Volume 106 · Issue 35 · 2026

The Diabetic Foot Group of the Chinese Diabetes Society, Chinese Medical Association was founded in 1995 and renamed the Diabetes Foot and Peripheral Vascular Disease Group (hereinafter referred to as the Group) in 2012. Over the past 30 years, through the persistent efforts of successive generations of specialists, the Group has achieved fruitful outcomes in clinical practice, scientific research, talent cultivation, international academic exchanges and other fields. This paper reviews the developmental course of the Group, summarizes the work accomplished by its seven successive committees, analyzes the gaps between domestic research on diabetic foot and peripheral vascular diseases in China and the advanced international standards, and puts forward proposals for the future development of the Group.

Hemophagocytic lymphohistiocytosis (HLH) is a severe inflammatory response syndrome caused by inherited or acquired dysregulation of immune function. In recent years, with the continuous advancement of basic and clinical research on HLH, novel diagnostic and therapeutic concepts as well as new therapeutic agents have emerged, and international clinical practice guidelines have been updated successively. To promote standardized management of the disease, academic organizations including the Lymphocyte Group of Hematology Branch of the Chinese Medical Association, Professional Committee of Oncological Hematology of the China Anti-Cancer Association, Hematology Group of the Pediatrics Branch of the Chinese Medical Association, Infectious Diseases Branch of the Chinese Medical Association, and National Clinical Research Center for Rheumatic and Autoimmune Diseases jointly initiated the guideline revision. A panel of 80 domestic experts from hematology, pediatrics, infectious diseases, and rheumatology and immunology disciplines was assembled to revise the 2022 edition of Chinese Guidelines for the Diagnosis and Treatment of HLH, on the basis of the latest domestic and international research advances and current evidence-based medical data. The guidelines provides 16 recommendations covering 11 aspects including HLH classification, diagnostic criteria, laboratory testing, therapeutic strategies and efficacy evaluation, aiming to improve the diagnosis and treatment of HLH in China and optimize patients′ clinical outcomes.

To further standardize the prevention and management of lung cancer in China, improve the level of diagnosis and treatment, enhance patient prognosis, and provide evidence-based professional recommendations for clinical practitioners at all levels, the Oncology Society of Chinese Medical Association organized experts from respiratory medicine, medical oncology, thoracic surgery, radiation oncology, radiology, and pathology to develop the "Oncology Society of Chinese Medical Association guideline for clinical diagnosis and treatment of lung cancer (2026 edition)" through a consensus conference. Compared with the 2025 edition, the 2026 edition incorporates updates and refinements in several aspects. In the lung cancer screening section, quality control requirements for low-dose computed tomography screening have been further detailed, and the introduction and scope of application of opportunistic screening and artificial intelligence technologies in lung cancer screening have been added. In the pathology section, on the basis of the latest clinical research findings and newly approved indications by the National Medical Products Administration (NMPA), the recommendations for molecular pathological testing have been supplemented, with several new gene testing-related recommendations added. In the treatment section, perioperative neoadjuvant and adjuvant treatment regimens for non-small cell lung cancer have been updated according to newly approved drugs and indications; additional options for consolidation immunotherapy after concurrent or sequential chemoradiotherapy for unresectable stage Ⅲ non-small cell lung cancer have been incorporated; and first-line and subsequent-line treatment strategies for patients with advanced epidermal growth factor receptor (EGFR)-mutations have been further refined. In addition, treatment recommendations for patients with non-small cell lung cancer harboring molecular subtypes such as anaplastic lymphoma kinase (ALK) fusion, KRAS G12C mutation, human epidermal growth factor receptor 2 (HER-2) mutations, and MET amplification have also been updated based on the approval of novel agents. This guideline adheres to NMPA-approved indications as the core principle, is grounded in drugs practically available in China and integrates recommendations from international guidelines as well as the current status of clinical practice in China. It synthesizes the latest evidence-based medical advances in recent years covering lung cancer screening, diagnosis, pathology, genetic testing, immunologic and molecular biomarker testing, treatment modalities, and follow-up, with the aim of providing reasonable and practical recommendations for clinicians at all levels, as well as professionals in radiology, laboratory medicine, and related disciplines.

