Disease Markers最新文献

[This retracts the article DOI: 10.1155/2020/7815214.].

[This retracts the article DOI: 10.1155/2021/9953234.].

[This retracts the article DOI: 10.1155/2022/1758113.].

Background: Liver hepatocellular carcinoma (LIHC) is the most frequently seen type of primary liver cancer. Cuproptosis is a novel form of cell death highly associated with mitochondrial metabolism. However, the clinical impact and pertinent mechanism of cuproptosis genes in LIHC remain largely unknown.

Methods: From public databases, we systematically assessed common genes from LIHC differentially expressed genes (DEGs) and cuproptosis-related genes using bioinformatics analysis. These common genes were then analyzed by enrichment analysis, mutation analysis, risk score model, and others to find candidate hub genes related to LIHC and cuproptosis. Next, hub genes were determined by expression, clinical factors, immunoassay, and prognostic nomogram.

Results: Based on 129 cuproptosis-related genes and 3492 LIHC DEGs, we totally identified 21 downregulated and 18 upregulated common genes, and they were enriched in pathways, such as zinc ion homeostasis and oxidative phosphorylation. In the mutation analysis, missense mutation was the most common type in LIHC patients, and the common gene F5 had the highest mutation frequency. After LASSO-Cox regression analysis and prognostic analysis, CDK1, ABCB6, LCAT, and COA6 were identified as prognostic signature genes. Among them, ABCB6 and LCAT were lowly expressed in tumors, and CDK1 and COA6 were highly expressed in tumors. In addition, ABCB6 and LCAT were negatively correlated with 6 kinds of immune cells, while CDK1 and COA6 were positively correlated with them. CDK1 and COA6 were identified as hub genes related to LIHC by Cox regression analysis and prognostic nomogram.

Conclusion: CDK1 and COA6 are two oncogenes in LIHC, which are involved in the molecular mechanism of cuproptosis and LIHC. Besides, CDK1 and COA6 can positively regulate the expressions of immune cells in LIHC. In clinical practice, they can be used as immunotherapeutic targets and prognostic predictors in LIHC, which sheds new light on the scientific fields of cuproptosis and LIHC.

Objective: This study is to investigate the difference in HIV-1 RNA pol gene expression in AIDS patients before and after antiviral treatment and its effect on the expression level of CD4⁺/CD8⁺ T cells in peripheral blood.

Methods: The participants included 200 AIDS patients who had undergone antiviral medication, and the quantity of HIV-1 RNA pol gene was determined using nested polymerase chain reaction (nPCR). The levels of CD3+, CD4+, and CD8+ T lymphocytes in peripheral blood were measured by flow cytometry before and after therapy. The receiver operating characteristics (ROC) curve was used to assess the impact of HIV-1 RNA pol gene expression and the CD4+/CD8+ ratio on the prognosis of AIDS patients.

Results: After three months of therapy, the levels of HIV-1 RNA and viral load in the patients showed a drastic decline, while the levels of CD4+/CD8+ were markedly elevated (P < 0.05). Logistic analysis revealed that patients' viral loads were positively correlated with HIV-1 RNA and negatively correlated with CD4+/CD8+ (P < 0.05). The alanine aminotransferase (ALT), white blood cell (WBC) count, Serum creatinine (Cr), total cholesterol (TC), triglyceride (TG), and platelet (PLT) levels significantly increased following a 24-month therapy, while no significant changes were observed in the level of aspartate aminotransferase (AST), red blood cell (RBC), and neutrophil (NEU) (%). (P > 0.05).

Conclusion: Antiviral drugs significantly inhibit the HIV-1 RNA POL gene expression and viral load in AIDS patients but upregulate the expression level of CD4⁺/CD8⁺ T cells in peripheral blood.

Background: Asthma is one of the most common respiratory diseases and one of the largest burdens of health care resources across the world. This study is aimed at using bioinformatics methods to find effective clinical indicators for asthma and conducting experimental validation.

