Proceedings of the Conference on Emerging Economic Issues in a Globalizing World

The challenges facing Þanlýurfa are not unique, they are the same challenges found in rural areas all around the world. Agriculture is still the most important sector in Þanlýurfa, but it is generating fewer and fewer jobs. New approaches used in regional development shift from a focus on individual sectors (such as agriculture policy) to one based on a comprehensive multisectoral approach in which agriculture is conceived as one component sector of a comprehensive regional development policy. Within this framework, there are two major aims of this study. The first aim is to identify the high point sectors (key industries) by using LQ analysis in Þanlýurfa province and 11 districts. The analysis encompasses all sectors of industry and services thus excluding agriculture. On the other hand the economy of Þanlýurfa, endowed with very rich arable land resources and irrigation facilities, thanks to GAP-(South Eastern Anatolian Project), is mainly based on agriculture. Accordingly the second aim of this paper is to analyze the development potentials of “clusters of agro-industries based on organic agriculture products” in the region. The findings of the analysis reveal that the key sectors identified in industry and services (food and textiles industries and retail and wholesale of food stuff) provide inputs from the main agricultural products in the region. On the other hand considering the availability of land and other facilities for organic agricultural products the findings of the study strongly supports development of “clusters of organic - agro industries” in Þanlýurfa Region.regional development, clusters

Usefulness of LDAEP to Predict Tolerability to SSRIs in Major Depressive Disorder: A Case Report

We report here a patient with major depressive disorder who experienced severe adverse effects after the administration of SSRIs (serotonin selective reuptake inhibitors) without improvement of his depressive symptoms. These adverse effects disappeared and his depressive symptoms improved after discontinuation of the SSRIs and the administration of tianeptine. The patient exhibited a low value for the loudness dependent of auditory evoked potentials (LDAEP) -0.14 at baseline, which means that his central serotonergic neurotransmission was already highly active. We assumed that it was this high serotonergic activity that rendered him unresponsive to SSRIs, and brought on him the adverse effects, and that the tianeptine was effective due to the lack of serotonin reuptake inhibitory action. Thus, we suggest that LDAEP can be used to predict an individual patient's tolerability and clinical response to SSRIs in major depression

Evidence for the gastric cytoprotective effect of centrally injected agmatine

Agmatine (decarboxylated arginine) exerts cytoprotective action in several tissues, such as in the brain, heart or kidneys, but there is still controversy over the effects of agmatine on the gastric mucosa. The aim of the present study was to reveal the potential gastroprotective action of agmatine by using an acid-independent ulcer model to clarify which receptors and peripheral factors are involved in it. Gastric mucosal damage was induced by acidified ethanol. Mucosal levels of calcitonin gene-related peptide (CGRP) and somatostatin were determined by radioimmunoassay. For analysis of gastric motor activity the rubber balloon method was used. It was found that agmatine given intracerebroventricularly (i.c.v., 0.044-220nmol/rat) significantly inhibited the development of ethanol-induced mucosal damage, while in the case of intraperitoneal injection (0.001-50mg/kg i.p.) it had only a minor effect. The central gastroprotective action of agmatine was completely antagonized by mixed alpha2-adrenoceptor and imidazoline I1 receptor antagonists (idazoxan, efaroxan), but only partially by yohimbine (selective alpha2-adrenoceptor antagonist) and AGN 192403 (selective I1 receptor ligand, putative antagonist). It was also inhibited by the non-selective opioid-receptor antagonist naloxone and the selective δ-opioid receptor antagonist naltrindole, but not by β-funaltrexamine and nor-Binaltorphimine (selective μ- and κ-opioid receptor antagonists, respectively). Furthermore, the effect of agmatine was antagonized by bilateral cervical vagotomy and by pretreatment with indomethacin and NG-nitro-l-arginine. Agmatine also reversed the ethanol-induced reduction of gastric mucosal CGRP and somatostatin content, but did not have any significant effect on gastric motor activity. These results indicate that agmatine given centrally induces gastric cytoprotection, which is mediated by central imidazoline I1 receptors, alpha2-adrenoceptors and δ-opioid receptors. Activation of these receptors induces the release of different mucosal protective factors, such as NO, prostaglandins, CGRP and somatostatin by a vagal-dependent mechanism. Alterations of gastric motility are not likely to contribute to the observed protective effect

