The aim of this study was to investigate expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in invasive pituitary adenomas (IPAs). The streptavidin peroxidase immunohistochemical method was employed to detect their expression in 40 cases of IPA and 40 of non-invasive pituitary adenoma (NIPA). TNF-α and IL-6 were found to be upregulated in IPA tissue compared with that of NIPA (P
The aim of this study was to observe the influence of gap junction (GJ) functional changes on the hepatotoxicity of TNF-α. Three different methods were employed to study functional effects of the GJ inhibition: 1) pretreatment with a GJ inhibitor; 2) inoculation of cells at high and low densities; and 3) inhibition of the expression of connexin 32 (Cx32) by small inhibitory RNA transfection. We then observed the influence of these treatments on hepatotoxicity following treatment with different concentrations of TNF-α for various duration.
Thermotherapy has been proven to be effective for the treatment of various tumors, including glioma. We determined whether tumor necrosis factor-alpha (TNF-α) is involved in the regulation of the biological processes of glioma development. Reverse transcription-polymerase chain reaction (RT-PCR) and immunocytochemistry were used to investigate the levels of TNF-α mRNA and heat shock factor-1 (HSF1) protein, respectively, in glioma cells. Radioimmunoassay was used to dynamically monitor the contents of TNF-α in the nutrient fluid of C6 cells after thermotherapy treatment.
We integrated all the eligible studies and investigated whether the TNF-α 308G/A polymorphism correlates with urogenital cancer risk. Tumor necrosis factor-α (TNF-α) is a risk factor for some urogenital cancers; however, in prostate and bladder cancers the results are controversial. PubMed, EMBASE, Web of Science, the Cochrane Library, the Chinese Biomedical Literature Database, and the Wanfang Database were searched for all case-control studies on the relationship between the TNF-α 308G/A polymorphism and susceptibility to urogenital cancer between January 1994 and January 2015.
The aim of this research was to study polymorphisms in the genes encoding cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) in patients with celiac disease (CD) antigens DQ2 (DQ2-positive) or DQ8 (DQ8-positive). We compared the results with healthy controls to determine whether any of the polymorphisms have a role in susceptibility to CD. A case-control of 192 patients with CD (96 DQ2-positive and 96 DQ8-positive) and 96 healthy controls from northeast Italy were included in the study.
We investigated the diagnostic values of microRNA-31 in peripheral blood mononuclear cells (PBMCs) for pediatric pulmonary tuberculosis in Chinese patients. Sixty-five children with TB were selected for this study, which was conducted at the Department of Infectious Diseases People’s Hospital of Laiwu City between December 2013 and December 2014. Sixty healthy children, selected in parallel, served as the control group. Real-time PCR was used to detect miR-31 expression in PBMCs. Serum levels of IL-6, TNF-α, NF-κB, and IFN-γ was detected by ELISA.
Type 1 diabetes mellitus (T1D) is a complex disorder characterized by an autoimmune response against human pancreatic beta-cells. Patients with T1D can also develop a response toward one or more other factors, such as in autoimmune thyroiditis (AITD) and celiac disease (CD). In the presence of T1D + AITD, the patient is diagnosed with autoimmune polyglandular syndrome type III (APSIII); patients with APSIII may also present with CD. These diseases have a strong genetic component and share many susceptibility genes, suggesting potentially overlapping pathogenic pathways.
Tumor necrosis factor-α (TNF-α) is an important pro-apoptotic cytokine, which performs a broad range of immune and inflammatory functions in several vital processes. TNF-α-induced apoptosis has been confirmed, however, relatively little is known regarding the role of forkhead box class-O 1 (FOXO1) in mediating TNF-α-induced apoptosis in cervical cancer. In our study, we used the well-characterized cervical cancer cell line C-33A to investigate the role of FOXO1.