Sleep Architecture in Patients With Primary Snoring and Obstructive Sleep Apnea.

INTRODUCTION: This study aimed to investigate sleep architecture in patients with primary snoring and obstructive sleep apnea. METHODS: In this study, we analyzed polysomnographic data of 391 clients who referred to Sleep Disorders Research Center (SDRS). These people were classified into three groups based on their Apnea-Hypopnea Index (AHI) and snoring; control, Primary Snoring (PS), and Obstructive Sleep Apnea (OSA) group. Sleep architecture variables were then assessed in all groups. RESULTS: The results of this study indicated a decrease in deep sleep or Slow Waves Sleep (SWS) and increase in light sleep or stage 1 of non-REM sleep (N1) in OSA patients compared with the control and PS groups. After controlling the effects of confounding factors, i.e. age and Body Mass Index (BMI) (which was performed through multiple regression analysis) significant differences were observed among the three groups with regard to N1. However, with regard to SWS, after controlling confounding variables (age and BMI), no significant difference was found among the groups. CONCLUSION: The results indicated that OSA, regardless of age and BMI, may increase light (N1) sleep possibly via a decline in blood oxygen saturation (SpO2 ). Such increase in N1 may be responsible for brain arousal. In addition, by controlling confounding factors (age and BMI), OSA did not affect SWS in OSA patients. However, further research is necessary to determine sleep architecture in more detail in the patients with OSA.

The Effect of Empowerment Program on Maternal Discharge Preparation and Neonatal Length of Hospital Stay: A Randomized Controlled Trial.

BACKGROUND: Despite the increased survival of premature infants, many infants are discharged from the hospital while they still require care and follow-up. The present study aimed to determine the effect of empowerment program on maternal discharge preparation and infants' length of hospital stay. MATERIALS AND METHODS: In this pretest-posttest clinical trial, 60 premature infants along with their mothers were selected from the neonatal intensive care unit (NICU) of a teaching hospital in Kermanshah in 2016 via convenience sampling and were allocated to experimental and control groups. Mothers in the control group performed routine care and those in experimental group, in addition to the routine care, performed an intervention program, training sessions including touching and massage, bathing, infection prevention, warning signs, and neonatal resuscitation. Data were collected by a maternal and neonatal demographic questionnaire and a discharge preparation checklist, performed twice (at admission and before discharge), by the researcher. The collected data were analyzed by independent and paired t-test. RESULTS: The mean (standard deviation) of the total score of maternal discharge preparation in intervention group 44.65 (3.90) was significantly higher than that of the control group 33.00 (8.28) (t = -6.58, p <0.001). The mean length of neonatal hospitalization in the intervention group (14.79 days) was significantly shorter than that of the control group (20.43 days) (p = 0.020). CONCLUSIONS: The increasing maternal discharge readiness and reducing the length of neonatal hospital stay would decrease the medical costs and supply more beds for admission of other infants.

Lovastatin prevents bleomycin-induced DNA damage to HepG2 cells.

Lovastatin as a member of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors is used as a lipid-lowering agent. It can also inhibit the formation of hydrogen peroxide and superoxide anion and finally leads to decline in oxidative stress processes. Here, we evaluated whether lovastatin can increase DNA damage resistance of HepG2 cells against genotoxicity of the anticancer drug bleomycin (BLM). HepG2 cells were incubated with different concentrations of lovastatin (0.1, 0.5, 1, 5 µM) before exposure to BLM (0.5 µg/mL for one h). The genotoxic dose of BLM and lovastatin was separately determined and comet assay was used to evaluate the genotoxicity. After trapping cells in agarose coated lames, they were lysed and the electrophoresis was done in alkaline pH, then colored and monitored by florescent microscope. The results of this study indicated that lovastatin in doses lower than 5 µM has genoprotective effect and in doses higher than 50 µM is genotoxic. In conclusion, lovastatin is able to protect genotoxic effects of BLM in HepG2 cells. Further studies are needed to elucidate the mechanism(s) involved in this process.

Satureja bachtiarica ameliorate beta-amyloid induced memory impairment, oxidative stress and cholinergic deficit in animal model of Alzheimer's disease.

Extracellular deposition of Beta-amyloid peptide (Aß) is the main finding in the pathophysiology of Alzheimer's disease (AD), which damages cholinergic neurons through oxidative stress and reduces the cholinergic neurotransmission. Satureja bachtiarica is a medicinal plant from the Lamiaceae family which was widely used in Iranian traditional medicine. The aim of the present study was to investigate possible protective effects of S. bachtiarica methanolic extract on Aß induced spatial memory impairment in Morris Water Maze (MWM), oxidative stress and cholinergic neuron degeneration. Pre- aggregated Aß was injected into the hippocampus of each rat bilaterally (10 µg/rat) and MWM task was performed 14 days later to evaluate learning and memory function. Methanolic extract of S.bachtiarica (10, 50 and 100 mg/Kg) was injected intraperitoneally for 19 consecutive days, after Aß injection. After the probe test the brain tissue were collected and lipid peroxidation, Acetylcholinesterase (AChE) activity and Cholin Acetyl Transferees (ChAT) immunorectivity were measured in the hippocampus. Intrahipocampal injection of Aß impaired learning and memory in MWM in training days and probe trail. Methanolic extract of S. bachtiarica (50 and 100 mg/Kg) could attenuate Aß-induced memory deficit. ChAT immunostaining revealed that cholinergic neurons were loss in Aß- injected group and S. bachtiarica (100 mg/Kg) could ameliorate Aß- induced ChAT reduction in the hippocampus. Also S. bachtiarica could ameliorate Aß-induced lipid peroxidation and AChE activity increase in the hippocampus. In conclusion our study represent that S.bachtiarica methanolic extract can improve Aß-induced memory impairment and cholinergic loss then we recommended this extract as a candidate for further investigation in treatment of AD.

