Low Antioxidant Enzyme Levels and Oxidative Stress in Laryngopharyngeal Reflux (LPR) Patients.

OBJECTIVE: Laryngopharyngeal reflux disease (LPR) is a characterized by symptoms different from gastroesophageal reflux disease (GERD). LPR can causes chronic mucosal inflammation which may lead to an increase in cytokine production, and a systemic decrease in antioxidant enzyme levels. Our aim in this study is to evaluate antioxidant enzyme levels in patients with LPR. METHODS: Reflux Symptom Index (RSI) questionnaire, extraesophageal symptom questionnaire which is included in RSI and Reflux Finding Score (RFS) evaluation with 70° rigid laryngoscope were performed to patients who applied to the otolaryngology clinic with a typical LPR complaint, and 60 patients who had an RSI score above 13 and an RFS score above 7 were included in the study. Thirty people consisting of healthy volunteers were included in the control group. Antioxidant enzyme SOD, GSH-Px and CAT levels were measured in the blood serum of the patients and compared with the control group. Results obtained from biochemical tests were expressed as mean ± SE. Descriptive statistical methods (mean ± standard error) were used for the independent t test for the control and study group. P < 0.05 was considered statistically significant. RESULTS: In the LPR group, 28 (46%) were women, 32 (53%) were men, and age range was 21-60, average age was 36.45 ± 1.147.There was no significant difference between LPR and control group in terms of age, gender and Body Mass Index (BMI). In the LPR group, the lowest score for RSI was 14 and the highest score was 39. The average RSI was 23.67. RFS ranges from 8-22. The mean RFS was 13.50. A highly significant statistical correlation was observed between RSI and total RFS (P < 0.001). There was a significant difference between the antioxidant enzyme levels of the control group and the LPR group. Antioxidant enzyme levels of the control group were SOD 274.10 ± 26.836 U / L, GSH-Px 174.20 ± 20.699 µU / mL and CAT 42.2898 ± 20.699 KU / L. Antioxidant enzyme level results of the LPR group were SOD 147 ± 14.022 U / L (P < 0.01), GSH-Px 88.28 ± 9.113 µU / mL (P < 0.01) and CAT 12.67 ± 0.799 KU / L (P < 0.001). The RSI results ranges from 4 to 39 and the RFS from 8 to 22. Antioxidant enzyme levels demonstrated fairly consistent reliability with individual variables from both RFS and RFS. There was also a highly significant statistical correlation between RSI and RFS. CONCLUSION: We found that the antioxidant enzymes SOD, GPX and catalase enzyme levels were significantly lower in LPR patients. Treatment modalities to reduce oxidative stress (OS) in LPR should be investigated.

Plasma Asymmetric Dimethylarginine (ADMA) and Nitric Oxide (NO) Levels in Patients with Chronic Pansinusitis.

Chronic pansinusitis is a mucosal inflammation of the nose and all paranasal sinuses with severe inflammation of the upper airways. Asymmetric dimethylarginine (ADMA) is associated with oxidative stress. In this study, we aimed to examine the plasma levels and importance of ADMA and nitric oxide (NO) in patients with chronic pansinusitis. The study was conducted with a total of 64 patients. The study group included a total of 40 patients with chronic pansinusitis. (18 females, 22 males) (mean age 32.27 ± 10.02). The control group consisted of 24 patients (11 females and 13 males). The mean age of the patients in the control group was 31.35 ± 6.05 years. Nasal endoscopic examinations were performed in patients with a history of chronic pansinusitis and symptoms of chronic pansinusitis. Later, the diagnosis of chronic pansinusitis was confirmed with coronal paranasal sinus Computed tomography scans. Plasma ADMA levels were measured by ELISA method and NO levels were measured by Griess method. Plasma ADMA and NO levels of the patients and healthy volunteers were measured and the mean plasma levels of the two groups were compared. ADMA levels were significantly higher in the group with chronic pansinusitis compared to the control group (1.23 ± 0.41 µM and 0.28 ± 0.06 µM, respectively) (p < 0.001), while NO levels were significantly lower in the patient group compared to the control group (7.06 ± 1.07 µM and 12.25 ± 0.95, µM, respectively) (p < 0.001). Our results show that the increase in ADMA levels and the decrease in NO levels are associated with chronic pansinusitis. According to these results, increased plasma levels of ADMA in chronic pansinusitis may be useful in clinical use as a sign of increased oxidative stress.

