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The EU Statistics on Income and Living Conditions (EU-SILC) has provided annual estimates of the number of labour market indicators for EU countries since 2003, with an almost exclusive focus on national rates. However, it is impossible to obtain reliable direct estimates of labour market statistics at low levels based on the EU-SILC survey. In such cases, model-based small area estimation can be used. In this paper, the low work intensity indicator for the spatial domains in Poland between 2005-2012 was estimated. The Rao and You (1994), Fay and Diallo (2012), and Marhuenda, Molina and Morales (2013) models were applied. The bootstrap MSE for the discussed methods was proposed. The results indicate that these models provide more reliable estimates than direct estimation.

New data sources, namely big data and the Internet, have become an important issue in statistics and for official statistics in particular. However, before these sources can be used for statistics, it is necessary to conduct a thorough analysis of sources of nonrepresentativeness.In the article, we focus on detecting correlates of the selection mechanism that underlies Internet data sources for the secondary real estate market in Poland and results in representation errors (frame and selection errors). In order to identify characteristics of properties offered online we link data collected from the two largest advertisements services in Poland and the Register of Real Estate Prices and Values, which covers all transactions made in Poland. Quarterly data for 2016 were linked at a domain level defined by local administrative units (LAU1), the urban/rural distinction and usable floor area (UFA), categorized into four groups. To identify correlates of representation error we used a generalized additive mixed model based on almost 5,500 domains including quarters.Results indicate that properties not advertised online differ significantly from those shown in the Internet in terms of UFA and location. A non-linear relationship with the average price per m2can be observed, which diminishes after accounting for LAU1 units.

Heart failure (HF) causes a decline in the function of the pacemaker of the heart—the sinoatrial node (SAN). The aim of the study was to investigate HF-induced changes in the expression of the ion channels and related proteins underlying the pacemaker activity of the SAN.

Transient ischemia has been shown to impair endothelium-dependent, but not endothelium-independent, coronary vasodilation, indicating selective endothelial dysfunction. Here a hypothesis was tested that agonist mediated activation of protein kinase C (PKC) and the related overproduction of the oxidative species contribute to the mechanism of the endothelial dysfunction. Perfused guinea-pig hearts were subjected either to 30 min global ischemia/30 min reperfusion or to 30 min aerobic perfusion with a PKC activator, phorbol ester (1 n M, PMA). Coronary flow responses to a bolus of acetylcholine (ACh) and sodium nitroprusside (SNP) were used as measures of endothelium-dependent and endothelium-independent vascular function, respectively. Salicylate hydroxylation was used as the assay for the myocardial hydroxyl radical (·OH) formation. Both ischemia/reperfusion and PMA impaired the ACh response and augmented the myocardial ·OH production. The effect of ischemia/reperfusion on the ACh response: (i) was fully prevented by a PKC inhibitor, chelerythrine (2μM) and a mixed endothelin blocker, bosentan (20μM); (ii) was partially prevented by an endothelin converting-enzyme inhibitor, phosphoramidon (40μM), and superoxide dismutase (150–500 U/ml, SOD) and (iii) was affected neither by catalase (600 U/ml) nor by losartan (20μM) and captopril (250μM), nor by prazosin (10μM). SOD, but not bosentan, partially prevented the effect of PMA on the ACh response. None of the interventions studied affected the SNP response. The reperfusion-induced ·OH release was attenuated by chelerythrine and bosentan, was not affected by prazosin and was increased by SOD. These results implicate the following sequence of events in the mechanism of the post-ischemic endothelial dysfunction: ischemia/reperfusion, endothelin-induced PKC activation, increased production of superoxide and/or some of its toxic metabolite, damage to the endothelium and endothelial dysfunction. The results argue against the contribution of angiotensin II, adrenergicα1-receptors and kinins in the mechanism of the post-ischemic endothelial dysfunction in guinea-pig hearts.

The role of adenosine and ATP-sensitive potassium channels (KATP) in the mechanism of ischemic preconditioning (IPC)-induced protection against the post-ischemic endothelial dysfunction was studied. Langendorff-perfused guinea-pig hearts were subjected either to 40 min of global ischemia and 40 min reperfusion or were preconditioned prior to the ischemia/reperfusion with three cycles of either 5 min ischemia/5 min reperfusion (IPC) or 5 min infusion/5 min wash-out of adenosine, adenosine A1receptor agonist, N6-cyclohexyladenosine (CHA) or KATPopener, pinacidil. The magnitude of coronary flow reduction caused by NO-synthase inhibitor, Nω-nitro-l-arginine methyl ester (l-NAME), served as an index of a basal endothelium-dependent vasodilator tone. Coronary overflows produced by a bolus of acetylcholine (ACh) and sodium nitroprusside (SNP) were used as measures of agonist-induced endothelium-dependent and endothelium-independent vascular function, respectively. The coronary flow, LVDP, ACh response andl-NAME response were reduced by 8, 32, 41 and 54%, respectively, while SNP response was not changed in the hearts subjected to ischemia/reperfusion. ACh response was fully restored,l-NAME response was partially restored, and SNP response was not affected in the hearts subjected to IPC. The post-ischemic recoveries of coronary flow and LVDP were not improved by IPC. The protective effect of IPC on the ACh response was mimicked by adenosine, CHA, and pinacidil. The protective effect of IPC, CHA and pinacidil was abolished by KATPantagonist, glibenclamide. The IPC protection was affected neither by a non-specific adenosine antagonist, 8-p-sulfophenyltheophylline, nor by a specific adenosine A1receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). Our data indicate that: (1) IPC affords endothelial protection in the mechanism that involves activation of KATP, but not adenosine A1receptors; (2) exogenous adenosine and A1receptor agonist afford the protection, which might be of a potential clinical significance; (3) the endothelial dysfunction is not involved in the mechanism of myocardial stunning in guinea-pig hearts.

