Klassiõpetajate õpetamistegevused mõistete kujundamisel põhikooli II kooliastme emakeeletundides

http://www.ester.ee/record=b4602359*es

Liberaalse rahvusluse õigustused immigratsiooni piiramisele: David Milleri "Strangers in our midst" (2016) näitel

2015. aasta põgenikekriisi kaudu taas avalikku arutellu jõudnud immigratsioon on tundlik teema, mis mõjutab inimelusid, ühiskonna toimimise alusväärtuseid ning paneb riike proovile immigratsioonipoliitikates kokkulepete jõudmisel. Seetõttu on põhjust uurida, millised on erinevate rahvusluse vormide suhtumine immigrantide vastuvõtmisele. Poliitikateooria valdkonda kuuluvas bakalaureusetöös keskendutakse liberaalsele rahvuslusele. Uuritakse, millised on liberaalse rahvusluse teooria hoiakud immigratsiooni suhtes ning kuidas õigustab teooria, mis rõhutab rahvuslike väärtuste vastavust liberaalsete alusväärtustega, immigratsiooni piiramist. Töös uuritakse esmalt liberaalse rahvusluse teooriat ning selle peamisi alaliike, mida esindavad on David Miller (autor, kellele valdavalt töös keskendutakse) ning Yael Tamir. Uuritakse, milliseid eesmärke täidab liberaalne rahvuslus ning millised on selle kesksed väärtused. Seejärel antakse ülevaade erinevatest käsitlustest immigratsioonist, nii rahvusvaheliste organisatsioonide kui David Milleri käsitluses. Immigratsiooni piiramise uurimisel tuginetakse David Milleri peamiselt teosele „Strangers in Our Midst“ (2016). Uuritakse, millised on Milleri peamised argumendid immigratsiooni piiramise kasuks ning seostatakse need Milleri varasema käsitlusega liberaalsest rahvuslusest, uurides Milleri erinevate käsitluse vahelist vastavust ja järjepidevust. Viimaks antakse Milleri käsitlusele kriitiline hinnang, tuginedes Chandran Kukathase ja töö autori kriitikale. Peamiste järeldustena selgub Milleri kogukondlikku heaolu säilitamist väärtustav positsioon, mille kaudu käsitluses immigratsiooni piiramist õigustatakse. Lisaks näib argumente immigratsiooni piiramisest liberaalse rahvusluse teooriaga seostades, et Milleri käsitlus on aja jooksul muutunud ning ettevaatlikuma hoiakuga. See aga ei anna põhjust arvata, et Milleri käsitlus immigratsioonist on vastuolus liberaalsete väärtustega: kõrvutades Milleri käsitlust Tamiriga ning Kukathase kriitikaga selgub, et Milleri käsitlus on poliitilisem ning ühiskondlikule toimimisele suunatud, mitte niivõrd indiviidi perspektiivist kirjeldatud teooria, mis võtaks arvesse immigratsiooni piiramise tagajärgi üksikisikutele.https://www.ester.ee/record=b5240830*es

Predicting global invasion risks: a management tool to prevent future introductions

Predicting regions at risk from introductions of non-native species and the subsequent invasions is a fundamental aspect of horizon scanning activities that enable the development of more effective preventative actions and planning of management measures. The Asian cyprinid fish topmouth gudgeon Pseudorasbora parva has proved highly invasive across Europe since its introduction in the 1960s. In addition to direct negative impacts on native fish populations, P. parva has potential for further damage through transmission of an emergent infectious disease, known to cause mortality in other species. To quantify its invasion risk, in regions where it has yet to be introduced, we trained 900 ecological niche models and constructed an Ensemble Model predicting suitability, then integrated a proxy for introduction likelihood. This revealed high potential for P. parva to invade regions well beyond its current invasive range. These included areas in all modelled continents, with several hotspots of climatic suitability and risk of introduction. We believe that these methods are easily adapted for a variety of other invasive species and that such risk maps could be used by policy-makers and managers in hotspots to formulate increased surveillance and early-warning systems that aim to prevent introductions and subsequent invasions

Plakophilin-2 truncating variants impair cardiac contractility by disrupting sarcomere stability and organization

Progressive loss of cardiac systolic function in arrhythmogenic cardiomyopathy (ACM) has recently gained attention as an important clinical consideration in managing the disease. However, the mechanisms leading to reduction in cardiac contractility are poorly defined. Here, we use CRISPR gene editing to generate human induced pluripotent stem cells (iPSCs) that harbor plakophilin-2 truncating variants (PKP2tv), the most prevalent ACM-linked mutations. The PKP2tv iPSC–derived cardiomyocytes are shown to have aberrant action potentials and reduced systolic function in cardiac microtissues, recapitulating both the electrical and mechanical pathologies reported in ACM. By combining cell micropatterning with traction force microscopy and live imaging, we found that PKP2tvs impair cardiac tissue contractility by destabilizing cell-cell junctions and in turn disrupting sarcomere stability and organization. These findings highlight the interplay between cell-cell adhesions and sarcomeres required for stabilizing cardiomyocyte structure and function and suggest fundamental pathogenic mechanisms that may be shared among different types of cardiomyopathies

Plakophilin-2 truncating variants impair cardiac contractility by disrupting sarcomere stability and organization

