Age work in organizations: maintaining and disrupting institutionalized understandings of higher age

Age diversity research calls for new approaches in explaining the persistence of age inequalities, which integrate different levels of analysis and display greater context sensitivity. Concurrently, neoinstitutionalist research interested in social inequalities calls for merging institutional theory with critical perspectives and to account for issues of power. In this study, we address the calls of both research streams through developing the concept of ‘age work’: the institutional work actors undertake on age as a social institution. Applying our novel concept to a multi-actor study of four German organizations known for their age management, we come across a counterintuitive insight regarding actors’ age work: maintaining stereotypical age images can serve to counter age inequalities, whereas deconstructing age images can reinforce age inequalities. The multi-actor perspective of our study allows us to categorize different forms of power-laden and interest-driven age work and to portray the reproduction of age inequalities as a result of actors’ age work, embedded in different contexts and complex power relations. Comparing employees’ forms of age work across sectors and organizations, we detail how notions of masculinity as well as income and job security shaped the categorized forms of age work

Interaction of CO and O₂ with Pt Studied by Field Ion Appearance Energy Spectroscopy

Using field ion appearance energy spectroscopy we have examined the interaction of CO and 02 with stepped platinum surfaces in the presence of electrostatic fields ranging between 10 and 20 V/nm. Mass-to-charge resolved retarding potential analyses have been carried out for single sites of [001] and [111]-oriented Pt field emitter exposed to a continuous flow of CO and 02. Applying a thermionic cycle, binding energies of molecularly adsorbed CO and O2, were derived from the appearance energies of field desorbed CO+ and O+2 . The data reveal an effect of the high field on the molecule-surface interaction, which is most pronounced for COPt(111) steps. Implications for FIM studies of catalytic CO and H2, oxidation reactions are discussed

BubR1 allelic effects drive phenotypic heterogeneity in mosaic-variegated aneuploidy progeria syndrome

Mosaic-variegated aneuploidy (MVA) syndrome is a rare childhood disorder characterized by biallelic BUBR1, CEP57, or TRIP13 aberrations; increased chromosome missegregation; and a broad spectrum of clinical features, including various cancers, congenital defects, and progeroid pathologies. To investigate the mechanisms underlying this disorder and its phenotypic heterogeneity, we mimicked the BUBR1(L1012P) mutation in mice (BubR1(L1002P)) and combined it with 2 other MVA variants, BUBR1(X753) and BUBR1(H), generating a truncated protein and low amounts of wild-type protein, respectively. Whereas BubR1(X753/L1002P) and BubR1(H/X753) mice died prematurely, BubR1(H/L1002P) mice were viable and exhibited many MVA features, including cancer predisposition and various progeroid phenotypes, such as short lifespan, dwarfism, lipodystrophy, sarcopenia, and low cardiac stress tolerance. Strikingly, although these mice had a reduction in total BUBR1 and spectrum of MVA phenotypes similar to that of BubR1(H/H) mice, several progeroid pathologies were attenuated in severity, which in skeletal muscle coincided with reduced senescence-associated secretory phenotype complexity. Additionally, mice carrying monoallelic BubR1 mutations were prone to select MVA-related pathologies later in life, with predisposition to sarcopenia correlating with mTORC1 hyperactivity. Together, these data demonstrate that BUBR1 allelic effects beyond protein level and aneuploidy contribute to disease heterogeneity in both MVA patients and heterozygous carriers of MVA mutations

Erratum:BubR1 allelic effects drive phenotypic heterogeneity in mosaic-variegated aneuploidy progeria syndrome (Journal of Clinical Investigation (2020) 130:1 (171-188) DOI: 10.1172/JCI126863)

During the preparation of this manuscript, the same sample was inadvertently included for the +/L1002P and +/– images in Figure 2E. The authors were able to use the original samples to prepare a corrected version. The correct figure is below. The description in Methods for this panel has also been corrected, as below: To assess the mitotic index of spontaneous lymphatic tumors, mitotic cells were visualized by IF labelling of at least 1 paraffin section for pHH3 (EMD Millipore, catalog 06-570), as described (6, 46). The online version of the article has been updated with the corrected information. The authors regret the errors

Rare mutations in SQSTM1 modify susceptibility to frontotemporal lobar degeneration

