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In this paper, we provide a macro-comparative assessment of welfare state convergence. Using the welfare state regime approach, the paper analyses the development of main welfare state indicators within in the enlarged European Union. In this study we capitalize on descriptive statistics and a single convergence analysis based on standard deviation in order to capture alterations in national welfare models of 26 European countries and among acknowledged welfare regimes. Our fundamental aim is to seize on long-term processes (convergence, divergence, or persistence), so we cover almost a two-decade period starting at 2000. Our results, in general, suggest that convergence among welfare states (different indicator of social spending) of European countries is particularly weak, however convergence inside welfare regimes is significantly stronger apart from the Anglo-Saxon group. The pre-crisis period was characterized by a stronger convergence among European countries as a consequence of economic prosperity and intense EU intervention. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S) and NO are important gasotransmitters, but how endogenous H2S affects the circulatory system has remained incompletely understood. Here, we show that CTH or CSE (cystathionine γ-lyase)-produced H2S scavenges vascular NO and controls its endogenous levels in peripheral arteries, which contribute to blood pressure regulation. Furthermore, eNOS (endothelial NO synthase) and phospho-eNOS protein levels were unaffected, but levels of nitroxyl were low in CTH-deficient arteries, demonstrating reduced direct chemical interaction between H2S and NO. Pretreatment of arterial rings from CTH-deficient mice with exogenous H2S donor rescued the endothelial vasorelaxant response and decreased tissue NO levels. Our discovery that CTH-produced H2S inhibits endogenous endothelial NO bioavailability and vascular tone is novel and fundamentally important for understanding how regulation of vascular tone is tailored for endogenous H2S to contribute to systemic blood pressure function. [ABSTRACT FROM AUTHOR]

The aim of our research project was to investigate the effect of different construction waste materials on the strength and durability of normal concrete. Construction waste materials were applied as supplementary material. 10% by mass (relative to the cement amount) of cellular concrete powder or powdered clay brick were used in the mixes, which were compared with a reference mix (without any supplementary material) and with a mix that contained air-entraining agent. The application of air-entraining agent in concrete is frequently recommended to increase the durability of concrete. Standard cubes with 100 mm of edge length were casted, and after 28 days a compressive strength test was done on three cubes from every mix. The durability of the concrete was investigated with two different methods. First the cubes were subjected to 0, 50, 100 and 150 cycles of freezing then the weight and strength loss of the samples were measured. Besides that, the freeze-thaw scaling resistance of the specimen was investigated by applying 7, 14, 21 up to 56 cycles of freeze-thaw scaling. All the applied methods were carried out in compliance with the recommendation of the CEN/TS 12390- 9:2007 standard. [ABSTRACT FROM AUTHOR]

Background Postconditioning may prove to be a suitable method to decrease ischemia-reperfusion injury of intestine after mesenteric arterial occlusion. Toll-like-receptor-4 is involved in the pathophysiology of organ damage after ischemia-reperfusion; therefore, the aim of our study was to investigate the effect of postconditioning on the mucosal expression of toll-like-receptor-4. Methods Male Wistar rats ( n = 10/group) underwent 60 minutes of superior mesenteric artery occlusion followed by 6 hours of reperfusion in 3 groups: sham-operated, ischemia-reperfusion, and a postconditioned group. Postconditioning was performed by 6 alternating cycles of 10 seconds of reperfusion/reocclusion. Blood and tissue samples were collected at the end of reperfusion. Intestinal histopathologic changes and immunohistochemical expression of mucosal caspase-3, antioxidant status, and protein levels of high-mobility group box-1 and toll-like-receptor-4 were assessed. Immunofluorescent labeling and confocal microscopic analysis of toll-like-receptor-4 were performed. Mucosal and serum levels of interleukin-6 and tumor necrosis factor-α protein were measured. Results Histologic alterations in the postconditioned group were associated with decreased caspase-3 positivity, less toll-like-receptor-4 mRNA, and less protein expression of high-mobility group box-1 and toll-like-receptor-4 in the intestinal villi compared with the ischemia-reperfusion group. Furthermore, a significantly improved antioxidant state of the intestinal mucosa and less mucosal and serum protein levels of interleukin-6 and tumor necrosis factor-α were detected in the postconditioned group. Conclusion Small intestinal ischemia-reperfusion injury in male Wistar rats caused by the occlusion of the superior mesenteric artery was ameliorated by the use of postconditioning, showing a more favorable inflammatory response, which may be attributed to the decreased mucosal expression of toll-like-receptor-4. [ABSTRACT FROM AUTHOR]

