These data suggest that SSRIs have a negative effect on testicular tissues. This negative impact is markedly greater in the paroxetine group. To determine the exact mechanism of action of these drugs on testicular tissue, well-designed randomized controlled clinical studies are needed on a larger population.

Our findings show that patients with SCF have significantly increased RDW and serum uric acid levels. This may help throw more light on the pathophysiological basis of SCF.

We aimed to determine the protective effects of thymoquinone (TQ), against ischaemia-reperfusion (I/R) injury in the testis tissue of rats. Twenty-seven male Wistar albino rats were randomly divided into three equal groups as follows: Group I, sham group; Group II, torsion group; and Group III, torsion + thymoquinone group. The ischaemia period was 2 h, and orchiectomy was performed after 30 min of detorsion. Testis tissue sections were analysed with the terminal transferase mediated dUTP-nick end labelling (TUNEL) assay to determine in situ apoptotic DNA fragmentation. Additionally, Caspase 3 and Bax proteins were analysed immunohistochemically. The superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) activity levels in the testis tissue were also measured. The superoxide dismutase activity and malondialdehyde levels in the torsion group were significantly higher than those of the sham group (P < 0.05). Thymoquinone administration significantly reduced these levels. Torsion significantly increased active-Caspase 3 and Bax expression, which was decreased by thymoquinone. The apoptotic index of the torsion group was significantly higher than that of the control group. However, thymoquinone significantly reduced the apoptotic index (P < 0.05). Our results indicate that thymoquinone plays a protective role in oxidative stress induced ischaemia-reperfusion in the testis tissue of rats.

We found higher levels of PAPP-A and CRP and the presence of a good correlation between CRP and MAP in pre-eclampsia.

Objective:Contrast-induced nephropathy (CIN) is one of the most common causes of acute renal failure in hospitalized patients. The direct toxic effect of contrast media; ischemic damage caused by reactive oxygen species; increased perivascular hydrostatic pressure; high viscosity and changes in the activity of vasoactive substances play important roles in the pathogenesis. Tadalafil inhibits the phosphodiesterase enzyme which destroys nitric oxide. Nitric oxide causes renal vasodilatation, increases renal medullar blood flow and mediates the removal of free oxygen radicals. Drugs that increase levels of nitric oxide are expected to reduce the development of contrast nephropathy due to contrast media. We aimed to test the hypothesis that tadalafil reduces the development of contrast nephropathy due to contrast toxicity.Methods:A total of 24 female Wistar albino rats, three groups of eight, were included in the study. After 48 hours of dehydration, contrast media (meglumine diatrozoate, 6 mL/kg) was administered to the first group, and contrast media with tadalafil (10 mg/kg) was administered to the second group. The third group served as the control group. Blood and tissue samples were taken 48 hours after this procedure.Results:Serum cystatin C, serum creatinine and blood urea nitrogen (BUN) values were significantly lower in the contrast with tadalafil group compared to the group given only contrast. Serum and tissue malondialdehyde (MDA) levels were significantly lower in the contrast with tadalafil group than in the contrast only group.Conclusion:These results demonstrate the protective effect of tadalafil in the prevention of CIN in rats.