Role of CENPF and NDC80 in the rehabilitation nursing of hepatocellular carcinoma and cirrhosis: An observational study.

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors globally and often develops on the foundation of chronic liver disease or cirrhosis. Cirrhosis is a clinically prevalent chronic progressive liver disease characterized by diffuse liver damage resulting from long-term or repeated actions of 1 or more etiological factors. However, the impact of CENPF and nuclear division cycle 80 (NDC80) genes on rehabilitation nursing of HCC and cirrhosis remains unclear. HCC and cirrhosis datasets GSE63898 and GSE89377 profile files were downloaded from the gene expression omnibus database generated on platforms GPL13667 and GPL6947, respectively. Differentially expressed genes (DEGs) screening, weighted gene co-expression network analysis (WGCNA), construction and analysis of protein-protein interaction (PPI) networks, functional enrichment analysis, gene set enrichment analysis (GSEA), survival analysis, immune infiltration analysis, and comparative toxicogenomics database (CTD) analysis were conducted. Gene expression heatmaps were plotted. miRNAs regulating central DEGs were selected through TargetScan. A total of 626 DEGs were identified. According to gene ontology (GO) analysis, they were primarily enriched in small molecule metabolic processes, drug metabolic processes, binding of identical proteins, and lipid metabolic processes. Kyoto Encyclopedia of Gene and Genome (KEGG) analysis results indicated that the target genes were mainly enriched in metabolic pathways, phagosomes, glycine, serine, and threonine metabolism. The construction and analysis of the PPI network revealed 3 core genes (NDC80, CENPF, RRM2). Gene expression heatmaps showed that core genes (CENPF, NDC80) were highly expressed in HCC and cirrhosis samples. CTD analysis found that 2 genes (CENPF and NDC80) were associated with liver, jaundice, ascites, fever, dyspepsia, and hepatic encephalopathy. CENPF and NDC80 are highly expressed in HCC and cirrhosis, and CENPF and NDC80 might be the biomarkers of rehabilitation nursing of HCC and cirrhosis.

MYC and NCAPG2 as molecular targets of colorectal cancer and gastric cancer in nursing.

Colorectal cancer is a common malignant tumor in intestinal tract, the early symptoms are not obvious. Gastric cancer is a malignant tumor originating from the gastric mucosal epithelium. However, the role of MYC and non-SMC condensin II complex subunit G2 (NCAPG2) in colorectal cancer and gastric cancer remains unclear. The colorectal cancer datasets GSE49355 and gastric cancer datasets GSE19826 were downloaded from gene expression omnibus database. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis (WGCNA) was performed. Functional enrichment analysis, gene set enrichment analysis (GSEA) and immune infiltration analysis was performed. Construction and analysis of protein-protein interactions (PPI) network. Survival analysis and comparative toxicogenomics database (CTD) were performed. A heat map of gene expression was drawn. A total of 751 DEGs were obtained. According to the gene ontology (GO) analysis, in Biological process (BP) analysis, they are mainly enriched in cell differentiation, cartilage development, and skeletal development. In cellular component (CC) analysis, they are mainly enriched in the cytoskeleton of muscle cells and actin filaments. In molecular function (MF) analysis, they are mainly concentrated in Rho GTPase binding, DNA binding, and fibronectin binding. In Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis, they are mainly enriched in the MAPK signaling pathway, apoptosis, and cancer pathways. The soft threshold power for WGCNA analysis was set to 9, resulting in the generation of 40 modules. Ultimately, 2 core genes (MYC and NCAPG2) were identified. The heatmap of core gene expression showed high expression of MYC and NCAPG2 in colorectal cancer tissue samples and low expression in normal tissue samples, while they were core molecules in gastric cancer. Survival analysis indicated that MYC and NCAPG2 were risk factors, showing an upregulation trend with increasing risk scores. CTD analysis revealed associations of MYC and NCAPG2 with colorectal cancer, gastric cancer, inflammation, and immune system diseases. MYC and NCAPG2 are highly expressed in colorectal cancer. The higher the expression of MYC and NCAPG2, the worse the prognosis. MYC and NCAPG2 are core molecules in gastric cancer.

Mining and exploration of rehabilitation nursing targets for colorectal cancer.

