Introduction Robotic surgery is a safe approach for gastric cancer. Most available evidence originates from East Asia, while data from European centers remain limited. This study aims to compare surgical and oncological outcomes between different countries, focusing on the number of lymph node retrieved. Materials and Methods We included adult patients who underwent curative-intent distal or total robotic gastrectomy for gastric cancer between 2017 and 2024 at specialized centers in Tuscany (Italy) and the Seoul National University Hospital (South Korea). Results A total of 700 patients were enrolled, including 232 Italian and 468 Korean patients. Western patients were older, had a higher comorbidity burden, and had more advanced disease (64.7% vs. 28.6%). Neoadjuvant chemotherapy and D2 lymphadenectomy were more frequently performed in Western centers, whereas D1+ was preferred in Eastern centers (p<0.001). Median node retrieved was 34 (West 38 vs. East 33 nodes), exceeding oncological thresholds (>15) across all pathological stages. Lymph node retrieved increased with pT stage and was independent of age, while higher BMI was associated with lower nodal retrieval (31 vs. 35 nodes). Postoperative surgical complications were higher in the Western cohort (13.4% vs. 8.1%, p=0.029), with an increased rate of anastomotic leakage (p<0.001). Length of stay and perioperative mortality were comparable between centers. Conclusion Robotic gastrectomy ensures adequate lymphadenectomy and acceptable perioperative outcomes in both Italian and Korean centers. Observed differences in operative efficiency, morbidity, and survival mainly reflect variations in patient selection and disease stage rather than surgical quality, supporting centralization and earlier diagnosis at Western populations.

BACKGROUND:Robotic systems may facilitate the double-flap technique (DFT) after proximal gastrectomy (PG), yet the superiority of robotic DFT following PG (RPG-DFT) over laparoscopic PG with DFT (LPG-DFT) remains unclear. METHODS:Seventy-three gastric cancer patients (28 RPG-DFT, 45 LPG-DFT) were compared for baseline characteristics, perioperative outcomes, and 3-month postoperative data. Gastroesophageal Reflux Disease-Health Related Quality of Life (GERD-HRQL) and weight loss are postoperative primary endpoints. RESULTS:RPG-DFT had significantly longer operative time (308.3 vs. 204.5 min, p < 0.0001) but shorter postoperative hospital stay (6.21 vs. 8.13 days, p < 0.0001). By postoperative day 3, RPG-DFT showed faster decline in inflammatory markers (NLR, PLR, MLR, SII). No significant differences were observed in reflux symptoms or anastomotic stenosis rates. CONCLUSION:Compared to LPG-DFT, RPG-DFT facilitates accelerated patient recovery, as evidenced by a rapid decline in inflammatory markers and reduced length of hospital stay.

Osteosarcoma is the most common primary malignant bone tumor in children and adolescents. The purpose of this study is to explore the regulatory mechanism of LINC01116 in osteosarcoma metastasis and its potential association with the urea cycle and chemoresistance. Transcriptomic profiling was performed, and the results were validated by qRT-PCR in 6 paired osteosarcoma and adjacent non-tumor tissues. Functional assays including in vivo xenograft models were used to verify the effect of LINC01116 on osteosarcoma cell proliferation. RNA-protein interaction studies and ChIRP-MS assays were conducted to confirm the binding between LINC01116 and CPS1.LINC01116 was significantly upregulated in metastatic osteosarcoma lesions. Silencing LINC01116 inhibited osteosarcoma cell proliferation both in vitro and in vivo. Mechanistically, LINC01116 directly binds to CPS1 -the rate-limiting enzyme of the urea cycle, which was confirmed by ChIRP-MS. Perturbing the LINC01116/CPS1 axis reduced citrulline levels, indicating impaired urea cycle function. Additionally, CPS1 silencing enhanced osteosarcoma cell sensitivity to cisplatin. This study identifies a novel LINC01116/CPS1 axis that drives osteosarcoma metastasis by regulating the urea cycle. Targeting this axis can sensitize osteosarcoma to cisplatin treatment, which highlights its potential as a therapeutic target for osteosarcoma.