Assessment of the deoxyribonucleic acid damage caused by occupational exposure to chemical compounds in Isfahan Polyacryl Company.

BACKGROUND: Chemical pollutants found in industrial environments can cause chronic genotoxicity in vulnerable individuals during the long-term exposure. The primary purpose of the present study was to assess the deoxyribonucleic acid (DNA) damage caused by occupational exposure to industrial chemicals and secondary purpose is to investigate the effect of possible risk factors of genotoxicity. MATERIALS AND METHODS: The blood samples of the workers of Isfahan Polyacryl Company were evaluated in terms of genotoxicity using the comet assay method. The percentage of DNA in the tail and tail moment were measured and DNA damage was evaluated. Furthermore, the effect of age, smoking, duration of working in the company and working in two parts of the company on the degree of vulnerability to genotoxicity was assessed. RESULTS: The amount of DNA damage in the target group (the production line workers) was significantly higher than the control group (the staffs), 3.87 versus 1.52 as tail moment, (P < 0.0001). DNA damage was significantly higher in smoker groups compared with non-smoker target group and control group, 4.18 versus 3.07 and 1.52 respectively as tail moment, (P < 0.0001). Furthermore, it was higher in person working in two different parts of the company compared to those work in one part and control group, 4.63 versus 3.74 and 1.52 respectively as tail moment, (P < 0.0001). CONCLUSION: Occupational exposure to Polyacryl caused DNA damage. Smoking and working in two parts of the company may have a significant role in DNA damage.

Interactive effects of a protein kinase AII inhibitor and testosterone on spatial learning in the Morris water maze.

Neurohormones such as testosterone (TE) are important in modulation of learning and memory. In the present study, we investigated the interactive effects of pre-training bilateral intra-hippocampal infusions of testosterone and H-89, a selective PKAII inhibitor, on spatial acquisition in the Morris water maze (MWM). Different doses of TE (20, 40 and 80 µg/side) and H-89 (5 and 10 µM/side) were administered 30 min before start of the training each day. Control animals received bilateral intra-hippocampal infusions of DMSO as vehicle for TE and H-89. Animals were trained for 4 days and each day included one block of four trials. The results of this study showed that bilateral infusion of TE (40 and 80 µg/side) or H-89 (10 µM/side) impaired spatial learning as indicated by significant increases in escape latency and traveled distance compared to the control group. Although pre-training bilateral infusions of a low concentration of either TE (20 µg/side) or H-89 (5 µM/side) into the CA1 region of the hippocampus did not affect learning capabilities, but the combination of the low doses of the drugs led to significant deficits in spatial acquisition. Overall, our data suggest that spatial acquisition was affected by PKAII inhibition or TE administration. Moreover, when co-administered, these drugs had a negative synergistic impact on acquisition.

Inhibition of PKA attenuates memory deficits induced by ß-amyloid (1-42), and decreases oxidative stress and NF-κB transcription factors.

Alzheimer's disease (AD), the most relevant cause of dementia in elderly, is characterized by amyloid ß (Aß) containing plaques and neurofibrillatory tangles, synaptic and neuronal loss, along with progressive cognitive impairment in short-term memory. However, mechanistic links between protein kinase A (PKA), oxidative stress and memory loss in response to Aß remain elusive. In the present study, we examined the effects of post-training bilateral intra-hippocampal infusions of the specific protein kinase AII inhibitor, H-89, on memory deficits induced by Aß (1-42) in Aß-pretreated rats. H-89 and Aß were administered immediately after completion of training. All animals were trained for 4 consecutive days and tested 9 and 19 days after the infusions. Significant differences were observed in the time and distance of finding the hidden platform in Aß treated animals after 19 days. Interestingly, intra-hippocampal infusion of H-89 (5µM/side) significantly prevented the Aß-induced memory impairment. Furthermore, evaluation of NFκB (nuclear factor-κB), and antioxidant enzymes, such as γ-GCS (glutamylcysteine synthetase), HO-1 (hemeoxygenase-1), GSH (glutathione), and SOD (superoxide dismutase) confirmed the protective effect of H-89. Given the possible neuroprotective effects of H-89 on Aß-induced memory impairment, our results may open a new avenue for the prevention of AD by PKAII signaling pathway inhibitor.