The paper will address the development of housing regimes in the new EU member states,introducing the analytical framework of a housing sector matrix to classifyforms of housing by tenure andintegration mechanism. Thus, ourhousing sector matrixcombines two common approaches: thestructure of housing provision (Ball and Harloe 1992) and the tenure-focused approach (Kemeny 1981, 1995). Starting from this rough typology of housing provisions, we also take further factors that have a major impact on the behaviour of stakeholders/actors into consideration, namely the legal/regulatory environment and the subsidy/tax system, to define the housing regimes. In its analysing of the development of the new member states the paperdifferentiates between global factors (economic development model, countries’ position in global economic structures, etc.) and local factors like the political/power structure, mainstream social ideology, the interplay betweendifferent stakeholders, etc. Institutional analyses (Bengtsson and Ruonavaara 2010) that take path-dependent factors into account are thus best able to address the process by which new housing regimes emerged in post-socialist countries and the degree to which we find convergence/divergence trends. The paper analyses three junctures in the development process after 1990: radical changes after the collapse of the old system; the development of the mortgage market and the regulation of the social sector at the turn of 2000; and reactions to the financial crisis of 2008. The paper concludes that the new member states are following the same trajectory despite their institutional differences.
Intraspecific variation in genome size makes it possible to study ongoing processes of genome size evolution. Although there are over 200 papers on intraspecific variation in genome size, there is still limited understanding of this phenomenon, especially as many of these papers are based on weak methodology and therefore report biased or false evidence of the extent of intraspecific variation. In this paper the recent progress in understanding the spatio-temporal dynamics of intraspecific variation in genome size caused by the gradual accumulation of mutations is reviewed. The results of the case studies on Microseris douglasii, Zea mays, Silene latifolia, Hordeum spontaneum and Lolium hybrids, and in particular that on Festuca pallens, are discussed. The variation in genome size that occurs within species is caused mainly by differences in the content of repetitive DNA, in particular it is a consequence of the dynamics of transposable elements. Variation may be induced and maintained polytopically.We assume that it is probably more frequent in groups of young radiating species. Even in the initial stages, the variation in genome size generated within a population seems to be restricted by selection, which is also important in stabilizing genome size within species. The long-term persistence of the variation within a population and its further accumulation may be enhanced by gametes with different genome sizes, produced by the segregation of unequally sized homeologous chromosomes. Over large geographical scales and across contrasting environmental gradients, the distribution of genome sizes within species may be influenced by the nucleotype effect, with smaller genomes being more successful at higher latitudes and altitudes and under stressful conditions. However, the small differences in genome size within species seem generally to be of minor importance relative to other components of plant fitness that may be selectively favourable under particular environmental or habitat conditions. The processes generating variation in genome size may be associated with phenotypic variation. While the shift in the genome size of a population through selection enables adaptive evolution of genome size in a newly arising species, the spatio-temporal variation in genome size within an ancestral species allows for a rapid multiple genome size divergence of related species through random drift in genome size (founder effect, bottleneck effect) during range fragmentation, hybridization and/or polyploidization.
In this article we show that significant differences between the foreign currency mortgage agreements in Hungary and Poland led to significant differences in monthly mortgage payments after the Global Financial Crisis (GFC) erupted. Hungarian banks were able to add a variable markup to the LIBOR3M that was connected to bank risk on top of the usual fixed markup. We compare the monthly mortgage payments and LTV levels of people who took out a CHF mortgage with those who obtained a local currency mortgage during the mortgage boom years of 2006–2008. We find that in the initial years of the mortgage CHF mortgages were cheaper than local currency mortgages, which allowed more people to buy housing. However, the GFC led to a deterioration of the exchange rate, and monthly payments and LTV levels (consequently?) increased. We analyse the mortgage costs and LTV levels of the 2006-2008 foreign currency (FX) mortgage vintages in Hungary and Poland between 2006 and 2020 and compare them to local currency mortgages. We also simulate the effects of changing housing prices and wages on mortgages in the cities of Budapest and Warsaw.
Traditionally, lecithinxholesterol acyltransferase (LCAT) role in the reverse cholesterol transport (RCT) has been considered "antiatherogenic" as the cholesterol esterification is the prerequisite for the formation of mature high density lipoprotein (HDL) particles and may create a gradient necessary for the flow of unesterified cholesterol (UC) from tissues to plasma. However, newer data suggest that a higher esterification rate is not necessarily protective. Here we review the available data on the role of LCAT in RCT and propose that the LCAT-mediated esterification of plasma cholesterol promotes RCT only in the presence of sufficient concentrations of HDL2 while this reaction may be atherogenic in the presence of high concentration of plasma low density lipoprotein (LDL) cholesteroL Thus, the "protective" or potentially "atherogenic" role of LCAT depends on the quality of HDL and concentration of LDL. This hypothesis is consistent with the known high predictive value of LDL/HDL cholesterol ratio.