The management of traumatic brain injury (TBI) in mass casualty incidents (MCI) is characterized by strong time dependence, complex injury patterns, and acute strain of medical resources, rendering it substantially more challenging than routine clinical practice. Currently, most existing domestic and international TBI guidelines and consensus statements are developed for daily medical scenarios, and lack systematic full-process standard tailored to the resource-constrained MCI environment. To fill this gap, the Chinese Neurosurgical Society convened a multidisciplinary expert panel covering neurosurgery, critical care medicine and evidence-based medicine and other disciplines. In strict accordance with international methodological standards for guideline development, the panel systematically searched the literature, completed evidence quality appraisal and subsequently formulated the Expertconsensus on the management of traumatic brain injury in mass casualty incidents (2026 edition). This consensus covers the entire process of TBI care in MCI treatment: general principles and emergency response system, safety and protection of rescue personnel and professional team development, on-site triage and emergency life support, safe transport and tiered triage, in-hospital standardized treatment and priority management, intracranial pressure monitoring and standardized management, in-hospital complication prevention and comprehensive management, and early rehabilitation and psychological support. The panel graded the quality of evidence and strength of recommendations using the Oxford University centre for evidence-based medicine levels of evidence framework (2009) and reached a consensus through Delphi expert consultation, forming in 42 recommendations. Guided by the core principle of "maximizing treatment outcomes with limited resources", this consensus defines tiered decision-making rules based on injury severity, clarifies triage priorities for mass casualties, and specifies full-process care protocols. It can provide evidence-based reference and practical basis for medical institutions at all levels and health administrative authorities in China to construct MCI-TBI emergency response systems, standardize clinical practice, and carry out specialized personnel training.

To evaluate the value of the Nutritional Risk Screening 2002 (NRS2002) and the Mini-Nutritional Assessment Short-Form (MNA-SF) in assessing nutritional status, disease progression, and prognosis in adult patients with amyotrophic lateral sclerosis (ALS).

Baseline data of 148 ALS patients who visited Peking University Third Hospital from January to December 2024 were prospectively collected. Patients were divided into malnutrition group and normal group based on the presence of nutritional risk. Assessments were conducted every 3 months over a 1-year follow-up period, during which ALSFRS-R scores, body mass index (BMI), and nutritional scale scores were recorded. The rates of ALSFRS-R score decline (δFS) and BMI change (δBMI) were calculated as (baseline ALSFRS-R score-follow-up ALSFRS-R score)/follow-up months and (baseline BMI-follow-up BMI)/follow-up months, respectively. The primary endpoint events were death or tracheostomy. Clinical data were compared between patients with different nutritional statuses. Spearman and Pearson correlation analyses were used to explore the correlations between scale scores and various indicators. Cohen′s Kappa coefficient was used to evaluate the inter-rater consistency between the two scales. Linear mixed-effects models were applied to assess the relationships between nutritional risk and changes in δFS and δBMI.

A total of 148 ALS patients were collected in this study, including 96 males and 52 females, with the age [M(Q₁, Q₃)] of 56.0 (49.0, 61.0) years. A total of 4 enrolled patients were excluded from the NRS2002 assessment owing to missing BMI data, which resulted from the inability to measure height and weight in these bedridden individuals. Based on the NRS2002 and MNA-SF, patients were classified into the malnutrition group (NRS2002 malnutrition group, n=45; MNA-SF malnutrition group, n=59) and the normal group (NRS2002 normal group, n=99; MNA-SF normal group, n=89). The Kappa values for the consistency between NRS2002 and MNA-SF at baseline, 3, 6, 9, and 12 months were 0.726, 0.713, 0.698, 0.648, and 0.769, respectively (all P<0.001). NRS2002 was negatively correlated with BMI (r=-0.413, P<0.001), body weight (r=-0.442, P<0.001), prealbumin (r=-0.253, P<0.001), creatinine (r=-0.139, P=0.049), and triglycerides (r=-0.228, P=0.003); MNA-SF was positively correlated with BMI (r=0.573, P<0.001), body weight (r=0.514, P<0.001), prealbumin (r=0.277, P<0.001), creatinine (r=0.233, P=0.002), and triglycerides (r=0.289, P<0.001). After adjusting for confounders using linear mixed-effects models, a higher NRS2002 score was identified as a risk factor for increases in δFS (β = 0.127, 95%CI: 0.065-0.189, P<0.001) and δBMI (β=0.150, 95%CI: 0.104-0.197, P<0.001), whereas a higher MNA-SF score served as a protective factor against increases in δFS (β=-0.090, 95%CI:-0.116 to -0.064, P<0.001) and δBMI (β=-0.092, 95%CI:-0.113 to -0.071, P<0.001).