Background:Severe fever with thrombocytopenia syndrome (SFTS) is a highly fatal infectious disease characterized by cytokine storm and multiple organ dysfunction. Stress hyperglycemia is common in severe infections, but its clinical significance in SFTS remains unclear. Objective:To evaluate blood glucose alterations in SFTS and their associations with disease severity, inflammation, and outcomes. Methods:We retrospectively analyzed 172 SFTS patients. Blood glucose levels, HbA1c, and the stress hyperglycemia ratio (SHR) were assessed at various time points during hospitalization, and their correlations with disease severity, prognosis, and laboratory parameters, including inflammatory cytokines, were analyzed. Results:Admission blood glucose and SHR were significantly elevated in SFTS patients compared with controls. Severe and non-surviving patients showed higher blood glucose and SHR levels than mild and surviving patients. Longitudinal analysis revealed persistently elevated or increasing blood glucose levels in non-survivors, whereas survivors showed a declining trend. Blood glucose was positively correlated with viral load, organ dysfunction indicators, coagulation abnormalities, platelet changes, and inflammatory cytokines (IL-1β, IL-6, TNF-α). Conclusion:Stress hyperglycemia is common in SFTS and is associated with disease severity, inflammatory responses, and adverse clinical outcomes. Blood glucose and SHR may serve as useful markers reflecting disease severity and clinical status in patients with SFTS.

ABSTRACT Gastric cancer (GC) remains an aggressive malignancy with limited effective therapeutic options. Integrated single‐cell and bulk transcriptomic analyses identify protein disulfide isomerase A6 (PDIA6) as a tumor epithelial–enriched gene associated with advanced tumor‑ node‑metastasis (TNM) stage and unfavorable survival. Multi‐omics profiling reveals that PDIA6 drives lipid metabolic reprogramming by sustaining the monounsaturated fatty acid (MUFA)–enriched neutral lipid pools required for lipid droplet homeostasis and redox balance. Mechanistically, PDIA6 directly associates with stearoyl‐CoA desaturase 1 (SCD1) through a structure‐defined interface centered on Asp44 of SCD1, thereby restricting its ubiquitin–proteasome–mediated degradation and maintaining SCD1‐dependent fatty acid desaturation. In vivo, PDIA6 knockdown suppresses tumor growth and liver metastasis, and synergistic SCD1 inhibition (CAY10566) yields efficacy superior to monotherapies. Upstream, tumor–stromal interactions may contribute to PDIA6 upregulation, as cancer‐associated fibroblast‐derived C‐X‐C motif chemokine ligand 12 (CXCL12) activated C‐X‐C chemokine receptor 4 (CXCR4)‐dependent signal transducer and activator of transcription 3 (STAT3) signaling in vitro. These findings establish the PDIA6–SCD1 axis as a targetable lipid metabolic dependency in GC and position PDIA6 as a candidate therapeutic vulnerability for precision oncology.

The present study investigated the relationship between serum Matrix metalloproteinase-3 (MMP3) levels in Primary Sjögren's syndrome (pSS) patients and disease activity, clinical parameters, and different clinical manifestations of pSS. Serum samples were obtained from 77 pSS patients and 77 healthy controls (HC). MMP3 levels were detected using a biochemical analyzer. Disease activity was assessed using the Sjögren's Syndrome Disease Activity Index (SSDAI) and the EULAR Sjögren's Syndrome Disease Activity Index (ESSDAI). Pearson correlation analysis was employed to evaluate the relationship between MMP3 levels and clinical parameters. Serum MMP3 levels in pSS patients were significantly elevated compared to HC (P < 0.0001). Serum MMP3 levels were significantly positively correlated with WBC counts (r = 0.564, P < 0.0001), neutrophil counts (r = 0.5225, P < 0.0001), and serum LDH levels (r = 0.459, P < 0.0001). Moreover, MMP3 levels were significantly positively correlated with both SSDAI scores (r = 0.407, P = 0.002) and ESSDAI scores (r = 0.3061, P = 0.0068). Serum MMP3 levels are significantly elevated in pSS patients and show significant positive correlations with both SSDAI and ESSDAI scores, as well as key inflammatory parameters (WBC, neutrophil counts, LDH). In conclusion, these consistent associations suggest the potential of serum MMP3 as a biomarker for tracking disease activity in pSS.