BACKGROUND: There are often subtle early symptoms of colorectal cancer, a common malignancy of the intestinal tract. However, it is not yet clear how MYC and NCAPG2 are involved in colorectal cancer. METHOD: We obtained colorectal cancer datasets GSE32323 and GSE113513 from the Gene Expression Omnibus (GEO). After downloading, we identified differentially expressed genes (DEGs) and performed Weighted Gene Co-expression Network Analysis (WGCNA). We then undertook functional enrichment assay, gene set enrichment assay (GSEA) and immune infiltration assay. Protein-protein interaction (PPI) network construction and analysis were undertaken. Survival analysis and Comparative Toxicogenomics Database (CTD) analysis were conducted. A gene expression heat map was generated. We used TargetScan to identify miRNAs that are regulators of DEGs. RESULTS: 1117 DEGs were identified. Their predominant enrichment in activities like the cellular phase of the cell cycle, in cell proliferation, in nuclear and cytoplasmic localisation and in binding to protein-containing complexes was revealed by Gene Ontology (GO). When the enrichment data from GSE32323 and GSE113513 colon cancer datasets were merged, the primary enriched DEGs were linked to the cell cycle, protein complex, cell cycle control, calcium signalling and P53 signalling pathways. In particular, MYC, MAD2L1, CENPF, UBE2C, NUF2 and NCAPG2 were identified as highly expressed in colorectal cancer samples. Comparative Toxicogenomics Database (CTD) demonstrated that the core genes were implicated in the following processes: colorectal neoplasia, tumour cell transformation, inflammation and necrosis. CONCLUSIONS: High MYC and NCAPG2 expression has been observed in colorectal cancer, and increased MYC and NCAPG2 expression correlates with worse prognosis.

Overexpression of ZNF169 promotes the growth and proliferation of colorectal cancer cells via the upregulation of ANKZF1.

Colorectal cancer (CRC) is one of the most common malignancies worldwide. The 5­year survival rate of patients diagnosed with the early stages of the disease is markedly higher than that of patients in the advanced stages. Therefore, identifying novel biomarkers and drug targets for CRC is critical for clinical practice. Zinc finger protein 169 (ZNF169) is a crucial transcription factor, and its role in CRC remains to be explored. The present study aimed to investigate the clinical relevance, function and underlying mechanisms of ZNF169 in CRC growth and proliferation. The Cancer Genome Atlas (TCGA) database was utilized to analyze the clinical relevance of ZNF169 in patients with CRC. Immunohistochemical staining was performed on tissue samples from patients with CRC to detect the expression of ZNF169. The HCT­116, HT­29 and RKO cell lines were employed for in vitro experiments. The overexpression and knockdown of ZNF169 were achieved by transfecting the cells with lentivirus and small interfering RNAs, respectively. Cell Counting Kit­8, colony formation and EdU staining assays were applied to investigate the function of ZNF169 in CRC cells. Dual luciferase activity and chromatin immunoprecipitation (ChIP)­quantitative PCR (qPCR) assays were performed to identify the regulatory effects of ZNF169 on the ankyrin repeat and zinc­finger domain­containing 1 (ANKZF1; also known as ZNF744) gene. Reverse transcription­quantitative PCR and western blot analysis were performed to measure mRNA and protein expression, respectively. The analysis of TCGA data revealed a positive correlation between ZNF169 and ANKZF1, with the overexpression of ANKZF1 being associated with a poor prognosis of patients with CRC. The experimental results demonstrated that ZNF169 was expression upregulated in CRC tissue compared with that in normal colon tissue. Gain­of­function and loss­of­function experiments revealed that ZNF169 enhanced the intensity of EdU staining, promoting the growth and proliferation of CRC cells. Furthermore, the overexpression of ZNF169 potentiated the transcriptional activity of the ANKZF1 gene, while the knockdown of ZNF169 produced the opposite results. ChIP­qPCR confirmed the interaction between ZNF169 and the promoter sequence of ANKZF1. Rescue experiments revealed that ZNF169 accelerated CRC cell growth and proliferation through the upregulation of ANKZF1. Furthermore, there was a positive correlation identified between ZNF169 and ANKZF1, and upregulation of ANKZF1 expression was associated with the poor prognosis of patients with CRC. On the whole, the present study demonstrates that ZNF169 contributes to CRC malignancy by potentiating the expression of ANKZF1. Thus, the regulation of ZNF169 and/or ANKZF1 expression may represent a viable strategy for the treatment patients with CRC with a high expression of ZNF169.

Complementary biomarkers of computed tomography for diagnostic grading of gastric cancer: DSCC1 and GINS1.