NRS2002 and MNA-SF demonstrate good consistency in nutritional risk assessment among ALS patients. The scores of both scales are correlated with traditional nutritional indicators including BMI, body weight, prealbumin, creatinine, and triglycerides, and are associated with the rates of ALSFRS-R and BMI changes in these patients.

To investigate the influencing factors for cardiovascular autonomic neuropathy (CAN) in patients with type 2 diabetes mellitus (T2DM) and to develop a predictive model.

A retrospective analysis was performed on clinical data of 831 patients with T2DM hospitalized in the Suqian Hospital Affiliated to Xuzhou Medical University from September 2024 to December 2025. Patients were divided into a training set (n=581) and a validation set (n=250) at a 7∶3 ratio using a random number table method. According to the presence of CAN, patients in the training set were further classified into the non-CAN group (n=307) and the CAN group (n=274). Compare the differences in various indicators between the two groups. Least absolute shrinkage and selection operator (LASSO) regression and multivariate logistic regression models were used to analyze influencing factors for CAN in patients with T2DM, and a nomogram prediction model was constructed. The area under the receiver operating characteristic curve (AUC), calibration curve and decision curve analysis were adopted to evaluate the predictive performance, accuracy and clinical applicability of the model.

In the training set, patients in the CAN group presented higher age, diabetes duration, glycated hemoglobin (HbA_1c), neutrophil count, platelet count, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio, systemic immune-inflammation index (SII), and systemic inflammatory response index compared with the non-CAN group. By contrast, height, body weight, total bilirubin, direct bilirubin, alanine aminotransferase, aspartate aminotransferase, fasting C-peptide and fasting insulin were lower in the CAN group (all P<0.05). The proportions of diabetic nephropathy, diabetic retinopathy (DR), diabetic peripheral neuropathy, history of hypertension, history of cardiovascular disease, history of stroke, anti-platelet agent use and insulin use were higher in the CAN group than in the non-CAN group (all P<0.05). Seven variables were screened out via LASSO regression analysis, including DR, age, diabetes duration, HbA1c, NLR, PLR and SII. Multivariate logistic regression analysis revealed that DR (OR=2.29, 95%CI: 1.48-3.56), longer diabetes duration (OR=1.04, 95%CI: 1.01-1.08), advancing age (OR=1.06, 95%CI: 1.04-1.09), elevated HbA_1c (OR=1.23, 95%CI: 1.13-1.36), increased NLR (OR=2.23, 95%CI: 1.36-3.69) and elevated PLR (OR=1.01, 95%CI: 1.00-1.02) were influencing factors for CAN in patients with T2DM. The nomogram prediction model constructed with the above 6 variables yielded AUC values of 0.839 (95%CI: 0.807-0.871) and 0.787 (95%CI: 0.732-0.843) for predicting CAN among T2DM patients in the training set and validation set, respectively. The corresponding sensitivity was 81.4% and 71.3%, and the specificity was 71.7% and 73.3%. Calibration curves demonstrated good agreement between predicted and observed CAN outcomes in both the training and validation sets. The Hosmer-Lemeshow test showed satisfactory calibration for the training set (χ²=6.701, P=0.461) and validation set (χ²=12.139, P=0.096). The decision curve analysis demonstrated that the model exhibits favorable clinical applicability when the threshold probability of the training set ranges from 1% to 88%, and that of the validation set ranges from 3% to 80%.