Objective: A proposal that injury in ischaemic/reperfused rat heart is critically dependent on the availability of free iron rather than on the efficiency of O₂ and H₂O₂ production was examined. Methods: Isolated working rat hearts from 152 male Wistar rats (200-250 g weight), subjected to 20-40 min of global ischaemia and reperfused for 30 min, were perfused with 10 µmol·litre–1 Fe [III] or Fe [11] and/or 0.6 mmol·litre–1 desferrioxamine, 10 mmol·litre–1 dimethylthiourea, and 1 mmol·litre–1 allopurinol. Curves relating the recoveries of haemodynamic functions and the reperfusion lactate dehydrogenase release to the duration of the preceding ischaemic period were constructed. Morphological examination was also performed. Results: In the untreated hearts, the duration of ischaemia resulting in 50% loss of cardiac output was 29 min. This time was decreased to 24 min and 20 min by Fe[III] and Fe[II], respectively, and was increased to 36 min and 37 min by desferrioxamine and dimethylthiourea, respectively. Desferrioxamine prevented the effect of Fe [III] but not that of Fe[II], whereas dimethylthiourea prevented the effect of Fe [II]. Neither the effect of Fe [III] nor that of Fe [II] was prevented by allopurinol which, however, proved to be beneficial in the untreated hearts. Conclusions: The beneficial effect of desferrioxamine and dimethylthiourea suggest that it is intensification of the Fenton reaction by iron which accounts for iron induced aggravation of the reperfusion injury. Thus we speculate that the availability of free iron, rather than O₂ and H₂O₂, is a limiting factor in the development of injury in an ishaemic/reperfused rat heart. What remains unclear is why allopurinol is unable to prevent iron induced changes.

Study objective — The aim was to evaluate the regulation of contractility by autonomic stimulation in the necrotic stage of cardiomyopathy in male Syrian hamsters. Design — The electrical and contractile activity of isolated intracellularly stimulated ventricular myocytes has been recorded and dose-response curves to [Ca2+]o, and to β adrenergic, α adrenergic, and muscarinic agonists and antagonists were examined. Experimental material — Ventricular cardiomyocytes were isolated by enzymatic dissociation of hearts from 90 to 120 day old cardiomyopathic hamsters CHF 147 and from age matched non-myopathic controls: CHF 148 or golden hamsters. Measurements and main results — The membrane potential was recorded by suction (patch) electrodes. The contractile activity was recorded by a video system as the shortenings of the myocytes. The contractile response (EC50) to β adrenergic stimulation (isoprenaline) showed a bimodal distribution: 60% of the myopathic myocytes responded like the controls, while in the remaining 40% the sensitivity was significantly decreased. The electrical activity and β adrenergic receptor density were not different from the controls. The α adrenergic stimulation (by phenylephrine) was enhanced, while response to the muscarinic agonist carbachol (in the presence of isoprenaline) was attenuated in the myopathic cells. Sensitivity to [Ca2+]o was unchanged. Conclusions — Profound changes occur in the contractile response of myocytes from cardiomyopathic hamster to stimulation by mediators of the autonomic nervous system, which at this necrotic stage are not related to any significant changes in basal contractile response to [Ca2+]o, to the electrical activity, or to the number of β adrenergic receptors.

Study objective – It has been proposed that oxygen free radicals trigger reperfusion arrhythmias. The mechanism of these arrhythmias is not clear. Thus, the effect of H2O2 on cellular action potentials was examined. Design – Trabecular muscles were superfused either with H2O2 alone or with H2O2 in combination with iron ions or an iron chelating agent or various scavengers of oxygen free radicals. The effect of reduction of the superfusate calcium from 1.8 to 0.2 mmol·litre−1 on H2O2 induced changes was also studied. Experimental material – Thin trabecular muscles isolated from the hearts of guinea pigs (200-300 g) of either sex were used. Measurements and main results – H2O2 (0.6 mmol·litre−1) caused a reproducible sequence of changes consisting of an initial increase in plateau height and in action potential duration, followed after 12-14 min by rapid action potential shortening accompanied by resting membrane depolarisation, reduction in action potential amplitude and dV/dtmax, and by occasional appearance of late afterdepolarisations, leading finally to loss of excitability. This sequence of changes was: (1) accelerated by higher concentrations of H2O2, FeCl3 (0.1 mmol·litre−1), and FeCl2 (0.1 mmol·litre−1); (2) prevented by dimethylthiourea (10 mmol·litre−1) and desferrioxamine (2 mmol·litre−1); (3) not influenced by superoxide dismutase (150 units·ml−1), mannitol (5-50 mmol·litre−1) or PBN (50 μmol·litre−1); and (4) not prevented by a reduction of the superfusate calcium. Conclusions – The electrophysiological alterations induced by H2O2 are caused by a hydroxyl radical formed intracellularly in the iron catalysed Fenton reaction.