Evaluering av assistansebestemmelsen i valgloven

Denne rapporten evaluerer praktiseringen av assistansebestemmelsen i valgloven, etter lovendringen i 2021. Hovedtemaer er valgmedarbeidernes og velgernes kjennskap til og erfaringer med assistansebestemmelsen. Datamaterialet består av en spørreundersøkelse til valgansvarlige for lokalvalget 2023 og kvalitative intervjuer med valgmedarbeidere og velgere, samt kommunale råd og nasjonale organisasjoner som representerer ulike grupper med nedsatt funksjonsevne. Intervjuene våre tyder på at lovendringen ennå ikke er godt kjent blant velgere med behov for assistanse. Hovedinntrykket er at assistansebestemmelsen er godt kjent i kommunene, men våre funn viser at det fremdeles er tilfeller hvor regelendringen ikke er kjent og praktiseres rett. Det er fortsatt behov for å informere velgere og valgmedarbeiderne om retten til selvvalgt hjelper.Evaluering av assistansebestemmelsen i valglovenpublishedVersio

Eldre ledere : ressurser og karrierealternativer : en utredning skrevet for K-bank

Alle ledere stilles overfor en rekke karrieremessige utfordringer. For eldre ledere vil omstillinger og økt konkurranse stille krav til kompetanse og lederstil som mange kan finne vanskelig å imøtekomme. Omstruktureringer kan føre til at en del stillinger blir overflødige, og at motivasjonen til å endre og utvikle seg for å møte nye krav svekkes mot slutten av den yrkesaktive karrieren. Det kan derfor være ønskelig både fra bedriftens og lederens side å reorientere karrieren. Denne rapporten gir en oppsummering av forskning og praktiske erfaringer som finnes om eldre lederes karriereløp. Det finnes lite forskning som relaterer seg til eldre ledere spesielt, men en kan slå fast at de har en rekke ressurser som kan utnyttes bedre enn det gjøres i dag. Skal en få til økt mobilitet er det ingen lettvinte løsninger. En må legge om store deler av personalpolitikken til å bli mer eldrevennlig, og vise dette gjennom handling. Institusjonelle barrierer knyttet til trygdesystem og pensjonspolitikk, markedet for deltidsarbeid og aldersdiskriminering må brytes ned. Personalpolitikken må endres slik at de individuelle barrierene – sosial status og verdighet – får mindre betydning ved skifte av stilling og ansvarsområde

NR4A2 is regulated by Gastrin and involved in gastrin-induced migration and invasion of gastric adenocarcinoma cells

The peptide hormone gastrin is known to play a role in differentiation, growth and apoptosis of cells in the gastric mucosa. In this study we demonstrate that gastrin induces Nuclear Receptor 4A2 (NR4A2) expression in the adenocarcinoma cell lines AR42J and AGS-GR, which both possess the gastrin/CCK2 receptor. In vivo, NR4A2 is strongly expressed in the gastrin responsive neuroendocrine ECL cells in normal mucosa, whereas gastric adenocarcinoma tissue reveals a more diffuse and variable expression in tumor cells. We show that NR4A2 is a primary early transient gastrin induced gene in adenocarcinoma cell lines, and that NR4A2 expression is negatively regulated by inducible cAMP early repressor (ICER) and zinc finger protein 36, C3H1 type-like 1 (Zfp36l1), suggesting that these gastrin regulated proteins exert a negative feedback control of NR4A2 activated responses. FRAP analyses indicate that gastrin also modifies the nucleus-cytosol shuttling of NR4A2, with more NR4A2 localized to cytoplasm upon gastrin treatment. Knock-down experiments with siRNA targeting NR4A2 increase migration of gastrin treated adenocarcinoma AGS-GR cells, while ectopically expressed NR4A2 increases apoptosis and hampers gastrin induced invasion, indicating a tumor suppressor function of NR4A2. Collectively, our results uncover a role of NR4A2 in gastric adenocarcinoma cells, and suggest that both the level and the localization of NR4A2 protein are of importance regarding the cellular responses of these cells

NR4A2 is regulated by Gastrin and involved in gastrin-induced migration and invasion of gastric adenocarcinoma cells