OBJECTIVE: Computed tomography (CT) is an important tool for grading gastric cancer. Gastric cancer typically originates from epithelial cells of gastric mucosa. However, complementary markers for gastric cancer, relationship between DSCC1, GINS1 and gastric cancer remain unclear. METHODS: Gastric cancer data were obtained from gene expression omnibus (GEO). Differentially expressed genes (DEGs) were identified, weighted gene co-expression network analysis (WGCNA) was conducted. Protein-protein interaction (PPI) network was constructed and analyzed. Functional enrichment analysis, gene set enrichment analysis (GSEA), gene expression heatmaps, immune infiltration analysis were performed. The most relevant diseases related to core genes were identified using Comparative Toxicogenomics Database (CTD). TargetScan was used to screen miRNAs. Validation was carried out using Western blotting (WB) and reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: 1243 DEGs were identified. Gene ontology (GO) and Kyoto Encyclopedia of Gene and Genome (KEGG) analyses revealed significant enrichment in cell cycle regulation, macrophage migration control, basement membrane, extracellular regions, growth factor binding, protein complex binding, P53 signaling pathway, protein digestion and absorption, metabolic pathways. Immune infiltration analysis indicated that high expression of activated Mast cells and Neutrophils, with a strong positive correlation between them, may influence progression of gastric cancer. CTD analysis revealed associations between DSCC1, GINS1 and gastric tumors, gastrointestinal diseases, tumors, gastritis, inflammation, necrosis. WB and RT-PCR results demonstrated high expression of DSCC1 and GINS1 in gastric cancer. CONCLUSION: The expressions of DSCC1 and GINS1 are up-regulated in gastric cancer, which can be used as supplementary markers for CT diagnostic grading of gastric cancer.

Role of PAX6, TRPA1, BCL11B, MCOLN2, CUX1, EMX1 in colorectal cancer and osteosarcoma.

Colorectal cancer is a cancer that arises from the abnormal growth of cells in the colon or rectum. Osteosarcoma (OS) is a common primary bone tumor with high degree of malignancy. The configuration files for colorectal cancer dataset GSE142279 and OS datasets GSE197158 and GSE206448 were downloaded from Gene Expression Omnibus database using the platforms GPL20795, GPL20301, and GPL24676. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis (WGCNA) was performed. Construction and analysis of protein-protein interactions (PPI) network. Functional enrichment analysis, gene set enrichment analysis (GSEA) were performed. A heat map of gene expression was drawn. The Comparative Toxicogenomics Database (CTD) was used to find the diseases most associated with the core genes. TargetScan was used to screen miRNAs regulating DEGs. According to the Gene Ontology (GO) analysis, DEGs are mainly enriched in acetylcholine binding receptor activity involved in Wnt signaling pathway, cell polarity pathway, PI3K-Akt signaling pathway, receptor regulator activity, cytokine-cytokine receptor interaction, transcriptional misregulation in cancer, and inflammation-mediated regulation of tryptophan transport. In the Metascape enrichment analysis, GO enrichment items related to the regulation of Wnt signaling pathway, regulation of muscle system process, and regulation of actin filament-based movement. Eight core genes (CUX1, NES, BCL11B, PAX6, EMX1, MCOLN2, TRPA1, TRPC4) were identified. CTD showed that 4 genes (CUX1, EMX1, TRPA1, BCL11B) were associated with colorectal neoplasms, colorectal tumors, colonic diseases, multiple myeloma, OS, and inflammation. PAX6, TRPA1, BCL11B, MCOLN2, CUX1, and EMX1 are highly expressed in colorectal cancer and OS, and the higher the expression level, the worse the prognosis.

Analysis of factors related to thrombosis in patients with PICC placements.

This study aimed to investigate the conditions of patients with peripherally inserted central catheter (PICC) placements, analyze the risk factors influencing thrombosis in PICC-placed patients, and formulate more accurate and effective PICC management strategies. A total of 147 patients undergoing PICC placements were selected as the study subjects. Clinical data were collected, and the patients were divided into thrombosis and non-thrombosis groups. Detect levels of bilirubin, white blood cells, venous pressure, heparin concentration, blood flow, citric acid, and platelets. Pearson chi-square test, Spearman correlation analysis, as well as univariate and multivariate logistic regression were employed to analyze independent risk factors. Among the 147 patients with PICC placements, there were 84 males and 63 females. Thrombosis occurred in 116 cases, with an incidence rate of 78.91%. Pearson chi-square test showed a significant correlation between citric acid, blood flow, platelets and frailty (P < .001) with thrombosis formation. Spearman correlation analysis revealed a significant correlation between citric acid (ρ = -0.636, P < .001), blood flow (ρ = 0.584, P < .001), platelet count (ρ = 0.440, P < .001), frailty (ρ = -0.809, P < .001) and thrombosis in PICC placement patients. Univariate logistic regression analysis indicated a significant correlation between thrombosis formation and citric acid (OR = 0.022, 95% CI = 0.006-0.08, P < .001), blood flow (OR = 33.973, 95% CI = 9.538-121.005, P < .001), platelet count (OR = 22.065, 95% CI = 5.021-96.970, P < .001), frailty (OR = 0.003, 95% CI = 0.001-0.025, P < .001). Multivariate logistic regression analysis also showed a significant correlation between thrombosis formation and citric acid (OR = 0.013, 95% CI = 0.002-0.086, P < .001), blood flow (OR = 35.064, 95% CI = 6.385-192.561, P < .001), platelet count (OR = 4.667, 95% CI = 0.902-24.143, P < .001), frailty (OR = 0.006, 95% CI = 0.001-0.051, P < .001). However, gender (OR = 0.544, 95% CI = 0.113-2.612, P = .447), age (OR = 4.178, 95% CI = 0.859-20.317, P = .076), bilirubin (OR = 2.594, 95% CI = 0.586-11.482, P = .209), white blood cells (OR = 0.573, 95% CI = 0.108-3.029, P = .512), venous pressure (OR = 0.559, 95% CI = 0.129-2.429, P = .438), and heparin concentration (OR = 2.660, 95% CI = 0.333-21.264, P = .356) showed no significant correlation with thrombosis formation. Patients with PICC placements have a higher risk of thrombosis, citric acid, blood flow, platelet count and frailty are the main risk factors.

