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While serum NSE, MBP, and S100B values cannot be considered as biomarkers for ASD, GFAP may be a biomarker and is suggested as a possible indicator of autism severity.

Aim:URS is a very commonly used procedure for treatment of ureter stones. Increased hydrostatic pressure in the collecting system linked to fluids used during the procedure may cause harmful effects on the kidney. The aim of this study is to determine whether the URS procedure has a negative effect on the kidney by investigating NGAL, KIM-1, FABP and Cys C levels in urine.Material and Methods:This study included 30 patients undergoing ureterorenoscopy (URS) for ureter stones. Urine samples were collected 5 times; before the URS procedure (control) and at 1, 3, 5 and 12 hours following the procedure. NGAL, KIM-1, FBAP and Cys C levels were measured in urine and compared with the control values.Results:The NGAL levels in urine before the procedure and at 1, 3, 5 and 12 hours after the procedure were 34.59±35.34; 62.72±142.32; 47.15±104.48; 45.23±163.16 and 44.99±60.79ng/mL, respectively (p=0.001). Similarly, the urinary KIM-1, FABP and Cys C levels were found to increase compared to control values; however this increase did not reach statistical significance (p >0.05).Conclusions:After the URS procedure, there were important changes in NGAL, FABP, KIM-1 and Cys C levels. These changes reached statistical significance for NGAL, but did not reach significance for the other parameters. In conclusion, the URS procedure significantly affects the kidney; however, this effect disappears over time.

Cadmium (Cd) toxicity was produced in male rats to study the role of cholinoceptors in Cd-induced endothelial dysfunction. The changes in the tension of the aortic rings to constrictor and dilator agonists were compared with those of controls. A Cd-induced significant increase in phenylephrine response was associated with a decrease in basal dilator prostanoid release. In Cd-exposed rings, despite an obvious depression in the acetylcholine (ACh) response, the receptor-independent dilation to the calcium ionophore A23187, which elicits a receptor-independent endothelial relaxation, was slightly elevated (p<0.01), but the smooth muscle cell response to the NO donor, sodium nitroprusside (SNP) remained unaltered. Cadmium decreased both the maximal response to ACh (10(-5) M) and its pirenzepine (Prz) sensitive component. The M1 type cholinoceptor-mediated response to ACh decreased in Cd-exposed rings to 10.30 +/- 5.00% from 38.40 +/- 6.90% (p<0.001). Cadmium also reduced the share of indomethacin 1.64% to 13.92 +/- 2.89% (p<0.01), which correlated well with the changes in the M1-mediated response (r=0.991, p<0.0001). Most of the deleterious effect of Cd appears to be restricted to the M1-dependent ACh response. These findings suggest that Cd produces an endothelial dysfunction by impairing the M1 type cholinoceptor mediated response, which seems to be involved in prostanoid release.

Introduction Sepsis is an inflammatory reaction to bacteria involving the whole body and is a significant cause of mortality and economic costs. The purpose of this research was to determine whether tadalafil exhibits a preventive effect on sepsis in a septic model induced in rats with cecal ligation and puncture (CLP).Materials and Methods Rats were randomly separated into groups, 10 rats in each: (i) a sham (control) group, (ii) an untreated sepsis group, (iii) a sepsis group treated with 5mg/kg tadalafil and (iv) a sepsis group treated with 10mg/kg tadalafil. A polymicrobial sepsis model was induced in rats using CLP. Rats were sacrificed after 16h, and blood and kidney tissues were collected for biochemical and histopathological study.Results Levels of the inflammatory parameter IL-6 decreased significantly in the sepsis groups receiving tadalafil in comparison with the untreated sepsis group (p<0.05). In terms of histopathology, inflammation scores investigated in kidney tissues decreased significantly in the sepsis groups receiving tadalafil compared to the untreated sepsis group (p<0.05). In addition, levels of creatinine and cystatin C measured in septic rats receiving tadalafil were lower by a clear degree than in septic rats (p<0.05).Conclusion In this study, tadalafil exhibited a preventive effect for sepsis-related damage by suppressing inflammation in serum and kidney tissue of septic rats in a polymicrobial sepsis model induced with CLP.

