Aim To assess kallikrein ( KLK ) expression in recurrent and non-recurrent prostate tumors and adjacent healthy prostate tissues. Methods The expression levels of 15 KLK genes in 34 recurrent and 36 non-recurrent prostate cancer samples and 19 adjacent healthy prostate tissue samples was assessed with quantitative reverse-transcription polymerase chain reaction. The samples were obtained from Baylor College of Medicine, Houston, TX, USA between 2013 and 2016 . Results Compared with controls, prostate cancer samples showed a strong decrease in KLK1, KLK4, KLK9, and KLK14 . Recurrent samples were negative for KLK1 , KLK2, and KLK14 but demonstrated higher levels of KLK3, KLK4, and KLK9 than controls. Other KLK s were not significantly expressed. Conclusion This study for the first time showed a difference in the expression levels of the KLK gene family in recurrent prostate cancer. KLK s could be used as recurrence markers for prostate cancer.

Aim To perform a mutation analysis of FK506 binding protein-like (FKBPL) in patients with azoospermia.Methods DNA samples were isolated from the peripheral blood of 30 azoospermic male patients with normal 46 XY karyotype and 10 healthy controls. Multiplex polymerase chain reaction assays were used to evaluate Y microdeletions, and the patients without deletions were further analyzed. Sanger sequencing was used for mutation analysis. ResultsA heterozygous adenine to guanine substitution was observed at position c.28 (c.28A>G) (one patient), guanine to adenine substitution at c.90 (c.90G>A) (three patients), and a novel insertion mutation of TCTCATAAGTCT at c. 229_240dup (two patients), all in FKBPL exon 2. Furthermore, four different benign variants were observed in the same gene. ConclusionOur study supports the literature on the etiologic effects of changes on autosomal chromosomes and highlights the importance of molecular analysis of all known and unknown genes that could be involved in male sexual development and function.

Background/Aim:Currently, there is not any specific treatment for chronic pancreatitis (CP). It was aimed to investigate the effects of melatonin administration on endoplasmic reticulum (ER) stress, oxidative stress, fibrosis, biochemical and histopathological parameters and Abcc2,Abcc5 and Abcg2 gene levels in an experimental rat CP model. Methods: Forty rats were randomized into five groups: Sham, CP, CP+25 mg/kg melatonin, CP+50 mg/kg melatonin, and CP+placebo. In all rats except the sham group, a model of chronic pancreatitis was accomplished with intraperitoneal caerulein administration. In treatment groups, melatonin was used as a therapeutic agent. Serum TGF-β, TNF-α, MDA and GPx levels were studied. Pancreatic tissues were evaluated histopathologically. The expression levels of αSma,IR1α,Perk,Abcc2,Abcc5 and Abcg2 genes were measured with the qRT-PCR.Results: Biochemical results of the melatonin groups exhibited favorable changes compared to the CP and placebo groups. αSma,IR1α,Perk expression levels were significantly lower in the melatonin groups. The expression levels of Abcc2, Abcc5 and Abcg2 were significantly higher in the CP group compared to the sham group and these gene levels were significantly lower in the melatonin groups compared to the CP group (p<0.01, p<0.05, p<0.05, respectively). Conclusion:In light of these favorable positive results, melatonin may be a useful preventive agent in the course of CP.

Aim In this study, it was aimed to investigate the relationship between expression levels of micro‐RNAs, endoplasmic reticulum (ER) stress, apoptosis and oxidative stress markers in hepatic ischaemia–reperfusion (IR) injury. Methods Sixteen rats were randomised into two groups: Sham and IR groups. In the IR group, portal vein and hepatic artery were totally clamped with an atraumatic microvascular clamp and 60 minutes later unclamped and finally IR model was accomplished (60 minutes ischaemia and 60 minutes reperfusion). After sacrification, serum insulin‐like growth factor‐1 (IGF‐1), tumour necrosis factor‐α (TNF‐α), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Liver tissue samples were evaluated histopathologically. The expression levels of IR1‐alpha, Perk, Catalase, Gpx‐1, Caspase‐3, Bcl‐2 genes and miR‐33a, miR‐221, miR‐190b, miR‐363‐3p, miR‐200c, miR‐223, miR‐133b were measured by quantitative real‐time polymerase chain reaction method. Results Biochemical parameters of the IR group showed significantly higher changes compared with the Sham group (P < .01). Histological tissue damage was significantly prominent in the IR group. ER stress, oxidative stress and apoptosis gene expression levels were significantly higher in the IR group (P < .01). Expression levels of miR‐221, miR‐190b, miR‐363‐3p and miR‐200c were increased in the IR group compared with the Sham group. No significant difference was found between the two groups in terms of miR‐33a, miR‐133b and miR‐223 expression levels (P > .05). Conclusion There is a strong need to enlighten the physiopathological and molecular mechanisms of liver IR injury and to find more specific biomarkers for IR damage, and miR‐221, miR‐190b, miR‐363‐3p and miR‐200c maybe used as potential biomarkers of hepatic IR injury.