Evaluation of adipokines and inflammatory mediator expression levels in patients with periodontitis and peri-implantitis: a cross-sectional study

Clinical Oral Investigations - The aim of this study was to analyze the mRNA and protein expression of adiponectin, leptin, visfatin, tumor necrosis factor (TNF)-α, and interleukin (IL)-6...     

Structural variations and expression profiles of the SARS-CoV-2 host invasion genes in lung cancer

Recent days have seen growing evidence of cancer's susceptibility to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and of the effect of genomic differences on the virus' entrance genes in lung cancer. Genetic confirmation of the hypotheses regarding gene expression and mutation pattern of target genes, including angiotensin-converting enzyme-2 (ACE2), transmembrane serine protease 2 (TMPRSS2), basigin (CD147/BSG) and paired basic amino acid cleaving enzyme (FURIN/PCSK3), as well as correlation analysis, was done in relation to lung adenocarcinoma (LUAD) and lung squamous carcinoma (LUSC) using in silico analysis. Not only were gene expression and mutation patterns detected, but also there were correlation and survival analysis between ACE2 and other target genes expression levels. The total genetic anomaly carrying rate of target genes, including ACE2, TMPRSS2, CD147/BSG, and FURIN/PCSK3, was determined as 8.1% and 21 mutations were detected, with 7 of these mutations having pathogenic features. p.H34N on the RBD binding residues for SARS-CoV-2 was determined in our LUAD patient group. According to gene expression analysis results, though the TMPRSS2 level was statistically significantly decreased in the LUSC patient group compared to healthy control, the ACE2 level was determined to be high in LUAD and LUSC groups. There were no meaningful differences in the expression of CD147 and FURIN genes. The challenge for today is building the assessment of genomic susceptibility to COVID-19 in lung cancer, requiring detailed experimental laboratory studies, in addition to in silico analyses, as a way of assessing the mechanism of novel virus invasion that can be used in the development of effective SARS-CoV-2 therapy.     

Relationship of ultrasonographic findings with synovial angiogenesis modulators in different forms of knee arthritides

Angiogenesis is controlled by a variety of angiogenesis stimulators and inhibitors. The increased power Doppler (PD) signals determined by ultrasonography is an indirect marker of synovial vascularity in arthritis. We aimed to investigate relationship between ultrasonographic findings and synovial angiogenesis modulators. Thirteen Behcet’s disease (BD), 15 spondyloarthropathy, 21 rheumatoid arthritis (RA), and 15 osteoarthritis (OA) patients with knee arthritis were included. Cumulative effusion, synovial hypertrophy, and PD signal scores were calculated in arthritic joints. In synovial fluid samples, angiogenesis inhibitors (angiostatin, thrombospondin-1, and endostatin) and stimulators [bFGF (basic fibroblast growth factor), angiopoietin-1] were studied. The comparisons between groups were made by Kruskal–Wallis test, and correlation analysis was calculated with Pearson and Spearman tests. Effusion scores were significantly higher in inflammatory arthritis than in OA. Synovial hypertrophy scores were higher in RA and spondylarthritis than in OA and BD. PD scores were not different between the groups. Synovial angiostatin and bFGF levels were significantly higher in patients with inflammatory arthritis than in OA. Cumulative effusion scores were positively correlated with angiopoietin-1, angiostatin, and bFGF and negatively correlated with thrombospondin-1 levels. Synovial hypertrophy scores were positively correlated with angiostatin and bFGF levels and negatively correlated with thrombospondin-1. No correlation was found between PD scores and modulators of angiogenesis. In large joints like knee, detecting PD signals alone was not sufficient to assess the angiogenesis. However, cumulative activity scores were positively correlated with angiogenesis stimulators. Therefore, when investigating the angiogenesis, PD technique should be added to gray-scale examinations.     

Evaluation of heat shock protein 70 and toll-like receptor 4 expression in gingival crevicular fluid in response to orthodontic forces

Clinical Oral Investigations - The aim of this study was to assess the concentrations of heat shock protein 70 (HSP70) and toll-like receptor 4 (TLR4) during orthodontic tooth movement and to...     

Hypoxia and cytokines regulate carbonic anhydrase 9 expression in hepatocellular carcinoma cells in vitro

AIM: To study the expression of carbonic anhydrase (CA) 9 in human hepatocellular carcinoma (HCC) cells.METHODS: We studied CA9 protein, CA9 mRNA and hypoxia-inducible factor-1 alpha (HIF-1α) protein levels in Hep3B cells exposed in different parallel approaches. In one of these approaches, HCC cells were exposed to extreme in vitro hypoxia (24 h 0.1% O₂) without or with interleukin (IL)-1, IL-6, tumor necrosis factor-alpha (TNF-α) and transforming growth factor-beta (TGF-β) stimulation for the same hypoxic exposure time or exposed to normoxic oxygenation conditions without or with cytokine stimulation.RESULTS: The tumour cell line analysed showed a strong hypoxic CA9 mRNA expression pattern in response to prolonged severe hypoxia with cell-line specific patterns and a marked induction of CA9 protein in response to severe hypoxia. These results were paralleled by the results for HIF-1α protein under identical oxygenation conditions with a similar expression tendency to that displayed during the CA9 protein expression experimental series. Continuous stimulation with the cytokines, IL-1, IL-6, TNF-α and TGF-β, under normoxic conditions significantly increased the carbonic anhydrase 9 expression level at both the protein and mRNA level, almost doubling the CA9 mRNA and CA9 and HIF-1α protein expression levels found under hypoxia. The findings from these experiments indicated that hypoxia is a positive regulator of CA9 expression in HCC, and the four signal transduction pathways, IL-1, IL-6, TNF-α and TGF-β, positively influence CA9 expression under both normoxic and hypoxic conditions.CONCLUSION: These findings may potentially be considered in the design of anti- cancer therapeutic approaches involving hypoxia-induced or cytokine stimulatory effects on expression. In addition, they provide evidence of the stimulatory role of the examined cytokine families resulting in an increase in CA9 expression under different oxygenation conditions in human cancer, especially HCC, and on the role of the CA9 gene as a positive disease regulator in human cancer.