Aim: Despite the belief that silica (Si) is an inert and non-toxic ingredient, latest studies indicated that it is a potent mitochondria activator and Si-induced ROS generation is involved in the inflammatory reactions of silicotic lungs. Si cytotoxicity has been well studied in phagocytic cells, but its effects on the mitochondria of proximal tubule cells which are continuously exposed to filtered blood-borne soluble Si were not known. Methods: Using renal cortical slices and isolated mitochondria, the effect of high dietary Si on the mitochondrial functions of proximal tubule cells was studied in rats exposed to 50 mg/kg sodium metasilicate-containing water for 8 days. Results: Digested Si did not accumulate in kidney cortex, it was totally eliminated in the urine. Glomerular filtration rate as well as urine output were normal. Despite unaltered blood and cortex Si levels, ammonia production of cortical slices and isolated mitochondria was increased significantly and this was further increased by L-NAME pre-treatment. Elevated mitochondrial oxygen utilization was associated with increased ammonia production. Cyclosporin-A-sensitive mtPTP increase was associated with unchanged K_ATP channels in the mitochondria of Si-exposed rats. Conclusion: These results suggested that dietary Si increases both extracellular and intracellular ammoniagenesis by elevating mitochondrial oxygen utilisation.

Increased protease activity causes receptor dysfunction due to extracellular cleavage of different membrane receptors in hypertension. The vasodilatory effects of insulin-like growth factor-1 (IGF-1) are decreased in hypertension. Therefore, in the present study the association of an enhanced protease activity and IGF-1 receptor cleavage was investigated using the spontaneously hypertensive rats (SHRs) and their normotensive Wistar Kyoto (WKY) controls (n = 4). Matrix metalloproteinase (MMP) activities were determined using gelatin zymography on plasma and different tissue samples. WKY aorta rings were incubated in WKY or SHR plasma with or without MMP inhibitors, and immunohistochemistry was used to quantify the densities of the alpha and beta IGF-1 receptor (IGF-1R) subunits and to determine receptor cleavage. The pAkt and peNOS levels in the aorta were investigated using immunoblotting as a measure of IGF-IR function. Increased MMP-2 and MMP-9 activities were detected in plasma and peripheral tissues of SHRs. IGF-1R beta labeling was similar in both groups without plasma incubation, but the fraction of immunolabeled area for IGF-1R alpha was lower in the endothelial layer of the SHR aorta (p < 0.05). A 24-h incubation of WKY aorta with SHR plasma did not affect the IGF-1R beta labeling density, but reduced the IGF-1R alpha labeling density in the endothelium (p < 0.05). MMP inhibitors prevented this decrease (p < 0.01). Western blot analyses revealed that the pAkt and peNOS levels under IGF-1-stimulated and -unstimulated conditions were lower in SHRs (p < 0.05). A reduced IGF-1 cellular response in the aorta was associated with the decrease in the IGF-1R alpha subunit in the SHR hypertension model. Our results indicate that MMP-dependent receptor cleavage contributed to the reduced IGF-1 response in SHRs.

Considering the importance of nitric oxide generation in the regulation of vessel tone, reduced endothelial nitric oxide synthase (eNOS) expression in alveolar macrophages exposed to short-term silica (Si) suggests the possibility of Si-induced changes in endothelial functions. In this experimental study, the functional changes of the endothelial cells were investigated in the aortic rings of rats subjected to 50 mg Si/kg body weight in their drinking water for 8 days. Norepinephrine elicited contractility and dilation response to acetylcholine (ACh) was significantly high in the aortic rings of Si-treated group. Alteration in receptor-independent endothelial response to A23187 in the aortic rings of Si-exposed rats was less obvious, but sodium nitroprusside (SNP)-elicited dilation was reduced significantly. A23187-induced relaxation was fully eliminated with N-nitro-L-arginine methyl ester (L-NAME) pretreatment, whereas 19.24 +/- 4.36% of ACh response was L-NAME resistant and eliminated with 10-5 M tetraethylammonium (TEA). Despite a significant reduction in the share of NO, the contribution of indomethacine (IND)-sensitive relaxation to ACh response remained unchanged in Si group. As a result, our findings demonstrated that Si both modifies the characteristics of endothelial relaxants and attenuates smooth muscle cell responsiveness to NO. Si-induced reduced NO association with elevated endothelium-derived hyperpolarizing factor (EDHF) in response to ACh, together with reduced NO sensitization, might have clinical importance in cardiovascular pathology.