Cognitive and metacognitive aspects of the development of lifelong learning competencies in law students

Lifelong learning is one of the main trends in educational and social policy in Europe, aimed at ensuring professional realization and social integrity of an individual. The article describes cognitive and metacognitive aspects of the formation of learning competence, as well as predisposition of law students to lifelong learning. A survey of 218 students and masters was conducted, data on the most popular and effective forms of knowledge acquisition (experience of formal, nonformal and informal learning over the past year), plans for further education and career development were collected. The dynamics of learning at different years of study is described. A group of students with pronounced learning and focus on lifelong learning (45% of the sample) was identified. A comparative analysis of two samples was carried out and qualities that could be considered markers of the LLL orientation were identified: a high level of metacognitive knowledge and metacognitive activity, reflective competence (at the cognitive, metacognitive and personal level), internal involvement in learning, focus on achieving professionalism and personal development, general self-efficacy, the prevalence of progressive and creative motives over consumer ones. Conclusions are drawn about the predominant role of metacognitions and personality determinants in the formation of lifelong learning competency among students. Reflection aimed at recognizing one’s own cognitive processes and understanding their contribution to personal development is the main mechanism for the formation of meta-cognitive abilities. The results obtained in the study determine the ways of pedagogical support and psychological intervention to ensure the development of lifelong learning competencies in different categories of students

Exogenous nitric oxide reduces glucose transporters translocation and lactate production in ischemic myocardium in vivo

Nitric oxide (NO) inhibits myocardial glucose transport and metabolism, although the underlying mechanism(s) and functional consequences of this effect are not clearly understood. We tested the hypothesis that NO inhibits the activation of AMP-activated protein kinase (AMPK) and translocation of cardiac glucose transporters (GLUTs; GLUT-4) and reduces lactate production. Ischemia was induced in open-chest dogs by a 66% flow reduction in the left anterior descending coronary artery (LAD). During ischemia, dogs were untreated (control) or treated by direct LAD infusion of (i) nitroglycerin (NTG) (0.5 μg·kg(–1)·min(–1)); (ii) 8-Br-cGMP (50 μg·kg(–1)·min(–1)); or (iii) NO synthase inhibitor l-nitro-argininemethylester (40 μg·kg(–1)·min(–1); n = 9 per group). Cardiac substrate oxidation was measured with isotopic tracers. There were no differences in myocardial blood flow or oxygen delivery among groups; however, at 45 min of ischemia, the activation of AMPK was significantly less in NTG (77 ± 12% vs. nonischemic myocardium) and 8-Br-cGMP (104 ± 13%), compared with control (167 ± 17%). Similarly, GLUT-4 translocation was significantly reduced in NTG (74 ± 7%) and 8-Br-cGMP (120 ± 11%), compared with control (165 ± 17%). Glucose uptake and lactate output were 30% and 60% lower in NTG compared with control. Inhibition of NO synthesis stimulated glucose oxidation (67% increase compared with control) but did not affect AMPK phosphorylation, GLUT-4 translocation and glucose uptake. Contractile function in the ischemic region was significantly improved by NTG and l-nitro-argininemethylester. In conclusion, in ischemic myocardium an NO donor inhibits glucose uptake and lactate production via a reduction in AMPK stimulation of GLUT-4 translocation, revealing a mechanism of metabolic modulation and myocardial protection activated by NO donors