Війна в спортивній журналістиці з точки зору когнітивної теорії метафори. (The war in the transmission of sports journalism in terms of cognitive metaphor theory.)

У статті, на основі аналізу метафори війни, яка часто трапляється у спортивних газетних статтях, автор показує можливість використання товариством дослідницького апарату когнітивної лінгвістики. Шляхом виявлення механізмів дискусії про спортивні заходи та їх вплив на осмислення спорту автор намагається відповісти на питання про те, як з моральної точки зору повинно і не повинно говоритися про спорт. (An author of article, by interpretation metaphor of war occurs in many articles about sport, outlines how we can apply the cognitive linguistic research tools to social research. This article aimed at answering the question, how, of moral point of view we should, a how we shouldn't talk about sport.

The sources of moisture in the sand dunes – the example of the Western Sahara dune field

Climatic and meteorological conditions may limit the aeolian transport within barchans. An explanation of that issue was the main goal of the investigation held in Western Sahara dune fields located around Tarfaya and Laâyoune. Particular attention was paid to the factors causing the moisture content rising of the sand dune surface layer, which could influence the wind threshold shear velocity in the aeolian transport. The wetted surface layer of sand, when receiving moisture from precipitation or suspensions, reduces the aeolian transport, even in case of wind velocity above 4–5 m s–1. Fog and dew condensation does not affect the moisture of deeper sand layers, what occurs after rainfall

RACJONALNIE O ŚMIERCI. ZMAGANIA JULII HARTWIG Z TAJEMNICĄ PRZEMIJANIA

Artykuł został poświęcony wybranym utworom Julii Hartwig, w których poetka próbuje ująć w słowo – i bez wątpienia jest to próba udana – jedno z najbardziej nieuniknionych i tajemniczych prawideł ludzkiej egzystencji, a mianowicie konieczność umierania. Doświadczenie przemijania, a nawet stałej obecności śmierci wyraża poetka poprzez uważne przyglądanie się rzeczywistości widzialnej, oczywistej, a nawet banalnej, którą jednak każdorazowo przekracza, by uchwycić to, co tajemnicze i niewyrażalne. W poezji Julii Hartwig nie brakuje wizyt zmarłych w świecie żywych, zarówno na jawie, jak i we śnie, co jest dowodem na to, że owe dwa światy – żywych i umarłych przenikają się, a może nawet więcej, że świat umarłych i żywych stanowią nierozerwalną jedność. Ten splot nie jest dla poetki niczym nadzwyczajnym, dlatego owe przejawy śmierci w życiu, czy też świata zmarłych w świecie żywych opisuje w sposób zupełnie racjonalny

„DOPÓKI NARÓD POSŁUGUJE SIĘ WŁASNYM JĘZYKIEM, DOPÓTY ZACHOWUJE SAM SIEBIE…”

Recenzja książki Łarysy Masenko, Język i polityka, tłum. i red. nauk. A. Bracki, Wydawnictwo Athenae Gedanenses, Gdańsk 2012, ss. 173. W dalszej części recenzji przypisy do poszczególnych fragmentów Języka i polityki zostaną podane w tekście głównym w postaci odniesienia do konkretnych stron książki. Про автора: Моніка Жмудзька-Бродніцка, літературознавець, кандидат філологічних наук, випускниця Філософського факультету й Інституту польської філології Гданського університету. Займається філософією й етикою спорту, а також етикою мови з особливим врахуванням суспільної ролі мови в спортивних передачах

H_3 histamine receptor antagonist pitolisant reverses some subchronic disturbances induced by olanzapine in mice

The use of atypical antipsychotic drugs like olanzapine is associated with side effects such as sedation and depression-like symptoms, especially during the initial period of the use. It is believed that the occurrence of these undesirable effectsis mainly the result of the histamine H(1)receptors blockade by olanzapine. In addition, use of olanzapine increases the level of triglycerides in the blood, which correlates with growing obesity. The aim of this study was to investigate the influence of pitolisant – H(3) histamine antagonist - on subchronic olanzapine-induced depresion-like symptoms, sedation and hypertriglicerydemia. Forced swim test was conducted to determinate depressive-like effect of olanzapine and antidepressive-like activity during the co-administered pitolisant. The test was performed after the first and fifteenth day of the treatment of the mice. The spontaneous activity of the mice was measured on the fourteenth day of the treatment with a special, innovative RFID-system (Radio-frequency identification system) – TraffiCage (TSE-Systems, Germany). Triglyceride levels were determined on the sixteenth day of the experiment after 15 cycles of drug administration. Daily olanzapine treatment (4 mg/kg b.w., i.p., d.p.d) for 15 days significantly induces sedation (p < 0.05) and prolongs immobility time in forced swim tests (FST) in mice (p < 0.05); and also elevates the level of triglycerides (p < 0.05). Administration of pitolisant (10 mg/kg b.w., i.p.) subsequentto olanzapine normalizes these adverse effects. This study presents a promising alternative for counteracting some behavioral changes and metabolic disturbances which occur in the early period of treatment with antipsychotic drugs

Chemically homogenous compounds with antagonistic properties at all α1\alpha_{1}-adrenoceptor subtypes but not β1\beta_{1}-adrenoceptor attenuate adrenaline-induced arrhythmia in rats

