Browsing by Author "Erdem, S. Remzi"

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A Bayesian Estimation Framework for Pharmacogenomics Driven Warfarin Dosing: A Comparative Study
(2015) Oztaner, Serdar Murat; Temizel, Tugba Taskaya; Erdem, S. Remzi; Ozer, Mahmut; 0000-0002-7537-2170; 25020183; AAJ-2370-2021
The incorporation of pharmacogenomics information into the drug dosing estimation formulations has been shown to increase the accuracy in drug dosing and decrease the frequency of adverse drug effects in many studies in the literature. In this paper, an estimation framework based on the Bayesian structural equation modeling, which is driven by pharmacogenomics, is proposed. The results show that the model compares favorably with the linear models in terms of prediction and explaining the variations in warfarin dosing.
beta-Adrenoreceptor antagonists reduce cancer cell proliferation, invasion, and migration
(2014) Iseri, Ozlem Darcansoy; Sahin, Feride Iffet; Terzi, Yunus Kasim; Yurtcu, Erkan; Erdem, S. Remzi; Sarialioglu, Faik; 25026350
Context: Propranolol, atenolol, and ICI118,551 are non-selective beta-adrenergic receptor (AR), beta(1)-AR, and beta(2)-AR antagonists, respectively. Objective: We investigated the efficacy of propranolol, atenolol, and ICI118,551 on proliferation, migration, and invasion of non-stimulated breast (MCF7), colon (HT-29), and hepatocellular (HepG2) cancer cells. Materials and methods: beta-AR expression profiling of cells was performed by real time PCR. Cell proliferation was determined by MTT. Boyden chamber and scratch assays were performed to evaluate invasion and migration. Results and discussion: All cell lines expressed beta-ARs. ICI118,551 was the most cytotoxic, whereas atenolol was the least effective beta-AR antagonist for 24, 48, and 72 h. Cell invasion was inhibited by ICI118,551 (45, 46, and 50% for MCF7, HT29, and HepG2, respectively) and propranolol (72, 65, and 90% for MCF7, HT29, and HepG2, respectively). Propranolol, atenolol, and ICI118,551 reduced migration of MCF7, HT-29, and HepG2 cells to varying extents depending on the application concentration and duration. Propranolol and atenolol reduced migration of MCF7 and HT-29 in a concentration-dependent manner, whereas migration of these cells decreased after 48 and 72 h of ICI118,551 applications. Conclusion: Beta(2)-AR antagonist seemed to be the most cytotoxic beta-blocker on non-stimulated cancer cells. Propranolol and ICI118,551 were more effective than atenolol in inhibiting invasion and migration of non-stimulated MCF7 and HT-29 cells; ICI118,551 being the most potent. Concordantly, beta(2)-selective blockage seemed to be more effective for non-stimulated cells. Effect of the selective beta-AR antagonists showed variation depending on the concentration, incubation time, and histological origin of cells.
Effects of Sacral Neuromodulation on Isolated Urinary Bladder Function in a Rat Model of Spinal Cord Injury
(2015) Kumsar, Sukru; Keskin, Ulya; Akay, Alaaddin; Bilgilisoy, Ugur Taylan; Erdem, S. Remzi; Peskircioglu, C. Levent; Ozkardes, Hakan; 0000-0002-7277-449X; 24917133; AAH-1052-2020
IntroductionSacral neuromodulation has been considered as an effective treatment option for various types of chronic voiding dysfunction, but the mechanism of action has not been well understood. The aim of this study was to evaluate the effect of chronic sacral neuromodulation on isolated bladder functions in a rat model of spinal cord injury. Materials and MethodsFemale Sprague-Dawley rats (250-300g; N = 20) were assigned to four groups as follows: 1) control group (N = 6); 2) spinal cord transection group (SCT; N = 5); 3) spinal cord transection + sacral neuromodulation group (SCT + SNM; N = 5); 4) sham (spinal cord transection + electrode wire implantation without sacral neuromodulation; N = 4). The rats in the SCT, SCT + SNM, and sham groups were anesthetized with ketamine (60mg/kg, i.p.) and xylazine (7mg/kg, i.p.). The spinal cord was completely transected at T8-T9 level in SCT and SCT + SNM groups. Electrode wires were implanted into S3 dorsal foramina in both sham and SNM groups, but only the SNM group was subjected to electrical stimulation for four hours a day for three weeks. Twenty-one days later, the rats were sacrificed via anesthetic overdose, and isolated longitudinal bladder strip preparations were placed in organ baths for the investigation of their isometric responses to pharmacological agents. ResultsIn isometric contraction experiments, SCT was found to increase the contraction responses of the bladder strips to muscarinic stimulation, and SNM could not prevent this increase. In isometric relaxation experiments, SCT caused a decrease in -adrenergic relaxation responses, and SNM augmented the bladder's -adrenergic relaxation responses. Nitric oxide did not affect the relaxation responses. ConclusionIn our rat model of SCT, SNM seemed to alter adrenergic receptor function in the urinary bladder. Further studies are required to clarify the mechanism of these alterations at the level of bladder receptors following sacral neuromodulation.