of serum RANTES and LTC4 in predicting poor prognosis in AE patients. Results The serum RANTES and LTC4 decreased sequentially in AE group, VE group and in control group (P＜0.05). The poor prognosis group had higher serum level of CRP, IL-6, TNF-α, RANTES, and LTC4 than the good prognosis group (P＜0.05). Serum RANTES and LTC4 were positively correlated with CRP, IL-6, and TNF-α(P＜0.05). Serum CRP, IL-6, TNF-α, RANTES, and LTC4 were influencing factors for poor prognosis in AE patients (P＜0.05). The union of serum RANTES and LTC4 had a higher predictive value for poor prognosis in AE patients than individual predictions(Z_RANTES-union=2.722, P_RANTES-union＜0.01; Z_LTC4-union=2.343, P_LTC4-union＜0.05). Conclusions Serum level of RANTES and LTC4 is elevated in AE patients and closely related to the disease outcomes. The combination of serum level of RANTES and LTC4 has a high value in predicting poor prognosis in AE patients.

Association of preoperative hemoglobin glycation index with postoperative complication risk in diabetic patients undergoing non-cardiac surgery

ZHANG Yi, LAN Ling, ZHANG Yuelun, SHEN Le

2026, 46(5):  703-710.  doi:10.16352/j.issn.1001-6325.2026.05.0703

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Objective To investigate the association between preoperative hemoglobin glycation index (HGI) and postoperative complications in diabetic patients undergoing elective surgery. Methods This single-center retrospective cohort study included adult diabetic patients who underwent elective non-cardiac surgery between January 2013 and June 2024. Preoperative fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), and perioperative clinical data were collected. HGI was calculated as the difference between observed HbA1c and HbA1c predicted from FPG using a linear regression model. The primary outcome was postoperative complications during hospitalization. Multivariable logistic regression was used to evaluate the independent association between HGI and postoperative complications, and restricted cubic splines were applied to assess potential non-linear relationships. Results Total of 9 249 diabetic patients undergoing elective surgery were included, among whom 761 patients (8.2%) developed postoperative complications. Higher preoperative HGI was independently associated with an increased risk of postoperative complications (OR:1.099, 95% CI: 1.029-1.171; P=0.004). Restricted cubic spline analysis suggested a linear association between HGI and complication risk. Conclusions Preoperative HGI is an independent risk factor for in-hospital postoperative complications in diabetic patients following elective non-cardiac surgery. The linear dose-response relationship identified highlights its potential as a supplementary tool for perioperative risk assessment.

Mini Reviews

Role of histone modifications in regulating immune cell function in diffuse large B-cell lymphoma

JIAO Lichao, ZHU Yubing, WANG Cancan, FENG Ning, LI Xinxia

2026, 46(5):  711-716.  doi:10.16352/j.issn.1001-6325.2026.05.0711

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Diffuse large B-cell lymphoma (DLBCL) exhibits complex pathogenesis and significant heterogeneity. In DLBCL, histone modifications serve as a core mechanism of epigenetic regulation, dependent on the dynamic regulation of key modifying enzymes. Mutations or inactivation of key modifying enzymes such as KMT2D, EZH2, CREBBP, and EP300 lead to abnormal modifications at H3K4, H3K18, and H3K27 sites. These alterations mediate abnormal activation or suppression of downstream genes, ultimately affecting the expression of proteins like MYC, TP53 and BCL6 to promote cell proliferation and malignant transformation. Concurrently, histone modifications promote tumor-associated macrophages(TAMs) polarization by mediating signaling pathways like FBXW7/NOTCH/MYC/TGF-β1 and FBXW7/NOTCH/CCL2/CSF1. This suppresses T-cell activation and killing functions, disrupts anti-tumor immune homeostasis, and facilitates immune escape in DLBCL cells.

Research progress in retinoic acid in cognitive impairment disorders

ZHANG Tengyu, WU Ting, WU Xiang

2026, 46(5):  717-720.  doi:10.16352/j.issn.1001-6325.2026.05.0717

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Retinoic acid (RA), as the principal active metabolite of vitamin A, plays a critical role in regulating neurogenesis, synaptic plasticity, and anti-inflammatory responses. Maladjustment of acid signaling pathways is closely associated with the pathogenesis of various cognitive disorders, including Alzheimer′s disease(AD) and vascular dementia. RA modulates signaling molecules and pathways such as retinoic acid receptors, brain-derived neurotrophic factor (BDNF), and NF-κB, thereby optimizing synaptic plasticity,suppressing inflammatory responses, and reducing oxidative stress. These mechanisms collectively contribute to maintaining homeostasis within the nervous system and delaying the progression of cognitive decline.

