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  • Küçük Resim
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    Association of IL-1Β (-511 C /T) and IL-1Β (-31 T / C) gene polymorphism with endoplasmic reticulum stress marker levels in acute decompensated heart failure with low ejection fraction
    (Serbian Genetics Soc, 2022) Sabırlı, Ramazan; Koseler, Aylin; Mete, Ergun; Turkcuer, Ibrahim
    Inflammatory processes play an important role in the pathogenesis of heart failure. The accumulation of unfolded protiens in the endoplasmic reticulum lumen and the unfolded protien response signal path is activated. The IL-IB gene is located in the Chromsone 2.q14 region. -31 and -511 single nucleotide polymorphisms (SNPs) were detected in the IL-IB Promoter region. These two SNPs affect IL-1expression. This Study aims to investigate the presence of IL-IB (-511 C / T) and IL-IB (-31 T / C) gene polymorphisms and the relationship between ER Stress markers and the inflammatory markers. Patients who applied to the department of emergency medicine with the findings of acute decompensated heart failure. Polymorphic sites of the IL-IB gene were determined by DNA sequencing. In all study, individuals with IL-IB (-31 T / C) T allele have higher serum PERK, GRP-78, CHOP AND CRP levels median values than individuals with IL-IB (-31 T/C) C allele (p = 0.00001, p = 0.0002, p = 0.002 and p = 0.011, respectively). Serum ERK and GRP-78 Values in HF Group were higher in individuals with IL-IB (-31 T / C) T allele compared to individuals with C alle (p = 0.0001 and p = 0.0006). There was a statistically difference in serum CHOP levels in the control group with the IL-IB (-511 C / T) T allele and the individuals with the C allele in the HF group (p= 0.002). In Cnclusion we consider that the inflammatory response caused by IL-IB (-31 T / C) gene polymorphism increased and the ER stress response increased, inflammatory pathway and stress of having IL-IB (-31 T / C) T / T genotype or T allele.
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    Galectin-3 as a potential prognostic biomarker for COVID-19 disease: a case-control study
    (Cureus Inc, 2022) Karsli, Emre; Metin, Damla Anabarli; Canacik, Omer; Sabırlı, Ramazan; Kaymaz, Buse; Kurt, Ozgur; Koseler, Aylin
    Background Recent studies have investigated the importance of Galetin-3 in inflammation, fibrosis, cell proliferation, cardiac disease, diabetes, and tumor formation. Aims This study aims to investigate the role of the Galectin-3 level in the diagnosis of COVID-19 pneumonia and the value of the Galectin-3 level in predicting the clinical course of the patient. Methods This study employed a prospective, case-control study design and was conducted at Bakircay University Cigli Training and Research Hospital. A total of 100 patients (40 had moderate and 60 had severe/critical COVID-19 disease according to World Health Organisation guidelines) and 50 non-symptomatic healthy volunteers participated in the study. Blood samples were taken from patients at the time of hospital admission, after which serum was isolated. Following the isolation of serum, Galectin-3 levels were evaluated using the enzyme-linked immunosorbent assay (ELISA) method. Results The serum Galectin-3 level was measured as 13.57 (10.9-16.4) ng/mL in the control group, 13.52 (10.69-16.6) ng/mL in the moderate disease group, and 11.65 (6.09-14.33) ng/mL in the severe/critical disease group. Serum Galectin-3 levels were significantly lower in the severe/critical disease group compared to the control and moderate disease groups (p=0.001 and p=0.019, respectively). Using ROC analysis, a larger area under the curve (AUC) for the serum Galectin-3 levels of the control group (AUC-0.622, 95% CI =0.529-0.714; p=0.015) was calculated compared to the COVID-19 patient group for the diagnosis of COVID-19 disease. The Galectin-3 level was found to be 75% sensitive and 50% specific at a cut-off level of 11.3 ng/mL in predicting the need for ICU treatment. Conclusion Galectin-3 levels may be a beneficial biomarker in predicting the clinical severity of COVID-19 disease when used in conjunction with other known biomarkers, at the time of admission to the emergency department (ED).