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@#BACKGROUND. Prostaglandin E2 (PGE2) is the most abundant prostanoid and a very potent lipid mediator, and is produced predominantly from arachidonic acid by it’s tightly regulated cyclooxygenases (COXs) and prostaglandin E synthases. PGE2 is involved in regulating many different fundamental biological functions, including immune responses. Recently, we have demonstrated that bacterial LPS induces NO production in auditory cells via an inducible NO synthase expression. The LPS-induced production of an excessive NO amount is suggested to cause injury of auditory cells, followed by ototoxicity. Auditory cells injured by such an inflammatory response must be accompanied by tissue repair and remodeling. In order to clarify the production of PGE2 in auditory cells for regulation of inflammatory response or tissue repair AIM: We aimed to examine an effect of LPS on the production of prostaglandin E2 in auditory cells. MATERIALS AND METHODS: The murine auditory cell line HEI-OC1 was established from long-term cultures of immortomouse cochlea and used as conditionally-immortalized auditory cells. HEI-OC1 cells were stimulated with or without LPS. The concentration of PGE2, TNF-α, IL-1β in the culture supernatant was determined with ELISA. COX-2 protein expression and mRNA were measured by immunoblotting and reverse transcription PCR, respectively. The bands were quantified by densitometric analysis using ImageJ software. Statistical analysis was performed using Student’s t-test and P values < 0.05 were considered significant. All experiments were performed independently at least three times. Data represent the mean value of triplicates SD. RESULT: HEI-OC1 auditory cells constitutively produce a small amount of PGE2. LPS augmented the PGE2 production via enhanced cyclooxygenase 2 (COX2) expression. LPS-induced augmentation of COX2 expression was dependent on up-regulation of COX2 mRNA expression. LPS induced the production of TNF-a, but not IL-1b An anti-TNF-α neutralizing Ab significantly inhibited PGE2 production and COX2 mRNA expression in response to LPS. LPS-induced PGE2 production was prevented by a series of pharmacological signaling inhibitors to NF- κB and MAPKs. Pam3CSK4 as a TLR2 ligand, as well as LPS as a TLR4 ligand, augmented the PGE2 production. However, poly I:C as a TLR3 ligand, imiquimod as a TLR7 ligand and CpG DNA as a TLR9 ligand did not augment it. HEI-OC1 cells expressed TLR2, TLR4 and TLR9, but not TLR3 or TLR7. CONCLUSION: The auditory cells produce PGE2 in response to LPS via COX2 expression. The PGE2 production may be involved in tissue repair and remodeling in the organ of Corti. Auditory cells might be important effector cells in host response to infection and inflammation in the organ of Corti and cochleae.
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INTRODUCTION:In Mongolia, The anatomists researched morphometric measurements and blood supply ofheart in adult’s liver pancreas, spleen, Ren and spinal cord and etc... The study of morphometricmeasurements of the choroid plexus is not being taught in Mongolia.GOAL:To determine the structure of the choroid plexus of adult brain ventricle.MATERIALS AND METHODS:This study obtained choroid plexus size in 84 dead bodies, which is between the adult and childrenfrom cadavers. To determine the choroid plexus morphometric measurements, the total 336specimens were evaluated. The standards deviation of choroid plexus length and thickness werecomputed in different ages.RESULT:In present study, the maximum length and thickness were determined in ages from 22-60. In presentstudy, the minimum length and thickness were determined in ages 0-10day. In adult, the meanchoroid plexus length was 8.61±0.15 cm of the lateral ventricles and 4.47±0.02 cm of the fourthventricles and 0.56±0.140 cm of the third ventricle and the choroid plexus thickness was 0.5±0.03cm of the lateral ventricles and 0.29±0.01 cm of the fourth ventricles and 0.28±0.01 cm of the thirdventricle.CONCLUSIONS:In adult, the mean choroid plexus length was 8.61±0.15 cm of the lateral ventricles and 4.47±0.02cm of the fourth ventricles and 0.56±0.140 cm of the third ventricle and the choroid plexus thicknesswas 0.5±0.03 cm of the lateral ventricles and 0.29±0.01 cm of the fourth ventricles and 0.28±0.01cm of the third ventricle.The choroid plexus weight was 0.51±0.01 gm in the lateral ventricles and 0.42±0.014 gm in thefourth ventricle.
