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Almost eight million Ukrainians have fled their country to escape the Russian full-scale invasion. To provide empirical evidence on how beneficiaries of temporary protection who reside in the immediate proximity of Ukraine differ from those who went further and reside in Western European countries, two large-scale rapid-response surveys were conducted in Kraków, Poland, and Vienna, Austria, in spring 2022. Data include information on socio-demographic characteristics, human capital, and return intentions of 472 and 1,094 adult Ukrainian refugees in Poland and Austria, respectively. Contributing to the growing empirical evidence on consistent assortative patterns in refugee inflows into Europe, our findings show that regularities in patterns of self-selection also occur in forced migration contexts where legal routes to safety apply. According to the analysed convenience sample, a tentative conclusion is that the further Ukrainian refugees moved to the West, the more self-selected they tend to be in the key dimensions of formal educational attainment, previous employment, language skills, and urbanity. Results indicate that willingness to stay in Kraków is significantly lower than willingness to remain in Vienna. This suggests that public financial support and living conditions, rather than diaspora networks, are decisive factors in shaping the decision to stay, move to another location or return to Ukraine. The aim to start a new life elsewhere may drive the motivation to choose a more distant destination instead of a neighboring country that allows to return rather quickly. Host countries should be aware of these specific characteristics of their refugee populations and adapt their integration policies accordingly.

Aim: Slc26a9 is a member of the Slc26 multifunctional anion transporter family. Polymorphisms in Slc26a9 are associated with an increased incidence of meconium ileus and diabetes in cystic fibrosis patients. We investigated the expression of Slc26a9 in the murine pancreatic ducts, islets and parenchyma, and elucidated its role in pancreatic ductal electrolyte and fluid secretion and endocrine function. Methods: Pancreatic Slc26a9 and CFTR mRNA expression, fluid and bicarbonate secretion were assessed in slc26a9−/− mice and their age- and sex-matched wild-type (wt) littermates. Glucose and insulin tolerance tests were performed. Results: Compared with stomach, the mRNA expression of Slc26a9 was low in pancreatic parenchyma, 20-fold higher in microdissected pancreatic ducts than parenchyma, and very low in islets. CFTR mRNA was ~10 fold higher than Slc26a9 mRNA expression in each pancreatic cell type. Significantly reduced pancreatic fluid secretory rates and impaired glucose tolerance were observed in female slc26a9−/− mice, whereas alterations in male mice did not reach statistical significance. No significant difference was observed in peripheral insulin resistance in slc26a9−/− compared to sex- and aged-matched wt controls. In contrast, isolated slc26a9−/− islets in short term culture displayed no difference in insulin content, but a significantly reduced glucose-stimulated insulin secretion compared to age- and sex-matched wt islets, suggesting that the impaired glucose tolerance in the absence of Slc26a9 expression these is a pancreatic defect. Conclusions: Deletion of Slc26a9 is associated with a reduction in pancreatic fluid secretion and impaired glucose tolerance in female mice. The results underline the importance of Slc26a9 in pancreatic physiology.

Building upon results of prior focus group research, the present study employs online surveys about possible future developments of the vulnerability of families with children in Europe. In addition, respondents assessed the relevance of societal factors influencing future family well-being and the effectiveness of ten selected policy measures in preventing the intergenerational transfer of vulnerability. One survey was directed at scientists and practitioners who are family experts (N=175). Another survey aimed at exploring the thoughts of parents themselves (N=1,343). Results show that experts are rather pessimistic and even expect vulnerability to increase in the future. In their opinion, the most relevant forces driving future vulnerability seem to be economic development—manifesting itself in unemployment and earnings inequality—and family policy. As for policy measures, childcare availability, early childhood education, assistance for children with special needs and raising awareness of employers for work–family reconciliation were ranked highly for mitigating the reproduction of vulnerability. While parents largely share the opinions of experts with regard to forces relevant for future family well-being, they evaluate some of the policy measures differently: the main disparities concern the assessment of support for stay-at-home mothers and the weight given to education for children after school and during holidays.