The peptide hormone gastrin is known to play a role in differentiation, growth and apoptosis of cells in the gastric mucosa. In this study we demonstrate that gastrin induces Nuclear Receptor 4A2 (NR4A2) expression in the adenocarcinoma cell lines AR42J and AGS-GR, which both possess the gastrin/CCK2 receptor. In vivo, NR4A2 is strongly expressed in the gastrin responsive neuroendocrine ECL cells in normal mucosa, whereas gastric adenocarcinoma tissue reveals a more diffuse and variable expression in tumor cells. We show that NR4A2 is a primary early transient gastrin induced gene in adenocarcinoma cell lines, and that NR4A2 expression is negatively regulated by inducible cAMP early repressor (ICER) and zinc finger protein 36, C3H1 type-like 1 (Zfp36l1), suggesting that these gastrin regulated proteins exert a negative feedback control of NR4A2 activated responses. FRAP analyses indicate that gastrin also modifies the nucleus-cytosol shuttling of NR4A2, with more NR4A2 localized to cytoplasm upon gastrin treatment. Knock-down experiments with siRNA targeting NR4A2 increase migration of gastrin treated adenocarcinoma AGS-GR cells, while ectopically expressed NR4A2 increases apoptosis and hampers gastrin induced invasion, indicating a tumor suppressor function of NR4A2. Collectively, our results uncover a role of NR4A2 in gastric adenocarcinoma cells, and suggest that both the level and the localization of NR4A2 protein are of importance regarding the cellular responses of these cells

Negative regulation of gastrin-induced NR4A2 expression.

<p><b>A</b>: AGS-G_R cells transfected with NR4A2-luc and ICER expression plasmids or empty vector. Cells were treated with gastrin for 6 h prior to measurement of NR4A2 activity. Data shown represent mean ± SEM of five biological replicas (** p<0.03, * p = 0.06). <b>B</b>: AGS-G_R cells transfected with NBRE-luc and ICER expression plasmid or empty vector and treated with gastrin for 4 h prior to measurement of NBRE activity. Data shown represent mean ± SEM of four biological replicas (** p<0.03). <b>C</b>: AGS-G_R cells were transfected with pZfp36l1 expression plasmid or empty vector and treated with gastrin (5 nM) NR4A2 mRNA expression was measured by qRT-PCR. Data shown represent one of three biological replicas; mean ± SD of three technical replicas is shown. <b>D</b>: Cyclin L1 represents one of three control genes examined.</p

NR4A2 suppresses gastrin-induced migration and invasion.

<p><b>A</b>: Real-time cell migration monitored (0-24 h) in AGS-G_R cells transfected with siNR4A2 or siCtr, with or without gastrin treatment (10 nM). Results show one representative of three biological replicas; mean ±SD of three technical replicas. <b>B</b>: Invasion assay with AGS-G_R cells transfected with pCMX-NR4A2 or pCMX (control) was performed in 24-well plates containing 8-µm pore Matrigel-coated inserts (with or without 0.3 nM gastrin). Cells invading the lower surface of the membrane were stained with Reastain Quick-Diff reagents and total numbers of cells in 5 fields per membrane were counted. The mean of three independent experiments is shown.</p

Immunostaining of NR4A2 in gastric adenocarcinoma.

<p><b>A-B</b>: NR4A2 immunoreactivity in normal oxyntic mucosa showing strong intensity in scattered single cells (neuroendocrine cells) and weaker staining intensity in the other epithelial cells. <b>C-F</b>: NR4A2 immunoreactivity in gastric adenocarcinomas of intestinal (C-D) and diffuse (E-F) type, showing a general staining in tumor cells with mixed nuclear or cytoplasmic localization and variable intensities. (A, C, E at x200 magnification, with boxes representing B, D and F at x400 magnification).</p

NR4A2 activates NBRE promoter elements.

<p><b>A</b>: Gastrin-induced NBRE-luc activation. Data represent one of two biological replicas. <b>B</b>: The effect of NR4A2 siRNA on gastrin-induced NBRE activation. Data represent mean ± SEM of four biological replicas (** p<0.01, * p=0.1). <b>C-D</b>: Effect of specific inhibitors of PKA (H-89, 10µM), PI3K (LY 294002, 10µM) or PKC (GF 109203x, 3.5µM) on (<b>C</b>) gastrin-induced NR4A2 gene expression and (<b>D</b>) gastrin-induced NBRE activation. Data represent one of three biological replicas; mean ± SD of six technical replicas.</p

NR4A2 Is Regulated by Gastrin and Influences Cellular Responses of Gastric Adenocarcinoma Cells

<p>© 2013 Misund et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited</p