There are a lot of influencing factors of facial nerve palsy; experts believe that is most likely caused by a Virus (54%) and Bacterial infections. Noninfectious causes of facial nerve palsy induce tumors (28%) and less commonly influences head trauma (18%). The retrospective analysis of WHO, in 2012. There are some cases of postoperative complication in middle ear surgery is facial nerve palsy and the total recovery outcome of function was not good. From 2013 to 2016 in EMJJ hospital, Mongolia, we enrolled 16 cases with facial nerve damaged in intratympanic canal but we could not recruit some patients with facial palsy over 6 months. Each subject was tested with pure tone test, ABR, Tympanometry. These were performed for the detection of hearing loss after Temporal bone injury. Then we also investigated location of facial nerve damages of patients by MRI and CT before reconstructive surgery. After that surgery, all patients were given corticosteroid treatment (20mg/day) and physical therapy performed such as acupuncture for a week. Study results revealed that 6 cases after 18 days, 2 cases after 30 days, 1 patient after 45 days of reconstructive surgery regained good symmetry. Therefore, we considered that, postoperative treatments like physical therapy with B12, steroid had good benefits for operation result and to shorten the recovery time. There was a patient who had damaged facial nerve in the tympanic segment during Mastoidectomy. In that case, we performed cable nerve grafting using the r.auricularismagnium but we could not recover facial nerve function. Traumatic facial nerve paralysis is the second most common type. We discussed that performing reconstruction surgery within first 3 months after intratemporal facial nerve injury is extremely desirable and more effective. In our opinion, nerve recovery might be not successfully cause of injured myelin sheet of facial nerve during middle ear surgery.

BACKGROUND: Toll like receptors (TLRs) are a class of proteins that key role in the innate immune system. TLR7 is expressed on monocytes, macrophages and dendritic cells, T cell, B cell and eosinophiles. TLR7, originally identified as recognizing imidaquinoline, loxibrine, broprimine and ssRNA, ssRNA viruses such as vesicular stomatitis virus, influenza A virus and human immunodefiency virus. It is known that virus ssRNA affects signaling molecule of IFN-y. Objective: To determine gene and protein activation of IFN-y signal transduction by TLR7 ligand in the endothelial cells. MATERIAL: In study we used mouse aortic linear endothelial cell which is cultured (END-D) in 5% heat- inactivated fetal calf serum (FCS), medium (DMEM) containing antibiotic mix(penicillin G, streptomycin, amphotericin B) at 37°C (5% CO2). Endothelial cells treated with synthetic IFN-γ and imiquimodligands, then the NO (nitric oxide) concentration in the supernatant is determined by Griess reagent. Endothelial cells are cultured in 6 well cell culture plate and in each well 2*104cells are expected to be grown for 24 hours of culture. Then, the cells are treated with synthetic IFN-γ and имиквимод ligand for 6 hours and the NO signaling gene activation iNOS mRNA expression which is induced by IFN-γ is determined by RT-qPCR. Endothelial cells are cultured in 12 well cell culture plate and in each well 2*104 cells are expected to be grown for 18 hours of culture. Then, the cells are treated with synthetic IFN-γ and imiquimodligands for 24 hours and the NO signaling protein iNOS expression which is induced by IFN-γ is determined by western blotting. The experiment was conducted as representation mean of at least three test results. The difference between statistical probabilities is determined by the “Students” t test. The p<0.01 value is assumed to be statistically different. RESULTS: TLR7 ligand imiquimodaugmented interferon gamma induced nitric oxide production TLR7 ligand imiquimodincreased interferon gamma induced iNOS mRNA gene expression. TLR7 ilgand imiquimodup-regulated interferon gamma induced iNOS protein expression. CONCLUSIONS: TLR7 ligand imiquimod augments IFN-γ signaling in the endothelial cells. This synergistic effect has revealed in the levels of gene and protein expression.

Introduction: The aim of this research project is to elucidate the crosstalk of innate and adaptive immune reactions against the DNA containing bacteria. : This study held in the Core laboratory, Science Technology Center, Mongolian National University of Medical Sciences (MNUMS). Murine aortal endothelial cells, END-D cultured and the cell viability checked by MTT assay. In addition, the NO production, protein and gene expression studied by Griess Reagent assay, R.T-PCR and immunoblotting, respectively. Results: 0.1µM, 1µM and 10µM of TLR9 ligand exhibited no cytotoxic action against the cells by MTT assay. IFN-ү alone induced NO production in END-D cells. In the other hand, TLR9 ligand at 0.1µM, 1µM and 10µM up-regulated IFN-ү induced NO production in dose dependent manner. RTPCR results exhibit that TLR9 ligand up regulates iNOS mRNA. Immunoblotting analysis showed the enhanced iNOS protein expression and phosphorylation of STAT1 in cells pre-treated with TLR9 ligand. Discussion: We have demonstrated CpG DNA, TLR9 ligand, up-regulates IFN-ү induced NO via enhanced IFN-ү signaling. The result of Western Blotting and RT-PCR support the up-regulation of NO. CpG DNA can be used as agent against virus and bacteria. Further research need to be conducted. Conclusion TLR9 ligand, CpG DNA up-regulates IFN-ү induced NO production in time and dose dependent manner. TLR9 ligand augments the expression of iNOS mRNA and STAT1 phosphorylation in response to IFN-ү.