Background/Aims: Trafficking, brush border membrane (BBM) retention, and signal-specific regulation of the Na+/H+ exchanger NHE3 is regulated by the Na+/H+ Exchanger Regulatory Factor (NHERF) family of PDZ-adaptor proteins, which enable the formation of multiprotein complexes. It is unclear, however, what determines signal specificity of these NHERFs. Thus, we studied the association of NHE3, NHERF1 (EBP50), NHERF2 (E3KARP), and NHERF3 (PDZK1) with lipid rafts in murine small intestinal BBM. Methods: Detergent resistant membranes ('lipid rafts') were isolated by floatation of Triton X-incubated small intestinal BBM from a variety of knockout mouse strains in an Optiprep step gradient. Acid-activated NHE3 activity was measured fluorometrically in BCECF-loaded microdissected villi, or by assessment of CO2/HCO3 - mediated increase in fluid absorption in perfused jejunal loops of anethetized mice. Results: NHE3 was found to partially associate with lipid rafts in the native BBM, and NHE3 raft association had an impact on NHE3 transport activity and regulation in vivo. NHERF1, 2 and 3 were differentially distributed to rafts and non-rafts, with NHERF2 being most raft-associated and NHERF3 entirely non-raft associated. NHERF2 expression enhanced the localization of NHE3 to membrane rafts. The use of acid sphingomyelinase-deficient mice, which have altered membrane lipid as well as lipid raft composition, allowed us to test the validity of the lipid raft concept in vivo. Conclusions: The differential association of the NHERFs with the raft-associated and the non-raft fraction of NHE3 in the brush border membrane is one component of the differential and signal-specific NHE3 regulation by the different NHERFs.

We investigated the role of the Na+/H+ exchanger regulatory factor 1 (NHERF1) on intestinal salt and water absorption, brush border membrane (BBM) morphology, and on the NHE3 mRNA expression, protein abundance, and transport activity in the murine intestine. NHERF1-deficient mice displayed reduced jejunal fluid absorption in vivo, as well as an attenuated in vitro Na+ absorption in isolated jejunal and colonic, but not of ileal, mucosa. However, cAMP-mediated inhibition of both parameters remained intact. Acid-activated NHE3 transport rate was reduced in surface colonocytes, while its inhibition by cAMP and cGMP was normal. Immunodetection of NHE3 revealed normal NHE3 localization in the BBM of NHERF1 null mice, but NHE3 abundance, as measured by Western blot, was significantly reduced in isolated BBM from the small and large intestines. Furthermore, the microvilli in the proximal colon, but not in the small intestine, were significantly shorter in NHERF1 null mice. Additional knockout of PDZK1 (NHERF3), another member of the NHERF family of adaptor proteins, which binds to both NHE3 and NHERF1, further reduced basal NHE3 activity and caused complete loss of cAMP-mediated NHE3 inhibition. An activator of the exchange protein activated by cAMP (EPAC) had no effect on jejunal fluid absorption in vivo, but slightly inhibited NHE3 activity in surface colonocytes in vitro. In conclusion, NHERF1 has segment-specific effects on intestinal salt absorption, NHE3 transport rates, and NHE3 membrane abundance without affecting mRNA levels. However, unlike PDZK1, NHERF1 is not required for NHE3 regulation by cyclic nucleotides.

Background and aims: We investigated the role of the recently discovered, villous-expressed anion exchanger Slc26a6 (PAT1) and the predominantly crypt-expressed cystic fibrosis transmembrane regulator (CFTR) in basal and acid-stimulated murine duodenal HCO3− secretion in vivo, and the influence of blood HCO3− concentration on both. Methods: The proximal duodenum of anaesthetized mice was perfused in situ, and HCO3− secretion was determined by back-titration. Duodenal mucosal permeability was assessed by determining 51Cr-EDTA leakage from blood to lumen. Results: Compared with wild type (WT) littermates basal duodenal HCO3− secretory rates were slightly reduced in Slc26-deficient mice at low (∼21 mm), and markedly reduced at high blood HCO3− concentration (∼29 mm). In contrast, basal HCO3− secretion was markedly reduced in CFTR-deficient mice compared with WT littermates both at high and low blood HCO3− concentration. A short-term application of luminal acid increased duodenal HCO3− secretory rate in Slc26a6-deficient and WT mice to the same degree, but had no stimulatory effect in the absence of CFTR. Luminal acidification to pH 2.5 did not alter duodenal permeability. Conclusions: The involvement of Slc26a6 in basal HCO3− secretion in murine duodenum in vivo is critically dependent on the systemic acid/base status, and this transporter is not involved in acid-stimulated HCO3− secretion. The presence of CFTR is essential for basal and acid-induced HCO3− secretion irrespective of acid/base status. This suggests a coupled action of Slc26a6 with CFTR for murine basal duodenal HCO3− secretion, but not acid-stimulated secretion, in vivo.