Trends and inequality in the new active ageing and well-being index of the oldest old: a case study of Sweden

The policy discourse on active ageing and well-being at the European level tends to have a strong focus on the experiences of the ‘young old’. In this study the focus instead is on the oldest old (75 years and older). The theoretical framework is inspired by the Active Ageing Index and the Nordic welfare research tradition. Active ageing and well-being indicators and domains of high relevance for the oldest old are used and a new Active Ageing-Well Being Index (AA-WB Index) is developed. Our aim is to go beyond averages and analyse changes over time and inequality in the AA-WB Index. The prime data is derived from two waves, 2004 and 2014, of the Swedish Panel Study of Living Conditions of the Oldest Old (SWEOLD), a nationally representative sample of older people. The results show an overall improvement in most domains of the AA-WB index, especially in the indicator participation in cultural and leisure activities. The findings also show clear and consistent gender and educational inequalities. In addition, the different domains correlate, implying that inequality within a domain is aggravated by the inequality in another domain. The study highlights that measurements on active ageing and well-being should place a greater importance on the living conditions of the oldest old with a special focus on inequality

Bicycle Dynamics and Control

In this paper, the dynamics of bicycles is analyzed from the perspective of control. Models of different complexity are presented, starting with simple ones and ending with more realistic models generated from multibody software. Models that capture essential behavior such as self-stabilization as well as models that demonstrate difficulties with rear wheel steering are considered. Experiences using bicycles in control education along with suggestions for fun and thought-provoking experiments with proven student attraction are presented. Finally, bicycles and clinical programs designed for children with disabilities are described

К вопросу о формировании межкультурной коммуникативной компетенции обучаемых

Dagens redovisningsregler, som behandlar hur svenska bolag ska redovisa forskning och utveckling (FoU), inrymmer godtycklighet och förser företagsledningar med möjligheten att själva bedöma hur kostnadsposter ska redovisas. Detta öppnar för att företagsledare kan manipulera kostnaderna och vilseleda sina intressenter gällande företagets prestationer, vilket är ett utövande av Earnings Management (EM). I dagens konkurrensutsatta företagsklimat ställer investerare höga krav på att bolagen skall nå sina finansiella mål, vilket medför att företagsledningar kan använda EM som ett verktyg för att justera de finansiella rapporterna och undvika besvikna investerare. Utifrån ett investerarperspektiv och en kvantitativ metod undersöker denna studie om EM förekommer bland svenska noterade publika bolag genom omklassificering av rörelsekostnader till FoU-kostnader. Med utgångspunkt i teorier om EM och signalteorin baseras studien huvudsakligen på en metodologi tidigare initierad av Skaife et al. (2013b) på amerikanska företag. Modellerna framtagna av Skaife et al. (2013b) har inte prövats av andra forskare, varpå denna studies syfte är att göra en jämförbar studie med svenska företag som utgångspunkt. Då ett företags stigande FoU-kostnader inger förväntningar om framtida lönsamhet är även vår avsikt att undersöka om företag omklassificerar rörelsekostnader till FoU-kostnader när de inte når uppsatta resultatmål, med avsikten att kunna rättfärdiga svaga resultat. I våra statistiska hypotesprövningar och regressionsanalyser använder vi oss av paneldata från åren 2005-2013. Från den första hypotesprövningen kan det konstateras att svenska noterade publika bolag i hög grad omklassificerar rörelsekostnader till FoU-kostnader. Vi menar att en omklassificering av kostnader skett då den redovisade FoU-kostnaden inte överensstämmer med den prognostiserade (förväntade) FoU-kostnaden, framräknad genom modellen av Skaife et al. (2013b). Till följd av osignifikanta resultat i den andra hypotesprövningen kan vi inte uttala oss om i vilken utsträckning företag omklassificerar till FoU-kostnader när de missar uppsatta resultatmål. Däremot har vi signifikanta resultat som visar att de företag som omklassificerar rörelsekostnader till FoU-kostnader tenderar att ha en revisor från “Big Four”, tillhör någon av de 30 mest omsatta aktierna på Stockholmsbörsen (OMXS30) eller redovisar ett negativt resultat det aktuella året. Studiens resultat bidrar med praktisk kunskap till investerare samt till de som formger redovisningsreglerna, om hur företagsledare utnyttjar godtyckligheten i redovisningen av FoU. Beroende på i vilken utsträckning EM förekommer kan dess konsekvenser upplevas både positivt och negativt. Dock kvarstår det faktum att investerare utsätts för en ekonomisk risk när företagsledningen bryter mot gällande redovisningspraxis och redovisar vilseledande information, något som vi menar kan ses som ett oetiskt beteende från ett investerar- och samhällsperspektiv