Methods: We downloaded GSE64913 data and performed differentially expressed gene (DEG) screening. Weighted gene coexpression network analysis (WGCNA) on DEGs was applied to identify key module most associated with asthma for protein-protein interaction (PPI) analysis. According to the degree value, ten genes were obtained and subjected to expression analysis and receiver operating characteristic (ROC) analysis. Next, key genes were screened for expression analysis and immunological analysis. Finally, cell counting kit-8 (CCK-8) and qRT-PCR were also conducted to observe the influence of hub gene on cell proliferation and inflammatory cytokines.

Results: From the GSE64913 dataset, 711 upregulated and 684 downregulated DEGs were found. In WGCNA, the top 10 genes in the key module were examined by expression analysis in asthma, and CYCS was determined as an asthma-related oncogene with a good predictive ability for the prognosis of asthmatic patients. CYCS is significantly associated with immune cells, such as HHLA2, IDO1, TGFBR1, and CCL18 and promoted the proliferation of asthmatic cells in vitro.

Conclusion: CYCS plays an oncogenic role in the pathophysiology of asthma, indicating that this gene may become a novel diagnostic biomarker and promising target of asthma treatment.

Performing cardiopulmonary bypass (CPB) to reduce ischemic injury during surgery is a common approach to cardiac surgery. However, this procedure can lead to systemic inflammation and multiorgan dysfunction. Therefore, elucidating the molecular mechanisms of CPB-induced inflammatory cytokine release is essential as a critical first step in identifying new targets for therapeutic intervention. The GSE143780 dataset which is mRNA sequencing from total circulating leukocytes of the neonatorum was downloaded from the Gene Expression Omnibus (GEO) database. A total of 21 key module genes were obtained by analyzing the intersection of differentially expressed gene (DEG) and gene coexpression network analysis (WGCNA), and then, 4 genes (TRAF3IP2-AS1, PPARGC1B, CD4, and PDLIM5) were further confirmed after the least absolute shrinkage and selection operator (LASSO) and support vector machine recursive feature elimination (SVM-RFE) screening and were used as hub genes for CPB-induced inflammatory cytokine release in patients with congenital heart defects. The enrichment analysis revealed 21 key module genes mainly related to the functions of developmental cell growth, regulation of monocyte differentiation, regulation of myeloid leukocyte differentiation, ERK1 and ERK2 cascade, volume-sensitive anion channel activity, and estrogen receptor binding. The result of gene set enrichment analysis (GSEA) showed that the hub genes were related to different physiological functions of cells. The ceRNA network established for hub genes includes 3 hub genes (PPARGC1B, CD4, and PDLIM5), 55 lncRNAs, and 34 miRNAs. In addition, 4 hub genes have 215 potential therapeutic agents. Finally, expression validation of the four hub genes revealed that they were all significantly low expressed in the surgical samples than before.

Purpose: Keloid is a type of benign fibrous proliferative tumor characterized by excessive scarring. C1q/TNF-related protein 3 (CTRP3) has been proven to possess antifibrotic effect. Here, we explored the role of CTRP3 in keloid. In the current research, we examined the influence of CTRP3 on keloid fibroblasts (KFs) and investigated the potential molecular mechanism.

Methods: KF tissue specimens and adjacent normal fibroblast (NF) tissues were collected cultured from 10 keloid participants. For the TGF-β1 stimulation group, KFs were processed with human recombinant TGF-β1. Cell transfection of pcDNA3.1-CTRP3 or pcDNA3.1 was performed. The siRNA of CTRP3 (si-CTRP3) or negative control siRNA (si-scramble) was transfected into KFs.

Results: CTRP3 was downregulated in keloid tissues and KFs. CTRP3 overexpression significantly controlled TGF-β1-induced propagation and migration in KFs. Col I, α-SMA, and fibronectin mRNA and protein levels were enhanced by TGF-β1 stimulation, whereas they were inhibited by CTRP3 overexpression. In contrast, CTRP3 knockdown exhibited the opposite effect. In addition, CTRP3 attenuated TGF-β receptors TRI and TRII in TGF-β1-induced KFs. Furthermore, CTRP3 prevented TGF-β1-stimulated nuclear translocation of smad2 and smad3 and suppressed the expression levels of p-smad2 and p-smad3 in KFs.

Conclusion: CTRP3 exerted an antifibrotic role through inhibiting proliferation, migration, and ECM accumulation of KFs via regulating TGF-β1/Smad signal path.

