12 research outputs found
Activities in English classes inducing positive / negative emotions
Introduction. Emotions have been proven to have significant impact on cognitive and motivational aspects of learning. Choosing appropriate activities to stimulate learnersβ positive emotions can thus greatly promote learning.Aim. The present research is aimed to find out which learning activities induce positive / negative emotions among upper secondary level learners of English as a foreign language and the secondary aim was to identify the emotions experienced.Methodology and research methods. Methodological triangulation applying qualitative research methods (questionnaire, interview and observation) was conducted among 62 learners and their 2 English teachers. A complementary quantitative instrument (scale) was used to detect the subjective emotional comfort of learners during English lessons.Results. The findings revealed prevailing positive habitual comfort of learners and joy as their primary emotion incited mostly by communication activities. Negative emotions of fear and sadness were detected mainly during testing and evaluation.Scientific novelty. The combination of four research methods in a combined research design studying the complex scale of emotions related to learning a foreign language has not been applied yet.Practical significance. Greater understanding of the affective aspect in learning a foreign language which may help foreign language teachers and methodologists select the appropriate activities to effectively address the actual cognitive and affective needs of learners.ΠΠ²Π΅Π΄Π΅Π½ΠΈΠ΅. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ ΡΠΌΠΎΡΠΈΠΈ ΠΎΠΊΠ°Π·ΡΠ²Π°ΡΡ ΡΡΡΠ΅ΡΡΠ²Π΅Π½Π½ΠΎΠ΅ Π²Π»ΠΈΡΠ½ΠΈΠ΅ Π½Π° ΠΊΠΎΠ³Π½ΠΈΡΠΈΠ²Π½ΡΠ΅ ΠΈ ΠΌΠΎΡΠΈΠ²Π°ΡΠΈΠΎΠ½Π½ΡΠ΅ Π°ΡΠΏΠ΅ΠΊΡΡ ΠΎΠ±ΡΡΠ΅Π½ΠΈΡ. Π’Π°ΠΊΠΈΠΌ ΠΎΠ±ΡΠ°Π·ΠΎΠΌ, Π²ΡΠ±ΠΎΡ ΠΏΠΎΠ΄Ρ
ΠΎΠ΄ΡΡΠΈΡ
