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Introduction: SARS-CoV-2, as a major threat to human health and economy, has brought in uncertain consequences in the early decade of the 21st century. Since no antiviral therapy or effective vaccine against SARS-CoV-2 is currently available, deciphering the possible mechanisms by which the host responds to the virus seems critical, as it may affect the scientific community around the world toward the development of novel therapeutics. Here, we identified the key regulatory molecules modulating the host response to SARS-CoV-2 that affected the transcriptional profiles of respiratory infections in vitro. Materials and Methods: We used the data recently published on the effect of SARS-CoV-2 on two lung cell lines. We selected the shared differentially expressed genes (DEGs) between the two cell lines. To find the key regulatory molecules, we used transcription factors-miRNA-gene interaction databases and analyzed the data using the FANMOD software to detect the crucial regulatory motifs. Cytoscape was then applied to construct the network. We used the KEGG pathway and Gene Ontology (GO) enrichment analysis to predict the probable intermediating biochemical pathways and biological processes. Results: Our data demonstrated that four triangle-shaped (3edge) feed-forward loop motifs (FFLs) played significant roles, and the integrated FFLs subnetwork was constructed. STAT1, IRF9, IRF7, and PRK12 were the genes shared among them. The most important biological processes relating to the effect of the new virus were linked to response to cytokine, innate immune response, and adaptive immune response. Besides, significantly enriched pathways associated with other different viral infections included the nuclear factor κ-light-chain-enhancer of activated B cells (NF-kappa B) signaling pathway, the nucleotide-binding oligomerization domain-like (NOD-like) receptor signaling pathway, and the Jak-STAT signaling pathway. Conclusion: Most of the pathways were related to the cytokines storm that may contribute to different levels of lung injury. These regulatory motifs shed light on the transcriptional signature of the respiratory cells and may be responsible for the development of COVID-19 or can also be used as a potential target for further drug therapies or vaccines.

Introduction: Reprograming different cell to neuron have been yet remain attractive field in in regenerative medicine, so discovery new methods or improve exist methods could be helpful. In this study, we analysis the transcriptome data of glia and neuron cells to determine the different gene expression in both groups. Then based on this transcriptom data determine the gene chemical interaction to find the most important chemical structure which induce glia cell to neurons. Material and methods: Data extract from transcriptome database related rat cerebral cortex cells generated by RNAseq technique. By comparison neuron against glia cells (astrocyte, oligodenderocyte and microglia) determined different gene expression. In CTD database determined the most important chemical interact with this gene set. Then by using genetrail2 database determined mechanism of gene set associated to chemicals and miRNA enriched. Results: Result determined different chemical with risk factor and protective factor properties related to 500 genes that enriched in neuron in comparison with glia cells. Carbon nanotube is the first important chemicals that interact with 75 genes of 500. Gene ontology analysis determined carbon nanotube effect on genes that induce neurogenesis, neurodevelopment and differentiation. Genetrail2 release the 29 significant miRNAs enriched in gene interacts with carbon nanotube in which miR-34a and miR-449a are the most significant molecules. Network analysis on these genes represents Kit, Gria1, Syt1, Rab3c and Tubb3 have central roles in neurogenesis by carbon nanotube. Conclusion: In sum up, carbon nanotube is the electrical stimulation biomaterial that are biocompatible to induce glia cell to neuron which apply as devise lonely or combination with cell in damage part of neural tissue.

Introduction: Oral squamous cell carcinoma (OSCC) is the most abundant dysplasia in the oral cavity that aberrant expression of microRNA plays an important role in cancer progression. It is well known that microRNA-21 expression is oncogenes or tumor suppressor factor in malignancy formation of several cancers. In this study used OSCC tissues to investigate the expression of mir-21 in malignancy causes. Material and Methods: OSCC tissues and normal samples were collected from Amir Alam and Taleghani Hospitals as fresh and frozen samples. The Expression level of miR-21 in OSCC and normal tissues were measured by qRT-PCR. To find the targets related mir-21 used databases including TargetScan, GenTrail2, GO and STITCH online websites. Results: MiR-21 found significantly up-regulated in OSCC tissues compared to normal tissues (Fold-change=5.54). Targets of miR-21 derived from the TargetScan and GeneTrail2 analysis determined the most significant biological processes be associated with the epithelialization, differentiation, and morphogenesis. So overexpression of miR-21 could reverse this process and promote the cells to stemness and metastatic state. EGFR and PDCD4, two targets of miR-21, previously have been demonstrated that are important in OSCC invasion, metastasis, and differentiation. In addition study on targets genes to find anticancer drugs enriched CI-1033 as a tyrosine-kinase inhibitor that previously reported for the treatment of cancer. Conclusion: Our findings indicate miR-21 act as oncomiR in OSCC and may be considered as a biomarker for the development of OSCC treatment.