Background:Telomeres play a crucial role in chromosomal stability and cancer development. However, the prognostic significance of telomere-related genes (TRGs) in colon adenocarcinoma (COAD) remains unexplored. In this study, we aimed to establish a TRG-based prognostic model for COAD, explore its association with the tumor immune microenvironment and drug sensitivity, and offer new therapeutic targets. Methods:RNA sequencing (RNA‑Seq) data of COAD with corresponding patient survival data from The Cancer Genome Atlas (TCGA), and TRGs from TelNet were used. A prognostic model was created by univariate/multivariate Cox regression analyses. Meanwhile, a nomogram was created for overall survival (OS) prediction. In addition, immune microenvironment [Cell‑type Identification By Estimating Relative Subsets Of RNA Transcripts (CIBERSORT), Tumor Immune Dysfunction and Exclusion (TIDE), single‑sample Gene Set Enrichment Analysis (ssGSEA), and immune checkpoint gene analysis] and drug sensitivity [half‑maximal inhibitory concentration (IC50)] analyses were performed. Results:This identified six key TRGs (USP2, TRIM7, EPHA6, IP6K3, CALML6, and COCH) significantly associated with patient outcome. A nomogram incorporating these genes demonstrated robust predictive ability for OS, with areas under the curve (AUCs) of 0.746, 0.750, and 0.726 for 1-, 2-, and 3-year OS, respectively. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analyses revealed that these genes were involved in cancer‑related pathways. Furthermore, distinct immune infiltration patterns, characterized by significant negative correlations between risk scores and activated CD8+ T cells as well as Memory B cells, were observed between high- and low-risk patient groups. Dasatinib, docetaxel, erlotinib, and gefitinib were identified as potential therapeutic candidates for high-risk patients. Finally, the differential expression of EPHA6 between COAD and normal tissues was validated by immunohistochemical (IHC) staining and Western blotting. Conclusions:Our findings establish TRGs as critical genetic determinants and powerful predictors of COAD prognosis, offering insights into potential therapeutic targets.

Neoadjuvant chemoradiotherapy (nCRT) is standard for locally advanced rectal cancer but increases postoperative complication (POC) risks due to tissue fibrosis and immunosuppression. Existing models based on clinical parameters overlook nCRT-induced tissue changes. Radiomics and deep learning technologies have been widely applied in tumor-related predictive models in recent years, but their potential in predicting postoperative complications has not yet been fully explored. This study aimed to investigate the impact of neoadjuvant chemoradiotherapy on postoperative complications in rectal cancer patients and develop a deep learning–based predictive model integrating MRI radiomics and clinical features for early risk stratification. A retrospective, dual-center study included 695 patients, comprising 272 nCRT patients and 423 non-nCRT patients. Propensity score matching (PSM) balanced baseline covariates. Radiomics and deep learning features were extracted from preoperative MRI of the nCRT group, respectively. Six machine learning algorithms were evaluated for predictive performance. nCRT was identified as a risk factor for POC (OR 3.78, P < 0.001). The radiomics-deep learning combined model outperformed unimodal approaches, with an AUC of 0.82 in external validation. In conclusion, nCRT is a risk factor of POC in LARC patients and the multimodal deep learning model shows superior predictive accuracy, providing a clinically actionable tool for personalized perioperative management.