Klebsiella pneumoniae ST258 is a globally disseminated, extremely drug resistant, nosocomial clone with limited treatment options. We show that the vast majority of ST258 isolates express modified d -galactan-I lipopolysaccharide O-antigen, termed hereinafter as d -galactan-III. The genetic determinant required for galactan-III synthesis was identified as a distinct operon adjacent to the rfb ( wb ) locus encoding d -galactan-I synthesis. The three genes within the operon encode predicted glycosyltransferases. Testing an isogenic transformant pair revealed that expression of d -galactan-III, in comparison to d -galactan-I, conferred improved survival in the presence of human serum. Eighty-three percent of the more than 200 ST258 draft genome sequences currently available carries the corresponding operon and hence these isolates are predicted to express galactan-III antigens. A d -galactan-III specific monoclonal antibody (mAb) was shown to bind to extracted LPS from a panel of ST258 isolates. The same mAb confirmed accessibility of galactan-III in surface staining of ST258 irrespective of the distinct capsular antigens expressed by both clades described previously. Based on these data, the galactan-III antigen may represent an attractive target for active and passive immunization approaches against K. pneumoniae ST258. [ABSTRACT FROM AUTHOR]

Background Incretine hormone glucagon-like peptide-1 (GLP-1) causes dose-dependent relaxation of the thoracic aorta of rats and other arteries via nitric oxide (NO), cAMP and ATP-sensitive potassium channels, however, through a mechanism not thoroughly described. Hereby we aimed to determine the mediators involved in the vasoactive effect of liraglutide. Methods Isolated rat aortic rings and segments of the femoral artery were mounted in a wire myograph to study the vasoactive effect of liraglutide. Vessels were preincubated either with inhibitors of gasotransmitter-, prostaglandin- or reactive oxygen species-formation, or with inhibitors of protein kinases, potassium channels or the Na + /Ca 2+ -exchanger. Results According to our findings, liraglutide activates endothelial cells and vascular smooth muscle cells leading to the production of NO, carbon monoxide, hydrogen sulphide, superoxide anion, and hydrogen peroxide. Increased production of such relaxing factors promotes the activation of protein kinase– A and –G, resulting in the activation of potassium channels (ATP-sensitive-, voltage-gated-, large-conductance-calcium activated), which profoundly contributes to the activation of the Na + /Ca 2+ -exchanger, thereby leading to calcium efflux and smooth muscle relaxation and vasorelaxation. Conclusions We reveal the contribution of all gasotransmitters in the vasorelaxation induced by liraglutide. We provide ex vivo evidence that liraglutide is capable of causing vasodilatation in the central and peripherial vessels, thereby supporting the clinical observation that it lowers blood pressure. [ABSTRACT FROM AUTHOR]

