Латинська Америка в дослідженнях російських етнографів за останні тридцять років

Статья посвящена истории исследований в области латиноамериканистики российскими и советскими учёными на примере научной деятельности сотрудников Института этнографии им. Н. Н. Миклухо-Маклая АН СССР (московское и ленинградское отделения).The article is dedicated to the Latin American researches provided by the Russian and Soviet scientists illustrated with the scientific activities of the representatives of the Soviet Academy of Science’s Myklukho-Maklai Ethnographical Institute (Moscow and Leningrad branches)

Natuurontwikkeling in de EHS, nu zorgen voor kwaliteit!

Momenteel werken de provincies aan het nieuwe subsidiestelsel voor (agrarisch) natuurbeheer, dat het huidige Programma Beheer gaat vervangen. Het streven is het nieuwe stelsel geïmplementeerd te krijgen in 2009. Met het stelsel is veel bereikt, maar er zijn zeker ook kansen gemist, namelijk om de ecologische kwaliteit van de EHS te realiseren. In dit artikel wordt een voorzet gegeven voor het inbedden van het realiseren van ecologische kwaliteit in een nieuwe regelgeving. Er valt namelijk een kwaliteitsslag te behalen bij het omvormen van landbouwgrond naar natuu

Interaction of Cupidin/Homer2 with two actin cytoskeletal regulators, Cdc42 small GTPase and Drebrin, in dendritic spines

<p>Abstract</p> <p>Background</p> <p>Homer is a postsynaptic scaffold protein that links various synaptic signaling proteins, including the type I metabotropic glutamate receptor subunits 1α and 5, the inositol 1,4,5-trisphosphate receptor, Shank and Cdc42 small GTPase. Overexpression of Homer induces changes in dendritic spine morphology in cultured hippocampal neurons. However, the molecular basis underpinning Homer-mediated spine morphogenesis remains unclear. In this study, we aimed to elucidate the structural and functional properties of the interaction between Cupidin/Homer2 and two actin-cytoskeletal regulators, Cdc42 small GTPase and Drebrin.</p> <p>Results</p> <p>Cupidin/Homer2 interacted with activated Cdc42 small GTPase via the Cdc42-binding domain that resides around amino acid residues 191–283, within the C-terminal coiled-coil domain. We generated a Cupidin deletion mutant lacking amino acids 191–230 (CPDΔ191–230), which showed decrease Cdc42-binding ability but maintained self-multimerization ability. Cupidin suppressed Cdc42-induced filopodia-like protrusion formation in HeLa cells, whereas CPDΔ191–230 failed to do so. In cultured hippocampal neurons, Cupidin was targeted to dendritic spines, whereas CPDΔ191–230 was distributed in dendritic shafts as well as spines. Overexpression of CPDΔ191–230 decreased the number of synapses and reduced the amplitudes of miniature excitatory postsynaptic currents in hippocampal neurons. Cupidin interacted with a dendritic spine F-actin-binding protein, Drebrin, which possesses two Homer ligand motifs, via the N-terminal EVH-1 domain. CPDΔ191–230 overexpression decreased Drebrin clustering in the dendritic spines of hippocampal neurons.</p> <p>Conclusion</p> <p>These results indicate that Cupidin/Homer2 interacts with the dendritic spine actin regulators Cdc42 and Drebrin via its C-terminal and N-terminal domains, respectively, and that it may be involved in spine morphology and synaptic properties.</p

Exposure to challenging behaviours and burnout symptoms among care staff:the role of psychological resources

Background Staff supporting individuals with intellectual disabilities are at risk of burnout symptoms. Evidence suggests an association between exposure to challenging behaviours of individuals with intellectual disabilities and burnout symptoms of staff, but the protective role of staff psychological resources in this relation has been understudied. Method We investigated the association between exposure to challenging behaviours and burnout symptoms of staff and the direct and moderating effects of several psychological resources. Staff (N = 1271) completed an online survey concerning burnout symptoms (subscale Emotional Exhaustion of the Maslach Burnout Inventory), exposure to challenging behaviours and a range of potential psychological resources. We examined main and moderating effects with multilevel analyses. In order to control for the multiple comparisons, P values corrected for false discovery rate (P-FDR) were reported. Results We found a direct relation between exposure to challenging behaviours and increased levels of burnout symptoms in staff (b = .15, t(670) = 4.466, P-FDR <.0001). Perceived supervisor social support (b = -.97, t(627) = -7.562, P-FDR <.0001), staff self-efficacy (b = -.23, t(673) = -3.583, P-FDR <.0001), resilience (b = -.19, t(668) = -2.086, P-FDR <.05) and extraversion (b = -.20, t(674) = -3.514, P-FDR <.05) were associated with reduced burnout symptoms. None of the proposed psychological resources moderated the association between exposure to challenging behaviours and burnout symptoms of staff. Conclusions Of the psychological resources found to be associated with reduced risk of burnout symptoms, staff self-efficacy and access of staff to supervisor social support seem to be the factors that can be influenced best. These factors thus may be of importance in reducing the risk of developing burnout symptoms and improving staff well-being, even though the current study was not designed to demonstrate causal relations between psychological resources and burnout symptoms