This study explores the changes in thrombosis-related indicators in patients with severe fever with thrombocytopenia syndrome (SFTS), providing a basis for early diagnosis, treatment, and disease monitoring. The patients were divided into mild and severe groups, as well as survivor and non-survivor groups. Forty-five healthy individuals were included as a control group. We compared the activity of thrombosis-related markers in these groups. The risk of developing severe disease and death in patients was predicted using receiver operating characteristic (ROC) curve analysis. We also examined the correlation between thrombomodulin (TM) and clinical lab parameters in the plasma of SFTS patients. Comparison among the mild, severe, and healthy control groups revealed that the levels of TM, thrombin-antithrombin complex (TAT), plasmin-antiplasmin complex (PIC), and tissue plasminogen activator-plasminogen activator inhibitor complex (t-PAIC) were significantly higher in severe patients than in the healthy control group (P < 0.05). Comparison between the survivor and non-survivor groups showed that the levels of TM, TAT, and t-PAIC in the non-survivor group were higher than those in the survivor group, and the differences were statistically significant (P < 0.05). ROC analysis showed that TM had a higher predictive ability for the risk of severe disease (area under the ROC curve [AUROC] = 0.931). Additionally, TM (AUROC = 0.817) and t-PAIC (AUROC = 0.824) had higher predictive abilities for the risk of death. TM was positively correlated with thrombin time (TT), d-dimer (D-D), creatinine (CREA), total bile acid (TBA), and c-reactive protein (CRP), and negatively correlated with cholesterol (CHOL), high density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and platelet (PLT). Monitoring thrombosis-related indicators in SFTS patients is crucial for assessing disease severity. Early symptomatic treatment can significantly reduce the rate of severe cases and prevent patient mortality.

BACKGROUND:Controlled low central venous pressure is recommended for laparoscopic hepatectomy. This study aimed to evaluate the effects of esketamine-based opioid-free (OF) anesthesia on hemodynamic stability and perioperative safety during this procedure, particularly under controlled low central venous pressure conditions. MATERIALS AND METHODS:This prospective, randomized, double-blind, controlled trial was conducted from June 2024 to February 2025 at a university hospital in Nanjing. Participants scheduled for laparoscopic hepatectomy were randomly allocated to receive either esketamine-based opioid-free anesthesia (esketamine, lidocaine, dexmedetomidine) or opioid-inclusive anesthesia (sufentanil and remifentanil). All patients underwent surgery with controlled low central venous pressure management, including restrictive fluid therapy and intermittent Pringle maneuvers. The primary outcome was the change in the mean arterial pressure within 1 minute after the first Pringle maneuver release. Secondary outcomes included mean arterial pressure variation after the final release and intraoperative vasopressor requirements. RESULTS:A total of 146 patients [age, 59.0 (54.0-65.0) years] were included in the intention-to-treat analysis. Compared with the opioid-inclusive group, patients in the opioid-free group experienced significantly smaller mean arterial pressure reductions within 1 minute after the first Pringle maneuver release [mean (standard deviation), 0.8 (6.4) mm Hg vs 12.5 (7.5) mm Hg; mean difference, 11.64 mm Hg; 95% CI, 9.37-13.92, P < 0.001], as well as milder blood pressure fluctuations after the final release. Intraoperative vasoactive drug consumption was also significantly lower in the opioid-free group. CONCLUSIONS:In patients undergoing laparoscopic hepatectomy with controlled low central venous pressure, esketamine-based OF anesthesia significantly improved intraoperative hemodynamic stability and reduced vasopressor requirements. These findings support the use of OF anesthesia as a viable alternative to opioid-inclusive strategies in enhanced recovery protocols for hepatobiliary surgery.

BACKGROUND:Severe fever with thrombocytopenia syndrome (SFTS), caused by the Dabie bandavirus, is a fatal infectious disease with no specific vaccines or antiviral treatments. Early diagnosis and severity assessment are critical for clinical management. METHODS:This study analyzed peripheral blood samples from 81 SFTS patients and healthy controls, focusing on the distribution of CD4+, CD8+, CD4+CD8+ double-positive T (DPT) cells, and CD4-CD8- double-negative T (DNT) cells. The relationship between T cell subsets, clinical parameters, viral load, and cytokine levels was examined for diagnostic and prognostic potential. RESULTS:DPT cells were lower and DNT cells higher in SFTS patients compared to controls. DNT cell proportions were higher in severe and fatal cases, correlating positively with viral load, APTT, TT, D-dimer, ferritin, and LDH, and negatively with platelet count, HDL, and fibrinogen. DNT cells were also positively correlated with IFN-α and IFN-γ levels, and higher in patients with complications like shock and sepsis. Furthermore, Cox regression analysis revealed that an elevated DNT cell proportion was an independent risk factor for poor prognosis in SFTS patients. CONCLUSION:DNT cell proportion changes are linked to SFTS severity and prognosis, suggesting DNT cells as potential biomarkers for early diagnosis and prognosis assessment.