Progressive loss of cardiac systolic function in arrhythmogenic cardiomyopathy (ACM) has recently gained attention as an important clinical consideration in managing the disease. However, the mechanisms leading to reduction in cardiac contractility are poorly defined. Here, we use CRISPR gene editing to generate human induced pluripotent stem cells (iPSCs) that harbor plakophilin-2 truncating variants (PKP2tv), the most prevalent ACM-linked mutations. The PKP2tv iPSC-derived cardiomyocytes are shown to have aberrant action potentials and reduced systolic function in cardiac microtissues, recapitulating both the electrical and mechanical pathologies reported in ACM. By combining cell micropatterning with traction force microscopy and live imaging, we found that PKP2tvs impair cardiac tissue contractility by destabilizing cell-cell junctions and in turn disrupting sarcomere stability and organization. These findings highlight the interplay between cell-cell adhesions and sarcomeres required for stabilizing cardiomyocyte structure and function and suggest fundamental pathogenic mechanisms that may be shared among different types of cardiomyopathies

Hospitalization for acute heart failure during non-working hours impacts on long-term mortality: the REPORT-HF registry

Aims Hospital admission during nighttime and off hours may affect the outcome of patients with various cardiovascular conditions due to suboptimal resources and personnel availability, but data for acute heart failure remain controversial. Therefore, we studied outcomes of acute heart failure patients according to their time of admission from the global International Registry to assess medical practice with lOngitudinal obseRvation for Treatment of Heart Failure.Methods and results Overall, 18 553 acute heart failure patients were divided according to time of admission into morning (7:00-14:59), evening (15:00-22:59), and night (23:00-06:59) shift groups. Patients were also dichotomized to admission during working hours (9:00-16:59 during standard working days) and non-working hours (any other time). Clinical characteristics, treatments, and outcomes were compared across groups. The hospital length of stay was longer for morning (odds ratio: 1.08; 95% confidence interval: 1.06-1.10, P &amp;lt; 0.001) and evening shift (odds ratio: 1.10; 95% confidence interval: 1.07-1.12, P &amp;lt; 0.001) as compared with night shift. The length of stay was also longer for working vs. non-working hours (odds ratio: 1.03; 95% confidence interval: 1.02-1.05, P &amp;lt; 0.001). There were no significant differences in in-hospital mortality among the groups. Admission during working hours, compared with non-working hours, was associated with significantly lower mortality at 1 year (hazard ratio: 0.88; 95% confidence interval: 0.80-0.96, P = 0.003).Conclusions Acute heart failure patients admitted during the night shift and non-working hours had shorter length of stay but similar in-hospital mortality. However, patients admitted during non-working hours were at a higher risk for 1 year mortality. These findings may have implications for the health policies and heart failure trials.Funding Agencies|Novartis</p

Hospitalization for acute heart failure during non‐working hours impacts on long‐term mortality: the REPORT‐HF registry

Abstract Aims Hospital admission during nighttime and off hours may affect the outcome of patients with various cardiovascular conditions due to suboptimal resources and personnel availability, but data for acute heart failure remain controversial. Therefore, we studied outcomes of acute heart failure patients according to their time of admission from the global International Registry to assess medical practice with lOngitudinal obseRvation for Treatment of Heart Failure. Methods and results Overall, 18 553 acute heart failure patients were divided according to time of admission into ‘morning’ (7:00–14:59), ‘evening’ (15:00–22:59), and ‘night’ (23:00–06:59) shift groups. Patients were also dichotomized to admission during ‘working hours’ (9:00–16:59 during standard working days) and ‘non‐working hours’ (any other time). Clinical characteristics, treatments, and outcomes were compared across groups. The hospital length of stay was longer for morning (odds ratio: 1.08; 95% confidence interval: 1.06–1.10, P < 0.001) and evening shift (odds ratio: 1.10; 95% confidence interval: 1.07–1.12, P < 0.001) as compared with night shift. The length of stay was also longer for working vs. non‐working hours (odds ratio: 1.03; 95% confidence interval: 1.02–1.05, P < 0.001). There were no significant differences in in‐hospital mortality among the groups. Admission during working hours, compared with non‐working hours, was associated with significantly lower mortality at 1 year (hazard ratio: 0.88; 95% confidence interval: 0.80–0.96, P = 0.003). Conclusions Acute heart failure patients admitted during the night shift and non‐working hours had shorter length of stay but similar in‐hospital mortality. However, patients admitted during non‐working hours were at a higher risk for 1 year mortality. These findings may have implications for the health policies and heart failure trials

Plakophilin-2 truncating variants impair cardiac contractility by disrupting sarcomere stability and organization

Progressive loss of cardiac systolic function in arrhythmogenic cardiomyopathy (ACM) has recently gained attention as an important clinical consideration in managing the disease. However, the mechanisms leading to reduction in cardiac contractility are poorly defined. Here, we use CRISPR gene editing to generate human induced pluripotent stem cells (iPSCs) that harbor plakophilin-2 truncating variants (PKP2tv), the most prevalent ACM-linked mutations. The PKP2tv iPSC-derived cardiomyocytes are shown to have aberrant action potentials and reduced systolic function in cardiac microtissues, recapitulating both the electrical and mechanical pathologies reported in ACM. By combining cell micropatterning with traction force microscopy and live imaging, we found that PKP2tvs impair cardiac tissue contractility by destabilizing cell-cell junctions and in turn disrupting sarcomere stability and organization. These findings highlight the interplay between cell-cell adhesions and sarcomeres required for stabilizing cardiomyocyte structure and function and suggest fundamental pathogenic mechanisms that may be shared among different types of cardiomyopathies