Objective·To investigate the bidirectional causal relationships between celiac disease(CeD)and Hashimoto thyroiditis(HT)as well as Graves disease(GD),using a two-sample Mendelian randomization(MR)approach.Methods·Single nucleotide polymorphisms(SNPs)related to CeD,HT and GD were extracted from publicly available Genome-Wide Association Studies(GWAS)databases and used as instrumental variables.The inverse-variance weighted(IVW)method served as the primary analytical approach,supplemented by MR-Egger,weighted median(WME)and weighted mode(WMO)methods,to evaluate the causal associations between CeD and both HT and GD.Replication analyses using alternative GWAS datasets were conducted to validate the robustness of the results.Heterogeneity was assessed using Cochran's Q test,and pleiotropy was evaluated via MR-Egger intercept test.Leave-one-out analyses were performed to assess the impact of individual SNPs on the results.Results·The IVW analysis results indicated that genetically predicted CeD significantly increased the risk of HT[discovery group:OR=1.186(95%CI 1.114?1.262),P<0.001;replication group:OR=1.218(95%CI 1.090?1.361),P<0.001]and GD[discovery group:OR=1.214(95%CI 1.155?1.276),P<0.001;replication group:OR=1.273(95%CI 1.161?1.396),P<0.001].However,reverse MR analyses did not provide evidence for a causal relationship between HT and CeD,while genetically predicted GD significantly increased the risk of CeD[discovery group:OR=1.259(95%CI 1.006?1.576),P=0.044;replication group:OR=1.387(95%CI 1.233?1.560),P<0.001].Sensitivity analyses suggested that the results were not influenced by horizontal pleiotropy.Conclusion·CeD may be causally associated with a higher risk of HT and GD,while GD may increase the risk of developing CeD.HT does not appear to have an impact on CeD.

Objective:To investigate the anatomical feasibility of the endoscopic transorbital approach (ETOA) to the orbital apex and lateral middle cranial fossa, to identify stable and recognizable surgical landmarks under endoscopic visualization, and to provide morphometric data for preoperative planning and intraoperative navigation.Methods:Stepwise anatomical dissection was performed on five formalin-fixed cadaveric heads and one fresh arterially injected cadaveric specimen to simulate the ETOA using a 0° endoscope. Key structures and their anatomical relationships were observed and recorded. Additionally, high-resolution CT scans of 50 adults were retrospectively analyzed. Three-dimensional reconstructions and measurements were performed using Mimics 17.0 software. Spatial validation was performed using 17 dry skulls to verify the consistency and reliability of osseous anatomical landmarks.Results:Cadaveric dissection identified the meningo-orbital band, superior orbital fissure, optic canal, foramen rotundum, and foramen ovale as reliable surgical landmarks for the ETOA. A topographic map of the surgical region was established based on the endoscopic view. CT measurements revealed the following distances (Mean±SD): the midpoint of the supraorbital rim to the foramen rotundum (57.31±3.59) mm and foramen ovale (71.46±3.42) mm; the lateral orbital rim to the lateral edge of the superior orbital fissure (37.38±2.52) mm; the distance from the superior orbital fissure to the optic canal (9.98±1.49) mm; and the distance from the anterior ethmoidal artery to the optic canal (19.98±2.05) mm. These measurements were consistent with dry skull data, indicating that these osseous landmarks had stable spatial relationships and were suitable for intraoperative localization.Conclusions:The ETOA provides favorable anatomical accessibility and clinical feasibility for lesions involving the orbital apex and lateral skull base. Key osseous structures demonstrate high identifiability and stable spatial relationships, serving as critical references for intraoperative navigation and preoperative pathway planning. The quantitative anatomical framework established in this study provides critical morphometric support for minimally invasive surgery targeting lesions in this region.

As a key member of the insulin-like growth factor family， insulin-like growth factor-‍Ⅰ （IGF-‍Ⅰ） is mainly synthesized in the liver and is widely distributed in the human body， and it is involved in the physiological processes such as cell proliferation， differentiation， metabolism， and apoptosis. Studies have shown that the level of IGF-‍Ⅰ is negatively correlated with the severity of liver cirrhosis， and IGF-‍Ⅰ mainly affects the progression of liver cirrhosis by inhibiting liver fibrosis， promoting DNA damage repair， and regulating lipid metabolism. Monitoring of IGF-‍Ⅰ level is expected to provide an evaluation indicator for improving the prognosis of patients with liver cirrhosis， and stimulating the action pathway of IGF-‍Ⅰ or regulating its expression level may become a new method for the treatment of liver cirrhosis. This article reviews the research advances in IGF-‍Ⅰ in liver cirrhosis， in order to provide new ideas for the diagnosis and treatment of liver cirrhosis.