DR, longer diabetes duration, advanced age, elevated HbA_1c, increased NLR and elevated PLR are risk factors for CAN in patients with T2DM. The nomogram prediction model established based on these variables can intuitively and individually assess the risk of CAN in patients with T2DM.

To explore the related factors of patients with primary aldosteronism (PA) developing into stage 4 of cardiovascular-renal-metabolic syndrome (CKM).

A total of 397 patients diagnosed with PA from January 2016 to December 2024 were retrospectively enrolled. According to the CKM staging criteria, the patients were divided into the early stage group (stages 0-2), stage 3 group and stage 4 group. To analyze the differences in each indicator among the three groups. Multivariate logistic regression models were applied to analyze the correlation between each indicator and the occurrence of CKM stage 4 via stepwise adjustment for confounding factors. Subgroup analyses were further conducted by gender, age (≤50 years and >50 years) and PA subtypes [idiopathic hyperaldosteronism (IHA) and aldosterone-producing adenoma].

Among the 397 PA patients, 231 were males and 166 were females, with a confirmed diagnosis age of (51.1±10.9) years. There were 179 patients in the early CKM stage group (including 1 case in stage 0, 7 cases in stage 1, and 171 cases in stage 2), 107 patients in the CKM stage 3 group, and 111 patients in the CKM stage 4 group. There were statistically significant differences among the 3 groups in age, gender, PA subtype, body mass index, diastolic blood pressure, systolic blood pressure, hypertension duration, proportion of dyslipidemia, proportion of diabetes, proportion of atherosclerosis, proportion of chronic kidney disease, proportion of cerebral infarction, and proportion of coronary heart disease (all P<0.05). In terms of laboratory indicators, there were statistically significant differences among the 3 groups in fasting blood glucose, total cholesterol, low-density lipoprotein cholesterol, γ-glutamyl transferase, blood potassium, serum creatinine, urinary albumin/creatinine ratio (UACR), estimated glomerular filtration rate (eGFR), supine aldosterone, and aldosterone 2 hours after the captopril test (all P<0.05). Multivariate logistic regression showed that after adjusting for a series of influencing factors including gender, age, BMI, metabolic indicators, disease history and medication history, 2 h post-captopril aldosterone remained independently and positively correlated with the occurrence of CKM stage 4 in PA patients (OR=1.003, 95%CI: 1.001-1.005). Subgroup analyses revealed that the correlation between 2-hour post-captopril aldosterone and CKM stage 4 was more significant in the male subgroup (OR=1.005, 95%CI: 1.002-1.008),the subgroup aged ≤50 years (OR=1.006, 95%CI: 1.002-1.010) andthe IHA subgroup (OR=1.005, 95%CI: 1.002-1.008).

High aldosterone level is a factor associated with progression of CKM to the clinical event phase (CKM stage 4). Among aldosterone-related indicators, 2 h post-captopril aldosterone has the most stable predictive value, and this correlation presents heterogeneity across populations with different genders, ages and PA subtypes.

To explore the role and mechanism of G-protein coupled receptor kinase 2 (GRK2)-mediated phosphorylation of adiponectin receptor 1 (AdipoR1) in diabetic cardiomyopathy (DCM), and to verify the therapeutic effect of site-directed mutagenesis targeting serine at position 205 (Ser205) of AdipoR1.

