Rabbit Anti-Human F2 Polyclonal antibody

Background: DPOAEs are acoustic energy within the external auditory canal (EAC) arising from the non-linear interaction within the cochlea; of 2 pure tones presented simultaneously; of primary frequencies f1 and f2. DPOAEs are recorded in nearly any normal-hearing subject and in patients with hearing loss up to 50 dBHL while recordings may be deceiving in the presence of severe to profound hearing loss. Objective: To determine the intensity levels of f1 and f2 at which DPOAEs truly reflect the active metabolic processes within the cochlea. Setting: University Hospital Study: Prospective Methods: One-hundred and forty ears were categorized into three groups; A (n = 50), B (n = 50) and C (n = 40); according to subjects' age (12 to 18, 2 to 12 and <2 years, respectively). A fourth group D was included; which entailed recordings from a dummy cavity simulating a child's external auditory canal. Each group was further subdivided into two subgroups according to hearing levels; either normal or severe to profound hearing loss. DP-grams were interpreted at 3 points/octave steps for all groups and reviewed as 'Pass' or 'Fail' according to set criteria. Stimulus levels were adjusted such that L1 exceeded L2 by 10 dB. Start levels for L1 and L2 were 80 and 70 dBSPL. Levels were reduced simultanueously in 5 dB steps for the following recordings; to reach 65 and 55 for the last recording. Results: Using the higher three stimulation levels, all subgroups had 'Pass' DP grams. On using the last and lowest recording level, only subgroups of normal hearing ears had 'Pass' DP grams; while subgroups of ears with sensorineural hearing loss (SNHL) demonstrated 'Failed' DP grams at all frequencies. Conclusions: For audiometric screening purposes, DPOAEs show to be rather insensitive to hearing loss at higher stimulation levels and may reveal false positive results.

Background: Epilepsy is one of the most common neurological diseases. The underlying pathophysiological mechanisms in epilepsy are still unknown. Oxidative stress is believed to be one of the factors involved in the pathogenesis of epileptogenesis. In various pathophysiological conditions, reactive nitrogen species (RNS) such as nitrogen and peroxynitrite are produced and these RNSs can bind to free nucleosides and nucleotides or to nucleosides and nucleotides existing in the DNA/RNA structure. 8-Nitroguanine (8-NG) is a typical DNA nucleobase product of nitrosative damage generated by RNS. It has been proposed that F2-isoprostanes, in particular 8-iso-Prostaglandin F2a (8-isoPGF2a), are specific, reliable and non-invasive biomarkers of lipid peroxidation in vivo. In the present study, we compared the levels of lipid oxidative stress biomarker 8-isoPGF2a and nitrosative stress DNA biomarker 8-NG in patients with epilepsy undergoing antiepileptic drug (AEDs) treatment and with those in healthy participants. Methods: The present study comprised 90 patients aged between 17 and 53 who were admitted to the Neurology Clinic of Cumhuriyet University and diagnosed with epilepsy. The patients were assigned into the intervention (n = 45) and control (n = 45) groups. Of the participants in the intervention group, 37.7% (n = 17) were treated with levetiracetam (LEV), 33.3% (n = 15) with valproic acid (VA) and 29% (n = 13) with carbamazepine. Serum 8-iso-PGF2a and 8-NG levels of the participants in the intervention and control groups were determined by ELISA. Results: There was no significant difference between the medication (LEV, VA, Carbamazepine) used by the participants and their 8-iso-PGF2a and 8-NG levels (p> 0.05). However, 8-iso-PGF2a and 8-NG were significantly higher in the participants in the intervention than in the participants in the control group (p< 0.001). Conclusion: Our study demonstrated that there was an increase in oxidative and nitrosative stres markers in patients with epilepsy. There was no significant difference between the 8-iso-PGF2a and 8-NG levels of the participants taking three different AEDs.