Role of oxidative stress in the pathogenesis of acute cerebral injury

LIU Chengguo, LI Lu, ZOU Chuan

2026, 46(5):  721-725.  doi:10.16352/j.issn.1001-6325.2026.05.0721

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Acute cerebral injury (ACI), including stroke and traumatic brain injury, is characterized by high disability. Oxidative stress is the key pathological mechanism, caused by mitochondrial dysfunction and NADPH oxidase activation. This leads to excessive accumulation of ROS, triggering lipid per oxidation, neuronal apoptosis, and blood-brain barrier disruption. Targeting intervention approaches such as mitochondrial ROS scavengers (SkQ1) and Nrf2 pathway activators (desferrioxamine) could have therapeutic potential.

Research advances in endobronchial cryo-denervation for treatment of asthma patients

YUAN Lei

2026, 46(5):  726-729.  doi:10.16352/j.issn.1001-6325.2026.05.0726

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Bronchial cryo-denervation(BCD), an emerging therapeutic intervention for asthma, effectively reduces airway hyper-responsiveness by cryoablating nerve fibers within the bronchial wall. The mechanism of action of BCD, focuses primarily on its effects on airway hyper-responsiveness and airway inflammation. The present article will further summarize and analyze issues identified in clinical practice, while proposing insights and future directions for its application.

Medical Education

Teaching practice of clinical nutrition course for postgraduates majoring in clinical medicine

CHEN Moxi, LIU Chengyu, CHEN Wei, YU Jianchun

2026, 46(5):  730-735.  doi:10.16352/j.issn.1001-6325.2026.05.0730

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Objective To establish and optimize the graduates′ course of clinical nutrition and to clarify the necessity and importance of integrating clinical nutrition into education system for medical students. Methods The content of the clinical nutrition course for graduates majoring in clinical medicine was set according to the position paper of the European Society of Clinical Nutrition and Metabolism on nutrition education programs in medical schools. Clinical physicians from related departments such as basic surgery, clinical nutrition and gastroenterology were invited to participate in curriculum preparation and teaching. A small-scale teaching practice was conducted for graduates majoring in Chinese Academy of Medical Sciences and Peking Union Medical College, and students′ feedback on the course content and format was collected. Results The clinical nutrition-related education for graduates majoring in clinical medicine during their undergraduate studies was insufficient and failed to meet the needs of clinical performance. Systematic and comprehensive clinical nutrition course training can not only broaden students′ vision of clinical nutrition-related diagnosis and treatment methods, but also enhance their confidence in the rational use of relevant knowledge and skills in their study, work and life. Some experiences learned from this pilot study on course content and assessment methods, such as the emphasis on cases analysis and discussion, also provide references for the implementation of clinical nutrition courses in other colleges and universities in the future. Conclusions The graduates in clinical medicine have a high demand for clinical nutrition knowledge. Medical schools should introduce systematic clinical nutrition education courses at the graduate stage to support the capacity building for diagnosis and treatment and promote the construction and development of clinical nutrition disciplines in China.

A survey on the current status of perioperative communication between anesthesiologist and surgeon

CHEN Wen, GONG Yahong, XIA Di, ZHANG Yuelun

2026, 46(5):  736-742.  doi:10.16352/j.issn.1001-6325.2026.05.0736

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Objective To identify and fill the communication gaps among anesthesiologists in key peri-operative scenarios through a questionnaire survey conducted in multiple tertiary teaching hospitals in China in order to provide evidence for targeted training and safety culture improvement. Methods A cross-section questionnaire survey was conducted among active anesthesiologists of varying professional titles and educational backgrounds from institutions affiliated with the Committee of Anesthesiology of the Chinese Medical Association. Participation was anonymous. The survey focused on four key scenarios: preoperative assessment and preparation, intra-operative adverse events, collecting patient complaints, and peri-operative communication gaps between anesthesiologists and surgeons. Results A total of 356 valid questionnaires were collected (98.07% response rate). Analysis of single-choice and multiple-choice question data showed similarities and differences in communication capabilities between different subgroups of anesthesiologists and surgeons. The results indicated that communication effectiveness was influenced not only by individual skills and seniority but also by the combined effects of team psychological safety, organizational power structures, and institutional support. Conclusions Significant gaps remain in the cultivation of non-technical skills. It is recommended that hospitals improve the quality between anesthesiologist and surgeon communication by establishing interdisciplinary accountability mechanisms, adverse event analysis systems and by fostering a non-punitive safety culture.

Medical Supervision

Current status and optimization of strategy for postdoctoral trainees management in medical research institutes

LIU Haoyue, WANG Xiao, CHEN Houzao

2026, 46(5):  743-746.  doi:10.16352/j.issn.1001-6325.2026.05.0743

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Based on an analysis of the current status of postdoctoral management in medical research institutions, this article describes existing issues in areas such as talent positioning, support mechanisms, performance evaluation, and career development. Furthermore, it proposes systematic optimization strategy by drawing on management practice.