Глокалізація та освіта вчителів – етичні міркування у складні часи

The article emphasizes that global thinking begins at the structural level of educational programs on teacher preparation, and we offer the example of Ukraine, which recently underwent a large-scale reform of its higher education system towards international standardization, which included their educational program on teacher preparation. At the same time, the process of modernization of higher education in Ukraine has a somewhat one-sided focus on the global sphere and neglects some local features, which has led to the emergence of problems. This article explores the connection between glocalization and teacher education from methodological and ethical perspective. We argue that global competence helps teachers and future generations to develop a multi-perspective view to accurately respond to current and future challenges and understand the world in its complexity. This mindset also enables them to make thoughtful ethical decisions based on well-considered global principles. In addition, we argue that glocalization begins at the structural level, and offer the example of Ukraine, which recently underwent a large-scale reform of its education system, including teacher education. However, the reform focused mainly on the global sphere and neglected some local features, leading to numerous problems and challenges. To better understand the idea of glocalization in teacher education from the ethical perspective, future scientific researches can be focused on the study of the international teacher education programs, which find a balance between national traditions and international developments in education, so different systems can learn and enrich each other. Of course, the article does not cover all theoretical aspects of the considered problem and provides further scientific discussions about glocalization in teacher education.У статті досліджуєються зв’язок між глокалізацією та педагогічною освітою з етичної точки зору. Ми стверджуємо, що посилений акцент на концепції глокалізації в освіті вчителів краще підготує майбутні покоління до відповіді на поточні та майбутні виклики. Усвідомлення взаємозв’язку між локальною та глобальною сферами допомагає вчителям і, зрештою, учням зрозуміти світ у його складності. Глокальний спосіб мислення дозволяє їм приймати обдумані етичні рішення, які враховують різні точки зору. Такі рішення базуються на глобальних принципах, таких як соціальна відповідальність, справедливість і стійкість. У статті акцентовано, що глобальне мислення починається на структурному рівні освітніх програм з підготовки вчителів, і надаємо приклад України, яка нещодавно пройшла широкомасштабну реформу своєї системи вищої освіти в напрямку міжнародної стандартизації, яка включала їхню програму підготовки вчителів. Водночас, процес модернізації вищої освіти в Україні має дещо однобічний фокус на глобальній сфері та відюбувається нехтування деякими локальними обставинами, що призвело до виникнення проблем. У статті обговорюється зв’язок між глокалізацією та педагогічною освітою з методологічної та етичної точки зору. Ми стверджуємо, що глобальна компетентність допомагає вчителям і майбутнім поколінням розвивати багаторакурсний погляд, щоб точно реагувати на сучасні та майбутні виклики та розуміти світ у його складності. Таке мислення також дає їм змогу приймати обдумані етичні рішення, які ґрунтуються на добре зважених глобальних принципах. Крім того, ми стверджуємо, що глокалізація починається на структурному рівні, і наводимо приклад України, яка нещодавно пройшла широкомасштабну реформу своєї системи освіти, зокрема й педагогічної освіти. Тим не менш, реформа зосередилася в основному на глобальній сфері та знехтувала деякими місцевими обставинами, що призвело до численних проблем і викликів. Щоб краще зрозуміти ідею глокалізації в педагогічній освіті з етичної точки зору, майбутні наукові дослідження можуть зосереджуватись на вивченні міжнародних програм педагогічної освіти, які знаходять баланс між національними традиціями та міжнародними розробками в освіті, щоб різні освітні системи могли вчитися та збагачувати одна одну. Звісно, матеріал статті не вичерпує всіх теоретичних аспектів розглянутої проблеми і передбачає подальші наукові дискусія про глокалізацію в освіті вчителів

Vorzeitiger Berufseinstieg ins Lehramt. Risiken für die Profession

Aufgrund des aktuellen Lehrer*innenmangels arbeiten Lehramtsstudierende zunehmend als Lehrpersonen. Fraglich ist, ob dies zu einer eingeschränkten individuellen Professionalisierung sowie kollektiven Deprofessionalisierung des Lehrer*innenberufs führt und wie es infolge zu einer Reprofessionalisierung kommen kann. Bereits unterrichtende Lehramtsstudierende wurden leitfadengestützt zur eigenen Professionalisierung interviewt. Die Ergebnisse zeigen, dass Studierende den vorzeitigen Berufseinstieg als bereichernd wahrnehmen, jedoch eine Reflexion des eigenen Professionalisierungsprozesses fehlt. (DIPF/Orig.