TYROBP as a molecular target in cholangiocarcinoma, renal cancer and abdominal aortic aneurysm.

Cholangiocarcinoma occurs when there is a malignant tumor in the bile duct system. Renal cancer originates from renal tubular epithelial cells. Abdominal aortic aneurysm (AAA) is a permanently localized dilation caused by a lesion or injury to abdominal aortic wall. However, the relationship between TYROBP and cholangiocarcinoma, renal cancer and AAA remains unclear. The profiles of cholangiocarcinoma dataset GSE107943, renal cell carcinoma dataset GSE213324, and AAA dataset GSE47472 were downloaded from the GEO database using the platforms GPL18573, GPL24676, and GPL10558. DEGs were screened, WGCNA was performed as well as construction and analysis of PPI network. Functional enrichment analysis, GSEA, heat map of gene expression, survival analysis, and immune infiltration analysis were performed. The most relevant diseases to core genes were found by CTD. The GSE107943 dataset identified 3383 DEGs for cholangiocarcinoma, GSE47472 identified 95 DEGs for abdominal aortic aneurysm, and GSE213324 identified 10245 DEGs for renal cell carcinoma. For the GSE107943 cholangiocarcinoma dataset, GO analysis revealed enrichment in immune response, cell adhesion, extracellular space, and oxidoreductase activity. KEGG analysis indicated enrichment in metabolic pathways, the PI3K-Akt signaling pathway, cell apoptosis, the cell cycle, and the NF-kappa B signaling pathway. In the GSE47472 AAA dataset, GO analysis showed enrichment in neuroblast differentiation, cardiac muscle myofilament complex, and alkaline binding. KEGG analysis indicated enrichment in mRNA surveillance pathway and purine metabolism. In the GSE213324 renal cell carcinoma dataset, GO analysis indicated enrichment in immune system processes, cell adhesion, and membrane parts. KEGG analysis showed enrichment in cytokine-cytokine receptor interaction, calcium signaling pathway, and hematopoietic cell lineage. Furthermore, for cholangiocarcinoma (GSE107943), enriched terms associated with DEGs were in metabolic pathways, cell apoptosis, and the cell cycle. For AAA (GSE47472), enriched terms were in alkaline binding and cellular redox homeostasis. For renal cell carcinoma (GSE213324), enriched terms were in biological adhesion, regulation of immune system processes, and cell surface. Common core genes (ADH6, AGXT, CYP3A43, TYROBP) were identified for cholangiocarcinoma, renal cell carcinoma, and AAA. ADH6 and TYROBP were associated with cholangiocarcinoma, AAA, renal tumors, kidney diseases, atherosclerosis, and inflammation. TYROBP is abnormally expressed in cholangiocarcinoma, renal cancer and abdominal aortic aneurysm.

Hub biomarkers in ultrasound-guided bladder cancer and osteosarcoma: Myosin light chain kinase and caldesmon.