Alzheimer disease features amyloid-β (Aβ) peptide deposition in brain and blood vessels and is associated with hypertension. Aβ peptide can cause vasoconstriction and endothelial dysfunction. We observed that Aβ peptides exert a chronotropic effect in neonatal cardiomyocytes, similar to α1-adrenergic receptor autoantibodies that we described earlier. Recently, it was shown that α1-adrenergic receptor could impair blood-brain flow. We hypothesized that Aβ peptides might elicit a signal transduction pathway in vascular cells, induced by α1-adrenergic receptor activation. Aβ (25-35) and Aβ (10-35) induced a positive chronotropic effect in the cardiac contraction assay (28.75±1.15 and 29.40±0.98 bpm), which was attenuated by α1-adrenergic receptor blockers (urapidil, 1.53±1.17 bpm; prazosin, 0.30±0.96 bpm). Both Aβ peptides induced an intracellular calcium release in vascular smooth muscle cells. Chronotropic activity and calcium response elicited by Aβ (25-35) were blocked with peptides corresponding to the first extracellular loop of the α1-adrenergic receptor. We observed an induction of extracellular-regulated kinase 1/2 phosphorylation by Aβ (25-35) in Chinese hamster ovary cells overexpressing α1-adrenergic receptor, vascular smooth muscle cells, and cardiomyocytes. We generated an activation-state-sensitive α1-adrenergic receptor antibody and visualized activation of the α1-adrenergic receptor by Aβ peptide. Aβ (25-35) induced vasoconstriction of mouse aortic rings and in coronary arteries in Langendorff-perfused rat hearts that resulted in decreased coronary flow. Both effects could be reversed by α1-adrenergic receptor blockade. Our data are relevant to the association between Alzheimer disease and hypertension. They may explain impairment of vascular responses by Aβ and could have therapeutic implications. [ABSTRACT FROM AUTHOR]

Alzheimer disease features amyloid-β (Aβ) peptide deposition in brain and blood vessels and is associated with hypertension. Aβ peptide can cause vasoconstriction and endothelial dysfunction. We observed that Aβ peptides exert a chronotropic effect in neonatal cardiomyocytes, similar to α1-adrenergic receptor autoantibodies that we described earlier. Recently, it was shown that α1-adrenergic receptor could impair blood-brain flow. We hypothesized that Aβ peptides might elicit a signal transduction pathway in vascular cells, induced by α1-adrenergic receptor activation. Aβ (25-35) and Aβ (10-35) induced a positive chronotropic effect in the cardiac contraction assay (28.75±1.15 and 29.40±0.98 bpm), which was attenuated by α1-adrenergic receptor blockers (urapidil, 1.53±1.17 bpm; prazosin, 0.30±0.96 bpm). Both Aβ peptides induced an intracellular calcium release in vascular smooth muscle cells. Chronotropic activity and calcium response elicited by Aβ (25-35) were blocked with peptides corresponding to the first extracellular loop of the α1-adrenergic receptor. We observed an induction of extracellular-regulated kinase 1/2 phosphorylation by Aβ (25-35) in Chinese hamster ovary cells overexpressing α1-adrenergic receptor, vascular smooth muscle cells, and cardiomyocytes. We generated an activation-state-sensitive α1-adrenergic receptor antibody and visualized activation of the α1-adrenergic receptor by Aβ peptide. Aβ (25-35) induced vasoconstriction of mouse aortic rings and in coronary arteries in Langendorff-perfused rat hearts that resulted in decreased coronary flow. Both effects could be reversed by α1-adrenergic receptor blockade. Our data are relevant to the association between Alzheimer disease and hypertension. They may explain impairment of vascular responses by Aβ and could have therapeutic implications. [ABSTRACT FROM AUTHOR]

Abstract: The immune response elicited by Shigella infections is dominated by serotype-specific antibodies recognizing the LPS O-antigens. Although a marked antibody response to invasion plasmid antigens (Ipa-s) shared by all virulent strains is also induced, the varying level of immunity elicited by natural infections is serotype-restricted. Previous vaccines have tried to mimic and achieve this serotype-specific, infection-induced immunity. As, however, the four Shigella species can express 50 different types of O-antigens, current approaches with the aim to induce a broad coverage use a mixture of the most common O-antigens combined in single vaccines. In the current study we present data on an alternative approach to generate immunity protective against multiple serotypes. Mutants lacking both major immune-determinant structures (i.e. the Ipa and O-antigens) were not only highly attenuated, but, unlike their avirulent counterparts still expressing these antigens, elicited a protective immune response to heterologous serotypes in a murine model. Evidence is provided that protection was mediated by the enhanced immunogenic potential of minor conserved antigens. Furthermore, the rough, non-invasive double mutants triggered an immune response different from that induced by the smooth, invasive strains regarding the isotype of antibodies generated. These non-invasive, rough mutants may represent promising candidates for further development into live vaccines for the prophylaxis of bacillary dysentery in areas with multiple endemic serotypes. [Copyright &y& Elsevier]