Objective: To investigate the efficacy of butylphthalide combined with edaravone in the treatment of acute ischemic stroke and the effect on serum inflammatory factors.

Methods: One hundred and sixty patients with acute ischemic stroke who attended the neurovascular intervention department of our hospital from May 2020 to June 2022 were enrolled as study subjects for prospective analysis and were equally divided into a control group and an experimental group using the random number table method, with 80 cases in each group. The control group was treated with edaravone injection, while the experimental group was treated with butylphthalide combined with edaravone. The disease was recorded to compare the efficacy, erythrocyte sedimentation rate, homocysteine, serum inflammatory factors including tumor necrosis factor-α, C-reactive protein and interleukin-6 levels, and the incidence of adverse reactions between the two groups.

Results: The total effective rate of treatment in the experimental group was 90.0% (72/80), while that of the control group was 62.5% (50/80), the total effective rate of the experimental group was significantly higher than that of the control group, and the difference was statistically significant (P < 0.05). After treatment, the erythrocyte sedimentation rate, homocysteine level, and serum TNF-α, CRP, and IL-6 levels of patients in the experimental group improved compared with those before treatment, and the degree of improvement was better than that of the control group, and the difference was statistically significant (P < 0.05). After 3 months of treatment, a comparison of the incidence of adverse reactions in the two groups showed no statistically significant difference between the two groups (P > 0.05).

Conclusion: The treatment of acute ischemic stroke with butylphthalide combined with edaravone has positive significance in improving blood circulation regulation and serum inflammatory factor levels and is reliable and worthy of clinical promotion.

Objective: To investigate the relationship between changes in blood glucose and blood lipid levels and the risk of thyroid cancer in patients with type 2 diabetes mellitus.

Methods: A total of 159 patients with type 2 diabetes who were treated in our hospital between June 2018 and February 2021 were recruited and assigned into the observation group, including 136 patients with type 2 diabetes without thyroid cancer (nonthyroid cancer group) and 23 patients with type 2 diabetes complicated with thyroid cancer (thyroid cancer group), and 120 healthy subjects during the same period were selected as the control group. Glycated hemoglobin (HbAlc), total cholesterol (TC), triacylglycerol (TG), high density lipoprotein cholesterol (HDL-C), and low density lipoprotein cholesterol (LDL-C) were detected and compared. Pearson's method was conducted to analyze the correlation between serum HbAlc level and TC, TG, HDL-C, and LDL-C levels in patients with type 2 diabetes mellitus; multivariate logistic regression analysis was performed to analyze the influencing factors of thyroid cancer in patients with type 2 diabetes mellitus.

Results: The serum HbAlc level and the incidence of thyroid cancer in patients with type 2 diabetes mellitus in the observation group were significantly higher than those in the control group (P < 0.05). The levels of TC, TG, and LDL-C in patients with type 2 diabetes mellitus in the observation group were significantly higher than those in the control group, and the level of HDL-C was significantly lower than that in the control group (P < 0.05). The correlation analysis showed that serum HbAlc levels in patients with type 2 diabetes were positively correlated with TC and TG levels and negatively correlated with HDL-C levels (P < 0.05) and not correlated with LDL-C levels (P > 0.05). Compared with the type 2 diabetes patients without thyroid cancer, the serum HbAlc, TC, and TG levels of the patients with type 2 diabetes mellitus in the thyroid cancer group were significantly higher, and the levels of HDL-C were significantly lower (P < 0.05). There was no significant change in the level of LDL-C (P > 0.05). Multivariate logistic regression analysis showed that serum HbAlc, TC, and TC levels were all risk factors for thyroid cancer in patients with type 2 diabetes mellitus (P < 0.05), while serum HDL-C level was a protective factor for thyroid cancer in patients with type 2 diabetes mellitus (P < 0.05).

Conclusion: Thyroid cancer in type 2 diabetes patients may be linked to elevated levels of blood HbAlc, TC, and TG. HbAlc may raise the risk of thyroid cancer in type 2 diabetes patients by modulating blood lipid levels, which might serve as a marker to assess the risk of thyroid cancer in type 2 diabetes mellitus patients. However, since this study did not conduct in vitro and in vivo experim