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The most important side effect of gentamicin (GM) is nephrotoxicity. p-Coumaric acid (PCA) is a phenolic compound that scavenges free radicals, reduces fibrosis, and tissue damage. This study investigates the protective effect of PCA on tissue damage and kidney function in gentamicin-induced nephrotoxicity (GIN). Thirty-five rats were separated into five groups and each group contained seven animals: control group, ethanol group, GM group, PCA group, and GM + PCA group. At the end of the seven-day treatment, the rats were sacrificed after blood and kidney tissue samples were taken. While serum urea, creatinine, and neutrophil gelatinase-associated lipocalin (NGAL) levels increased significantly in the GM group compared to the control, they showed a significant decrease in the GM + PCA group compared to the GM. Serum tumor necrosis factor-α (TNF-α) and tissue malondialdehyde (MDA) levels were significantly increased in the GM group compared to the control. While the tissue total oxidant status (TOS) and oxidative stress index (OSI) values of the GM group were significantly higher than the control, they showed a significant decrease in the GM + PCA group compared to the GM. In the histopathological examination, significant tubular necrosis and tubulointerstitial inflammation were detected in the proximal tubules in the GM group compared to the control, while a significant decrease was observed in the severity of these findings in the GM + PCA group compared to the GM. This study shows that PCA has biochemical and histopathological ameliorating effects on GIN in the rat model.

Aim: Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease. The exact pathogenesis of NAFLD has not been fully elucidated. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a member of TNF superfamily and it has been implicated in the pathogenesis of several diseases including liver inflammation and fibrosis. Current study was conducted to evaluate serum sTWEAK levels in patients with NAFLD.Material and Methods: Seventeen patients with biopsy proven non-alcoholic steatohepatitis (NASH), 22 patients with simple hepatosteatosis and 30 healthy controls were included in the study and serum sTWEAK concentrations were measured using commercial ELISA kits.Results: Mean serum sTWEAK concentration was significantly lower in the NASH group when compared to the simple hepatosteatosis group and healthy controls (199.6±101.2 pg/mL, 246.1±65.7 pg/mL and 277.6±117.6 pg/mL respectively, p=0.029). ROC analyses for sTWEAK to differentiate NASH patients from healthy controls and from simple hepatosteatosis revealed that AUC for sTWEAK was 0.712 (%95 CI, 0.543-0.880). For the specified cut off value, 171.1 pg/mL positive and negative predictive values calculated were 64.3% and 85.5% respectively. Conclusion: Serum sTWEAK concentration is decreasedin patients with NASH when compared to patients with simple hepatosteatosis and healthy controls. Keywords: Nonalcoholic steatohepatitis; tumor necrosis factor-like weak inducer of apoptosis; sTWEAK; fibroblast growth factor-inducible 14; Fn 14.

WOS:000404381800035, PubMed ID: 28618749, Background/aim: Albumin is the most important protein synthesized by the liver. Posttranscriptional changes occur in the molecular structure of albumin due to various factors and isoforms arise. Ischemic modified albumin (IMA) is one such isoform. This study was conducted to evaluate serum IMA concentrations in patients with hepatitis B virus (HBV)-related chronic liver diseases. Materials and methods: This study included 74 treatment-naive chronic hepatitis B patients, 25 patients with HBV-related cirrhosis, and 49 healthy controls. Serum IMA concentration was measured spectrophotometrically using the albumin cobalt binding test. Results: The mean IMA concentrations in the chronic hepatitis B group and healthy controls were 0.33 ± 0.11 ABSU and 0.27 ± 0.70 ABSU, respectively, and the difference was statistically significant. Mean IMA/albumin ratios (IMAR) in the chronic hepatitis B and control groups were 0.08 ± 0.04 and 0.06 ± 0.17, respectively, and the difference was also statistically significant (P > 0.001). Higher serum IMA concentrations and IMAR were detected in patients with advanced fibrosis. Conclusion: Serum IMA concentration and IMAR are increased in patients with HBV-related chronic liver diseases and IMA and IMAR are associated with the degree of liver fibrosis. IMA and IMAR may have potential use as noninvasive markers of fibrosis in chronic hepatitis B patients.