Π·Π°Π½ΡΡΠΈΠΉ Π΄Π»Ρ ΡΡΠΈΠΌΡΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½ΡΡ
ΡΠΌΠΎΡΠΈΠΉ ΡΠΊΠΎΠ»ΡΠ½ΠΈΠΊΠΎΠ² ΠΌΠΎΠΆΠ΅Ρ Π² Π·Π½Π°ΡΠΈΡΠ΅Π»ΡΠ½ΠΎΠΉ ΡΡΠ΅ΠΏΠ΅Π½ΠΈ ΡΠΏΠΎΡΠΎΠ±ΡΡΠ²ΠΎΠ²Π°ΡΡ ΠΎΠ±ΡΡΠ΅Π½ΠΈΡ. Π¦Π΅Π»Ρ. ΠΡΠ½ΠΎΠ²Π½Π°Ρ ΡΠ΅Π»Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ Π·Π°ΠΊΠ»ΡΡΠ°Π»Π°ΡΡ Π² ΡΠΎΠΌ, ΡΡΠΎΠ±Ρ Π²ΡΡΡΠ½ΠΈΡΡ, ΠΊΠ°ΠΊΠΈΠ΅ Π²ΠΈΠ΄Ρ ΡΡΠ΅Π±Π½ΠΎΠΉ Π΄Π΅ΡΡΠ΅Π»ΡΠ½ΠΎΡΡΠΈ Π²ΡΠ·ΡΠ²Π°ΡΡ ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½ΡΠ΅, Π° ΠΊΠ°ΠΊΠΈΠ΅ β ΠΎΡΡΠΈΡΠ°ΡΠ΅Π»ΡΠ½ΡΠ΅ ΡΠΌΠΎΡΠΈΠΈ Ρ ΡΡΠ°ΡΡΠ΅ΠΊΠ»Π°ΡΡΠ½ΠΈΠΊΠΎΠ², ΠΈΠ·ΡΡΠ°ΡΡΠΈΡ
Π°Π½Π³Π»ΠΈΠΉΡΠΊΠΈΠΉ ΡΠ·ΡΠΊ ΠΊΠ°ΠΊ ΠΈΠ½ΠΎΡΡΡΠ°Π½Π½ΡΠΉ. ΠΡΠΎΡΠΎΡΡΠ΅ΠΏΠ΅Π½Π½ΠΎΠΉ ΡΠ΅Π»ΡΡ Π±ΡΠ»ΠΎ Π²ΡΡΠ²Π»Π΅Π½ΠΈΠ΅ ΠΈΡΠΏΡΡΡΠ²Π°Π΅ΠΌΡΡ
ΡΠΌΠΎΡΠΈΠΉ. ΠΠ΅ΡΠΎΠ΄ΠΎΠ»ΠΎΠ³ΠΈΡ ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. ΠΠ΅ΡΠΎΠ΄ΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠ°Ρ ΡΡΠΈΠ°Π½Π³ΡΠ»ΡΡΠΈΡ Ρ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ΠΌ ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ² ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ (Π°Π½ΠΊΠ΅ΡΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅, ΠΈΠ½ΡΠ΅ΡΠ²ΡΡ ΠΈ Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΠ΅) Π±ΡΠ»Π° ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½Π° ΡΡΠ΅Π΄ΠΈ ΡΡΠ°ΡΠΈΡ
ΡΡ (n = 62) ΠΈ ΠΈΡ
ΡΡΠΈΡΠ΅Π»Π΅ΠΉ Π°Π½Π³Π»ΠΈΠΉΡΠΊΠΎΠ³ΠΎ ΡΠ·ΡΠΊΠ° (n = 2). ΠΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΡΠΉ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΠΉ ΠΈΠ½ΡΡΡΡΠΌΠ΅Π½Ρ (ΡΠΊΠ°Π»Π°) ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π»ΡΡ Π΄Π»Ρ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΡ ΡΡΠ±ΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΠ³ΠΎ ΡΠΌΠΎΡΠΈΠΎΠ½Π°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΊΠΎΠΌΡΠΎΡΡΠ° ΡΠΊΠΎΠ»ΡΠ½ΠΈΠΊΠΎΠ² Π²ΠΎ Π²ΡΠ΅ΠΌΡ ΡΡΠΎΠΊΠΎΠ² Π°Π½Π³Π»ΠΈΠΉΡΠΊΠΎΠ³ΠΎ ΡΠ·ΡΠΊΠ°. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ ΠΏΠΎΠΊΠ°Π·Π°Π»ΠΈ, ΡΡΠΎ Ρ ΡΡΠ°ΡΠΈΡ
