Browsing by Author "Tuǧlu I."
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Item Insulin: Does it induce follicular arrest in the rat ovary?(Parthenon Publishing Group Ltd, 2002) Kuşcu N.K.; Koyuncu F.; Özbilgin K.; Inan S.; Tuǧlu I.; Karaer Ö.The goal of this study was to investigate histological changes of the rat ovary treated with either insulin or insulin plus human chorionic gonadotropin (hCG). The study was conducted in Celal Bayar University, School of Medicine, Animal Research Laboratory. Eighteen adult female Wistar rats were divided into three groups to receive saline, or insulin, or insulin plus hCG for 4 weeks. At the end of treatment the rats were sacrificed and the ovaries were evaluated with hematoxylin and eosin. There was no abnormal change in rats treated with saline. A thickened capsule, stromal hypertrophy and stromal cell hyperplasia, and no developing follicles, were observed in the insulin-only group. A thin capsule, developing follicles and corpora lutea, and normal theca cells and stroma were observed in the insulin-plus-hCG group. We conclude that insulin may lead to histological changes similar to stromal hyperthecosis and polycystic ovary syndrome, and may be one of the factors causing follicular arrest.Item Ischemic preconditioning - Association of reperfusion and brain damage with metabolic state; [İskemik ön tanitim-reperfüzyon ve beyin hasarinin metabolik durumu ile ilişkisi](2005) Tuǧlu I.; Vural K.; Cezayirli E.; Varol T.; Özbilgin K.Stroke and cardiac arrest, which are major causes of death and disability, affect millions of individuals around the world and are responsible for the leading health care costs of all diseases. The ischemia-induced neuronal death is an energy dependent process and is the result of activation of cascades of detrimental biochemical and histological events that include perturbion of calcium homeostasis leading to increased excitotoxicity, malfunction of endoplasmic reticulum and mitochondria, elevation of oxidative stress causing DNA damage, alteration in proapoptotic gene expression, and activation of the effector caspases and endonucleases leading to the final degradation of the genome. Ischemic preconditioning of the brain describes the neuroprotection induced by a short, conditioning ischemic episode to a subsequent severe ischemic episode. The tolerance of the brain to an ischemic injury depends not only on the duration and severity of insufficient blood flow but also on various pre- and post-ischemic factors that are able to influence the post ischemic outcome. Recent experimental studies focus on the preischemic factors, that can increase the ischemic tolerance, among which the suppression of metabolic rate, the increase of brain tissue energy reserves and the inhibition of membrane permeability of cations are of particular importance. During the induction phase, aspartate and adenosine receptors, and oxygen free radicals and conservation of energy metabolism are required. Protein kinases, transcription factors, and immediate early genes appear to transduce the signal into a tolerant response. The brain succumbs to ischemic injury as a result of loss of metabolic stores, excessive intracellular calcium accumulation, oxidative stress, and potentiation of the inflammatory response. Neurons can also die via necrotic or apoptotic mechanisms, depending on the nature and severity of the insult. While it has been widely held that ischemia is notable for cessation of protein synthesis, brain regions with marginal reduction in blood supply are especially capable of expressing a variety of genes, the functions of many of which are only beginning to be understood. Gene expression is also upregulated upon reperfusion and reoxygenation. Brain extracellular levels of glutamate, aspartate, GABA and glycine increase rapidly following the onset of ischemia, remain at an elevated level during the ischemia, and then decline following reperfusion. In the early stages neuronal responses to ischem ia are dependent on the modulation of ion channels. Reactive oxygen species generated during ische-mia-reperfusion contribute to the injury. Oxygen free-radicals serve as important signalling molecules that trigger inflammation and apoptosis. The use of appropriate animal models is essential to predict the value and effect of therapeutic approaches in human subjects. Animal models should be used to determine dosage and duration of therapy, which will vary with the pharmacokinetic properties of different agents. Finally, physiological monitoring for the metabolic condition such as cerebral blood flow, blood pressure and gazes, body temperature, glycemia, etc., should be performed to eliminate confounding variables and to observe adverse systemic effects. Therefore, it is very important to know the experimental process, survey of animals, neurologic scoring, histological methods which highly affect the explanation of the results. In this review, we discuss mechanisms of ischemic brain damage