Deficiency of epithelial-mesenchymal transition causes child indirect inguinal hernia.

INTRODUCTION: Epithelial-mesenchymal transition (EMT) describes rapid changes in cellular phenotype. During EMT, epithelial cells down-modulate cell-cell adhesion, alter polarity, reorganize cytoskeleton, become isolated, motile, and resistant to anoikis. Epithelial breakdown and epithelial cell migration are the key processes involved in the obliteration of processus vaginalis. The great majority of abnormalities are because of nonobliteration or incomplete fusion of PV. We aimed to analyze the quantitative changes of epithelial genes in adult/child patients and their controls to examine differences of the genesis of these hernias. We also aimed to investigate the potential epigenetic causes of indirect inguinal hernia in adult patients. METHODS: Ten adult, ten child indirect inguinal hernia sacs and ten adult, ten child parietal peritonea were used. Hernial sac samples were obtained from indirect inguinal hernia surgeries. Peritonea of adult patients who underwent open cholecystectomy for cholelithiasis via subcostal incision were included in the study as the healthy control groups. Ages of the children were selected to be between 0 and 5 whereas the age of adults was chosen as 35-55, respectively. Total RNA isolation and cDNA synthesis were made from hernia sacs and peritoneum samples. Relative Keratin 1, Keratin 15, Filaggrin2 and STAT3 expressions were analyzed via qPCR. Indirect inguinal hernia sac cells were seeded and grown in vitro. Child diseased cells were employed in immunocytochemistry (ICC) analysis for Cytokeratin 15, Filaggrin2 and Bcl-2. Adult indirect inguinal hernia cells were examined for H3 modifications through ICC. RESULTS: In child indirect inguinal hernia, Keratin expressions were found higher than their controls. They were meaningfully lower than the healthy group in adult indirect inguinal hernia. Keratin 15, Keratin 1 and Filaggrin2 expressions were all correlating since they are members of related pathways. STAT3 expressions were opposite to Keratin and Filaggrin expressions suggesting that adult cells might have a switch to the mesenchymal state from the epithelial state. Adult indirect inguinal hernia samples have switched to the mesenchymal state whereas child indirect inguinal hernia samples have shown lack of transition. CONCLUSION: Irregular changes of EMT associated genes act in the progression of indirect inguinal hernia. Hence, the information on the epigenetic regulation of EMT in patients with primary inguinal hernia can aid to comprehend the pathogenesis in adults and infers new therapeutic approaches for this disease. TYPE OF STUDY: Prognosis study. LEVEL OF EVIDENCE: Level 2.

In vitro artificial skin engineering by decellularized placental scaffold for secondary skin problems of meningomyelocele.

BACKGROUND: Meningomyelocele (MMC) is a condition that is originated by the fusion defect of the neural tube. It is a congenital anomaly and can be characterized by spinal cord defects and impaired skin integrity. It is very important to close the skin openings via three-dimensional artificial skin like construction for preventing infection and maintaining the healthy skin structure. Therefore, we aim to generate artificial skin like structures formed by the own cells of donor for treating the MMC-related skin disorder. METHODS: In this study, waste placental tissues were collected and decellularization process was applied. Decellularized and normal placental tissues were compared by immunohistochemistry (IHC). Donor's own placental stem cells were seeded onto biological scaffold and were differentiated into skin related cell types. Finally, gene expressions were evaluated, and the structural integrity were analyzed with IHC. Tube formation assay was also performed for examining the angiogenesis formation of the tissue in order to evaluate the possibility of a healthy organ development. RESULTS: Characterization experiments proved that the decellularized skin preserved a normal skin 3D construction and vasculature along with significant ECM arrangements. The well-kept placental ECM scaffold was cytocompatible, supportive of mesenchymal cell types. Native organ related scaffold is expected to carry a huge influence in skin tissue engineering via delivering a niche for skin-based cells and even for stem/progenitor cells. Regarding to the data obtained from this study, in vivo investigation the skin-like structure in animal models is thought to be the next step as a future prospect. CONCLUSION: This study is a reference investigation for skin engineering based on placental stem cells and biological scaffolds.