Twenty 4-week-old C57BL/6J mice were randomly assigned to the normal control (NC) group and the DCM model group using a random-number table, with 10 mice per group. The DCM model was established in the DCM group by high-fat diet (HFD) feeding combined with intraperitoneal injection of streptozotocin (STZ). After 21-week intervention, 6 mice from each group were selected using a random-number table for measurements of serum biochemical parameters, adiponectin (APN) levels and cardiac diastolic function. Following euthanasia, myocardial tissues were harvested for Masson′s trichrome staining to evaluate the degree of myocardial fibrosis. Co-immunoprecipitation and Western blot (WB) assays were performed to determine GRK2 expression, phosphorylated serine (p-Ser) levels, and the binding capacity between AdipoR1 and adaptor protein, phosphotyrosine-binding domain and leucine zipper motif 1 (APPL1). The remaining 4 mice per group were used for isolation of primary adult cardiomyocytes, which were treated with exogenous APN or phosphate-buffered saline (PBS). Phosphorylation status of the downstream adenosine monophosphate-activated protein kinase (AMPK)/protein kinase B (Akt) signaling pathway was subsequently detected. Twenty-eight 3-day-old AdipoR1-knockout neonatal mice were included in further experiments. Four of these AdipoR1-knockout neonatal mice were randomly selected by a random-number table to isolate primary cardiomyocytes. Plasmid co-transfection was conducted to assess AdipoR1-APPL1 interaction and downstream AMPK/Akt phosphorylation upon GRK2 overexpression. Four experimental subgroups were set: Adenovirus-empty(Ad-empty)+3×Flag-AdipoR1^WT, Ad-empty+3×Flag-AdipoR1^S205A, adenovirus-mediated GRK2(Ad-GRK2)+3×Flag-AdipoR1^WT, and Ad-GRK2+3×Flag-AdipoR1^S205A. This experiment aimed to identify whether Ser205 phosphorylation serves as the key molecular event whereby GRK2 blocks APN signaling. From the remaining 24 AdipoR1-knockout neonatal mice, 12 were randomly allocated into two groups (6 mice per group) using a random-number table. On postnatal day 3, mice received an injection of either adeno-associated virus serotype 9 (AAV9)-AdipoR1^WT or AAV9-AdipoR1^S205A. Ten weeks later, primary adult cardiomyocytes were isolated and divided into 4 subgroups: AAV9-AdipoR1^WT+Ad-empty, AAV9-AdipoR1^WT+Ad-GRK2, AAV9-AdipoR1^S205A+Ad-empty, and AAV9-AdipoR1^S205A+Ad-GRK2. GRK2 was overexpressed in vitro, and immunofluorescence co-localization was applied to quantify the co-localization of AdipoR1 and APPL1. The leftover 12 AdipoR1-knockout neonatal mice were randomized into two groups (6 mice per group) with a random-number table, and injected with the aforementioned viruses on postnatal day 3. Four weeks after virus injection, DCM was induced by HFD plus STZ administration, yielding two in-vivo groups: AAV9-AdipoR1^WT+DCM (wild-type group) and AAV9-AdipoR1^S205A+DCM (point-mutation group). APN was continuously delivered via osmotic minipumps. Eight weeks after APN intervention, cardiac function and myocardial fibrosis were evaluated.

In C57BL/6J mice, the DCM group exhibited significantly higher levels of blood glucose, triglycerides, low-density lipoprotein-cholesteral and adiponectin (APN) compared with the NC group (all P<0.001). Statistically significant differences were observed between the two groups in the E/A ratio, radial strain rate, reverse radial strain rate (rRSR), longitudinal strain rate (LSR), and reverse longitudinal strain rate (rLSR) (all P<0.05). The fraction of myocardial fibrotic area was larger in the DCM group than in the NC group (9.20±1.66 vs 1.24±0.51, P<0.001). Myocardial protein levels of GRK2 (4.81±0.46 vs 1.03±0.09, P<0.001) and p-Ser (1.75±0.21 vs 0.98±0.05, P<0.001) were elevated in the DCM group relative to the NC group. The binding ratio of APPL1 to AdipoR1 in myocardial tissue was decreased in the DCM group versus the NC group (0.398±0.085 vs 0.978±0.088, P<0.001). APN-stimulated AMPK/Akt phosphorylation was blunted in primary adult cardiomyocytes isolated from DCM-model C57BL/6J mice. In-vitro experiments using AdipoR1-knockout neonatal mouse cardiomyocytes demonstrated that following AdipoR1 Ser205 site mutation, the ratios of p-AMPK/AMPK (4.025±0.767 vs 1.003±0.087, P<0.001) and p-Akt/Akt (4.125±0.544 vs 0.990±0.034, P<0.001) were markedly increased in the 3×Flag-AdipoR1^S205A+APN group compared with the 3×Flag-AdipoR1^S205A+PBS group. In primary adult cardiomyocytes derived from AdipoR1-knockout mice, the AAV9-AdipoR1^S205A+Ad-GRK2 group restored the AdipoR1-APPL1 interaction in the presence of GRK2 when compared with the AAV9-AdipoR1^WT+Ad-GRK2 group (P=0.014). In the in-vivo DCM model established in AdipoR1-knockout mice, the AAV9-AdipoR1^S205A+DCM group displayed higher E/A ratio, rRSR, LSR and rLSR values, together with a lower myocardial fibrotic area fraction (all P<0.05), relative to the AAV9-AdipoR1^WT+DCM group.