ΡΡ ΠΏΡΠ΅ΠΎΠ±Π»Π°Π΄Π°ΡΡ ΠΏΠΎΠ·ΠΈΡΠΈΠ²Π½ΡΠΉ ΠΏΡΠΈΠ²ΡΡΠ½ΡΠΉ ΠΊΠΎΠΌΡΠΎΡΡ ΠΈ ΡΠ°Π΄ΠΎΡΡΡ ΠΊΠ°ΠΊ ΠΊΠ»ΡΡΠ΅Π²Π°Ρ ΡΠΌΠΎΡΠΈΡ, Π²ΡΠ·Π²Π°Π½Π½Π°Ρ Π² ΠΎΡΠ½ΠΎΠ²Π½ΠΎΠΌ ΠΊΠΎΠΌΠΌΡΠ½ΠΈΠΊΠ°ΡΠΈΠ²Π½ΠΎΠΉ Π΄Π΅ΡΡΠ΅Π»ΡΠ½ΠΎΡΡΡΡ. ΠΡΡΠΈΡΠ°ΡΠ΅Π»ΡΠ½ΡΠ΅ ΡΠΌΠΎΡΠΈΠΈ (ΡΡΡΠ°Ρ
ΠΈ ΠΏΠ΅ΡΠ°Π»Ρ) Π²ΡΡΠ²Π»ΡΠ»ΠΈΡΡ ΠΏΡΠ΅ΠΈΠΌΡΡΠ΅ΡΡΠ²Π΅Π½Π½ΠΎ Π²ΠΎ Π²ΡΠ΅ΠΌΡ ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΈ ΠΎΡΠ΅Π½ΠΈΠ²Π°Π½ΠΈΡ. ΠΠ°ΡΡΠ½Π°Ρ Π½ΠΎΠ²ΠΈΠ·Π½Π° ΡΠΎΡΡΠΎΠΈΡ Π² ΡΠΎΠΌ, ΡΡΠΎ Π²ΠΏΠ΅ΡΠ²ΡΠ΅ ΠΏΡΠΈΠΌΠ΅Π½ΡΠ»ΠΎΡΡ ΡΠΎΡΠ΅ΡΠ°Π½ΠΈΠ΅ ΡΠ΅ΡΡΡΠ΅Ρ
ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ² Π² ΠΊΠΎΠΌΠ±ΠΈΠ½ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΌ Π΄ΠΈΠ·Π°ΠΉΠ½Π΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ ΡΠ»ΠΎΠΆΠ½ΠΎΠΉ ΡΠΊΠ°Π»Ρ ΡΠΌΠΎΡΠΈΠΉ, ΡΠ²ΡΠ·Π°Π½Π½ΡΡ
Ρ ΠΈΠ·ΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΈΠ½ΠΎΡΡΡΠ°Π½Π½ΠΎΠ³ΠΎ ΡΠ·ΡΠΊΠ°.ΠΡΠ°ΠΊΡΠΈΡΠ΅ΡΠΊΠ°Ρ Π·Π½Π°ΡΠΈΠΌΠΎΡΡΡ. ΠΡΡΡΠ΅Π΅ ΠΏΠΎΠ½ΠΈΠΌΠ°Π½ΠΈΠ΅ Π°ΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΠ³ΠΎ Π°ΡΠΏΠ΅ΠΊΡΠ° Π² ΠΈΠ·ΡΡΠ΅Π½ΠΈΠΈ ΠΈΠ½ΠΎΡΡΡΠ°Π½Π½ΠΎΠ³ΠΎ ΡΠ·ΡΠΊΠ° ΠΌΠΎΠΆΠ΅Ρ ΠΏΠΎΠΌΠΎΡΡ ΠΏΠ΅Π΄Π°Π³ΠΎΠ³Π°ΠΌ ΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΈΡΡΠ°ΠΌ Π² Π²ΡΠ±ΠΎΡΠ΅ ΠΏΠΎΠ΄Ρ
ΠΎΠ΄ΡΡΠΈΡ
Π·Π°Π½ΡΡΠΈΠΉ Π΄Π»Ρ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΠ³ΠΎ ΡΠ΄ΠΎΠ²Π»Π΅ΡΠ²ΠΎΡΠ΅Π½ΠΈΡ ΡΠ΅Π°Π»ΡΠ½ΡΡ
ΠΊΠΎΠ³Π½ΠΈΡΠΈΠ²Π½ΡΡ
ΠΈ ΡΠΌΠΎΡΠΈΠΎΠ½Π°Π»ΡΠ½ΡΡ
ΠΏΠΎΡΡΠ΅Π±Π½ΠΎΡΡΠ΅ΠΉ ΡΡΠ°ΡΠΈΡ
ΡΡ.This work was supported by the Cultural and Educational Grant Agency of the Ministry of Education, Science, Research and Sport of the Slovak Republic (KEGA 002UKF-4/2020).Π‘ΡΠ°ΡΡΡ ΠΏΠΎΠ΄Π΄Π΅ΡΠΆΠ°Π½Π° ΠΠ³Π΅Π½ΡΡΡΠ²ΠΎΠΌ ΠΊΡΠ»ΡΡΡΡΠ½ΡΡ
ΠΈ ΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°ΡΠ΅Π»ΡΠ½ΡΡ
Π³ΡΠ°Π½ΡΠΎΠ² ΠΠΈΠ½ΠΈΡΡΠ΅ΡΡΡΠ²Π° ΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΡ, Π½Π°ΡΠΊΠΈ, ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΉ ΠΈ ΡΠΏΠΎΡΡΠ° Π‘Π»ΠΎΠ²Π°ΡΠΊΠΎΠΉ Π Π΅ΡΠΏΡΠ±Π»ΠΈΠΊΠΈ (KEGA 002UKF-4/2020)
Projekce balbuties do vychovne vzdelavaciho procesu deti skolniho veku a adolescentu.