Examination of age-dependent effects of fetal ethanol exposure on behavior, hippocampal cell counts, and doublecortin immunoreactivity in rats

WOS: 000333998100002PubMed ID: 24302592Ethanol is known as a potent teratogen having adverse effects on brain and behavior. However, some of the behavioral deficits caused by fetal alcohol exposure and well expressed in juveniles ameliorate with maturation may suggest some kind of functional recovery occurring during postnatal development. The aim of this study was to reexamine age-dependent behavioral impairments in fetal-alcohol rats and to investigate the changes in neurogenesis and gross morphology of the hippocampus during a protracted postnatal period searching for developmental deficits and/or delays that would correlate with behavioral impairments in juveniles and for potential compensatory processes responsible for their amelioration in adults. Ethanol was delivered to the pregnant dams by intragastric intubation throughout 7-21 gestation days at daily dose of 6 g/kg. Isocaloric intubation and intact control groups were included. Locomotor activity, anxiety, and spatial learning tasks were applied to juvenile and young-adult rats from all groups. Unbiased stereological estimates of hippocampal volumes, the total number of pyramidal and granular cells, and double cortin expressing neurons were carried out for postnatal days (PDs) PD1, PD10, PD30, and PD60. Alcohol insult during second trimester equivalent caused significant deficits in the spatial learning in juvenile rats; however, its effect on hippocampal morphology was limited to a marginally lower number of granular cells in dentate gyrus (DG) on PD30. Thus, initial behavioral deficits and the following functional recovery in fetal-alcohol subjects may be due to more subtle plastic changes within the hippocampal formation but also in other structures of the extended hippocampal circuit. Further investigation is required. (c) 2013 Wiley Periodicals, Inc. Develop Neurobiol 74: 498-513, 2014METU Scientific Research Fund; Turkish Scientific and Technical Council (TUBITAK) [SBAG-107S069]; TUBITAK PhD scholarshipTurkish Scientific and Technical Council (TUBITAK) [SBAG-107S069]Contract grant sponsor: METU Scientific Research Fund.; Contract grant sponsor: Turkish Scientific and Technical Council (TUBITAK); contract grant number: SBAG-107S069 (to E.J.D.).; Contract grant sponsor: TUBITAK PhD scholarship (to B.E.C.)

Effect of venlafaxine on bone loss associated with ligature-induced periodontitis in Wistar rats

<p>Abstract</p> <p>Background</p> <p>The present study investigated the effects of venlafaxine, an antidepressant drug with immunoregulatory properties on the inflammatory response and bone loss associated with experimental periodontal disease (EPD).</p> <p>Materials and Methods</p> <p>Wistar rats were subjected to a ligature placement around the second upper left molar. The treated groups received orally venlafaxine (10 or 50 mg/kg) one hour before the experimental periodontal disease induction and daily for 10 days. Vehicle-treated experimental periodontal disease and a sham-operated (SO) controls were included. Bone loss was analyzed morphometrically and histopathological analysis was based on cell influx, alveolar bone, and cementum integrity. Lipid peroxidation quantification and immunohistochemistry to TNF-α and iNOS were performed.</p> <p>Results</p> <p>Experimental periodontal disease rats showed an intense bone loss compared to SO ones (SO = 1.61 ± 1.36; EPD = 4.47 ± 1.98 mm, p < 0.001) and evidenced increased cellular infiltration and immunoreactivity for TNF-α and iNOS. Venlafaxine treatment while at low dose (10 mg/kg) afforded no significant protection against bone loss (3.25 ± 1.26 mm), a high dose (50 mg/kg) caused significantly enhanced bone loss (6.81 ± 3.31 mm, p < 0.05). Venlafaxine effectively decreased the lipid peroxidation but showed no significant change in TNF-α or iNOS immunoreactivity.</p> <p>Conclusion</p> <p>The increased bone loss associated with high dose venlafaxine may possibly be a result of synaptic inhibition of serotonin uptake.</p