GRK2-mediated phosphorylation of AdipoR1 at serine 205 triggers APN-AdipoR1 metabolic dysfunction, which represents a critical contributor to aggravated cardiac dysfunction in DCM. This mechanism is associated with the decoupling of AdipoR1 from APPL1. Targeted inhibition of AdipoR1 phosphorylation via site-directed mutagenesis restores APN-AdipoR1 signaling and ameliorates cardiac dysfunction in DCM.

To explore the molecular mechanisms by which ethionine induces neural tube defects (NTD) through regulating the lysine demethylase 5A (KDM5A)/trimethylated lysine 4 of histone H3 (H3K4me3) axis and modulating the Wnt/β-catenin signaling pathway.

Specific pathogen-free adult male and female C57BL/6 mice (80 females and 35 males) were housed overnight in a 2∶1 female-to-male ratio. Vaginal plugs were examined the following morning to confirm pregnancy. Pregnant mice were randomly divided into two groups: the ethionine experimental group (ethionine group) and the control group. At embryonic day 7.5 (E7.5), the ethionine group received a single intraperitoneal injection of ethionine (500 mg/kg) to establish the NTD model, while the control group was injected with an equal volume of normal saline, with 21 mice in each group. At E10.5, pregnant mice were sacrificed and embryos were collected for observation and photography under a stereomicroscope. Brain tissues from embryos of both groups were harvested for transcriptome sequencing. The expression levels of KDM5A, H3K4me3, Wnt/β-catenin pathway components [β-catenin, transcription factor 4 (TCF4), axis inhibition protein 2 (Axin2), phosphorylated glycogen synthase kinase 3β (p-GSK3β)], and cell proliferation-related proteins [G1/S-specific cyclin-D1 (Cyclin D1), proliferating cell nuclear antigen (PCNA), Myc oncogene (c-Myc)] were assessed by Western blotting, real-time quantitative polymerase chain reaction (RT-qPCR), and immunofluorescence. An additional KDM5A-specific inhibitor GSK-4J treatment group (GSK-4J group) and ethionine combined with GSK-4J treatment group (ethionine+GSK-4J group) were included to verify the regulatory role of the KDM5A/H3K4me3 axis. The pregnant mice in the GSK-4J group received intraperitoneal injection of GSK-4J (7 mg/kg) and the ethionine+GSK-4J group were injected with both 7 mg/kg GSK-4J and 500 mg/kg ethionine, with 12 mice in each group. Comparisons between the two groups were performed using independent samples t-test, one-way ANOVA was applied to evaluate the overall differences among multiple groups, and Tukey′s honestly significant difference test was adopted for pairwise post-hoc comparisons.

The ethionine treated group exhibited 48.79% (121/248) incidence of incomplete brain structure and morphological malformations, while the malformation rate in the control group was 3.73% (10/268), with a statistically significant difference (P<0.001). Compared with the control group, the ethionine group showed elevated KDM5A mRNA and protein levels, accompanied by reduced H3K4me3 modification levels (all P<0.001); protein expression of β-catenin, TCF4, and Axin2 were decreased (P<0.01, P<0.05), whereas p-GSK3β was increased (P<0.01). Following GSK-4J intervention, the expression of β-catenin, TCF4, and Axin2 was partially restored (all P<0.01), and the percentage of Cyclin D1-positive cells, as well as the expression of PCNA and c-Myc were increased (all P<0.05).