Laparoscopic distal gastrectomy is now widely used in East Asia and worldwide with different preferences and outcomes. This study aimed to compare the short- and long-term outcomes and preferences between two high-volume gastric cancer centers in Korea and China. Patients who underwent laparoscopic-assisted distal gastrectomy (LADG) and totally laparoscopic distal gastrectomy (TLDG) for gastric cancer from Seoul National University Hospital (SNUH) and the First Affiliated Hospital of Nanjing Medical University (NMUH) from 2017 to 2020 were enrolled in this study. A total of 1166 SNUH cases and 847 NMUH cases enrolled in this study. The overall complication rate of SNUH (14.49

BACKGROUND:Non-alcoholic fatty liver disease (NAFLD) is increasingly recognized for its role in the pathogenesis of various cancers. However, its impact on gastric cancer (GC) outcomes, particularly in patients undergoing laparoscopic distal gastrectomy (LDG), remains unclear. AIM:To investigate the clinical and prognostic impacts of NAFLD on GC patients undergoing LDG. METHODS:In this retrospective cohort study, we collected clinical data from 1122 GC patients who underwent LDG at the Gastric Cancer Center of the First Affiliated Hospital of Nanjing Medical University between January 2020 and December 2022. Propensity score-matching (PSM) was used to mitigate the bias to compare the oncological and surgical outcomes between the two groups. Survival analysis was also performed to evaluate NAFLD as a prognostic factor. RESULTS:PSM yielded a balanced cohort of 260 patients (52 with NAFLD and 208 controls) from the original cohort. No differences in clinicopathological characteristics, including surgery time, complications, T stage, N stage, p-tumor-node-metastasis stage, neural invasion, vascular invasion, total number of retrieved lymph nodes, positive retrieved lymph nodes and positive lymph nodes rate, were observed between the two groups. Overall survival was comparable between two groups (Log-rank P = 0.49), whereas progression-free survival (PFS) in the NAFLD group was inferior to that in the control group (Log-rank P = 0.016). Univariable Cox regression analysis further confirmed that NAFLD was an unfavorable prognostic factor for PFS. CONCLUSION:GC patients with NAFLD exhibited inferior PFS, suggesting that addressing NAFLD-related metabolic alterations may enhance clinical outcomes. Future investigations should explore the mechanistic links between NAFLD and GC progression and consider integrated therapeutic strategies.

Background: Chemoresistance severely deteriorates the prognosis of advanced gastric cancer (GC) patients. Several studies demonstrated that H. pylori (HP)-positive GC patients showed better outcomes after receiving chemotherapy than HP-negative ones. This study aims to confirm the role of HP in GC chemotherapy and to study the underlying mechanisms. Methods: The HP infection co-culture with GC cell lines were performed. The m6A-seq and NGS were used for bioinformatic analysis. Western Blot, qRT-PCR and IHC were adopted for expressions of METTL3, BRD2 and YTHDF2. The ATPGlow, flow cytometry and IF were used to detect the cell viability, DNA damage, apoptosis and pyroptosis. Luciferase reporter assay and CHIP were applied to explore the mechanisms. Results: The HP infection sensitized GC cells to 5-FU and induced expressions of METTL3 and YTHDF2. The HP infection promoted transcription of METTL3 through NF-kappa B pathway, therefore promoting the m6A modification level. METTL3 induced the m6A modification of BRD2 while YTHDF2 promoted the decay of mRNA of BRD2, both of which could promote the apoptosis and pyroptosis induced by 5-FU. In addition, BRD2 regulated the transcription of FLIP by importing FOXO4 into nucleus, thereby inhibiting the activation of Caspase-8, which was considered as the molecular switch of both apoptosis and pyroptosis. Conclusions: HP-induced m6A methylation could sensitize gastric cancers to 5-FU with activation of caspase-8 and induced apoptosis and pyroptosis. The Methylated BRD2 activated by NF-kappa B pathway regulates Caspase-8 by binding to FLIP-promoter FOXO4. This study provides new sights to the HP-positive gastric cancer chemotherapy.