Studies proved that among all α1-adrenoceptors, cardiac myocytes functionally express only α1A- and α1B-subtype. Scientists indicated that α1A-subtype blockade might be beneficial in restoring normal heart rhythm. Therefore, we aimed to determine the role of α1-adrenoceptors subtypes (i.e. α1A and α1B) in antiarrhythmic effect of six structurally similar derivatives of 2-methoxyphenylpiperazine. We compared the activity of studied compounds with carvedilol, which is β1- and α1-adrenoceptors blocker with antioxidant properties.To evaluate the affinity for adrenergic receptors, we used radioligand methods. We investigated selectivity at α1-adrenoceptors subtypes using functional bioassays. We tested antiarrhythmic activity in adrenaline-induced (20 µg/kg i.v.), calcium chloride-induced (140 and 25 mg/kg i.v.) and barium chloride-induced (32 and 10 mg/kg i.v.) arrhythmia models in rats. We also evaluated the influence of studied compounds on blood pressure in rats, as well as lipid peroxidation. All studied compounds showed high affinity towards α1-adrenoceptors but no affinity for β1 receptors. Biofunctional studies revealed that the tested compounds blocked α1A- stronger than α1B-adrenoceptors, but except for HBK-19 they antagonized α1A-adrenoceptor weaker than α1D-subtype. HBK-19 showed the greatest difference in pA2 values - it blocked α1A-adrenoceptors around sevenfold stronger than α1B subtype. All compounds showed prophylactic antiarrhythmic properties in adrenaline-induced arrhythmia, but only the activity of HBK-16, HBK-17, HBK-18 and HBK-19 (ED50=0.18-0.21) was comparable to that of carvedilol (ED50=0.36). All compounds reduced mortality in adrenaline-induced arrhythmia. HBK-16, HBK-17, HBK-18 and HBK-19 showed therapeutic antiarrhythmic properties in adrenaline-induced arrhythmia. None of the compounds showed activity in calcium chloride- or barium chloride-induced arrhythmias. HBK-16, HBK-17, HBK-18 and HBK-19 decreased heart rhythm at ED84. All compounds significantly lowered blood pressure in normotensive rats. HBK-18 showed the strongest hypotensive properties (the lowest active dose: 0.01 mg/kg). HBK-19 was the only compound in the group, which did not show hypotensive effect at antiarrhythmic doses. HBK-16, HBK-17, HBK-18, HBK-19 showed weak antioxidant properties.Our results indicate that the studied 2-methoxyphenylpiperazine derivatives that possessed stronger α1A-adrenolytic properties (i.e. HBK-16, HBK-17, HBK-18 and HBK-19) were the most compounds in adrenaline-induced arrhythmia. Thus, we suggest that the potent blockade of α1A-receptor subtype is essential to attenuate adrenaline-induced arrhythmia

HBK-17, a 5-HT1A Receptor Ligand With Anxiolytic-Like Activity, Preferentially Activates ß-Arrestin Signaling

Numerous studies have proven that both stimulation and blockade of 5-HT1A and the blockade of 5-HT7 receptors might cause the anxiolytic-like effects. Biased agonists selectively activate specific signaling pathways. Therefore, they might offer novel treatment strategies. In this study, we investigated the anxiolytic-like activity, as well as the possible mechanism of action of 1-[(2,5-dimethylphenoxy)propyl]-4-(2-methoxyphenyl)piperazine hydrochloride (HBK-17). In our previous experiments, HBK-17 showed high affinity for 5-HT1A and 5-HT7 receptors and antidepressant-like properties. We performed the four plate test and the elevated plus maze test to determine anxiolytic-like activity. Toward a better understanding of the pharmacological properties of HBK-17 we used various functional assays to determine its intrinsic activity at 5-HT1A, 5-HT2A, 5-HT7, and D2 receptors and UHPLC-MS/MS method to evaluate its pharmacokinetic profile. We observed the anxiolytic-like activity of HBK-17 in both behavioral tests and the effect was reversed by the pretreatment with WAY-100635, which proves that 5-HT1A receptor activation was essential for the anxiolytic-like effect. Moreover, the compound moderately antagonized D2, weakly 5-HT7 and very weakly 5-HT2A receptors. We demonstrated that HBK-17 preferentially activated ß-arrestin signaling after binding to the 5-HT1A receptor. HBK-17 was rapidly absorbed after intraperitoneal administration and had a half-life of about 150 min. HBK-17 slightly penetrated the peripheral compartment and showed bioavailability of approximately 45%. The unique pharmacological profile of HBK-17 encourages further experiments to understand its mechanism of action fully

Translational studies in the complex role of neurotransmitter systems in anxiety and anxiety disorders

Discovery of innovative anxiolytics is severely hampering. Existing anxiolytics are developed decades ago and are still the therapeutics of choice. Moreover, lack of new drug targets forecasts a severe jeopardy in the future treatment of the huge population of CNS-diseased patients. We simply lack the knowledge on what is wrong in brains of anxious people (normal and diseased). Translational research, based on interacting clinical and preclinical research, is extremely urgent. In this endeavor, genetic and genomic approaches are part of the spectrum of contributing factors. We focus on three druggable targets: serotonin transporter, 5-HT1A, and GABAA receptors. It is still uncertain whether and how these targets are involved in normal and diseased anxiety processes. For serotonergic anxiolytics, the slow onset of action points to indirect effects leading to plasticity changes in brain systems leading to reduced anxiety. For GABAA benzodiazepine drugs, acute anxiolytic effects are found indicating primary mechanisms directly influencing anxiety processes. Close translational collaboration between fundamental academic and discovery research will lead to badly needed breakthroughs in the search for new anxiolytics.</p