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This research attempted to elucidate the molecular components are involved in the pathogenesis of recurrent implantation failure (RIF). We initially identified that 386 mRNAs, 144 miRNAs and 2548 circRNAs were differentially expressed (DE) in RIF and then investigated the genetic cause of the observed abnormal expression by constructing a circRNA‐miRNA‐mRNA network considering the competing endogenous RNA theory. We further analysed the upstream transcription factors and related kinases of DEmRNAs (DEMs) and demonstrated that SUZ12, AR, TP63, NANOG, and TCF3 were the top five TFs binding to these DEMs. Besides, protein‐protein interaction analysis disclosed that ACTB, CXCL10, PTGS2, CXCL12, GNG4, AGT, CXCL11, SST, PENK, and FOXM1 were the top 10 hub genes in the acquired network. Finally, we performed the functional enrichment analysis and found that arrhythmogenic right ventricular cardiomyopathy (ARVC), hypertrophic cardiomyopathy (HCM), pathways in cancer, TNF signalling pathway and steroid hormone biosynthesis were the potentially disrupted pathways in RIF patients. Optimistically, our findings may deepen our apprehensions about the underlying molecular and biological causes of RIF and provide vital clues for future laboratory and clinical experiments that will ultimately bring a better outcome for patients with RIF.

BackgroundAlzheimer’s disease (AD) is a degenerative condition characterized by progressive cognitive impairment and dementia. Findings have revolutionized current knowledge of miRNA in the neurological conditions. Two regulatory mechanisms determine the level of mature miRNA expression; one is miRNA precursor processing, and the other is gene expression regulation by transcription factors. This study is allocated to the in-silico investigation of miRNA’s SNPs and their effect on other cell mechanisms.MethodsWe used databases which annotate the functional effect of SNPs on mRNA-miRNA and miRNA-RBP interaction. Also, we investigated SNPs which are located on the promoter or UTR region.ResultsmiRNA SNP3.0 database indicated several SNPs in miR-339 and miR-34a in the upstream and downstream of pre-miRNA and mature miRNAs. While, for some miRNAs miR-124, and miR-125, no polymorphism was observed, and also miR-101 with ΔG -3.1 and mir-328 with ΔG 5.8 had the highest and lowest potencies to produce mature microRNA. SNP2TFBS web-server presented several SNPs which altered the Transcription Factor Binding Sites (TFBS) or generated novel TFBS in the promoter regions of related miRNA. At last, RBP-Var database provided a list of SNPs which alter miRNA-RBP interaction pattern and can also influence other miRNAs’ expression.DiscussionThe results indicated that SNPs microRNA affects both miRNA function and miRNA expression. Our study expands molecular insight into how SNPs in different parts of miRNA, including the regulatory (promoter), the precursor (pre-miRNA), functional regions (seed region of mature miRNA), and RBP-binding motifs, which theoretically may be correlated to the Alzheimer’s disease.

Objective. Pregnancy can cause diabetic conditions and gestational diabetes is the most common metabolic disorder of the era. Scientific evidence suggests that obesity increases the incidence and severity of gestational diabetes. Adipokines are proteins secreted from adipose tissue in response to extracellular stimuli and altered metabolism. These hormones are involved in regulating the energy balance, lipid metabolism, and insulin sensitivity. One of the types of adipokines is called adiponectin, which has anti-diabetic, anti-inflammatory, and anti-atherogenic effects. Accordingly, this study is aimed to investigate the correlation between the serum adiponectin level with the gestational diabetes and the postpartum metabolic syndrome.Methods. This case-control study was carried out on 37 pregnant women (in Sari, Iran) with gestational diabetes and 37 non-diabetic pregnant women who were matched regarding age and body mass index (BMI). Serum adiponectin and glucose levels were measured. Finally, six weeks after termination of pregnancy, women in both groups were evaluated for metabolic syndrome. All statistical analyses of this study were performed using IBM SPSS software version 21 and, in all cases, the two-way p value less than 0.05 was considered statistically significant.Results. The mean age of pregnant women was 28.46±4.11 years in the non-diabetic group and 30.03±4.71 in the diabetic group. There was no statistically significant difference found between the mean age (p=0.123) and BMI (p=0.727) in two groups. Serum adiponectin levels in the diabetic group (5.51±3.15 µg/ml) were significantly lower than in the non-diabetic group (8.35±4.54 µg/ml) (p=0.003). In the diabetic group, serum adiponectin level did not correlate with the maternal age, maternal BMI, and postpartum metabolic syndrome (p>0.005).Conclusions. The results of the present study indicate a correlation of low adiponectin concentrations with gestational diabetes, but this association with postpartum metabolic syndrome is uncertain. However, to elucidate the mechanism of adiponectin in predicting gestational diabetes and postpartum metabolic syndrome further studies are required.

MicroRNAs (miRNAs) constitute a large family of small non-coding RNAs which regulate gene expression at the surface following transcription. They are widely involved in many physiological and pathological processes including polycystic ovarian syndrome (PCOS). PCOS is an endocrine disorder in women. Currently, there is no comprehensive information about the role of miRNAs in PCOS. Thus, this paper has attempted to collate studies on miRNAs in order to determine important changes in their miRNA expression profile in the total blood, serum, plasma, follicular fluid, and granulosa cells in PCOS patients alongside the genes which are targeted for regulation by these miRNAs. This study presents a new approach for using miRNAs and their target genes for diagnosing and treating PCOS.