miR-122 and miR-192 were investigated as indicators of toxic liver injury caused by acetaminophen, but their role in idiosyncratic toxic liver injury remains controversial.So, this work aimed to assess and compare the expressions of miR-122 and miR-192 in two different types of toxic liver injury (intrinsic [acetaminophen] and idiosyncratic [diclofenac]). Forty male adult Wistar albino rats were divided into equal five groups, in which serum liver enzymes; microRNAs (miRNAs) expressions (miR-122 and miR-192) and histopathological findings were studied. The present study showed that (1) miR-122 and miR-192 are good serum biomarkers of toxic liver injury whatever its etiology, as their serum levels exhibited a significantly earlier increase and earlier return to normal baseline levels as compared to serum aminotransferase levels;(2) miR-122 is more specific than miR-192; and (3) both serum levels of miR-122 and miR-192 showed non-significant differences in relation to the type of toxic liver injury. K E Y W O R D S biomarkers, hepatotoxicity, idiosyncratic, intrinsic, miR-122, miR-192, real-time polymerase chain reaction J Biochem Mol Toxicol. 2019;33:e22321. wileyonlinelibrary.com/journal/jbt

Problem statement: Thrombophilia has been recently implicated in early pregnancy loss and IVF implantation failure, by impairing the initial vascularization process occurring at implantation, which is necessary for a successful pregnancy. Approach: The aim of this study is to assess the presence possibility of mutation in thrombophilic genes [Factor V (FV) gene, Prothrombin (PT) gene and Methylenetetrahydrofolate Reductase (MTHFR) gene] in women with repeated IVF-embryo transfer failure with unknown causes. The study was performed on patients with two or more previously failed IVF-embryo transfer cycles with unknown causes. Women who conceived spontaneously with no previous history of miscarriage and women who have had successful pregnancy after their first IVF-embryo transfer cycle are included as control groups. Results: There are increase in allelic frequencies of thrombophilic genes (factor V, prothrombin and methylenetetrahydrofolate reductase) mutation, in addition to genotype frequencies (both homozygote and heterozygote) and increase in frequency of multiple gene mutations among women with IVF-embryo transfer failure. Conclusion: Thrombophilia has a significant role in IVF-embryo transfer implantation failure. Women with repeated IVF-embryo transfer failure should be screened for Thrombophilia to avoid repeated IVF-embryo transfer failure.

Growing evidence indicates that TNF-alpha is involved in the pathogenesis of POAG in several ways, primarly by induction of retinal ganglion cells apoptosis and therefore optic nerve degeneration. TNF-alpha and POAG relationship has been studied at the genetic level with variable results in different populations. The transcription rate and the release of the TNF-alpha cytokine have been reported to be affected by polymorphisms in the promoter of the TNF-alpha gene. Polymorphisms at positions -238 and -308 are the most frequent studied. Another polymorphism, at the position -863 in the promoter region, has been less studied, but a homozygous AA allele appears protective in a Chinese population. Our aim was to assess the potential association of -863C/A TNF-alpha gene promoter polymorphisms with POAG in an Egyptian group of subjects. Genotyping of the TNF-alpha (-863) polymorphism was done for 228 POAG patients and 230 control subjects using the PCRbased, Restriction Fragment Length Polymorphism (RFLP) assay. TNFalpha (-863) A/A genotype was absent in both groups. There was no significant difference between both groups as regards to TNF-α (-863) A allele carriage (6.14 versus 10.43%; p = 0. 099)). Also the genotype TNF-α (-863) C/C and the frequency of the tumor necrosis factor-alpha (-863) C allele did not significantly differ between both groups (93.86 versus 89.57%; p = 0. 099) and 96.93 versus 94.78%; p = 0. 107) respectively. Our data indicated that the TNF-alpha (-863) a allele is not linked with primary open angle glaucoma protection among Egyptian patients.

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Background & Aim: Fibroblast growth factor 21 (FGF21) is a peptide hormone recently discovered to be released from brown adipocytes. It plays an outstanding role in the metabolic homeostasis. Induction of brown-like adipocytes termed beige/brite within the white adipose tissue (WAT) by means of browning agents is known as "browning process". These beige/brite cells due to plenty of mitochondria and unique expression of uncoupling protein-1 (UCP1), promotes energy expenditure. Being the WAT is excessively expanded in adiposity, the browning agents have gained great interest to combat obesity. The browning effect of Sildenafil (Sild) in obese rats stills a matter of debate. So, we aimed to illustrate it. Method & Results: 3 groups of rats were conducted; control group fed standard diet for 9 weeks, obese non-treated group fed high-fat diet (HFD)-fed group for 9 weeks, and Sild-treated group fed HFD for 9 weeks and received Sild (20 mg /kg/s.c./each) twice daily in the last 3 weeks. Our findings revealed Sild reduced weight gain, fat depots weight, and adiposity index in spite of unchanged food intake. Additionally, it reduced serum triglycerides, free fatty acids, glucose, insulin, and insulin resistance index. The subcutaneous WAT of Sild-treated rats exhibited augmented UCP1, citrate synthase activity, and FGF21 and FGF21-Receptor1 expressions with the highest FGF21 serum levels. Conclusions: the present study suggested a protective impact of Sild against adiposity and insulin resistance through browning of WAT with enhanced FGF21-Receptor1 expression.