History of peripheral artery disease and cardiovascular risk of real-word patients with acute coronary syndrome: Role of inflammation and comorbidities.

BACKGROUND Patients with acute coronary syndromes (ACS) remain at risk of cardiovascular disease (CVD) recurrences. Peripheral artery disease (PAD) may identify a very high risk (VHR) group who may derive greater benefit from intensified secondary prevention. METHODS Among ACS-patients enrolled in the prospective multi-center Special Program University Medicine (SPUM), we assessed the impact of PAD on major cardiovascular events (MACE: composite of myocardial infarction, stroke and all-cause death) and major bleeding. Multivariate analysis tested the relation of each significant variable with MACE, as well as biomarkers of inflammation and novel markers of atherogenesis. RESULTS Out of 4787 ACS patients, 6.0% (n = 285) had PAD. PAD-patients were older (p < 0.001), with established CVD and signs of increased persistent inflammation (hs-CRP; 23.6 ± 46.5 vs 10.4 ± 27.2 mg/l, p < 0.001 and sFlt-1; 1399.5 ± 1501.3 vs 1047.2 ± 1378.6 ng/l, p = 0.018). In-hospital-death (3.2% vs 1.4%, p = 0.022) and -MACE (5.6% vs 3.0%, p = 0.017) were higher in PAD-patients. MACE at 1 year (18.6% vs 7.9%,p < 0.001) remained increased even after adjustment for confounders (Adj. HR 1.53, 95% CI: 1.14-2.08, p = 0.005). Major bleeding did not differ between groups (Adj. HR 1.18; 95% CI 0.71-1.97, p = 0.512). Although PAD predicted MACE, PAD-patients were prescribed less frequently for secondary prevention at discharge. CONCLUSIONS In this real-world ACS patient cohort, concomitant PAD is a marker of VHR and is associated with increased and persistent inflammation, higher risk for MACE without an increased risk of major bleeding. Therefore, a history of PAD may be useful to identify those ACS patients at VHR who require more aggressive secondary prevention

Occlusion of the infarct-related coronary artery presenting as acute coronary syndrome with and without ST-elevation: impact of inflammation and outcomes in a real-world prospective cohort

Background Patients with ST-segment elevation typically feature total coronary occlusion (TCO) of the infarct-related artery (IRA) on angiography, which may result in worse outcomes. Yet, relying solely on electrocardiogram (ECG) findings may be misleading and those presenting with non-ST-segment elevation acute coronary syndromes (NSTE-ACSs) may have TCO as well. Herein, we aimed to delineate clinical characteristics and outcomes of patients with ACS stratified by IRA location. Methods A total of 4787 ACS patients were prospectively recruited between 2009 and 2017 in SPUM-ACS (ClinicalTrials.gov Identifier: NCT01000701). The primary endpoint was major adverse cardiovascular events (MACEs), a composite of all-cause death, non-fatal myocardial infarction and non-fatal stroke at 1 year. Multivariable-adjusted survival models were fitted using backward selection. Results A total of 4412 ACS patients were included in this analysis, 56.0% (n = 2469) ST-elevation myocardial infarction (STEMI) and 44.0% (n = 1943) NSTE-ACS. The IRA was the right coronary artery (RCA) in 33.9% (n = 1494), the left-anterior descending coronary artery (LAD) in 45.6% (n = 2013), and the left circumflex (LCx) in 20.5% (n = 905) patients. In STEMI patients, TCO (defined as TIMI 0 flow at angiography) was observed in 55% of cases with LAD, in 63% with RCA, and in 55% with LCx. In those presenting with NSTE-ACS, TCO was more frequent in those with LCx and RCA as compared to the LAD (27 and 24%, respectively, vs. 9%, P &lt; 0.001). Among patients with NSTE-ACS, occlusion of the LCx was associated with an increased risk of MACE during 1 year after the index ACS (fully adjusted hazard ratio 1.68, 95% confidence interval 1.10–2.59, P = 0.02; reference: RCA and LAD). Features of patients with NSTE-ACS associated with TCO of the IRA included elevated lymphocyte and neutrophil counts, higher levels of high-sensitivity C reactive protein (hs-CRP) and high-sensitivity cardiac troponin T, lower eGFR, and notably a negative history of MI. Conclusion In NSTE-ACS, both LCx and RCA involvement was associated with TCO at angiography despite the absence of ST-segment elevation. Involvement of the LCx, but not the LAD or RCA, as the IRA represented an independent predictor of MACE during 1-year follow-up. Hs-CRP, lymphocyte, and neutrophil counts were independent predictors of total IRA occlusion, suggesting a possible role of systemic inflammation in the detection of TCO irrespective of ECG presentation