Prolongation of working life and its effect on mortality and health in older adults : propensity score matching

Many countries are raising the age of pension eligibility because of increases in life expectancy. Given the social gradient in life expectancy and health, it is important to understand the potential late-life health effects of prolonging working life and whether any effects differ by socioeconomic position. We examined the effect of prolonging working life beyond age 65 on mortality and a series of indicators of late-life physical health (the ability to climb stairs without difficulty, self-rated health, ADL limitations, and musculoskeletal pain) in a representative sample of the Swedish population. In addition to average effects, we also examined heterogeneous effects, for instance by occupational social class. To do this, we use propensity score matching, a method suitable for addressing causality in observational data. The data came from two linked Swedish longitudinal surveys based on nationally representative samples with repeated follow-ups; The Swedish Level of Living Survey and the Swedish Panel Study of Living conditions of the Oldest Old, and from national income and mortality registries. The analytical sample for the mortality outcome included 1852 people, and for late-life physical health outcomes 1461 people. We found no significant average treatment effect on the treated (ATT) of working to age 66 or above on the outcomes, measured an average of 12 years after retirement: mortality (ATT -0.039), the ability to climb stairs (ATT -0.023), self-rated health (ATT -0.009), ADL limitations (ATT -0.023), or musculoskeletal pain (ATT -0.009) in late life. Analyses of whether the results varied by occupational social class or the propensity to prolong working life were inconclusive but suggest a positive effect of prolonging working life on health outcomes. Accordingly, more detailed knowledge about the precise mechanisms underlying these results are needed. In conclusion, working to age 66 or above did not have effect on mortality or late-life physical health

Att mäta korruption

I denna uppsats genomförs en statistisk analys där fyra socialpolitiska teoriers förklaringskraft vad gäller förekomsten av korruption testas. Det huvudsakliga materialet utgörs av data från Quality of Government, Transparency International samt teorier från vetenskapliga artiklar. Uppsatsen är begränsad till EU-27-länderna för vilka data har sammanställts och redovisats i grafer. Teorierna testas mot ett korruptionsindex (CPI) och därefter följer en analys av respektive teori. Uppsatsen påvisar att det finns starka samband mellan samtliga teorier och korruptionsindex. Avslutningsvis konstateras att inga nya empiriska slutsatser kan dras, men att de uppmärksammade teoriernas validitet har stärkts. En diskussion om metodologiska överväganden och tillägg inför vidare forskning förs i slutet av uppsatsen

Physical functioning as a predictor of retirement: Has its importance changed over a thirty-year period in Sweden?

Open access funding provided by Karolinska Institute. This work was supported by the Social Inequalities in Ageing (SIA) project, funded by NordForsk, [74637] and the Swedish Research Council for Health, Working Life and Welfare (FORTE) (2019-01100). The financial sponsors played no role in the design, execution, data analysis and interpretation, nor in the writing of the study.Peer reviewe

Enforcing the Federal Water Resource Servitude on Submerged and Riparian Lands

The epidermal growth factor receptor (EGFR) is frequently overexpressed in colorectal cancer and is therefore an attractive target for treatment. (ZEGFR:1907)2 is a newly developed dimeric affibody molecule with high affinity to the extracellular part of EGFR. In this study, we evaluated the cytotoxic effects of (ZEGFR:1907)2 in combination with external radiation and the possible inhibitory effects in the EGFR signalling pathways in the colon cancer cell lines HT-29 and HCT116. The effects were compared with an EGFR antibody (cetuximab) and the tyrosine kinase inhibitors (erlotinib and sunitinib). These cell lines are genotypically different with respect to e.g. KRAS and BRAF mutational status, recently shown to be of clinical significance for therapeutic effects. Both cell lines express approximately 100,000-150,000 EGFRs per cell but differ in the radiation response (HCT116, SF2=0.28 and HT-29, SF2=0.70). Exposure to (ZEGFR:1907)2 produced a small, but significant, reduction in survival in HCT116 but did not affect HT-29 cells. Similar results were obtained after exposure to EGF and the EGFR antibody cetuximab. The EGFR tyrosine kinase targeting inhibitor erlotinib and the multi-tyrosine kinase inhibitor sunitinib reduced survival in both cell lines. However, none of the drugs had any significant radiosensitizing effects in combination with radiation. Akt and Erk are central proteins in the EGFR downstream signalling and in the cellular response to ionizing radiation. The activation of Akt (Ser 473) and Erk (Thr202/Tyr204) by radiation was both dose- and time-dependent. However the activation of EGFR was not clearly affected by radiation. Neither (ZEGFR:1907)2 nor any of the other drugs were able to completely inactivate Akt or Erk. On the contrary, erlotinib stimulated Akt phosphorylation in both cell lines and in HCT116 cells Erk was activated. Overall the results illustrate the complexity in response to radiation and drugs in cells with differential phenotypic status.Online ISSN:1791-2423</p

Do cognitively stimulating activities affect the association between retirement timing and cognitive functioning in old age?