Ethionine participates in NTD development by upregulating KDM5A to decreased H3K4me3 levels, inhibiting Wnt/β-catenin signaling pathway, and reducing neuroepithelial cell proliferation. Thus, targeting the KDM5A/H3K4me3 axis may provide a new strategy for the prevention and treatment of NTD.

To systematically evaluate the clinical efficacy and safety of endoscopic submucosal dissection (ESD) versus surgical resection for early gastric cancer (EGC) in patients aged 75 years and above.

A systematic search was conducted in PubMed, Embase, Cochrane Library, and CNKI from the inception of the database to April 2026, to include relevant literature on ESD and surgery for aged 75 years and above patients with EGC. The experimental group consisted of patients aged≥75 years treated with ESD (ESD group), while the control group included those treated with surgery (surgery group). According to inclusion and exclusion criteria, two researchers independently performed literature screening, data extraction using the Newcastle-Ottawa Scale, and conducted meta-analysis using RevMan 5.4 and Stata 18.0 software to assess heterogeneity using I². Outcome measures included the 5-year survival rate, recurrence rate, recurrence-related mortality rate, and tumor incidence rates across different mucosal layers in both groups of patients. Funnel plots and leave-one-out analysis were adopted for publication bias analysis and sensitivity analysis.

A total of 6 studies involving 2 045 patients were included, with 988 in the ESD group and 1 057 in the control group. The 5-year survival rate (82.9% vs 77.4%, OR=1.29, 95%CI: 1.01-1.65, P=0.040, I²=0) and gastric cancer recurrence rate (8.5% vs 4.3%, OR=2.39, 95%CI: 1.37-4.14, P=0.002, I²=24%) were higher in the ESD group than those in the surgical group, whereas the recurrence-related mortality rate was lower in the ESD group (1.9% vs 4.9%, OR=0.47, 95%CI: 0.25-0.86, P=0.020, I²=34%). Subgroup analysis by tumor incidence rates across different mucosal layers showed that the proportion of mucosal tumors was higher in the ESD group than that in the surgical group (78.8% vs 38.3%, OR=3.40, 95%CI: 1.15-10.07, P=0.030, I²=95%), whereas the proportion of submucosal tumors was lower in the ESD group than in the surgical group (20.7% vs 61.4%, OR=0.29, 95%CI: 0.10-0.87, P=0.030, I²=95%). Funnel plot analysis showed that the studies were generally symmetrically distributed on both sides of the pooled effect size (log OR), forming an inverted funnel shape; sensitivity analysis demonstrated that the point estimates of individual studies fluctuated slightly around the original pooled effect size (log OR=1.05).

For EGC patients aged 75 years and above, ESD demonstrates superior clinical efficacy and safety compared to surgical treatment.

Seven patients with lower urinary tract dysfunction who developed skin erosion after implant surgery at Beijing Hospital between June 2022 and November 2025 were prospectively studied. Follow-up was conducted at 1 month postoperatively (outpatient visit), and at 3, 6, and 12 months, and annually thereafter via telephone interviews, to assess wound healing, device function (where applicable), and complications. The age was (50.6±25.2) years. Time since implantation [M (Q₁,Q₃)] was 15 (12, 36) months, with erosion duration of 0.50 (0.17, 1.00) months. All patients were Clavien-Dindo grade Ⅲ. Three had artificial urethral sphincter (AUS) erosion: 2 with control pump extrusion underwent device-preserving debridement and revision; 1 developed urethral injury, scrotoperineal abscess, and systemic infection from catheterization with the AUS activated, requiring device removal, partial urethrectomy, and end-to-end anastomosis. Four had sacral neuromodulation (SNM) erosion: three with surgical-site breakdown and pulse generator exposure underwent device-preserving revision; 1 with fluctuance, tenderness, and purulent discharge required SNM explantation. Median follow-up was 14 (1, 23) months. Both AUS-preserved patients recovered uneventfully, with device reactivation at 6 weeks and social continence at last follow-up; the AUS-removed patient returned to pre-implant incontinence levels. All 3 SNM-preserved patients healed well with normal device function; the SNM-explanted patient returned to pre-SNM symptom levels. No surgery-related complications occurred by December 2025. Device-preserving revision is feasible for implant erosion without abscess or systemic infection and with adequate subcutaneous fat, provided risks are thoroughly discussed and informed consent is obtained.