Loss of autophagy protein ATG5 impairs cardiac capacity in mice and humans through diminishing mitochondrial abundance and disrupting Ca2+Ca^{\text{2+}} cycling

Aims Autophagy protects against the development of cardiac hypertrophy and failure. While aberrant Ca2+ handling promotes myocardial remodelling and contributes to contractile dysfunction, the role of autophagy in maintaining Ca2+ homeostasis remains elusive. Here, we examined whether Atg5 deficiency-mediated autophagy promotes early changes in subcellular Ca2+ handling in ventricular cardiomyocytes, and whether those alterations associate with compromised cardiac reserve capacity, which commonly precedes the onset of heart failure. Methods and results RT–qPCR and immunoblotting demonstrated reduced Atg5 gene and protein expression and decreased abundancy of autophagy markers in hypertrophied and failing human hearts. The function of ATG5 was examined using cardiomyocyte-specific Atg5-knockout mice (Atg5−/−). Before manifesting cardiac dysfunction, Atg5−/− mice showed compromised cardiac reserve in response to β-adrenergic stimulation. Consequently, effort intolerance and maximal oxygen consumption were reduced during treadmill-based exercise tolerance testing. Mechanistically, cellular imaging revealed that Atg5 deprivation did not alter spatial and functional organization of intracellular Ca2+ stores or affect Ca2+ cycling in response to slow pacing or upon acute isoprenaline administration. However, high-frequency stimulation exposed stunted amplitude of Ca2+ transients, augmented nucleoplasmic Ca2+ load, and increased CaMKII activity, especially in the nuclear region of hypertrophied Atg5−/− cardiomyocytes. These changes in Ca2+ cycling were recapitulated in hypertrophied human cardiomyocytes. Finally, ultrastructural analysis revealed accumulation of mitochondria with reduced volume and size distribution, meanwhile functional measurements showed impaired redox balance in Atg5−/− cardiomyocytes, implying energetic unsustainability due to overcompensation of single mitochondria, particularly under increased workload. Conclusion Loss of cardiac Atg5-dependent autophagy reduces mitochondrial abundance and causes subtle alterations in subcellular Ca2+ cycling upon increased workload in mice. Autophagy-related impairment of Ca2+ handling is progressively worsened by β-adrenergic signalling in ventricular cardiomyocytes, thereby leading to energetic exhaustion and compromised cardiac reserve

Low-density lipoprotein electronegativity and risk of death after acute coronary syndromes: A case-cohort analysis.

BACKGROUND AND AIMS Low-density lipoprotein (LDL)-cholesterol (LDL-C) promotes atherosclerotic cardiovascular disease (ASCVD), with changes in LDL electronegativity modulating its pro-atherogenic/pro-thrombotic effects. Whether such alterations associate with adverse outcomes in patients with acute coronary syndromes (ACS), a patient population at particularly high cardiovascular risk, remains unknown. METHODS This is a case-cohort study using data from a subset of 2619 ACS patients prospectively recruited at four university hospitals in Switzerland. Isolated LDL was chromatographically separated into LDL particles with increasing electronegativity (L1-L5), with the L1-L5 ratio serving as a proxy of overall LDL electronegativity. Untargeted lipidomics revealed lipid species enriched in L1 (least) vs. L5 (most electronegative subfraction). Patients were followed at 30 days and 1 year. The mortality endpoint was reviewed by an independent clinical endpoint adjudication committee. Multivariable-adjusted hazard ratios (aHR) were calculated using weighted Cox regression models. RESULTS Changes in LDL electronegativity were associated with all-cause mortality at 30 days (aHR, 2.13, 95% CI, 1.07-4.23 per 1 SD increment in L1/L5; p=.03) and 1 year (1.84, 1.03-3.29; p=.04), with a notable association with cardiovascular mortality (2.29; 1.21-4.35; p=.01; and 1.88; 1.08-3.28; p=.03). LDL electronegativity superseded several risk factors for the prediction of 1-year death, including LDL-C, and conferred improved discrimination when added to the updated GRACE score (area under the receiver operating characteristic curve 0.74 vs. 0.79, p=.03). Top 10 lipid species enriched in L1 vs. L5 were: cholesterol ester (CE) (18:2), CE (20:4), free fatty acid (FA) (20:4), phosphatidyl-choline (PC) (36:3), PC (34:2), PC (38:5), PC (36:4), PC (34:1), triacylglycerol (TG) (54:3), and PC (38:6) (all p < .001), with CE (18:2), CE (20:4), PC (36:3), PC (34:2), PC (38:5), PC (36:4), TG (54:3), and PC (38:6) independently associating with fatal events during 1-year of follow-up (all p < .05). CONCLUSIONS Reductions in LDL electronegativity are linked to alterations of the LDL lipidome, associate with all-cause and cardiovascular mortality beyond established risk factors, and represent a novel risk factor for adverse outcomes in patients with ACS. These associations warrant further validation in independent cohorts