Acute Ethanol Inhibition of γ Oscillations Is Mediated by Akt and GSK3β

Hippocampal network oscillations at gamma band frequency (γ, 30–80 Hz) are closely associated with higher brain functions such as learning and memory. Acute ethanol exposure at intoxicating concentrations (≥50 mM) impairs cognitive function. This study aimed to determine the effects and the mechanisms of acute ethanol exposure on γ oscillations in an in vitro model. Ethanol (25–100 mM) suppressed kainate-induced γ oscillations in CA3 area of the rat hippocampal slices, in a concentration-dependent, reversible manner. The ethanol-induced suppression was reduced by the D1R antagonist SCH23390 or the PKA inhibitor H89, was prevented by the Akt inhibitor triciribine or the GSk3β inhibitor SB415286, was enhanced by the NMDA receptor antagonist D-AP5, but was not affected by the MAPK inhibitor U0126 or PI3K inhibitor wortmanin. Our results indicate that the intracellular kinases Akt and GSk3β play a critical role in the ethanol-induced suppression of γ oscillations and reveal new cellular pathways involved in the ethanol-induced cognitive impairment

A new target for diagnosis and treatment of CNS disorders: Agmatinergic system.

A polyamine agmatine is produced through decarboxylation of L -arginine by the enzyme arginine decarboxylase and is a new neurotransmitter in central nervous system (CNS). It has been suggested that agmatine has analgesic, anxiolytic and antidepressant activities in animals. In experimental studies, it also generates some favorable effects on cerebral damages and withdrawal syndromes involved in addictive drugs. Furthermore, it modulates some processes of learning and memory. Thus, agmatine may be an important target for the treatment of CNS disorders. However, the abnormal release and transmission of agmatine in brain may also be related to some CNS disorders, such as schizophrenia. Interaction of agmatine with other central neurotransmitter systems, such as the glutamatergic and nitrergic systems, seems to be very important. According to the current literature, we can expect that the central agmatinergic system may be a new key target in development of novel approaches for understanding the etiopathogenesis of CNS disorders and their treatment with drugs. The main goal of this article is to evaluate the effects of agmatine in CNS and underline its pharmacological actions in CNS and drug development

The pharmacological importance of agmatine in the brain

Agmatine is a polyamine that is produced via decarboxylation of l-arginine by the enzyme arginine decarboxylase. It binds to various receptors and has been accepted as a novel neurotransmitter in brain. In experimental studies, agmatine exhibited anticonvulsant, antinociceptive, anxiolytic and antidepressantlike actions. Furthermore, it has some beneficial effects on cerebral ischemia models in animals. Agmatine interacts with the mechanisms of withdrawal syndromes for several addictive agents. It also modulates some processes involved in learning and memory. Thus, agmatine seems to be a valuable agent for the treatment of behavioral and neurodegenerative disorders. However, the aberrant release and transmission of agmatine in the central nervous system (CNS) may be associated with mechanisms of several CNS disorders, such as psychosis. Interactions between agmatine and other central neurotransmitter systems, such as the glutamatergic and nitrergic systems, are also very important. In light of the current literature on agmatine, we can anticipate that the central agmatinergic system may be an important target in development of novel strategies and approaches for understanding the etiopathogenesis of some important central disorders and their pharmacological treatments. The main objective of this review is to investigate and update the information on effects of agmatine in CNS and highlight its pharmacological importance in central disorders