Human personality with disturbed speed fluency is stroken in all spheres of their social existence. Specialized literature is concerned with the balbuties' problematics in the education and training context only marginally. The presented publication reflects the speech fluency disorders penetrations into the field of education and training of children of the age range between 6 and 18 years. The theoretical part of the presented publication summarizes the actual knowledge in the balbutology field. The educational and training process with all specifications in persons with disturbed communication ability is analyzed. The theoretical part is completed by a chapter dealing with evolutional aspects in persons of the age between 6 and 18 years. The practical part of the dissertation was based on a questionnaire distributed to primary schools, pedagogic-psychological consulting rooms, educational care centres, children's homes with a school and educational institution. The aim of this inquiry is to refer on specifics of the educational and training process of school-aged children and adolescents. The educational factor oriented on the school success of balbutics is analyzed. The publication is also engaged in the educative level formation.Available from STL Prague, CZ / NTK - National Technical LibrarySIGLECZCzech Republi
Melatonin as a Potential Approach to Anxiety Treatment
Anxiety disorders are the most common mental diseases. Anxiety and the associated physical symptoms may disturb social and occupational life and increase the risk of somatic diseases. The pathophysiology of anxiety development is complex and involves alterations in stress hormone production, neurosignaling pathways or free radical production. The various manifestations of anxiety, its complex pathophysiological background and the side effects of available treatments underlie the quest for constantly seeking therapies for these conditions. Melatonin, an indolamine produced in the pineal gland and released into the blood on a nightly basis, has been demonstrated to exert anxiolytic action in animal experiments and different clinical conditions. This hormone influences a number of physiological actions either via specific melatonin receptors or by receptor-independent pleiotropic effects. The underlying pathomechanism of melatonin’s benefit in anxiety may reside in its sympatholytic action, interaction with the renin–angiotensin and glucocorticoid systems, modulation of interneuronal signaling and its extraordinary antioxidant and radical scavenging nature. Of importance, the concentration of this indolamine is significantly higher in cerebrospinal fluid than in the blood. Thus, ensuring sufficient melatonin production by reducing light pollution, which suppresses melatonin levels, may represent an endogenous neuroprotective and anxiolytic treatment. Since melatonin is freely available, economically undemanding and has limited side effects, it may be considered an additional or alternative treatment for various conditions associated with anxiety
Effect of Ivabradine on a Hypertensive Heart and the Renin-Angiotensin-Aldosterone System in L-NAME-Induced Hypertension
Ivabradine, the selective inhibitor of the If current in the sinoatrial node, exerts cardiovascular protection by its bradycardic effect and potentially pleiotropic actions. However, there is a shortage of data regarding ivabradine’s interaction with the renin-angiotensin-aldosterone system (RAAS). This study investigated whether ivabradine is able to protect a hypertensive heart in the model of L-NAME-induced hypertension and to interfere with the RAAS. Four groups (n = 10/group) of adult male Wistar rats were treated as follows for four weeks: control, ivabradine (10 mg/kg/day), L-NAME (40 mg/kg/day), and L-NAME plus ivabradine. L-NAME administration increased systolic blood pressure (SBP) and left ventricular (LV) weight, enhanced hydroxyproline concentration in the LV, and deteriorated the systolic and diastolic LV function. Ivabradine reduced heart rate (HR) and SBP, and improved the LV function. The serum concentrations of angiotensin Ang 1–8 (Ang II), Ang 1–5, Ang 1–7, Ang 1–10, Ang 2–8, and Ang 3–8 were decreased in the L-NAME group and ivabradine did not modify them. The serum concentration of aldosterone and the aldosterone/Ang II ratio were enhanced by L-NAME and ivabradine reduced these changes. We conclude that ivabradine improved the LV function of the hypertensive heart in L-NAME-induced hypertension. The protective effect of ivabradine might have been associated with the reduction of the aldosterone level
Sacubitril/Valsartan and Ivabradine Attenuate Left Ventricular Remodelling and Dysfunction in Spontaneously Hypertensive Rats: Different Interactions with the Renin–Angiotensin–Aldosterone System
This study investigated whether sacubitril/valsartan and ivabradine are able to prevent left ventricular (LV) fibrotic remodelling and dysfunction in a rat experimental model of spontaneous hypertension (spontaneously hypertensive rats, SHRs) and whether this potential protection is associated with RAAS alterations. Five groups of three-month-old male Wistar rats and SHRs were treated for six weeks as follows: untreated Wistar controls, Wistar plus sacubitril/valsartan, SHR, SHR plus sacubitril/valsartan, and SHR plus ivabradine. The SHRs developed a systolic blood pressure (SBP) increase, LV hypertrophy and fibrosis, and LV systolic and diastolic dysfunction. However, no changes in serum RAAS were observed in SHRs compared with the controls. Elevated SBP in SHRs was decreased by sacubitril/valsartan but not by ivabradine, and only sacubitril/valsartan attenuated LV hypertrophy. Both sacubitril/valsartan and ivabradine reduced LV collagen content and attenuated LV systolic and diastolic dysfunction. Sacubitril/valsartan increased the serum levels of angiotensin (Ang) II, Ang III, Ang IV, Ang 1-5, Ang 1-7, and aldosterone, while ivabradine did not affect the RAAS. We conclude that the SHR is a normal-to-low serum RAAS model of experimental hypertension. While the protection of the hypertensive heart in SHRs by sacubitril/valsartan may be related to an Ang II blockade and the protective Ang 1-7, the benefits of ivabradine were not associated with RAAS modulation