Endothelial SIRT6 deficiency promotes arterial thrombosis in mice

OBJECTIVE Arterial thrombosis may be initiated by endothelial inflammation or denudation, activation of blood-borne elements or the coagulation system. Tissue factor (TF), a central trigger of the coagulation cascade, is regulated by the pro-inflammatory NF-κB-dependent pathways. Sirtuin 6 (SIRT6) is a nuclear member of the sirtuin family of NAD$^{+}$-dependent deacetylases and is known to inhibit NF-κB signaling. Its constitutive deletion in mice shows early lethality with hypoglycemia and accelerated aging. Of note, the role of SIRT6 in arterial thrombosis remains unknown. Thus, we hypothesized that endothelial SIRT6 protects from arterial thrombosis by modulating inhibition of NF-κB-associated pathways. APPROACH AND RESULTS Using a laser-induced carotid thrombosis model, in vivo arterial occlusion occurred 45% faster in 12-week-old male endothelial-specific Sirt6$^{-/-}$ mice as compared to Sirt6$^{fl/fl}$ controls (n ≥ 9 per group; p = 0.0012). Levels of procoagulant TF were increased in animals lacking endothelial SIRT6 as compared to control littermates. Similarly, in cultured human aortic endothelial cells, SIRT6 knockdown increased TF mRNA, protein and activity. Moreover, SIRT6 knockdown increased mRNA levels of NF-κB-associated genes tumor necrosis factor alpha (TNF-α), poly [ADP-ribose] polymerase 1 (PARP-1), vascular cell adhesion molecule 1 (VCAM-1), and cyclooxygenase-2 (COX-2); at the protein level, COX-2, VCAM-1, TNF-α, and cleaved PARP-1 remained increased after Sirt6 knockdown. CONCLUSIONS Endothelium-specific Sirt6 deletion promotes arterial thrombosis in mice. In cultured human aortic endothelial cells, SIRT6 silencing enhances TF expression and activates pro-inflammatory pathways including TNF-α, cleaved PARP-1, VCAM-1 and COX-2. Hence, endogenous endothelial SIRT6 exerts a protective role in experimental arterial thrombosis

Mentoring als Entwicklungsfeld (in) der Profession: Professionalisierung durch phasenübergreifende Zusammenarbeit über die Konzeptualisierung durch Entwicklungsaufgaben

Im vorliegenden Beitrag wird Mentoring in der Lehrer*innenbildung am Beispiel der Situation in Österreich als ein aktuell hoch relevantes und dynamisches Entwicklungsfeld in der und für die Profession verstanden. Im Setting des Mentorings, in dem Lehrkräfte in ihrer ersten beruflichen Phase begleitet werden, werden zentrale wissensbasiert-theoretische und handlungsorientiert-praktische Aspekte des Lehrer*innenberufs sichtbar und bearbeitbar. Mentoring hat eine Schnittstellen- und Übergangsfunktion im Professionskontinuum inne, wirkt personal (Mentor*innen, Mentees), inhaltlich (Mentoring-Curriculum) und auf Systemebene (professionsstabilisierend). Eine Möglichkeit der Konzeptualisierung bieten professionsspezifische Entwicklungsaufgaben (im Mentoring). Diese werden methodologisch rekonstruktiv modelliert. Damit eröffnet sich ein fruchtbares Potenzial für die Weiterentwicklung des Mentorings und die der Profession über das Mentoring im Gefolge der zweiten empirischen Wende

Rezeptedidaktik in der LehrerInnenbildung? Kritik und Würdigung einer pädagogischen (Un-)Praxis

Heinrich M. Rezeptedidaktik in der LehrerInnenbildung? Kritik und Würdigung einer pädagogischen (Un-)Praxis. In: Kraler C, Schratz M, eds. Ausbildungsqualität und Kompetenz im Lehrerberuf. Österreichische Beiträge zur Bildungsforschung. Vol 4. Wien: Lit-Verlag; 2007: 140-156