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- Demir, Ahmet U., et al.
(författare)
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Prevalence of sleep disorders in the Turkish adult population epidemiology of sleep study
- 2015
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Ingår i: Sleep and Biological Rhythms. - : Springer Science and Business Media LLC. - 1446-9235 .- 1479-8425. ; 13, s. 298-308
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Tidskriftsartikel (refereegranskat)abstract
- © 2015 Japanese Society of Sleep Research. Sleep disorders constitute an important public health problem. Prevalence of sleep disorders in Turkish adult population was investigated in a nationwide representative sample of 5021 Turkish adults (2598 women and 2423 men, response rate: 91%) by an interviewer-administered questionnaire. Insomnia was defined by the DSM-IV criteria, habitual snoring and risk for sleep-related breathing disorders (SDB) by the Berlin questionnaire, excessive daytime sleepiness (EDS) by the Epworth sleepiness scale score, and restless legs syndrome (RLS) by the complaints according to the International Restless Legs Syndrome Study Group criteria. Mean age of the participants was 40.7 ± 15.1 (range 18 to 90) years. Prevalence rates (men/women) were insomnia 15.3% (10.5%/20.2%; P < 0.001), high probability of SDB 13.7% (11.1%/20.2%; P < 0.001), EDS 5.4% (5.0%/5.7%; P: 0.09), RLS 5.2% (3.0%/7.3%; P < 0.001). Aging and female gender were associated with higher prevalence of sleep disorders except for habitual snoring. Prevalence rates of the sleep disorders among Turkish adults based on the widely used questionnaires were close to the lower end of the previous estimates reported from different parts of the world. These findings would help for the assessment of the health burden of sleep disorders and addressing the risk groups for planning and implementation of health care. Sleep and Biological Rhythms
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| 2. |
- Hannan, Johanna L., et al.
(författare)
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Inhibition of Rho-Kinase Improves Erectile Function, Increases Nitric Oxide Signaling and Decreases Penile Apoptosis in a Rat Model of Cavernous Nerve Injury
- 2013
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Ingår i: Journal of Urology. - : Elsevier. - 0022-5347 .- 1527-3792. ; 189:3, s. 1155-1161
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: Bilateral cavernous nerve injury results in up-regulation of ROCK signaling in the penis. This is linked to erectile dysfunction in an animal model of post-prostatectomy erectile dysfunction. We evaluated whether daily treatment with the ROCK inhibitor Y-27632 (Tocris Bioscience, Ellisville, Missouri) would prevent erectile dysfunction in a rat model of bilateral cavernous nerve injury.Materials and Methods: Sprague-Dawley(R) rats underwent surgery to create sham (14) or bilateral (27) cavernous nerve injury. In the injury group 13 rats received treatment with Y-27632 (5 mg/kg twice daily) and 14 received vehicle. At 14 days after injury, rats underwent cavernous nerve stimulation to determine erectile function. Penes were assessed for neuronal and nitric oxide synthase membrane-endothelial nitric oxide synthase. ROCK2 was assessed by Western blot. Cyclic guanosine monophosphate was determined by enzyme-linked immunosorbent assay. Cavernous homogenates were tested for ROCK and protein kinase G enzymatic activity. Penile apoptosis was evaluated using the Apostain technique (Alexis, San Diego, California). Data were analyzed on ROCK using ANOVA and the t test.Results: While erectile function was decreased in rats with bilateral cavernous nerve injury, daily administration of Y-27632 improved erectile responses. Injury decreased neuronal and nitric oxide synthase membrane-endothelial nitric oxide synthase but ROCK2 was significantly increased. Y-27632 treatment restored neuronal nitric oxide synthase, nitric oxide synthase membrane-endothelial nitric oxide synthase and cyclic guanosine monophosphate levels, and protein kinase G activity. Treatment significantly decreased ROCK2 protein and ROCK activity. There were significantly fewer apoptotic cells after treatment than in injured controls.Conclusions: These results provide evidence for up-regulation of the RhoA/ROCK signaling pathway with detrimental effects on erectile function after bilateral cavernous nerve injury. ROCK inhibition improved erectile dysfunction associated with bilateral cavernous nerve injury by preserving penile nitric oxide bioavailability and decreasing penile apoptosis.
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| 3. |
- Hannan, Johanna L., et al.
(författare)
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Valproic acid prevents penile fibrosis and erectile dysfunction in cavernous nerve-injured rats
- 2014
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Ingår i: Journal of Sexual Medicine. - : Wiley-Blackwell. - 1743-6095 .- 1743-6109. ; 11:6, s. 1442-1451
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Tidskriftsartikel (refereegranskat)abstract
- Introduction Bilateral cavernous nerve injury (BCNI) causes profound penile changes such as apoptosis and fibrosis leading to erectile dysfunction (ED). Histone deacetylase (HDAC) has been implicated in chronic fibrotic diseases. Aims This study will characterize the molecular changes in penile HDAC after BCNI and determine if HDAC inhibition can prevent BCNI-induced ED and penile fibrosis. Methods Five groups of rats (8-10 weeks, n=10/group) were utilized: (i) sham; (ii and iii) BCNI 14 and 30 days following injury; and (iv and v) BCNI treated with HDAC inhibitor valproic acid (VPA 250mg/kg; 14 and 30 days). All groups underwent cavernous nerve stimulation (CNS) to determine intracavernosal pressure (ICP). Penile HDAC3, HDAC4, fibronectin, and transforming growth factor-1 (TGF-1) protein expression (Western blot) were assessed. Trichrome staining and the fractional area of fibrosis were determined in penes from each group. Cavernous smooth muscle content was assessed by immunofluorescence to alpha smooth muscle actin (-SMA) antibodies. Main Outcome Measures We measured ICP; HDAC3, HDAC4, fibronectin, and TGF-1 protein expression; penile fibrosis; penile -SMA content. Results There was a voltage-dependent decline (Pless than0.05) in ICP to CNS 14 and 30 days after BCNI. Penile HDAC3, HDAC4, and fibronectin were significantly increased (Pless than0.05) 14 days after BCNI. There was a slight increase in TGF-1 protein expression after BCNI. Histological analysis showed increased (Pless than0.05) corporal fibrosis after BCNI at both time points. VPA treatment decreased (Pless than0.05) penile HDAC3, HDAC4, and fibronectin protein expression as well as corporal fibrosis. There was no change in penile -SMA between all groups. Furthermore, VPA-treated BCNI rats had improved erectile responses to CNS (Pless than0.05). Conclusion HDAC-induced pathological signaling in response to BCNI contributes to penile vascular dysfunction. Pharmacological inhibition of HDAC prevents penile fibrosis, normalizes fibronectin expression, and preserves erectile function. The HDAC pathway may represent a suitable target in preventing the progression of ED occurring post-radical prostatectomy.
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