Elevated expression of Aiolos family zinc finger 3 (IKZF3), a transcription factor crucial for lymphocyte maturation, is observed in hematological cancers. However, its role in gastric cancer (GC) remains unclear. We detect the increased IKZF3 levels in GC tissues using immunohistochemical, qRT-PCR and western blot analysis. The function of IKZF3 in GC cells is further studied through CCK-8, Transwell, colony formation, scratch wound healing, and flow cytometry assays. IKZF3 overexpression significantly promotes GC cell invasion, migration, and proliferation, whereas IKZF3 knockdown induces cell cycle arrest at the G1/S phase. Flow cytometry confirms these alterations in cell cycle dynamics. Using the JASPAR database, we determine that IKZF3 binds to the SMO promoter region, thereby activating SMO expression. Notably, the SMO inhibitor SANT-1 effectively reverses IKZF3-mediated effects. Furthermore, IKZF3 promotes GC tumor growth in xenograft models. Our findings highlight the pivotal role of IKZF3 in GC progression by modulating SMO expression and activating the Hedgehog signaling pathway. Therapeutically, targeting IKZF3 with SANT-1 is promising for mitigating GC proliferation and invasion. This study provides insights into potential therapeutic approaches targeting IKZF3 for GC treatment.

Helicobacter pylori (H. pylori) is carcinogenic and has the potential to cause progressive gastric lesions and gastric cancer (GC), which also represents one of the essential constituents of the tumor microenvironment (TME) of GC. The infiltration and functional status of tumor-infiltrating lymphocytes (TILs) in the TME affect the anti-tumor function of the body. However, the impact of H. pylori on anti-tumor immunity and prognosis of GC is still unclear. In this study, we constructed a tissue microarray (TMA) consisting of GC tissues from patients with or without H. pylori infection. We evaluated the status of TILs and the expression of CD3, CD8 and PD-L1 by Hematoxylin-eosin (H E) staining and immunohistochemical (IHC) staining, respectively. Correlation, Cox regression, and survival analyses were performed. We found that TIL, CD3, and CD8 were negatively correlated with H. pylori infection. In addition, TILhigh and CD8+TILs status were positively associated with better survival. Simultaneously, patients with H. pylori-positive status had decreased survival compared to those in the H. pylori-negative group. Our study supports the hypothesis that H. pylori infection was positively correlated with less TILs and CD8+TILs, which may contribute to anti-tumor immune escape, thus lead to a poor prognosis of GC.

Background: The short-term and long-term outcomes of laparoscopic-assisted distal gastrectomy (LADG) and totally laparoscopic distal gastrectomy (TLDG) have been subject to controversy with various reconstruction techniques of Billroth-I, Billroth-II, Roux-en-Y, and Uncut. This study aims to compare the short-term and long-term outcomes of LADG and TLDG as well as the outcomes of different anastomoses. Methods: This study enrolled patients with gastric cancer at the First Affiliated Hospital of Nanjing Medical University (NMUH) between 2017 and 2021. Postoperative complications were classified according to the Clavien-Dindo grade. Exclusion criteria included metachronous and synchronous malignancy and palliative surgery. The Kaplan-Meier analysis was applied to assess 5-year prognosis between two groups. Results: This study included 1221 cases with an overall complication rate of 17.37% for LADG, which was significantly higher than TLDG's 10.72%. The incidence of anastomosis-related complications was 4.79% for LADG and 1.13% lower for TLDG. LADG and TLDG did not show significant difference for Grade III-V complications and resected lymph nodes. The postoperative stay was shorter for TLDG than LADG, and R-Y had a longer postoperative stay than B-II and Uncut after combining LADG and TLDG. The operation time was shorter in TLDG cases than that in LADG cases. The 5-year OS of the TLDG group was not significantly better than that of the LADG group. Conclusion: TLDG is superior in overall complication rate, anastomosis-related complication rate, postoperative stay and operation time to LADG. No difference of OS was observed between LADG and TLDG. Four anastomoses had no convincing evidence of being superior in complications rates, post-op stay, and harvested lymph nodes to each other.