In response to the rising financial pressure on old-age pension systems in industrialised economies, many European countries plan to increase the eligibility age for retirement pensions. We used data from Sweden to examine whether (and if so, how) retirement after age 65 – the eligibility age for basic pension – compared to retiring earlier affects older adults’ (between ages 70 and 85) cognitive functioning. Using a propensity score matching (PSM) approach, we addressed the selection bias potentially introduced by non-random selection into either early or late retirement. We also examined average and heterogeneous treatment effects (HTEs). HTEs were evaluated for different levels of cognitive stimulation from occupational activities before retirement and from leisure activities after retirement. We drew from a rich longitudinal data-set linking two nationally representative Swedish surveys with a register data-set and found that, on average, individuals who retire after age 65 do not have a higher level of cognitive functioning than those who retire earlier. Similarly, we did not observe HTEs from occupational activities. With respect to leisure activities, we found no systematic effects on cognitive functioning among those working beyond age 65. We conclude that, in general, retirement age does not seem to affect cognitive functioning in old age. Yet, the rising retirement age may put substantial pressure on individuals who suffer from poor health at the end of their occupational career, potentially exacerbating social- and health-related inequalities among older people

Cover to Volume 3

The fibroblast mitogen platelet-derived growth factor -BB (PDGF-BB) induces a transient expression of the orphan nuclear receptor NR4A1 (also named Nur77, TR3 or NGFIB). The aim of the present study was to investigate the pathways through which NR4A1 is induced by PDGF-BB and its functional role. We demonstrate that in PDGF-BB stimulated NIH3T3 cells, the MEK1/2 inhibitor CI-1040 strongly represses NR4A1 expression, whereas Erk5 downregulation delays the expression, but does not block it. Moreover, we report that treatment with the NF-κB inhibitor BAY11-7082 suppresses NR4A1 mRNA and protein expression. The majority of NR4A1 in NIH3T3 was found to be localized in the cytoplasm and only a fraction was translocated to the nucleus after continued PDGF-BB treatment. Silencing NR4A1 slightly increased the proliferation rate of NIH3T3 cells; however, it did not affect the chemotactic or survival abilities conferred by PDGF-BB. Moreover, overexpression of NR4A1 promoted anchorage-independent growth of NIH3T3 cells and the glioblastoma cell lines U-105MG and U-251MG. Thus, whereas NR4A1, induced by PDGF-BB, suppresses cell growth on a solid surface, it increases anchorage-independent growth

Survival effect of PDGF-CC rescues neurons from apoptosis in both brain and retina by regulating GSK3β phosphorylation

Platelet-derived growth factor CC (PDGF-CC) is the third member of the PDGF family discovered after more than two decades of studies on the original members of the family, PDGF-AA and PDGF-BB. The biological function of PDGF-CC remains largely to be explored. We report a novel finding that PDGF-CC is a potent neuroprotective factor that acts by modulating glycogen synthase kinase 3β (GSK3β) activity. In several different animal models of neuronal injury, such as axotomy-induced neuronal death, neurotoxin-induced neuronal injury, 6-hydroxydopamine–induced Parkinson’s dopaminergic neuronal death, and ischemia-induced stroke, PDGF-CC protein or gene delivery protected different types of neurons from apoptosis in both the retina and brain. On the other hand, loss-of-function assays using PDGF-C null mice, neutralizing antibody, or short hairpin RNA showed that PDGF-CC deficiency/inhibition exacerbated neuronal death in different neuronal tissues in vivo. Mechanistically, we revealed that the neuroprotective effect of PDGF-CC was achieved by regulating GSK3β phosphorylation and expression. Our data demonstrate that PDGF-CC is critically required for neuronal survival and may potentially be used to treat neurodegenerative diseases. Inhibition of the PDGF-CC–PDGF receptor pathway for different clinical purposes should be conducted with caution to preserve normal neuronal functions