Summary: Background & aims: Ischemia–reperfusion (I–R) injury is responsible for the morbidity associated with liver surgery. Production of toxic free radicals influences the microcirculation. The aim of our study was to examine the effect of glutamine (Gln) supplementation—adminstered in alanyl-glutamine dipeptide form—on liver function, immuno/histopathology and the oxidative state of the liver after injury. Methods: Two-hundred and fifty grams male Wistar rats underwent normothermic, 60min, segmental liver ischemia followed by 6h of reperfusion. The animals (n=45) were divided into three groups: sham operated, I–R and parenteral Gln pretreatment. Hepatic microcirculation was monitored by laser Doppler flowmetry. At the 6h of reperfusion, histological alterations, TUNEL reaction, active caspase-3 reaction, serum and liver tissue antioxidant levels, serum ALAT, ASAT and TNF-α levels were measured. Results: Upon reperfusion, the Gln group had significantly (p<0.05) higher flow rates than the I–R group and, at the end of the 6h of reperfusion, significantly (p<0.05) lower serum ALAT and ASAT levels. The liver chemiluminescent intensity was lower, free SH-groups were elevated, while the reducing power was decreased in the Gln-pretreated group. Positive staining for caspase-3 after Gln pretreatment was significantly increased in contrast to the control tissues. Conclusion: Glutamine pretreatment is beneficial in supporting hepatic microcirculation and can prevent hepatocellular necrosis in liver reperfusion injury. [Copyright &y& Elsevier]

Introduction: Vitamin D may ameliorate hypertension and kidney disease through genomic and extra-genomic pathways. Several studies have shown that vitamin D levels can affect levels of circulating FoxP3-positive regulatory T-lymphocytes. Previously, our group has demonstrated that adoptive transfer of FoxP3-positive T-lymphocytes ameliorated the phenotype in a mouse model of angiotensin-II induced cardiac damage.Objective: To investigate the impact of vitamin D depletion in a transgenic rat model of angiotensin II-mediated hypertensive organ failure, and to investigate the possible association with levels of FoxP3 regulatory T-lymphocytes.Methods: In 4-week old age-matched rats overexpressing the human renin and angiotensinogen genes, group 1 (n=18) received vitamin D depleted chow, and group 2, (n=15) received chow with standard contents of vitamin D. Blood pressure (tail cuff) and 24-hour albuminuria were determined once weekly. After three weeks, animals were sacrificed. Heart tissue was examined for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) by RT-PCR. Lymphocytes from spleens were isolated, and the percentage of CD4+ cells, which were CD4+CD25+FoxP3-positive, was measured by flow cytometry. Mesenteric arteries were removed and stimulated with nitroprusside and acetylcholine to investigate the relaxation potential of the epithelium.Results: The vitamin D depleted group had higher blood pressure at all times (mean differences were 23.40 mmHg, 14.31 mmHg and 15.71 mmHg respectively, p<0.05), higher heart-to-body weight ratio, and higher ANP and BNP levels. No differences were found between groups in mortality or proteinuria. Neither the levels of CD4+CD25+FoxP3-positive cells in spleen, nor the relaxation potential measured in mesenteric arteries differed between groups.Conclusion: Short-term vitamin D depletion aggravated hypertension and end-organ damage in a rat model of angiotensin II-induced hypertension. However, the aggravated phenotype was not due to different levels of splenic FoxP3-positive activated T-lymphocytes or to higher endothelial resistance in arteries. [ABSTRACT FROM AUTHOR]

