Prognostic Factors Associated With Sleep Duration: Serum Pro-Oxidant/Antioxidant Balance and Superoxide Dismutase 1 as Oxidative Stress Markers and Anxiety/Depression.

Objectives: Sleep is a conserved vital behavior in humans, and insufficient sleep is associated with several disorders. Recent studies have investigated the association of sleep duration, oxidative stress markers, anxiety, and depression. Therefore, we aim to assess the relationship between sleep duration, serum pro-oxidant/antioxidant balance (PAB) and superoxide dismutase 1 (SOD1) levels as markers of oxidative stress, anxiety, and depression. Methods: Participants included in our cross-sectional analysis were recruited as part of the MASHAD study (n = 9,184). Nocturnal sleep duration was identified using a self-reported questionnaire, and serum pro-oxidant/antioxidant balance (PAB) and superoxide dismutase 1 (SOD1) levels were assessed using methods that have been previously reported. Results: Serum PAB, depression, and anxiety scores were found significantly higher in subjects with very short sleep duration. In an adjusted model using MANOVA regression analysis, serum PAB was significantly higher in the subjects with a very short sleep duration (p: 0.016 in depression and p: 0.002 in anxiety). Conclusion: The present cross-sectional study demonstrates a relationship between sleep duration, oxidative balance, and depression/anxiety, especially in anxiety subjects that might predict each other.

The visceral adiposity index and lipid accumulation product as predictors of cardiovascular events in normal weight subjects.

INTRODUCTION: Visceral adipose tissue (VAT) has an important role in the incidence of cardiovascular disease (CVD) than obesity by itself. The visceral adiposity index (VAI) and lipid accumulation product (LAP) are surrogate indices for measuring VAT. The aimed of this study was to investigate the association of these markers with cardiovascular events among populations with different BMI category in Mashhad, northeast of Iran. METHOD: The present study comprised a prospective cohort of 9685 men and women (35-65 years) who were recruited from MASHAD study. BMI category was defined as normal weight (BMI <25), over weight (25 ≤ BMI<30) and obese (BMI≥30). Demographic, laboratory evaluations, anthropometric and metabolic parameters were performed. Logistic and Cox regression analyses were used to determine the association and risk of cardiovascular events with VAT and LAP. RESULTS: The mean VAI and LAP in CVD patients were significantly higher than in healthy ones in all 3 groups. In terms of CVD event prediction, VAI and LAP had significant association with the incidence of CVD in the second (RR (95% CI): 2.132 (1.047-4.342) and 2.701 (1.397-5.222), respectively) and third tertiles (RR (95% CI): 2.541 (1.163-5.556) and 2.720 (1.159-6.386), respectively) in the normal group, but this association was only found in the third tertiles (RR (95% CI): 2.448 (1.205-4.971) and 2.376 (1.086-5.199), respectively) in the overweight group. The result couldn't find this association for the obese group. CONCLUSION: In this study, we found that there was a significant association between LAP and VAI and cardiovascular events in normal weight and over-weight groups; however, no significant relationship was found in the obese group.

Protective Effects of Leukadherin1 in a Rat Model of Targeted Experimental Autoimmune Encephalomyelitis (EAE): Possible Role of P47phox and MDA Downregulation.

BACKGROUND: Reactive oxygen and nitrogen species (ROS and RNS) are involved in pathologic mechanisms underlying demyelination and exacerbation in multiple sclerosis (MS) lesions. P47phox is the most important subunit of an ROS-producing enzyme (NADPH oxidase) which is reportedly upregulated in MS plaques due to the intense activity of infiltrated immune cells and resident microglia. Leukadherin1 is a specific CD11b/CD18 agonist that inhibits signaling and transmigration of inflammatory cells to sites of injury. Based on this mechanism, we evaluated therapeutic effects of leukadherin1 in an animal model of targeted experimental autoimmune encephalomyelitis (EAE) through focal injection of inflammatory cytokines to the spinal cord. METHODS: For model induction, Lewis rats were first immunized with 15µg MOG 1-125 emulsion. Twenty days later, animals were subjected to stereotaxic injection of IFNγ and TNFα to the specific spinal area (T8). One day after injection, all animals presented EAE clinical signs, and their behaviors were monitored for eight days through open-field locomotion and grid-walking tests. Leukadherin1-treated animals received daily intraperitoneal injections of 1mg/kg of the drug. The specific spinal tissues were extracted on day 5 in order to measure nitric oxide (NO), malon di-aldehyde (MDA), and TNFα concentrations alongside P47phox real-time PCR analysis. In addition, spinal sections were prepared for immunohistochemical (IHC) observation of infiltrated leukocytes and activated microglia. RESULTS: Leukadherin1 exhibited promising improvements in EAE clinical scores and behavioral tests. Demyelination, CD45+ leukocyte infiltration, and Iba1+ microglia activation were reduced in spinal tissues of leukadherin1-treated animals. Furthermore, P47phox expression levels, MDA, and NO amounts were decreased in treated animals. However, TNFα concentrations did not differ following treatment. CONCLUSION: Based on our results, we suggest that leukadherin1 may be used as a novel therapeutic agent in tackling the clinical challenge of multiple sclerosis, especially during the acute phase of the disease. This effect was possibly mediated through decreased leukocyte infiltration and oxidative stress.