Clinical characterization of 66 patients with congenital retinal disease due to the deep-intronic c.2991+1655A>G mutation in CEP290

Purpose: To describe the phenotypic spectrum of retinal disease caused by the c.2991+1655A>G mutation in CEP290 and to compare disease severity between homozygous and compound heterozygous patients. Methods: Medical records were reviewed for best-corrected visual acuity (BCVA), age of onset, fundoscopy descriptions. Foveal outer nuclear layer (ONL) and ellipsoid zone (EZ) presence was assessed using spectral-domain optical coherence tomography (SD-OCT). Differences between compound heterozygous and homozygous patients were analyzed based on visual performance and visual development. Results: A total of 66 patients were included. The majority of patients had either light perception or no light perception. In the remaining group of 14 patients, median BCVA was 20/195 Snellen (0.99 LogMAR; range 0.12-1.90) for the right eye, and 20/148 Snellen (0.87 LogMAR; range 0.22-1.90) for the left. Homozygous patients tended to be more likely to develop light perception compared to more severely affected compound heterozygous patients (P = 0.080) and are more likely to improve from no light perception to light perception (P = 0.022) before the age of 6 years. OCT data were available in 12 patients, 11 of whom had retained foveal ONL and EZ integrity up to 48 years (median 23 years) of age. Conclusions: Homozygous patients seem less severely affected compared to their compound-heterozygous peers. Improvement of visual function may occur in the early years of life, suggesting a time window for therapeutic intervention up to the approximate age of 17 years. This period may be extended by an intact foveal ONL and EZ on OCT

Book Review of Serendipity: An Ecologist’s Quest to Understand Nature

A common thought among graduate students is: “how do established scientists get where they are today?” In Serendipity: An Ecologist’s Quest to Understand Nature, James Estes offers a personal reflection on research experiences spanning his 50-year career, beginning as a Ph.D. student in 1970 and concluding with recognition as a member of the National Academy of Sciences in 2014. Estes chronologically outlines the foundational trophic cascade ecology research that he and colleagues conducted in the Aleutian Islands, examining key relationships among kelp forests, sea otters, sea urchins, and killer whales through anecdotal stories of achievement and challenge. Estes’ 3 main goals in writing this book are to: (1) recount what he had learned from 50 years of research; (2) provide a larger story of how predators and prey interact with one another; and (3) explain how science “really happens.

Genetic Risk in Families with Age-Related Macular Degeneration

PURPOSE: To determine the contribution of common and rare genetic risk variants in families with age-related macular degeneration (AMD). DESIGN: Case-control study. PARTICIPANTS: A family cohort (355 affected and 342 unaffected family members from 144 families with AMD) and an unrelated case-control cohort (1078 patients, 952 controls), recruited from the European Genetic Database. METHODS: Genetic data of both cohorts were filtered for carriership of rare genetic variants in the coding and splice-site regions of the complement factor H (CFH) and complement factor I (CFI) genes, and 52 AMD-associated variants were extracted for calculation of genetic risk scores (GRS). To compare GRSs between familial and nonfamilial rare CFH and CFI variant carriers and noncarriers and between AMD disease stages, we performed a 2-way analysis of variance, with Bonferroni correction for multiple testing. Within families with AMD carrying rare CFH and CFI variants, we analyzed segregation patterns by calculating the proportion of affected among carriers. MAIN OUTCOME MEASURES: GRSs and segregation of rare CFH and CFI variants. RESULTS: We observed higher GRSs in familial versus nonfamilial individuals without rare CFH and CFI variants: mean GRS, 1.76 (standard error [SE], 0.08) versus 0.83 (SE, 0.03; P < 0.001). In 51 of 144 families (35.4%), rare CFH and CFI variants were identified. Within the AMD family cohort, carriers of rare CFH and CFI variants showed lower GRSs compared with noncarriers (mean GRS, 1.05 [SE, 0.23] vs. 1.76 [SE, 0.08]; P = 0.02). The proportion of affected family members with a high GRS was 57.3% (176/307). Of the affected family members with a low or intermediate GRS, 40.0% carried rare CFH or CFI variants. Among carriers of 11 rare CFH or CFI variants, the proportion affected by AMD was more than 75%. CONCLUSIONS: Genetic risk in families with AMD often is attributed to high GRSs based on common variants. However, in part of the families with a low or intermediate GRS, rare CFH and CFI variants contributed to disease development. We recommend computing GRSs and sequencing the CFH and CFI genes in families with AMD, in particular in the light of ongoing gene-specific clinical trials