BackgroundHoylesella marshii can be isolated from human oral cavities affected by dental pulp and periodontal infections, as well as from the dental plaque of healthy individuals, making it a common bacterium within the oral microbiota. However, its role in causing pleural infections in humans is rare.Case presentationA case of purulent pleural effusion occurred shortly after discharge in an elderly patient who had undergone surgery for gastric cancer. The infection was identified as being caused by an obligate anaerobe through laboratory culture, and was further identified as Hoylesella marshii causing pleural infection through 16 S rRNA gene sequence analysis. Susceptibility testing guided precise treatment with cefoperazone-sulbactam and metronidazole. The patient's clinical symptoms improved rapidly, laboratory test indicators gradually returned to normal, and the patient ultimately recovered.ConclusionHoylesella marshii can cause pleural infections in humans. Clinical microbiology laboratories should pay special attention to the cultivation of obligate anaerobes when routine aerobic cultures do not show bacterial growth but bacteria are visible on smear staining, and when conventional identification methods fail to identify the bacterium, analysis based on the highly conserved 16 S rRNA gene sequence can accurately and specifically identify the bacterium, guiding clinicians in formulating precise anti-infection strategies.

Gastric cancer (GC) ranks as the fifth most common cancer and the fourth leading cause of cancer-related deaths globally. Despite advancements in molecular profiling, the mechanisms driving GC proliferation and metastasis remain unclear. This study identifies Early 2 Factor 4 (E2F4) as a key transcription factor that promotes GC cell proliferation, migration, and invasion by upregulating DNA Replication and Sister Chromatid Cohesion 1 (DSCC1) expression. Bioinformatics and transcription factor analyses revealed E2F4 as a significant regulator of DSCC1. Functional assays confirmed E2F4's role in enhancing GC cell malignancy in vitro and in vivo. Knockdown and overexpression experiments demonstrated that E2F4 positively regulates DSCC1 at the transcriptional level, with ChIP-qPCR and dual luciferase reporter assays validating the binding sites on the DSCC1 promoter. These findings highlight the E2F4-DSCC1 axis as a potential therapeutic target to mitigate GC progression.

Background: Gastric cancer (GC) continues to be one of the leading causes of cancer-related deaths globally. Diet significantly influences the incidence and progression of GC. However, the relationship between dietary intake and GC is inconsistent.Methods: A study was conducted with adults who participated in the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2016 to investigate possible associations between 32 dietary factors and GC. To further detect potential causal relationships between these dietary factors and the risk of GC, a two-sample Mendelian randomization (MR) analysis was conducted. The primary method employed was the inverse variance weighted (IVW) analysis, and its results were further validated by four other methods.Results: Of the 35,098 participants surveyed, 20 had a history of GC. Based on the results of weighted logistic multivariate analysis, it was observed that there was a positive correlation between total fat intake [odds ratio (OR) = 1.09, 95% confidence interval (CI): (1.01–1.17), p = 0.03] and GC as well as negative association of dietary monounsaturated fatty acids (MUFAs) intake [OR = 0.83, 95% CI: (0.76–0.92), p < 0.001]. Further evaluations of the odds of GC across the quartiles of dietary MUFAs showed that the top quartile of total MUFA intake was associated with a lower likelihood of GC in three different models [model1: OR = 0.03, 95% CI: (0.00–0.25), p < 0.01; model2: OR = 0.04, 95% CI: (0.00–0.38), p = 0.01; model3: OR = 0.04, 95% CI: (0.00–0.40), p = 0.01]. For the MR analyses, genetic instruments were selected from the IEU Open GWAS project; IVW analysis showed that GC risk was not associated with MUFAs [OR = 0.82, 95% CI: (0.59–1.14), p = 0.23] or the ratio of MUFAs to total fatty acids [OR = 1.00, 95% CI: (0.75–1.35), p = 0.98]. Similar results were observed when using the other MR methods.Conclusion: The NHANES study revealed that consuming MUFAs was linked to a lower risk of GC, although the results of MR analyses do not provide evidence of a causal relationship. Additional research is therefore necessary to clarify these findings.