Bladder cancer and osteosarcoma are 2 types of cancers that originate from epithelial tissues inside the bladder and bone or muscle tissues. Ultrasound-guided biopsies provide crucial support for the diagnosis and treatment of bladder cancer and osteosarcoma. However, the relationship between myosin light chain kinase (MYLK) and caldesmon (CALD1) and bladder cancer and osteosarcoma remains unclear. The bladder cancer datasets GSE65635 and GSE100926, the osteosarcoma dataset GSE39058, were obtained from gene expression omnibus. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis was performed. The construction and analysis of protein-protein interaction network, functional enrichment analysis, gene set enrichment analysis. Gene expression heat map was drawn and immune infiltration analysis was performed. The comparative toxicogenomics database analysis were performed to find disease most related to core gene. Western blotting experiments were performed. TargetScan screened miRNAs that regulated central DEGs. We obtained 54 DEGs. Functional enrichment analysis revealed significant enrichment in terms of cellular differentiation, cartilage development, skeletal development, muscle actin cytoskeleton, actin filament, Rho GTPase binding, DNA binding, fibroblast binding, MAPK signaling pathway, apoptosis, and cancer pathways. Gene set enrichment analysis indicated that DEGs were primarily enriched in terms of skeletal development, cartilage development, muscle actin cytoskeleton, MAPK signaling pathway, and apoptosis. The immune infiltration analysis showed that when T cells regulatory were highly expressed, Eosinophils exhibited a similar high expression, suggesting a strong positive correlation between T cells regulatory and Eosinophils, which might influence the disease progression in osteosarcoma. We identified 6 core genes (SRF, CTSK, MYLK, VCAN, MEF2C, CALD1). MYLK and CALD1 were significantly correlated with survival rate and exhibited lower expression in bladder cancer and osteosarcoma samples compared to normal samples. Comparative toxicogenomics database analysis results indicated associations of core genes with osteosarcoma, bladder tumors, bladder diseases, tumors, inflammation, and necrosis. The results of Western blotting showed that the expression levels of MYLK and CALD1 in bladder cancer and osteosarcoma were lower than those in normal tissues. MYLK and CALD1 likely play a role in regulating muscle contraction and smooth muscle function in bladder cancer and osteosarcoma. The lower expression of MYLK and CALD1 is associated with poorer prognosis.

The occurrence and development of vertebral osteoporosis regulated by IL-8.

Vertebral osteoporotic fracture is a common type of fracture, and the incidence is higher in the elderly. However, the relationship between vertebral osteoporotic fractures and interleukin-8 (IL-8) remains unclear. A total of 163 patients with osteoporotic vertebral fractures were recruited. Clinical and follow-up data were recorded, and the expression levels of IL1, MMP9, IL-8, and C-reactive protein in blood were measured. Pearson Chi-square test and Spearman correlation coefficient were used to analyze the relationship between vertebral osteoporotic fractures and related parameters. Univariate and multivariate logistic regression and univariate and multivariate Cox proportional hazards regression were used for further analysis. Pearson chi-square test, Spearman correlation coefficient and Logistic regression analysis showed that IL1 and IL-8 were significantly associated with vertebral osteoporotic fractures. Univariate Cox regression analysis showed that age and IL-8 expression level were significantly associated with maintenance time from recovery to recurrence of vertebral osteoporotic fractures. Multivariate Cox regression analysis showed that IL-8 expression level was significantly associated with maintenance time from recovery to recurrence of vertebral osteoporotic fractures. The higher the expression level of IL-8, the more likely it is to develop vertebral osteoporotic fracture, and the more likely it is to relapse in a short time.

The role of CD14 and CSF1R in osteoarthritis and gastritis.

Osteoarthritis (OA) is a non-inflammatory degenerative joint disease that mainly involves articular cartilage damage and involves the whole joint tissue. Gastritis is a common stomach disorder, typically referring to inflammation or lesions of the gastric mucosa. However, the relationship between CD14 and colony stimulating factor-1 receptor (CSF1R) and these 2 diseases is not yet clear. OA datasets GSE46750, GSE82107 and gastritis datasets GSE54043 profiles were downloaded from gene expression omnibus databases generated by GPL10558 and GPL570.The R package limma was used to screen differentially expressed genes (DEGs). Weighted gene co-expression network analysis was performed. The construction and analysis of protein-protein interaction network, functional enrichment analysis, gene set enrichment analysis and comparative toxicogenomics database analysis were performed. TargetScan was used to screen miRNAs regulating central DEGs. A total of 568 DEGs were identified. According to the gene ontology (GO) and biological processes analysis, they were mainly enriched in ATP metabolism negative regulation, toll-like receptor TLR1:TLR2 signaling pathway, and intracellular transport. The enrichment terms for OA and gastritis were similar to the GO and Kyoto encyclopedia of gene and genome enrichment terms of DEGs, mainly enriched in ATP metabolism negative regulation, secretion granules, transmembrane receptor protein kinase activity, cytokine-cytokine receptor interaction, Toll-like receptor signaling pathway, MAPK signaling pathway, and TGF-ß signaling pathway. In the Metascape enrichment projects, GO enrichment projects showed functions related to cell-cell receptor interaction, cell secretion, and growth. Two core genes were identified through the construction and analysis of the protein-protein interaction network. The core genes (CD14 and CSF1R) exhibited high expression in OA and gastritis samples and low expression in normal samples. Comparative toxicogenomics database analysis revealed associations between core genes (CD14 and CSF1R) and diseases such as OA, osteoporosis, gastritis, juvenile arthritis, diarrhea, and inflammation. CD14 and CSF1R are highly expressed in OA and gastritis, making them potential therapeutic targets for both diseases.