This article reports the diagnosis and treatment of a patient with common variant immunodeficiency disease (CVID) complicated with cytomegalovirus (CMV) gastroenteritis. The patient started with chronic diarrhea and multiple gastrointestinal ulcers, and was misdiagnosed as inflammatory bowel disease in the early stage. After administration of hormones and immunosuppressants, the condition worsened, and multiple perforations of the small intestine and septic shock occurred. Surgical repair and small intestinal ostomy were performed in the emergency department. Combined with immunoglobulin levels, viral serological indicators and histopathology, CVID combined with CMV gastroenteritis was confirmed. Immunoglobulin replacement therapy, rapid reduction and discontinuation of immunosuppressants, standardized anti-infection, combined with extracorporeal intestinal fluid reinfusion, intestinal mucosal repair and stepped nutritional support, can relieve intestinal stenosis in stages and complete stoma recovery. During the follow-up period of up to 6 years, the patient's condition was generally stable, but recurrent respiratory tract and CMV infections still occurred. This case suggests that patients with atypical gastrointestinal ulcers and recurrent infections should be vigilant against primary immunodeficiency and avoid blind immunosuppressive treatment; When combined with serious complications, it is necessary to rely on a multidisciplinary model to implement comprehensive management to improve the long-term prognosis.

Lipotoxicity refers to dysfunction caused by elevated circulating lipid levels and is one of the key factors driving the development of insulin resistance. Studies have shown that its effect is not simply caused by lipid accumulation, but by ectopic deposition in multiple organs such as liver, skeletal muscle, adipose tissue and islet β cells, forming harmful lipid intermediates, interfering with insulin signaling, inducing inflammatory response and organelle response damage, and amplifying each other in all dimensions to jointly promote insulin resistance. This paper systematically reviews the correlation between lipotoxicity and insulin resistance and its intrinsic regulatory mechanisms, elucidates the differences in the response mechanisms of different metabolic organs to lipotoxicity, and explores the organ response and molecular mechanism network of lipotoxicity-induced insulin resistance from the dimensions of abnormal accumulation of lipid intermediates, activation of inflammatory pathways, endoplasmic reticulum stress, and mitochondrial dysfunction, providing new ideas for the intervention of diseases such as type 2 diabetes, fatty liver, and metabolic syndrome.

The patient, a 33-year-old female, presented to the Endocrinology Department of the Air Force Specialized Medical Center for "recurrent tetany for 28 years". The patient developed tetany without obvious cause from the age of 5, which was relieved after calcium supplementation, and the symptoms recurred. He was diagnosed with hypoparathyroidism at the age of 6. The first grand mal seizure occurred at the age of 7, with intermittent seizures, and no further seizures occurred after the age of 12. Growth and development are normal, menarche begins at the age of 15, and tetany is prone to occur on cloudy days or during menstruation. She gave birth to a son by cesarean section at the age of 28, and the son is in good health. His father and sister are in good health, while his mother suffers from diabetes. Physical examination: no special physical appearance, normal hearing and vision, positive for Chvostek sign and Trousseau sign. Daily supplementation of elemental calcium 1 200 mg, calcitriol 0.5 μg, blood calcium 1.8 mmol/L, blood phosphorus 1.9 mmol/L, vitamin D3 64.86 nmol/L, parathyroid hormone<5.05 ng/L, 24 h urine calcium 5.44 mmol, urine phosphorus 14.72 mmol. Plain CT scan of the skull revealed multiple patchy calcifications in the bilateral cerebellar hemispheres, basal ganglia, thalamus, dentate nucleus, radiation crown area, and brain, which were symmetrically distributed with clear boundaries (Figure 1). This patient had recurrent tetany, multiple seizures, low blood calcium, high blood phosphorus, and low parathyroid hormone, which was consistent with primary hypoparathyroidism. Cranial CT findings suggested hypoparathyroidism encephalopathy.