Aim Vasopressin exerts robust influences on social communication and behavior in humans. Apelin is a relatively novel neuropeptide that could counteract vasopressin's actions and has been shown to be closely related with a broad range of physiological functions. Abnormalities in vasopressin and apelin have been detected in a variety of psychiatric disorders, but their relation to attention-deficit hyperactivity disorder (ADHD) is unknown. In the present study, we explored the plasma levels of vasopressin and apelin-13 in children with ADHD. Methods Thirty-four children with ADHD and 36 healthy controls were enrolled in this study. The severity of ADHD symptoms was assessed via Conners’ Parent Rating Scale and Conners’ Teacher Rating Scale. Plasma levels of vasopressin and apelin-13 were measured using commercial enzyme-linked immunosorbent assay kits. Results The mean plasma apelin-13 levels were significantly higher in male children with ADHD than in male control subjects; no significant difference was found between the groups for plasma apelin-13 levels in girls or in the entire subject cohort. Plasma vasopressin levels did not show any significant differences between groups. There were no significant correlations between plasma levels of these neuropeptides and scores for Conners’ Parent Rating Scale and Conners’ Teacher Rating Scale. Conclusion Our results suggest a sex-specific association between plasma apelin-13 levels and ADHD. Apelin-13 may play a role in the etiopathogenesis of ADHD either with a direct impact on the apelin receptor or via its opposing effect on the vasopressinergic system.

Abstract. Vitamin D deficiency is associated with several non-homeostatic conditions and/or diseases like inflammation, atherosclerosis, cardiovascular disease and mortality. YKL-40 is a glycoprotein, secreted by macrophages, neutrophils and different cell types and it is also associated with inflammation and pathological tissue remodeling. In this study, we aimed to evaluate relationship between the proinflammatory biomarkers YKL-40 and hs-CRP levels and vitamin D deficiency. Our study group includes 45 subjects with vitamin D deficiency (Group 1) (20 M, 25 F; mean age 37.72 ± 7.70 years) and 40 age and sex-matched healthy subjects with normal serum levels of vitamin D (Group 2) (19 M, 21 F; mean age 39.26 ± 7.41 years). Plasma 25 (OH) vitamin D levels were measured by liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. Plasma YKL-40 analysis was performed by ELISA. Serum hs-CRP levels were measured by nephelometric method. Plasma vitamin D levels below 20 ng/mL were accepted as vitamin D deficiency. Although we could not find any significant differences by means of serum hs-CRP levels between Group 1 and Group 2 (2.21 (0.27–11.70); 1.79 (0.16–9.85) mg/L, p = 0.247), plasma YKL-40 levels were significantly higher in group 1 than group2 (70.47 (17.84–198.50); 47.14 (4.80–135.48) ng/mL, p = 0.047). In literature, vitamin D deficiency is associated with inflammation. In our study, we found similar hs-CRP levels between groups and higher YKL-40 levels in group 1. Vitamin D deficiency may be related to high YKL-40 levels in terms of causing chronic inflammation.

The constriction of vessels due to atherosclerotic lesions causes hypoxia/ischemia and oxidative changes resulting in transformation of free albumin to ischemia-modified albumin (IMA) in the circulation and increased carotid intima–media thickness (cIMT). We investigated the reliability of IMA increase in evaluating atherosclerosis in patients with familial Mediterranean fever (FMF) compared with cIMT. Patients with FMF (n = 58) diagnosed by the Tel-Hashomer criteria in attack-free period and 38 healthy people were included in the study. Patient demographics as well as the clinical and laboratory characteristics of the healthy controls and patients with FMF were noted. The IMA levels and cIMT in patients with FMF were 0.30 ± 0.09 absorbance units (ABSUs) and 1.12 ± 0.27 mm, respectively, and in the control group, IMA levels and cIMT were 0.25 ± 0.07 ABSU and 0.74 ± 0.26 mm, respectively. The IMA levels and cIMT were significantly higher in patients with FMF than in controls ( P = .020 and P < .0001, respectively). The IMA values showed positive correlation with cIMT in patients with FMF( r = .302, P = .041). Our results reveal that IMA—an oxidative stress marker—may be an indicator of atherosclerosis in patients with FMF. This finding deserves further investigation.