Roles of DSCC1 and GINS1 in gastric cancer.

Gastric carcinoma is a common malignant tumor originating from gastric mucosal epithelium. However, role of DS-cell cycle-dependent protein 1 (DSCC1) and GINS1 in gastric carcinoma remains unclear. The gastric carcinoma datasets GSE79973 and GSE118916 were downloaded from gene expression omnibus. Multiple datasets were merged and batched. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis was performed. Functional enrichment analysis, gene set enrichment analysis and immune infiltration analysis were performed. Construction and analysis of protein-protein interaction Network. Survival analysis and comparative toxicogenomics database were performed. A heat map of gene expression was drawn. Target Scan screen miRNAs regulating DEGs. Two thousand forty-four DEGs were identified. According to gene ontology analysis, in biological process, they were mainly enriched in cell migration, transforming growth factor ß receptor signaling pathway, angiogenesis, and steroid metabolism process. In cellular component, they were mainly enriched in extracellular vesicles, basement membrane, endoplasmic reticulum lumen, and extracellular space. In molecular function, they focused on extracellular matrix structural components, protein binding, platelet-derived growth factor binding, and catalytic activity. In Kyoto encyclopedia of genes and genomes, they were mainly enriched in protein digestion and absorption, metabolic pathways, fatty acid degradation, Glycerophospholipid metabolism, ether lipid metabolism. Gene set enrichment analysis showed that DEGs were mainly enriched in transforming growth factor ß receptor signaling pathway, steroid metabolism process, basement membrane, endoplasmic reticulum lumen, structural components of extracellular matrix, platelet-derived growth factor binding, Glycerophospholipid metabolism, ether lipid metabolism. The results of immune infiltration analysis showed that expression of T cell CD4 memory resting was lower in the samples of gastric cancer. The core genes (TRIP13, CHEK1, DSCC1, GINS1) are protective factors, their expression shows a downward trend with increase of risk score. Comparative toxicogenomics database analysis showed that TRIP13, CHEK1, DSCC1, GINS1 were related to gastric tumors, gastric diseases, tumors, inflammation, and necrosis. DSCC1 and GINS1 are highly expressed in gastric cancer. Higher expression levels of DSCC1 and GINS1, worse the prognosis.

Metabolomics analyses of cancer tissue from patients with colorectal cancer.

The alteration of metabolism is essential for the initiation and progression of numerous types of cancer, including colorectal cancer (CRC). Metabolomics has been used to study CRC. At present, the reprogramming of the metabolism in CRC remains to be fully elucidated. In the present study, comprehensive untargeted metabolomics analysis was performed on the paired CRC tissues and adjacent normal tissues from patients with CRC (n=35) using ultra­high­performance liquid chromatography­mass spectrometry. Subsequently, bioinformatic analysis was performed on the differentially expressed metabolites. The changes in these differential metabolites were compared among groups of patients based on sex, anatomical tumor location, grade of tumor differentiation and stage of disease. A total of 927 metabolites were detected in the tissue samples, and 24 metabolites in the CRC tissue were significantly different compared with the adjacent normal tissue. The present study revealed that the levels of three amino acid metabolites were increased in the CRC tissue, specifically, N­α­acetyl­Îµ­(2­propenal)­Lys, cyclo(Glu­Glu) and cyclo(Phe­Glu). The metabolites with decreased levels in the CRC tissue included quinaldic acid (also referred to as quinoline­2­carboxilic acid), 17α­ and 17ß­estradiol, which are associated with tumor suppression activities, as well as other metabolites such as, anhydro­ß­glucose, Asp­Arg, lysophosphatidylcholine, lysophosphatidylethanolamine (lysoPE), lysophosphatidylinositol, carnitine, 5'­deoxy­5'­(methylthio) adenosine, 2'­deoxyinosine­5'­monophosphate and thiamine monophosphate. There was no difference in the levels of the differential metabolites between male and female patients. The differentiation of CRC also showed no impact on the levels of the differential metabolites. The levels of lysoPE were increased in the right side of the colon compared with the left side of the colon and rectum. Analysis of the different tumor stages indicated that 2­aminobenzenesulfonic acid, P­sulfanilic acid and quinoline­4­carboxylic acid were decreased in stage I CRC tissue compared with stage II, III and IV CRC tissue. The levels of N­α­acetyl­Îµ­(2­propenal)­Lys, methylcysteine and 5'­deoxy­5'­(methylthio) adenosine varied at different stages of tumorigenesis. These differential metabolites were implicated in multiple metabolism pathways, including carbohydrate, amino acid, lipid, nucleotide and hormone. In conclusion, the present study demonstrated that CRC tumors had altered metabolites compared with normal tissue. The data from the metabolic profile of CRC tissues in the present study provided supportive evidence to understand tumorigenesis.