Esophageal cancer cases in China account for more than 50% of the world, among which approximately 90% are histological subtypes of esophageal squamous cell carcinoma. Over 50% of esophageal cancer patients are initially diagnosed at locally advanced or advanced stages. The R0 resection rate with surgical treatment alone is relatively low, and local recurrence and distant metastasis are prone to occur, resulting in a low 5-year survival rate. Recent research has focused on neoadjuvant therapy for esophageal cancer, but the most effective form of such therapy remains undetermined. Immunotherapy is currently the most active research field in tumor treatment. Further exploration of the treatment model combing immunotherapy with neoadjuvant chemotherapy or chemoradiotherapy is expected to improve the therapeutic effect and survival benefit in patients with locally advanced resectable esophageal squamous cell carcinoma.

Objective·To investigate the bidirectional causal relationships between celiac disease(CeD)and Hashimoto thyroiditis(HT)as well as Graves disease(GD),using a two-sample Mendelian randomization(MR)approach.Methods·Single nucleotide polymorphisms(SNPs)related to CeD,HT and GD were extracted from publicly available Genome-Wide Association Studies(GWAS)databases and used as instrumental variables.The inverse-variance weighted(IVW)method served as the primary analytical approach,supplemented by MR-Egger,weighted median(WME)and weighted mode(WMO)methods,to evaluate the causal associations between CeD and both HT and GD.Replication analyses using alternative GWAS datasets were conducted to validate the robustness of the results.Heterogeneity was assessed using Cochran's Q test,and pleiotropy was evaluated via MR-Egger intercept test.Leave-one-out analyses were performed to assess the impact of individual SNPs on the results.Results·The IVW analysis results indicated that genetically predicted CeD significantly increased the risk of HT[discovery group:OR=1.186(95%CI 1.114?1.262),P<0.001;replication group:OR=1.218(95%CI 1.090?1.361),P<0.001]and GD[discovery group:OR=1.214(95%CI 1.155?1.276),P<0.001;replication group:OR=1.273(95%CI 1.161?1.396),P<0.001].However,reverse MR analyses did not provide evidence for a causal relationship between HT and CeD,while genetically predicted GD significantly increased the risk of CeD[discovery group:OR=1.259(95%CI 1.006?1.576),P=0.044;replication group:OR=1.387(95%CI 1.233?1.560),P<0.001].Sensitivity analyses suggested that the results were not influenced by horizontal pleiotropy.Conclusion·CeD may be causally associated with a higher risk of HT and GD,while GD may increase the risk of developing CeD.HT does not appear to have an impact on CeD.

Objective:To investigate the anatomical feasibility of the endoscopic transorbital approach (ETOA) to the orbital apex and lateral middle cranial fossa, to identify stable and recognizable surgical landmarks under endoscopic visualization, and to provide morphometric data for preoperative planning and intraoperative navigation.Methods:Stepwise anatomical dissection was performed on five formalin-fixed cadaveric heads and one fresh arterially injected cadaveric specimen to simulate the ETOA using a 0° endoscope. Key structures and their anatomical relationships were observed and recorded. Additionally, high-resolution CT scans of 50 adults were retrospectively analyzed. Three-dimensional reconstructions and measurements were performed using Mimics 17.0 software. Spatial validation was performed using 17 dry skulls to verify the consistency and reliability of osseous anatomical landmarks.Results:Cadaveric dissection identified the meningo-orbital band, superior orbital fissure, optic canal, foramen rotundum, and foramen ovale as reliable surgical landmarks for the ETOA. A topographic map of the surgical region was established based on the endoscopic view. CT measurements revealed the following distances (Mean±SD): the midpoint of the supraorbital rim to the foramen rotundum (57.31±3.59) mm and foramen ovale (71.46±3.42) mm; the lateral orbital rim to the lateral edge of the superior orbital fissure (37.38±2.52) mm; the distance from the superior orbital fissure to the optic canal (9.98±1.49) mm; and the distance from the anterior ethmoidal artery to the optic canal (19.98±2.05) mm. These measurements were consistent with dry skull data, indicating that these osseous landmarks had stable spatial relationships and were suitable for intraoperative localization.Conclusions:The ETOA provides favorable anatomical accessibility and clinical feasibility for lesions involving the orbital apex and lateral skull base. Key osseous structures demonstrate high identifiability and stable spatial relationships, serving as critical references for intraoperative navigation and preoperative pathway planning. The quantitative anatomical framework established in this study provides critical morphometric support for minimally invasive surgery targeting lesions in this region.

