Purpose: Lung cancer is frequently observed as a second primary malignancy following gastric cancer, yet the genetic causality between them remains uncertain. This study aims to evaluate the causal relationship between gastric and lung cancers using Mendelian randomization (MR) analysis. Materials and Methods: Single nucleotide polymorphisms associated with gastric and lung cancers were selected from genome-wide association study in East Asian and European populations as instrumental variables. The causal effects between gastric and lung cancers were evaluated using univariable and multivariable MR analysis, with the inverse variance weighted (IVW) method serving as the primary criterion. Heterogeneity and sensitivity analyses were performed to ensure the robustness of the findings. Results: Univariable MR analysis demonstrated that genetic susceptibility to gastric cancer in the European population was significantly associated with an increased risk of lung cancer (IVW: odds ratio [OR], 1.285; 95% confidence interval [CI], 1.072 to 1.541; p=6.83E-03), which was consistently validated in the East Asian population (IVW: OR, 1.356; 95% CI, 1.114 to 1.651; p=2.40E-03). Multivariable MR analysis further indicated that the significant positive causal relationship between gastric cancer and lung cancer persisted in both populations after adjusting for confounding factors (all p < 0.05). Conversely, no significant causal relationship was observed for the risk of developing gastric cancer following the diagnosis of lung cancer in either population (p > 0.05). Conclusion This study confirms that genetic susceptibility to gastric cancer increases the risk of lung cancer. This finding provides a theoretical basis for exploring the underlying biological mechanisms and suggests that enhancing lung cancer screening in patients with gastric cancer may be necessary to improve patient prognosis.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Dendritic cells （DCs）， as key regulatory cells in the immune system， play a significant role in the pathogenesis of autoimmune diseases. This article reviews the mechanism of action of DCs and related research advances in autoimmune liver diseases （including autoimmune hepatitis， primary biliary cholangitis， and primary sclerosing cholangitis） and autoimmune pancreatitis. By summarizing the functions and heterogeneity of DCs in these diseases， this article reveals the crucial role of DCs in the imbalance of immune tolerance and chronic inflammation. Related research findings provide an important basis for a deep understanding of the role of DCs in autoimmune liver diseases and autoimmune pancreatitis and lay a foundation for the development of precise treatment strategies.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Objective With the development of manned space missions to the moon and space exploration,extravehicular activities become more frequent and extravehicular mission become more complex,which puts forward higher requirements for the extravehicular spacesuit.In order to ensure the ergonomics of spacesuit,the flexible joints are usually adopted in the limbs of spacesuit.The structural design of large angle of movement and low resistance joints is the basic for ensuring the ergonomics of spacesuit.Methods This study established a method of spacesuit joint structure to analysis the motion characteristic of typical joints.Firstly,the structure and activity characteristics of the spacesuit and lunar space suits were comprehensively analyzed,and the activity characteristics of different typical structure are qualitatively analyzed based on existing empirical method.Then,the dynamics of typical structure was analyzed by finite element model.By studying the change trend of motion of spacesuit joint with motion angle,and the motion characteristic curve was obtained.Finally,the model was studied according to different structural size parameters.The influence of structural parameters on the motion characteristics was analyzed,and the curves was obtained to provide a basis for design of spacesuit motion joint structure.Results Through the above analysis,the motion characteristics of different typical structure are obtained qualitatively.And the influence of different structure parameters on the motion characteristics was analyzed.This establishes the method basis for structure design.Conclusion The study was carried out a method based on finite element model for joint motion analysis,which is suitable for the design of typical joint structure of spacesuit.