Background:Acute diarrheal disease and urinary tract infection are leading causes of childhood morbidity and mortality in the developing world. Diarrheagenic Escherichia coli (DEC) has been identified as a major etiologic agent of diarrhea worldwide, and urinary tract infection (UTI) caused by uropathogenic Escherichia coli (UPEC) is one of the most common bacterial infections among human beings. Quick and precise detection of these bacteria help provide more effective intervention and management of infection.Objectives:In this study we present a precise and sensitive typing and phylogenetic study of UPEC and DEC using multiplex PCR in order to simplify and improve the intervention and management of diarrheal and UT infections.Materials and Methods:In total, 100 urinary tract infection samples (UTI) and 200 specimens from children with diarrhea, which had been diagnosed with E. coli as the underlying agent by differential diagnosis using MacConkey’s agar and biochemical study, were submitted for molecular detection. Pathotyping of E. coli pathotypes causing urinary tract infection and diarrhea were examined using a two set multiplex PCR, targeting six specific genes. Phylogenetic typing was done by targeting three genes, including ChuA, YjaA and TspE4C2.Results:Overall, 88% of DEC and 54% of UTI isolates were positive for one or more of the six genes encoding virulence factors. Prevalence of the genes encoding virulence factors for DEC were 62%, 25%, 24%, 13%, 7% and 5% for ST (ETEC), LT (ETEC), aggR (EAggEC), daaD (DAEC), invE (EIEC) and eae (EPEC), respectively; whereas, the prevalence rates for the UTI samples were 23%, 14%, 6%, 6% and 4% for aggR (EAggEC), LT (ETEC), daaD (DAEC), invE (EIEC) and ST (ETEC), respectively. No coding virulence factors were detected for eae (EPEC). Group B2 was the most prevalent phylogroup and ST was the most frequently detected pathotype in all phylogroups.Conclusions:ETEC and EAggEC were the most detected E. coli among stool and UTI samples, emphasizing the need to dedicate more health care attention to this group. In addition, our phylogenetic study may be helpful in figuring out the infection origin and for epidemiological studies. Nonetheless, more research studies with larger sample sizes are suggested for confirming our results.

Recently, ST18 polymorphism has played a role in increasing the risk of pemphigus among some populations such as Egyptian and Jewish. In addition, a variant within the ST18 promoter gene was shown to induce ST18 upregulation and cytokine secretion leading to keratinocyte susceptibility to anti-desmoglein antibodies. Thus, the present study aimed to assess the ST18 single nucleotide polymorphisms (SNP) relationship with pemphigus, disease severity and family history among Iranian population. A total of 111 pemphigus patients and 201 healthy controls were genotyped for three ST18 SNPs rs2304365, rs10504140 and rs4074067 by using TETRA-ARMS PCR method. The results indicated that risk allele A in rs2304365 was significantly higher in pemphigus patients, compared with the amount in the control group (OR = 2.43 CI = 1.49-3.975, P < 0.001). Thus, A allele represents a risk factor for pemphigus. Further, the patients carrying the risk allele had a more severe disease and a higher age of disease onset while no relationship was observed between the number of relapses and positive family history of pemphigus with the risk allele. Finally, dominant model was regarded as the strongest inheritance model for the associated risk. The present study confirmed the relationship between ST18 gene with pemphigus disease, a more severe disease, and a higher age of disease onset.

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A growing amount of evidence has revealed that long noncoding RNAs (lncRNAs) play significant roles in malignancies through different mechanisms especially the competing endogenous RNA (ceRNA). They have also been shown to have the potential diagnostic, prognostic and therapeutic biomarker capacity in oncology research. Recently, lncRNA Alu-mediated p21 transcriptional regulator (APTR) has been proposed as an oncogenic lncRNA in development and clinical outcome of some cancers. However, clinical and molecular importance in breast cancer (BC) is still unclear. The purpose of this study was to examine the APTR expression and its potential roles in BC. The 47 BC tumors and 47 tumor adjacent normal tissues were obtained from the study subjects. Real-time PCR was applied for the analysis of APTR expression in breast tumors compared with paired adjacent normal tissues. Then, we used bioinformatics approach to investigate the potential ceRNA activity of APTR in APTR-microRNAs-mRNAs axes and with focus on ErbB signaling pathway in BC. Our results demonstrated that APTR expression was significantly upregulated in BC tumors compared with the adjacent normal tissues. Besides, APTR over-expression was related to a larger tumors size. Finally, bioinformatics analysis indicated that APTR could influence cell proliferation through dysregulating the oncogenes working in ErbB signaling pathway by sponging some tumor suppressive microRNAs (miRNAs). Current work provided some clues for the involvement of APTR in physiopathology of the breast tumors. However, other aspects of these findings need to be further elucidated by future functional studies.

RNAs have long been described as the mediators of gene expression; they play a vital role in the structure and function of cellular complexes. Although the role of RNAs in the prokaryotes is mainly confined to these basic functions, the effects of these molecules in regulating the gene expression and enzymatic activities have been discovered in eukaryotes. Recently, a high-resolution analysis of the DNA obtained from different organisms has revealed a fundamental impact of the RNAs in shaping the genomes, heterochromatin formation, and gene creation. Deep sequencing of the human genome revealed that about half of our DNA is comprised of repetitive sequences (remnants of transposable element movements) expanded mostly through RNA-mediated processes. ORF2 encoded by L1 retrotransposons is a cellular reverse transcriptase which is mainly responsible for RNA invasion of various transposable elements (L1s, Alus, and SVAs) and cellular mRNAs in to the genomic DNA. In addition to increasing retroelements copy number; genomic expansion in association with centromere, telomere, and heterochromatin formation as well as pseudogene creation are the evolutionary consequences of this RNA-based activity. Threatening DNA integrity by disrupting the genes and forming excessive double strand breaks is another effect of this invasion. Therefore, repressive mechanisms have been evolved to control the activities of these invasive intracellular RNAs. All these mechanisms now have essential roles in the complex cellular functions. Therefore, it can be concluded that without direct action of RNA networks in shaping the genome and in the development of different cellular mechanisms, the evolution of higher eukaryotes would not be possible.