and reperfusion related to metabolic condition and histology.Item Cell surface glycosylation diversity of embryonic thymic tissues(Elsevier GmbH, 2008) Balcan E.; Tuǧlu I.; Şahin M.; Toparlak P.In the thymus, glycosylation status of many cell surface molecules changes during the thymocyte maturation and selection processes. In this study, we evaluated the glycosylation changes and possible relationships with programmed cell death in the thymic tissues from mouse embryos at the days 14 (E14), 15 (E15), 16 (E16), 17 (E17) and 18 (E18) of embryonic development. In order to determine glycosylation changes we used three different plant lectins: peanut agglutinin (PNA), Maackia amurensis leucoagglutinin (MAL or MAAI) and Sambucus nigra agglutinin (SNA), which recognize core disaccharide galactose (1-3) N-acetylgalactosamine [Galβ(1→3)GalNAc], sialic acid linked (2→3) to galactose [SAα(2→3)Gal] and sialic acid linked to galactose [SAα(2→6)Gal] structures, respectively. Our lectin histochemistry and lectin blotting studies indicated that glycosylation pattern was modified in thymocytes at the embryonic developmental stages analyzed. The immature cortical thymocytes were labeled by PNA, whereas medullary thymocytes were positive for MAL and SNA binding. Many medullary thymocytes exhibited α(2→6)-linked sialic acid on their surface and this increased throughout the gestational stages. In the lectin blotting studies, different protein bands of various molecular weights were identified in thymocytes. Two of them were putatively identified as CD43 and CD45 glycoproteins. In addition, TUNEL (deoxynucleotdyltransferase-mediated dUDP nick end labeling) indicated that only PNA-positive cortical thymocytes were deleted in all embryonic stages. These results indicate that the glycosylation pattern was modified in thymocytes at all embryonic developmental stages, and these modifications can affect the T cell deletion, probably via the galectin-1 molecule in the embryonic thymus. © 2007 Elsevier GmbH. All rights reserved.Item Histopathological alterations in gobius niger (black goby) due to pollution of the izmir bay(2012) Katalay S.; Minareci E.; Tuǧlu I.; Segner H.The present study aims to investigate the possible impact of aquatic pollution of Izmir Bay on resident fish. Gobius niger were sampled from two stations of the Izmir Bay, and gills and liver were examined histopathologically. The presence of pathological lesions in gills and liver of the fish as possible result of pollutant exposure was evaluated by semiquantitative analyses. The only histopathological changes found were hyperplasia, hypertrophy (12.5%, 18.8%), epithelial degeneration (18.8%, 25%) in gill and fatty livers (12.5%, 25%) of the fishes from both study sites, respectively. The moderate manifestation of pathological lesions in organs of Gobius niger from the presumably Bostanh site may be either the result of substantial protective and detoxification capabilities of this fish species, or from recent measures to reduce water pollution in Izmir Bay such as the installment of wastewater treatment plants.Item Attachment and growth of dental pulp stem cells on dentin in presence of extra calcium(Elsevier Ltd, 2016) Özdal-Kurt F.; Şen B.H.; Tuǧlu I.; Vatansever S.; Türk B.T.; Deliloǧlu-Gürhan I.Objective We aimed to differentiate dental pulp stem cells (DPSC) to odontoblast-like cells (ODPSC) and to investigate their attachment and growth on dentin in the presence of extra calcium by colorimetric assay and scanning electron microscopy (SEM). Methods After isolation of DPSC, they were differentiated to ODPSC. Standard dentin discs from human molar teeth were prepared. While the dentin discs in Group 1 did not receive any extra treatment, the discs in Group 2 were treated with acidic calcium phosphate precipitation (CPP) solution. In Group 3, the discs were suspended in phosphate buffered saline containing calcium. DPSC or ODPSC (3 × 104 cells/mL) were seeded on all discs and incubated for 7, 14 or 21 days. Attachment and growth of 7-day cell cultures on extra dentin samples were examined by SEM. MTT assay showed that number of cells on dentin surfaces was increased by time periods regardless of type of treatment and cells (p < 0.05). Results While DPSC and ODPSC showed similar proliferation rates at 7 and 14 days (p > 0.05), the number of ODPSC was higher than DPSC in 21-day samples (p = 0.039). MTT assay showed that number of cells on dentin surfaces was increased by time periods regardless of type of treatment and cells (p < 0.05). Calcium-treated dentin surfaces always had lower number of cells; being significant for only CPP-treated surfaces (p < 0.01). Both types of cells demonstrated good attachment and proliferation on dentin surfaces regardless of type of dentin treatment. Conclusions Because the nature of dentin surface itself showed good adhesive characteristics with ODPSC and DPSC, additional calcium treatment of dentin surfaces may not be necessary. © 2016 Published by Elsevier Ltd.