Effect of platelet content on occurrence and prognosis of distal radius fracture.

Fractures of the distal radius are a common fracture with an increasing incidence. However, the underlying factors for distal radius fractures (DRFs) remain unclear. A total of 123 patients with distal radial fractures were recruited. To document clinical and follow-up data, and measure the levels of white blood cells, hemoglobin, platelets, and red blood cells in the bloodstream for qualitative observation of their expression effects within the human body, specifically assessing whether the magnitudes of these indicators are associated with potential factors influencing DRF. Pearson chi-square test and Spearman correlation were used to analyze the relationship between DRF and related parameters. Univariate and multivariate logistic regression and multivariate Cox proportional risk regression were used for further analysis. Pearson chi-square test and Spearman correlation analysis showed a significant correlation between platelet and red blood cell levels and the occurrence of DRFs. Univariate logistic regression analysis demonstrated a significant correlation between platelet count (OR [odds ratio] = 6.286, 95% CI [confidence interval]: 2.862-13.808, P < .001) and red blood cell count (OR = 2.780, 95% CI: 1.322-5.843, P = .007) with DRFs. Increasing levels of both indicators were associated with a higher susceptibility to DRFs. Multivariate logistic regression showed that platelets (OR = 6.344, 95% CI: 2.709-14.855, P < .001) were significantly associated with DRFs. Multivariate Cox regression analysis showed sex (HR [hazard ratio] = 0.596, 95% CI: 0.381-0.931, P = .023) and platelet (HR = 3.721, 95% CI: 2.364-5.855, P < .001) were significantly associated with maintenance time from recovery to recurrence (MTRR) of DRFs. In other words, the platelet content in the body of different genders is different, and the MTRR of DRF is different. Platelets were significantly associated with DRFs. The higher the platelet count, the higher the risk of DRF and the shorter the time of DRF recurrence.

CD3D and CD247 are the molecular targets of septic shock.

Septic shock is a serious systemic disease with circulatory failure and abnormal cell metabolism caused by sepsis. However, the relationship between CD3D and CD247 and septic shock remains unclear. The septic shock datasets GSE33118 and GSE142255 profiles were generated from the gene expression omnibus databases GPl570, GPl17586. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis was performed. The construction and analysis of protein-protein interaction (PPI) network, functional enrichment analysis, gene set enrichment analysis (GSEA) were performed. Gene expression heat map was drawn. Immune infiltration analysis was performed. Comparative toxicogenomics database (CTD) analysis were performed to find the disease most related to the core gene. Targets can was used to screen miRNAs regulating the hub DEGs. 467 DEGs were identified. According to the gene ontology analysis, they were mainly enriched in the regulation of immune response, cell activation, signaling receptor activity, enzyme binding. Kyoto encyclopedia of genes and genomes analysis showed that they were mainly enriched in the TCR signaling pathway, Fc epsilon RI signaling pathway. GSEA showed that the DEGs were mainly enriched in immune response regulation, cell activation, TCR signaling pathway, Fc epsilon RI signaling pathway. Positive regulation of Fc receptor signaling pathway, PID IL12 2 pathway, immune response was observed in go enrichment items in the enrichment items of metascape. PPI networks got 5 core genes. Gene expression heat map showed that 5 core genes (CD247, Lck, cd3e, cd3d, ITK) were lowly expressed in the sepsis shock samples and highly expressed in the normal samples. CTD analysis showed that 5 core genes (CD247, Lck, cd3e, cd3d, ITK) were found to be associated with hemorrhage and necrosis. Low expression of cd3d, CD247 was observed in septic shock, and the lower the level of cd3d, CD247, the worse the prognosis.

Role of SNAP25 on the occurrence and development of eosinophilic gastritis.