In recent years, numerous studies have elucidated the correlation between DNA methylation and gastric cancer (GC) from the perspectives of early diagnosis, targeted therapy, and prognosis assessment. However, the clinical understanding of their relationship remains incomplete and insufficiently explored. This review will summarize the research progress on the role of DNA methylation in GC, focusing on methylation biomarkers currently approved for GC detection, DNA methylation-based diagnostic markers utilizing liquid biopsy techniques, as well as the relationship between DNA methylation and GC treatment and prognosis. The aim is to provide further insights for the clinical diagnosis and treatment of GC.

  Objective  To establish a model that can predict the occurrence of acute kidney disease (AKD) in liver cirrhotic patients and evaluate its performance.  Methods  Liver cirrhotic patients who hospitalized in the department of gastroenterology of the First Hospital of Lanzhou University from January 2017 to January 2022 were retrospectively included. They were divided into AKD and non-AKD groups according to whether they were combined with AKD during hospitalization, and were randomized into training and validation sets in a 7∶3 ratio. The clinical data of patients in the two groups were collected, and LASSO regression and multifactorial Logistic regression were used to screen the influencing factors for the occurrence of AKD in patients with liver cirrhosis and to establish a prediction model. The model was then evaluated by using the receiver operating characteristic curve, the calibration curve and the clinical decision curve.  Results  A total of 796 cases of liver cirrhotic patients who met the inclusion and exclusion criteria were enrolled. Among them, 103 cases were in the AKD group and 693 cases were in the non-AKD group; 561 cases were in the training set and 235 cases were in the validation set. The results of LASSO regression and multifactorial Logistic regression showed that a history of diabetes (OR=2.922, 95% CI: 1.290-6.564, P=0.009), hepatic encephalopathy (OR=6.210, 95% CI: 2.278-17.479, P < 0.001), gastrointestinal bleeding (OR=2.501, 95% CI: 1.236-5.073, P=0.011), ascites (OR=3.219, 95% CI: 1.664-6.539, P < 0.001), male (OR=0.477, 95% CI: 0.254-0.879, P=0.019), hemoglobin (OR=0.987, 95% CI: 0.975-0.999, P=0.044), albumin (OR=0.952, 95% CI: 0.911-0.991, P=0.023), and prothrombin time (OR=0.865, 95% CI: 0.779-0.920, P < 0.001) were the independent influences on the occurrence of AKD in liver cirrhotic patients, and were used to construct a prediction model. The area under the curve of the model in the training set and validation set for predicting the occurrence of AKD in liver cirrhotic patients was 0.895 (95% CI: 0.865-0.925) and 0.869 (95% CI: 0.807-0.930), respectively. The calibration curves showed that the model had good fit and consistency and the clinical decision curves showed that the use of the model for predicting the risk of AKD could benefit liver cirrhotic patients overall.  Conclusions  A prediction model for the occurrence of AKD in liver cirrhotic patients was established based on eight influencing factors, including gender, history of diabetes, and hepatic encephalopathy. It was validated to have good discrimination, calibration, and clinical utility, and is expected to assist in the clinical early screening and identification of liver cirrhosis-associated AKD.

Hepatocellular carcinoma is one of the common causes of tumor-related death, and it has high morbidity and mortality rates in China. Recent studies have shown that platelets are closely associated with the development of hepatocellular carcinoma. Literature review shows that platelets not only participate in hemostasis, but also act on liver cells and tumor microenvironment, promote the formation of new blood vessels, and participate in the development and progression of hepatocellular carcinoma as a cell mediator through immune response and other pathways. In addition, platelets and their derivatives can be used as potential therapeutic targets for hepatocellular carcinoma. Therefore, antiplatelet therapy is expected to become a new adjuvant strategy for the treatment of hepatocellular carcinoma, which has important clinical significance.

Steroid-induced avascular necrosis of the femoral head (SANFH) is the death of the femoral head caused by long-term use of glucocorticoid (GC). Its pathological manifestations are mainly trabecular bone collapse and increased empty bone lacunas, osteocyte apoptosis rate and autophagy rate. Its pathogenesis is complicated, and the exact pathogenesis is still unclear. MicroRNAs (miRNAs) are a group of endogenous, non-coding small RNAs with an average length of 23 nucleotides. They are responsible for negatively regulating gene expression after transcription by inhibiting target messenger RNAs (mRNAs). MiRNAs play an important role in physiological processes, including cell development, proliferation, differentiation, metabolism, migration and apoptosis. According to bioinformatics analysis, MiRNAs play an important role in regulating gene expression, and it is estimated that more than one-third of human genes are regulated by them. In the past few years, more and more miRNAs have been found to be related to osteonecrosis, such as regulating the proliferation and differentiation of mesenchymal stem cells and osteoblasts. This article aims to review the relationship between steroid-induced femoral head necrosis and miRNAs.