Alzheimer disease (AD) features β-amyloid peptide (Aβ) deposition in brain and blood vessels and is associated with hypertension. Aβ can cause vasoconstriction and endothelial dysfunction. Recently, we could show that Aβ peptides elicit a signal transduction pathway in vascular smooth muscle cells and cardiomyocytes, induced by α1-adrenergic receptor activation. We hypothesized that the Aβ vasoactivity is also induced by activation of the α1-adrenoreceptor. Mouse aortic Rings were incubated for 24 h with 1 μmol/l Aβ (25-35). The influence of Aβ (25-35) on vasoconstriction of mouse aortic rings was studied in the additional presence and absence of α1-adrenergic receptor blocker prazosin. Vasoactivity in isolated aortic rings was measured using an isometric myograph. Vasoconstriction to 5-hydroxytryptamine was significantly increased (P0.001) in aortic rings by Aβ (25-35) pretreatment. This vasoactive effect was improved by the presence of α1-adrenergic receptor blocker during the Aβ (25-35) pretreatment. Rat middle cerebral artery (MCA) segments were treated with either 0.1μmol/L Aβ (25-35) or 0.1μmol/L of a negative control peptide with a reverse amino acid sequence (Aβ rev.) of Aβ (25-35) for 4h. Constriction of the middle cerebral artery was measured in dual vessel chamber. Incubation with Aβ (25-35) significantly enhanced (P0.0005) response of middle cerebral artery segments to the α1-agonist phenylephrine induced contractions. In a further ex vivo model of Langendorff-perfused rat hearts Aβ (25-35) also induced vasoconstriction of coronary arteries that resulted in decreased coronary flow. These effects could also be reversed by α1-adrenergic receptor blockade. Furthermore we analyzed the brain of hypertensive dTGR animals and in human arteriosclerotic plaques for the presence of Aβ amyloid. Amyloid deposits are present in cerebral cortex of hypertensive dTGR animals with damaged blood-brain barrier and in human arteriosclerotic plaques. Our data are relevant to the association between AD and hypertension. They may serve to explain impaired of vascular responses by Aβ and could have therapeutic implications. [ABSTRACT FROM AUTHOR]

Introduction: An excessive maternal systemic inflammatory response to pregnancy, as well as an imbalance between circulating angiogenic factors and their antagonists plays a central role in the pathogenesis of preeclampsia. The complement system, as part of innate immunity, is fundamental to the host’s immune defense against microbial pathogens, apoptotic and necrotic cells. Both of its excessive activation and deficiencies can lead to various disorders. Objectives: The aim of this study was to determine circulating levels of components of the complement system and their relationship to those of angiogenic factors in normal pregnancy and preeclampsia. Methods: Sixty preeclamptic patients, 60 healthy pregnant women and 59 healthy non-pregnant women were involved in this case–control study. Circulating levels of C1rC1sC1-inh, C3bBbP, C4d, C3a, SC5b9, ficolin-2, ficolin-3, soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF), as well as activity of the complex of mannose-binding lectin and mannose-binding lectin-associated serine protease 2 (MBL–MASP2 complex) were measured. For statistical analyses, non-parametric methods were applied. Results: Circulating levels of C3bBbP, C4d, C3a, SC5b9, sFlt-1, PlGF, as well as MBL–MASP2 activity were significantly higher, while ficolin-2 concentrations were significantly lower in healthy pregnant than in healthy non-pregnant women. Furthermore, preeclamptic patients had significantly higher C1rC1sC1-inh, C3bBbP, C4d, C3a, SC5b9 and sFlt-1 levels and significantly lower ficolin-2, ficolin-3 and PlGF concentrations than healthy pregnant women. In the groups of healthy pregnant women and preeclamptic patients, plasma ficolin-2 levels showed a significant positive correlation with serum PlGF concentrations and a significant inverse correlation with serum levels of sFlt-1. There was no other relationship between complement components and angiogenic factors in either study group. Conclusion: Elevated levels of activation products in the systemic circulation indicate complement activation with increased terminal complex formation in preeclampsia, which seems to be independent from alterations in circulating angiogenic factors. Nevertheless, low ficolin-2 concentrations might contribute to the angiogenic imbalance in preeclampsia by impaired removal of the sFlt-1-containing trophoblast-derived material released into the maternal circulation by the hypoxic and oxidatively stressed preeclamptic placenta. [Copyright &y& Elsevier]