Eosinophilic gastritis is characterized by gastrointestinal symptoms accompanied by peripheral eosinophilia. This study aims to explore the association between eosinophilic gastritis and Synaptosome Associated Protein 25 (SNAP25), and provide a new direction for the diagnosis and treatment of eosinophilic gastritis. GSE54043 was downloaded from the gene expression omnibus database. Differentially expressed genes (DEGs) were screened. The functions of common DEGs were annotated by Database for Annotation, Visualization and Integrated Discovery and Metascape. The protein-protein interaction network of common DEGs was obtained by Search Tool for the Retrieval of Interacting Genes and visualized by Cytoscape. Significant modules were identified from the protein-protein interaction network. A total of 186 patients with eosinophilic gastritis were recruited. The clinical data were recorded and the expression levels of CPE, SST, PCSK2, SNAP25, and SYT4 were detected. Pearson chi-square test and Spearman correlation coefficient were used to analyze the relationship between eosinophilic gastritis and related parameters. Univariate and multivariate Logistic regression were used for further analysis. 353 DEGs were presented. The top 10 genes screened by cytoHubb were shown, and Veen diagram figured out 5 mutual genes. Pearson's chi-square test showed that SNAP25 (P < .001) was significantly associated with eosinophilic gastritis. Spearman correlation coefficient showed a significant correlation between eosinophilic gastritis and SNAP25 (ρ = -0.569, P < .001). Univariate logistic regression analysis showed that SNAP25 (OR = 0.046, 95% CI: 0.018-0.116, P < .001) was significantly associated with eosinophilic gastritis. Multivariate logistic regression analysis showed that SNAP25 (OR = 0.024, 95% CI: 0.007-0.075, P < .001) was significantly associated with eosinophilic gastritis. The low expression of SNAP25 gene in eosinophilic gastritis is associated with a higher risk of eosinophilic gastritis.

Increased NOX1 and DUOX2 expression in the colonic mucosa of patients with chronic functional constipation.

To determine whether oxidative stress and inflammation are associated with constipation by examining the expression of the main producers of reactive oxygen species, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, and pro-inflammatory cytokines in the colon of patients with chronic functional constipation. The colonic biopsies were collected from 32 patients with chronic functional constipation and 30 healthy subjects who underwent colonoscopy. Colonic mucosal histology was observed. Interleukin (IL)-1ß, IL-6, IL-8 messenger RNA (mRNA), and 4 members of NADPH oxidase (NOX1, NOX2, DUOX2, and NOX4) protein and mRNA were assessed by immunohistochemistry, western blotting, and reverse transcription polymerase chain reaction. The tissues from both patients and healthy subjects showed normal histological structure without increase of inflammatory cells. NOX1 protein and mRNA levels were significantly increased compared to controls (P < .05). DUOX2 protein, but not mRNA, was increased by 2-fold compared to controls (P < .05). The levels of NOX2 and NOX4 protein and mRNA demonstrated no significant difference between patients and control subjects. The levels of IL-1ß and IL-6 mRNA were significantly higher in constipation patients (P < .05), while IL-8 mRNA level was no different between the 2 groups. NADPH oxidase and pro-inflammatory cytokine might be involved in the pathogeneses of chronic functional constipation.

The Efficacy of Percutaneous Transhepatic Gallbladder Drainage Combined with Gallbladder-Preserving Cholecystolithotomy in High-Risk Patients with Acute Calculous Cholecystitis.

Objective: This study aimed to investigate the value of combining percutaneous transhepatic gallbladder drainage (PTGD) with gallbladder-preserving cholecystolithotomy (GPC) in high-risk patients with acute calculous cholecystitis. Methods: Clinical data from 74 high-risk patients with acute calculous cholecystitis, admitted to our hospital between October 2018 and September 2021, were analyzed retrospectively. All the patients underwent PTGD, and 59 of them underwent delayed cholecystectomy, while 14 patients were subjected to GPC 8-12 weeks after the PTGD; one patient, whose life expectancy was fewer than 6 months, was not treated for gallstones after PTGD. Results: In all 74 patients, symptom remission was achieved after the PTGD therapy, and the incidence of catheter-related complications was 10.8%. Among the 59 patients who underwent delayed cholecystectomy (DC) after PTGD, there was a complication incidence of 6.8%. Of the 14 patients who underwent GPC after the PTGD, 13 patients were subjected to the removal of drainage tubes, 1 patient received cholecystostomy catheter draining externally, and two patients (14.3%) had complications. There were no perioperative deaths. Conclusion: Percutaneous transhepatic gallbladder drainage, combined with GPC, is a safe and effective treatment that is suitable for high-risk patients with acute calculous cholecystitis who cannot receive DC. This combined method allows for early acute cholecystitis to settle, helps to remove gallstones at a later stage, and solves the problem of long-term tube drainage after PTGD.