Mutations in the gene coding for Sequestosome 1 (SQSTM1) have been genetically associated with amyotrophic lateral sclerosis (ALS) and Paget disease of bone. In the present study, we analyzed the SQSTM1 coding sequence for mutations in an extended cohort of 1,808 patients with frontotemporal lobar degeneration (FTLD), ascertained within the European Early-Onset Dementia consortium. As control dataset, we sequenced 1,625 European control individuals and analyzed whole-exome sequence data of 2,274 German individuals (total n = 3,899). Association of rare SQSTM1 mutations was calculated in a meta-analysis of 4,332 FTLD and 10,240 control alleles. We identified 25 coding variants in FTLD patients of which 10 have not been described. Fifteen mutations were absent in the control individuals (carrier frequency < 0.00026) whilst the others were rare in both patients and control individuals. When pooling all variants with a minor allele frequency < 0.01, an overall frequency of 3.2 % was calculated in patients. Rare variant association analysis between patients and controls showed no difference over the whole protein, but suggested that rare mutations clustering in the UBA domain of SQSTM1 may influence disease susceptibility by doubling the risk for FTLD (RR = 2.18 [95 % CI 1.24-3.85]; corrected p value = 0.042). Detailed histopathology demonstrated that mutations in SQSTM1 associate with widespread neuronal and glial phospho-TDP-43 pathology. With this study, we provide further evidence for a putative role of rare mutations in SQSTM1 in the genetic etiology of FTLD and showed that, comparable to other FTLD/ALS genes, SQSTM1 mutations are associated with TDP-43 pathology

The Vehicle, Spring 1981

Vol. 22, No. 2 Table of Contents Old Farmers at the Arcade CafeJohn Stockmanpage 4 ConfettiCathy Georgepage 6 Ode to a Corned Beef SandwichJeff Bennettpage 6 The Ice on Kirschner\u27s CreekScott Fishelpage 7 Love Poem to LindaJohn Stockmanpage 7 Grandfather\u27s PortraitJames Marshpage 8 The MassageKathleen Alakspage 9 A Driving ForceSandy Youngpage 10 King DandelionNancy Siebenpage 12 One Afternoon - Contemplating HouseworkKelli Sanderpage 13 Tent WallsAndy Sudkamppage 14 The SentinelElise Hempelpage 16 Daddy\u27s AftershaveJeff Bennettpage 16 The WeddingChris Goerlichpage 17 UntitledCarol Hansenpage 17 Treasures in the YardScott Fishelpage 18 Hitchhiker\u27s BootsAndy Sudkamppage 20 The RaffleLaura Henrypage 21 A Walk at NightJudi Jinespage 24 Morning in the DumpJeff Bennettpage 24 In Praise of Chocolate Ice CreamJohn Stockmanpage 25 Summer on the Isle of PalmsElisabeth Cristpage 26 The WaveHerbert S. Demminpage 27 RememberingJohn Kleinsteiberpage 27 PotatoJohn Stockmanpage 28 Late ShowChris Goerlichpage 30 Love in Him - JoeDebbie Klinnertpage 31 ShoeScott Fishelpage 35 The DrinkerBob Huntpage 36 The WidowGeorge Ndu Igbudupage 37 ElectricityScott Fishelpage 37 Hatchet JackB.L. Davidsonpage 39 Walking Home LateJohn Stockmanpage 41 NovemberCindy Hubbarttpage 41 On the BusLaura Henrypage 42 HaikuJames Marshpage 43 SpillwayGloria Rhoadspage 43 Art Cover design by Linda Fraembs PhotographRobin Scholzpage 3 PhotographRobin Scholzpage 5 PhotographMichelle Glassmeyerpage 15 PhotographRobert Schinaglpage 19 PhotographTom Robertspage 38 PhotographRobert Schinaglpage 44https://thekeep.eiu.edu/vehicle/1039/thumbnail.jp

Brain age as a biomarker for pathological versus healthy ageing – a REMEMBER study

Objectives: This study aimed to evaluate the potential clinical value of a new brain age prediction model as a single interpretable variable representing the condition of our brain. Among many clinical use cases, brain age could be a novel outcome measure to assess the preventive effect of life-style interventions. Methods: The REMEMBER study population (N = 742) consisted of cognitively healthy (HC,N = 91), subjective cognitive decline (SCD,N = 65), mild cognitive impairment (MCI,N = 319) and AD dementia (ADD,N = 267) subjects. Automated brain volumetry of global, cortical, and subcortical brain structures computed by the CE-labeled and FDA-cleared software icobrain dm (dementia) was retrospectively extracted from T1-weighted MRI sequences that were acquired during clinical routine at participating memory clinics from the Belgian Dementia Council. The volumetric features, along with sex, were combined into a weighted sum using a linear model, and were used to predict ‘brain age’ and ‘brain predicted age difference’ (BPAD = brain age–chronological age) for every subject. Results: MCI and ADD patients showed an increased brain age compared to their chronological age. Overall, brain age outperformed BPAD and chronological age in terms of classification accuracy across the AD spectrum. There was a weak-to-moderate correlation between total MMSE score and both brain age (r = -0.38,p < .001) and BPAD (r = -0.26,p < .001). Noticeable trends, but no significant correlations, were found between BPAD and incidence of conversion from MCI to ADD, nor between BPAD and conversion time from MCI to ADD. BPAD was increased in heavy alcohol drinkers compared to non-/sporadic (p = .014) and moderate (p = .040) drinkers. Conclusions: Brain age and associated BPAD have the potential to serve as indicators for, and to evaluate the impact of lifestyle modifications or interventions on, brain health