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Objective:To investigate the clinical and endoscopic characteristics of patients with autoimmune gastritis (AIG).Methods:From January 1, 2013 to December 31, 2023, 73 AIG patients who visited Peking Union Medical College Hospital were retrospectively enrolled. The clinical data of all the patients were analyzed, including gender, age, symptoms, laboratory examination results (such as serum hemoglobin, vitamin B 12, serum iron, gastrin, anti-parietal cell antibody (APCA), anti-intrinsic factor antibody (AIFA), Helicobacter pylori ( HP) infection status; the indicators were judged based on the normal reference value), and endoscopic and histopathological examination results. Descriptive statistical methods were used for statistical analysis. Results:Among the 73 AIG patients, there were 27 males (37.0%) and 46 females (63.0%), with a median age of 57 years old (ranged from 25 to 85 years old). Among the 73 AIG patients, 68 patients received APCA test, with a positivity rate of 88.2% (60/68); 67 patients took the AIFA test, with a positivity rate of 52.2%(35/67); 62 patients underwent both APCA and AIFA tests, of which 22 patients (35.5%) showed double positive. Serum level of vitamin B 12 was detected in 59 patients, and decreased in 27 cases (median level: 0.100 ng/L, mean level: 0.102 ng/L). Gastrin level was detected in 58 patients, and increased in 55 cases (median level: 0.930 ng/L, mean level: 1.203 ng/L). The levels of serum iron and ferritin were tested in 52 patients, the level of serum iron of 5 cases decreased, and the level of ferritin of 17 cases decreased (median level: 780.0 and 26.0 μg/L, mean level: 807.8 and 76.0 ng/L, respectively).Among the 73 AIG patients, the urea breath test was performed in 12 patients, and the result was positive in 6 cases. Endoscopic rapid urease test was performed in 69 patients, and the result was positive in 11 cases (15.9%). Regular blood analysis was performed in 71 patients, 24 cases (33.8%) were diagnosed with anemia, the median age of patients with anemia was 55 years old, and male-to-female ratio was 1∶5. There were 6 cases of iron-deficiency anemia and 5 cases of pernicious anemia. The endoscopic examination results of 73 patients indicated that 65 cases (89.0%) with mucosal atrophy under endoscopy, including 47 cases (64.4%) with mucosal atrophy in the gastric fundus and body, and 18 cases (24.7%) with whole gastric atrophy, more obviously in the gastric body. The pathological examination results showed type Ⅰ gastric neuroendocrine tumor(g-NET) in 35 cases (47.9%). Conclusions:The early clinical symptoms of AIG patients are nonspecific, often present with anemia and vitamin B 12 deficiency. Close monitoring of serological markers including APCA, AIFA and gastrin is essential. For patients diagnosed or suspected with AIG, intervals of endoscopic surveillance should be shortened to prevent the genesis and development of neoplasms such as g-NET.

BACKGROUND:Cognitive impairment is the most common complication after stroke,and its severity is closely related to the patient's prognosis.The prognosis of patients can be significantly improved if the severity of their cognitive impairment is recognized and targeted early.OBJECTIVE:To initially explore potential biomarkers affecting the progression of post-stroke cognitive impairment,thereby providing a richer and unique reference for the study of their pathophysiological mechanisms.METHODS:Using ultra performance liquid chromatography-mass spectrometry,non-targeted metabolomics analysis was conducted on serum samples from patients with mild and moderate post-stroke cognitive impairment to identify differential metabolites between the two groups.To further validate the diagnostic efficacy of the differential metabolites,the receiver operating characteristic curve analysis was used to evaluate their accuracy and sensitivity in distinguishing disease severity.In addition,pathway analysis was conducted on the differential metabolites.RESULTS AND CONCLUSION:(1)There were significant differences in metabolic profiles between patients with mild and moderate post-stroke cognitive impairment,and 9 differential metabolites were screened by the receiver operating characteristic curve.(2)Differential metabolite pathway analysis revealed that the metabolic pathways affecting disease progression in patients with mild-to-moderate post-stroke cognitive impairment included tryptophan metabolism,D-amino acid metabolism,biotin metabolism,retinol metabolism,aminoacyl-tRNA biosynthesis,lysine degradation,protein digestion and uptake,pyrimidine metabolism,cysteine and methionine metabolism,ABC transporter proteins,amino acid biosynthesis,and 2-oxocarboxylic acid metabolism.To conclude,9 potential biomarkers affecting disease progression in patients with mild-to-moderate post-stroke cognitive impairment have been identified,involving 12 metabolic pathways including tryptophan metabolism,D-amino acid metabolism and retinol metabolism.