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Background:The cardiovascular disease especially coronary artery disease is the leading cause of mortality in worldwide. There is lack of research study which evaluated stenosis of coronary atherosclerosis. It is known that coronary stenosis is highly connected to the levels of biomarkers. Coronary atherosclerosis correlated with endothelin receptor type A (EDNRA) levels in a group of patients suspected of having coronary artery disease.Objective:The goal of this study was to evaluate the relation between the coronary atherosclerosis and levels of EDNRAMethods:A total of 311 participants were involved in this study. A case-control study was used in the study. The baselines data were collected from the department of Angiography at the National Third Central Hospital and National lilood Transfusion and Research center. We have determined the degree of coronary atherosclerosis using the Angiography machine and Elisa were used for detecting the blood endothelin levels in all groups.Results:98 participants were diagnosed with stenosis and occlusion. The blood endothelin levels were estimated to 6.32±0.64 pg/ml which refer to () degree of coronary stenosis, the first degree of stenosis of coronary atherosclerosis is estimated to 5.56±0.22pg/ml, the second degree of stenosis of coronary atherosclerosis is estimated to 5.42J0.34 pg/ml, the third degree of stenosis of coronary atherosclerosis is estimated to 5.87 H). 13 pg/ml, the fourth degree of stenosis of coronary atherosclerosis is I'SlilllSltll lo 5.69±0.09 pg/ml, it was estimated to 5.88±0.13 pg/ml in control groups. Level of EDNRA (occupying one segment of coronary artery) was estimated to 5.77±0.08 pg/ml. two segment involvement was estimated to 5.72±0.16 pg/ml, three segment involvement 5.73±0.19 pg/ml. four segments involvement 5.50±0.25 pg/ml, respectively.Conclusion:The blood endothelin level and coronary artery stenosis were not correlated statistically significant in control group of the study. However, blood endothelin levels were increased in patients who tend to experience the coronary artery stenosis.
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Background: The cardiovascular disease especially coronary artery disease is the leading cause of mortality in worldwide. There is lack of research study which evaluated stenosis of coronary atherosclerosis. It is known that coronary stenosis is highly connected to the levels of biomarkers. Coronary atherosclerosis correlated with endothelin receptor type A (EDNRA) levels in a group of patients suspected of having coronary artery disease. Objective: The goal of this study was to evaluate the relation between the coronary atherosclerosis and levels of EDNRA Methods: A total of 311 participants were involved in this study. A case-control study was used in the study. The baselines data were collected from the department of Angiography at the National Third Central Hospital and National lilood Transfusion and Research center. We have determined the degree of coronary atherosclerosis using the Angiography machine and Elisa were used for detecting the blood endothelin levels in all groups. Results: 98 participants were diagnosed with stenosis and occlusion. The blood endothelin levels were estimated to 6.32±0.64 pg/ml which refer to () degree of coronary stenosis, the first degree of stenosis of coronary atherosclerosis is estimated to 5.56±0.22pg/ml, the second degree of stenosis of coronary atherosclerosis is estimated to 5.42J0.34 pg/ml, the third degree of stenosis of coronary atherosclerosis is estimated to 5.87 H). 13 pg/ml, the fourth degree of stenosis of coronary atherosclerosis is I'SlilllSltll lo 5.69±0.09 pg/ml, it was estimated to 5.88±0.13 pg/ml in control groups. Level of EDNRA (occupying one segment of coronary artery) was estimated to 5.77±0.08 pg/ml. two segment involvement was estimated to 5.72±0.16 pg/ml, three segment involvement 5.73±0.19 pg/ml. four segments involvement 5.50±0.25 pg/ml, respectively. Conclusion: The blood endothelin level and coronary artery stenosis were not correlated statistically significant in control group of the study. However, blood endothelin levels were increased in patients who tend to experience the coronary artery stenosis.