Browsing by Author "Stojanovic, Jelena (58823726400)"

We investigated the effect of intense audiogenic stimulation (AGS) on rats treated with the antibiotic imipenem and dipeptidase inhibitor cilastatin (Imi/Cil). Under pentobarbital anesthesia (40 mg/kg) adult male Wistar rats were implanted with electrodes and cannulas were placed in the right lateral ventricle. Animals were divided into the following groups: (1) vehicle, (2) Imi/Cil 10 μg/10 μg, (3) Imi/Cil 25 μg/25 μg, (4) vehicle + AGS, (5) Imi/Cil 10 μg/10 μg + AGS, and (6) Imi/Cil 25 μg/25 μg + AGS. Imi/Cil was administered intracerebroventricularly in 5 μl of physiological saline. AGS (100 ± 3 dB, 60 seconds) was applied at 15-minute intervals after the injection. Imi/Cil-induced seizures (twitching, forelimb clonus, headnodding, rearing, and clonic convulsions) and Imi/Cil-audio-induced seizures (wild running, clonic and tonic convulsions) were scored according to appropriate rating scales. Imi/Cil provoked convulsions dose-dependently. Each behavioral seizure response had a characteristic EEG correlate. AGS by itself did not provoke seizures in untreated rats. Sound stimulation in Imi/Cil-injected rats elicited typical audiogenic seizures, which were induced during five AGS tests (75 minutes postinjection). In most cases audiogenic seizures were not associated with epileptiform activity in the EEG, indicating that spreading of seizures did not involve the cortex. Since Imi/Cil-induced and Imi/Cil-audio-induced seizures differed behaviorally and electroencephalographically, it is suggested that different neural pathways are responsible for these two types of seizures: neuronal networks in the cortex are involved in Imi/Cil-induced seizures, whereas audiogenic seizures use networks residing primarily in the brainstem. © 2003 Elsevier Inc. All rights reserved.

We investigated the effect of intense audiogenic stimulation (AGS) on rats treated with the antibiotic imipenem and dipeptidase inhibitor cilastatin (Imi/Cil). Under pentobarbital anesthesia (40 mg/kg) adult male Wistar rats were implanted with electrodes and cannulas were placed in the right lateral ventricle. Animals were divided into the following groups: (1) vehicle, (2) Imi/Cil 10 μg/10 μg, (3) Imi/Cil 25 μg/25 μg, (4) vehicle + AGS, (5) Imi/Cil 10 μg/10 μg + AGS, and (6) Imi/Cil 25 μg/25 μg + AGS. Imi/Cil was administered intracerebroventricularly in 5 μl of physiological saline. AGS (100 ± 3 dB, 60 seconds) was applied at 15-minute intervals after the injection. Imi/Cil-induced seizures (twitching, forelimb clonus, headnodding, rearing, and clonic convulsions) and Imi/Cil-audio-induced seizures (wild running, clonic and tonic convulsions) were scored according to appropriate rating scales. Imi/Cil provoked convulsions dose-dependently. Each behavioral seizure response had a characteristic EEG correlate. AGS by itself did not provoke seizures in untreated rats. Sound stimulation in Imi/Cil-injected rats elicited typical audiogenic seizures, which were induced during five AGS tests (75 minutes postinjection). In most cases audiogenic seizures were not associated with epileptiform activity in the EEG, indicating that spreading of seizures did not involve the cortex. Since Imi/Cil-induced and Imi/Cil-audio-induced seizures differed behaviorally and electroencephalographically, it is suggested that different neural pathways are responsible for these two types of seizures: neuronal networks in the cortex are involved in Imi/Cil-induced seizures, whereas audiogenic seizures use networks residing primarily in the brainstem. © 2003 Elsevier Inc. All rights reserved.

Background/aim: Type 2 diabetes mellitus (T2D) is a complex metabolic impairment. Beta cell (BC) failure is the most challenging among its pathogenetic mechanisms. Recognizing reversible contributors to BC failure could guide individualized approach to early T2D treatment. The aim of this study was to compare early short-term insulin treatment vs. glimepiride, both added to metformin, on BC function, glycemic and lipid control, during 12-month follow-up. Patients and methods: Eighty newly diagnosed T2D patients, 30–65 years of age, presenting with HbA1c ≥ 9% were enrolled in the study. They were randomly assigned to single-month initial insulin therapy (INS) added to metformin, or to glimepiride and metformin (OAD) as only treatment. Subjects assigned to initial insulin intervention were thereafter switched to OAD. C-peptide (C-Pep) was analyzed at baseline and 2 hours after standardized test meal (STM). All subjects were STM-retested after 3 and 12 months. HbA1c, serum lipids, BMI, HOMA IR, and HOMA B were assessed over follow-up. Results: HbA1c was lower in INS vs OAD at 3-months: 6.26 ± 0.18% vs 6.78 ± 0.10% (p = 0.016), remaining so by 12 months (p = 0.056). BMI-adjusted ΔC-Pep was greater in INS vs. OAD at 3 months (4.60 ± 0.59 vs. 3.21 ± 0.34 m2/kg; p = 0.044), persisting by 12 months (4.57 ± 0.56 vs. 3.04 ± 0.34 m2/kg; p = 0.023). Average ΔC-Pep improvement from recruitment to 3 months was 100.8% in INS, vs. 51.3% in OAD. Prevalence of STM-ΔC-Pep response greater than 2.4 ng/mL had risen 3.2-fold by 12 months in the INS, vs. 2.4-fold only in the OAD group (p = 0.018). Conclusion: Early short-term insulin intervention in newly diagnosed T2D improves beta cell function more than glimepiride, both added to metformin, resulting in a superior and longer lasting glycemic and lipid control. © TÜBİTAK.

The effects of phenytoin (PHT) and phenobarbital (PHB) on EEG activity and behavior was studied in the model of epilepsy induced by intracerebroventricular (i.c.v.) administration of imipenem/cilastatin (Imi/Cil). Under intraperitoneal (i.p.) sodium pentobarbital anesthesia adult male Wistar albino rats were implanted with electrodes and cannulas were placed into the right lateral ventricle. Animals were divided into groups : 1) Imi/Cil (100/100 μg, i.c.v.), 2) PHT (40 mg/kg) + Imi/Cil (100/100 μg, i.c.v.), 3) PHT (80 mg/kg) + Imi/Cil (100/100 μg, i.c.v.), 4) PHT (160 mg/kg) + Imi/Cil (100/100 μg, i.c.v.), 5) PHB (50 mg/kg) + Imi/Cil (100/100 μg, i.c.v.), and 6) PHB (80 mg/kg) + Imi/Cil (100/100 μg, i.c.v.). PHT and PHB were injected intraperitoneally (i.p.) 1 h before Imi/Cil. Seizures were scored according to the scale : 0 - normal behavior 1 - twitching, 2 - head nodding, forelimb clonus, 3 - rearing, and 4 - clonic-tonic convulsions. Imi/Cil provoked maximal seizures in all animals, and all rats died 10-18 min after the injection. Epileptiform activity preceded behavioral seizures. Clonic-tonic seizures were associated with continuous bursts of high-frequency high-amplitude spikes in the EEG. PHT and PHB suppressed Imi/Cil-induced seizures dose-dependently. PHB reduced epileptiform discharges during behavioral seizures elicited by Imi/Cil, while PHT had no effect on EEG epileptic phenomena. These results suggest that PHT acts as anticonvulsant, and PHB as anticonvulsant and antiepileptic agent in the model of epilepsy induced by Imi/Cil.