Lactacystin-Induced Model of Hypertension in Rats: Effects of Melatonin and Captopril
Lactacystin is a proteasome inhibitor that interferes with several factors involved in heart remodelling. The aim of this study was to investigate whether the chronic administration of lactacystin induces hypertension and heart remodelling and whether these changes can be modified by captopril or melatonin. In addition, the lactacystin-model was compared with NG-nitro-l-arginine-methyl ester (L-NAME)- and continuous light-induced hypertension. Six groups of three-month-old male Wistar rats (11 per group) were treated for six weeks as follows: control (vehicle), L-NAME (40 mg/kg/day), continuous light (24 h/day), lactacystin (5 mg/kg/day) alone, and lactacystin with captopril (100 mg/kg/day), or melatonin (10 mg/kg/day). Lactacystin treatment increased systolic blood pressure (SBP) and induced fibrosis of the left ventricle (LV), as observed in L-NAME-hypertension and continuous light-hypertension. LV weight and the cross-sectional area of the aorta were increased only in L-NAME-induced hypertension. The level of oxidative load was preserved or reduced in all three models of hypertension. Nitric oxide synthase (NOS) activity in the LV and kidney was unchanged in the lactacystin group. Nuclear factor-kappa B (NF-ΞΊB) protein expression in the LV was increased in all treated groups in the cytoplasm, however, in neither group in the nucleus. Although melatonin had no effect on SBP, only this indolamine (but not captopril) reduced the concentration of insoluble and total collagen in the LV and stimulated the NO-pathway in the lactacystin group. We conclude that chronic administration of lactacystin represents a novel model of hypertension with collagenous rebuilding of the LV, convenient for testing antihypertensive drugs or agents exerting a cardiovascular benefit beyond blood pressure reduction
Hypertension and Cardiovascular Remodelling in Rats Exposed to Continuous Light: Protection by ACE-Inhibition and Melatonin
Exposure of rats to continuous light attenuates melatonin production and results in hypertension development. This study investigated whether hypertension induced by continuous light (24 hours/day) exposure induces heart and aorta remodelling and if these alterations are prevented by melatonin or angiotensin converting enzyme inhibitor captopril. Four groups of 3-month-old male Wistar rats (10 per group) were treated as follows for six weeks: untreated controls, exposed to continuous light, light-exposed, and treated with either captopril (100βmg/kg/day) or melatonin (10βmg/kg/day). Exposure to continuous light led to hypertension, left ventricular (LV) hypertrophy and fibrosis, and enhancement of the oxidative load in the LV and aorta. Increase in systolic blood pressure by continuous light exposure was prevented completely by captopril and partially by melatonin. Both captopril and melatonin reduced the wall thickness and cross-sectional area of the aorta and reduced the level of oxidative stress. However, only captopril reduced LV hypertrophy development and only melatonin reduced LV hydroxyproline concentration in insoluble and total collagen in rats exposed to continuous light. In conclusion, captopril prevented LV hypertrophy development in the continuous light-induced hypertension model, while only melatonin significantly reduced fibrosis. This antifibrotic action of melatonin may be protective in hypertensive heart disease
Effect of Melatonin on the Renin-Angiotensin-Aldosterone System in l-NAME-Induced Hypertension
The renin-angiotensin-aldosterone system (RAAS) is a dominant player in several cardiovascular pathologies. This study investigated whether alterations induced by l-NAME, (NLG)-nitro-l-arginine methyl ester, a nitric oxide synthase inhibitor, and the protective effect of melatonin are associated with changes in the RAAS. Four groups of 3-month-old male Wistar rats (n = 10) were treated as follows for four weeks: untreated controls, rats treated with melatonin (10 mg/kg/day), rats treated with l-NAME (40 mg/kg/day), and rats treated with l-NAME + melatonin. l-NAME administration led to hypertension and left ventricular (LV) fibrosis in terms of enhancement of soluble, insoluble and total collagen concentration and content. Melatonin reduced systolic blood pressure enhancement and lowered the concentration and content of insoluble and total collagen in the LV. The serum concentration of angiotensin (Ang) 1β8 (Ang II) and its downstream metabolites were reduced in the l-NAME group and remained unaltered by melatonin. The serum aldosterone level and its ratio to Ang II (AA2-ratio) were increased in the l-NAME group without being modified by melatonin. We conclude that l-NAME-hypertension is associated with reduced level of Ang II and its downstream metabolites and increased aldosterone concentration and AA2-ratio. Melatonin exerts its protective effect in l-NAME-induced hypertension without affecting RAAS