The Effect of Hepcidin on Cardiac Ischemia-Reperfusion Injury

Background/aim: Hepcidin is the main hormone in the regulation of iron metabolism which is also released from the heart. The aim of our study was to investigate the effects of hepcidin on the cardiac ischemia-reperfusion injury. Materials and methods: In this study, 12 Wistar albino rats were divided into two groups (n = 6 each): 1) The ischemia-reperfusion group (Group 1); 2) Hepcidin-treated group (Group 2). Rat hearts were perfused on Langendorff system with KH (Krebs-Henseleit) and subjected to 30 min stabilization, 30 min global ischemia, and 30 min reperfusion. Hepcidin ((-) M) was applied to group 2 at the onset of ischemia. Malondialdehyde (MDA), glutathione (GSH), and nitric oxide (NOx) levels were measured in heart tissue for NOx levels, viscosity, and ion content of perfusate were collected before ischemia and the 1st, 5th, 10th, 20th, and 30th minutes of reperfusion were determined. Apoptosis in heart was evaluated. Results: NOx and MDA levels significantly decreased in heart tissue in Hepcidin-treated group. NOx and viscosity of perfusate were not significantly different between the groups. Perfusate iron, calcium, magnesium, potassium, and sodium levels in group 2 were more homogeneous. Histologic structures of heart tissue were regularly in group 2. Apoptosis were increased in control group compared to hepcidin treated group. Conclusion: These results suggest that hepcidin may have a protective effect on the heart for the ischemia-reperfusion injury

Structural Damage Detection by Fusion of GA and PSO

health monitoring. Abstract: In order to solve the inverse problem on structural damage detection (SDD) in the field of structural health monitoring (SHM), a FGAPSO algorithm is proposed by a fusion of the genetic algorithm (GA) and the particle swarm optimization (PSO) in this study. For improving the simple GA with drawbacks of easy precocious and of lower computation efficiency, the real-coded GA is implemented, the chaotic logistic mapping is chosen for initializing population, the self-adaptive crossover-mutation operators and elitist strategy are employed. The GA is then mixed with the PSO algorithm for the population diversity and convergence by exchanging genes between two new populations internally and the goal of improving GA is attained at last. Further, some numerical simulations on a 13-bar planar truss structure with several damage cases have been carried out for assessing the performance of the FGAPAO. The illustrated results show that the proposed FGAPSO algorithm is better than any of conventional GA and PSO. Even for the slight damage case, it is still more feasible and effective for SDD

Protective effects of Nigella sativa oil against carboplatin-induced liver damage in rats

Objective: This study aimed to investigate the protective effects of nigella saliva oil (NSO) against liver damage due to intraperitoneal (i.p.) usage of carboplatin which is commonly used as a chemotherapeutic agent. Material and Method: Twenty four female Wistar-albino rats (about 200-350 grams each) were divided into 4 groups. Group 1 (n = 6) was administered 4 ml/kg intraperitoneal (i.p.) saline 48 and 24 h before. Group 2 (n = 6) was i.p. administered 4 ml/kg NSO 48 h before and 4 ml/kg saline 24 h before. Group 3 (n = 6) was i.p. administered 4 ml/kg saline 48 h before and 80 mg/kg carboplatin 24 h before. Group 4 (n = 6) was i.p. administered 4 ml/kg NSO 48 h before and 80 mg/kg carboplatin 24 h before. M the end of 48 h, all rats were sacrificed, and liver tissues were put into 10\% neutral formalin. After the routine tissue follow-up, histopathological changes and collagen fiber density were evaluated with Hematoxylin-Eosin and Masson's Trichrome staining. Apoptotic index was determined with TUNEL staining. Results: The degeneration in hepatocytes, fiber distribution and density around central vein and portal space was observed in the carboplatin group compared to the control and NSO groups, hepatocyte cords preserved integrity, partial degeneration in hepatocytes and decreased collagen fiber distribution around central vein was noted in the NSO-carboplatin group compared to the carboplatin group. The apoptosis was lower in the NSO-carboplatin group compare with the carboplatin group, but no statistically significant difference was found between the two groups (p = 0.449). Conclusion: When used NSO before carboplatin exposure, it may protect against liver damage