2,076 research outputs found
Implicit Encoding Explored Through the Flankers Task
We examined the process of selective attention and its relation to implicit and explicit memory encoding. To further understand the mechanisms behind selective attention, we asked if implicit learning of irrelevant information is encoded differently than explicit learning. We used the flankers task to examine selective attention. This task involves responding to a center item (i.e. the target), while ignoring the irrelevant flankers. Participants completed the correlated flankers task as well as implicit and explicit memory tasks. The correlated flanker effect is the decreased reaction time on the trials in which the flankers that are correlated with the correct response are present versus uncorrelated trials (Miller, 1987). Results were contrary to what we expected and reasons as to why this occurred are discussed. Opportunity for participation in discussion is welcome
Anodic dissolution of metals in oxide-free cryolite melts
The anodic behavior of metals in molten cryolite-alumina melts has been investigated mostly for use as inert anodes for the Hall-Héroult process. In the present work, gold, platinum, palladium, copper, tungsten, nickel, cobalt and iron metal electrodes were anodically polarized in an oxide-free cryolite melt (11%wt. excess AlF3 ; 5%wt. CaF2) at 1273 K. The aim of the experiments was to characterize the oxidation reactions of the metals occurring without the effect of oxygen-containing dissolved species. The anodic dissolution of each metal was demonstrated, and electrochemical reactions were assigned using reversible potential calculation. The relative stability of metals as well as the possibility of generating pure fluorine is discussed
Ocean Model Formulation Influences Transient Climate Response
The transient climate response (TCR) is 20% higher in the Alfred Wegener Institute Climate Model (AWI-CM) compared to the Max Planck Institute Earth System Model (MPI-ESM) whereas the equilibrium climate sensitivity (ECS) is by up to 10% higher in AWI-CM. These results are largely independent of the two considered model resolutions for each model. The two coupled CMIP6 models share the same atmosphere-land component ECHAM6.3 developed at the Max Planck Institute for Meteorology (MPI-M). However, ECHAM6.3 is coupled to two different ocean models, namely the MPIOM sea ice-ocean model developed at MPI-M and the FESOM sea ice-ocean model developed at the Alfred Wegener Institute, Helmholtz Centre for Polar and Marine Research (AWI). A reason for the different TCR is related to ocean heat uptake in response to greenhouse gas forcing. Specifically, AWI-CM simulations show stronger surface heating than MPI-ESM simulations while the latter accumulate more heat in the deeper ocean. The vertically integrated ocean heat content is increasing slower in AWI-CM model configurations compared to MPI-ESM model configurations in the high latitudes. Weaker vertical mixing in AWI-CM model configurations compared to MPI-ESM model configurations seems to be key for these differences. The strongest difference in vertical ocean mixing occurs inside the Weddell and Ross Gyres and the northern North Atlantic. Over the North Atlantic, these differences materialize in a lack of a warming hole in AWI-CM model configurations and the presence of a warming hole in MPI-ESM model configurations. All these differences occur largely independent of the considered model resolutions
Alternativní zemědělství - informační bulletin č.7
Témata informačního bulletinu č.7 jsou:
Vyhodnocení výnosů zemědělských plodin v roce 1991 u organicky hospodařících zemědělců svazu PRO-BIO. Nutnost moření osiva z hlediska alternativního zemědělství. Využití přirozených surovin v alternativním zemědělství. Mechanická regulace plevelů. Možnosti realizace alternativního zemědělství z hlediska ochrany rostlin. Regulace hraboše polního bez chemie. Úvod k připravované knize "Ekologická východiska zemědělství". Stáj s hlubokou podestýlkou pro dojnice z hlediska etologie a ekonomiky. Zelené hnojení. Organické vinohradnictví
Seizures as an early symptom of autosomal dominant Alzheimer's disease
Our objective was to assess the reported history of seizures in cognitively asymptomatic mutation carriers for autosomal dominant Alzheimer's disease (ADAD) and the predictive value of seizures for mutation carrier status in cognitively asymptomatic first-degree relatives of ADAD patients. Seizure occurrence in the Dominantly Inherited Alzheimer Network observational study was correlated with mutation carrier status in cognitively asymptomatic subjects. Of 276 cognitively asymptomatic individuals, 11 (4%) had experienced seizures, and nine of these carried an ADAD mutation. Thus, in the Dominantly Inherited Alzheimer Network population, seizure frequency in mutation carriers was significantly higher than in noncarriers (p = 0.04), and the positive predictive value of seizures for the presence of a pathogenic mutation was 81.8%. Among cognitively asymptomatic ADAD family members, the occurrence of seizures increases the a priori risk of 50% mutation-positive status to about 80%. This finding suggests that ADAD mutations increase the risk of seizures
The Free Cued Selective Reminding Test detects episodic memory impairment in the presymptomatic period of familial frontotemporal dementia within the GENFI cohort
Social cognition impairment in genetic frontotemporal dementia within the GENFI cohort.
A key symptom of frontotemporal dementia (FTD) is difficulty interacting socially with others. Social cognition problems in FTD include impaired emotion processing and theory of mind difficulties, and whilst these have been studied extensively in sporadic FTD, few studies have investigated them in familial FTD. Facial Emotion Recognition (FER) and Faux Pas (FP) recognition tests were used to study social cognition within the Genetic Frontotemporal Dementia Initiative (GENFI), a large familial FTD cohort of C9orf72, GRN, and MAPT mutation carriers. 627 participants undertook at least one of the tasks, and were separated into mutation-negative healthy controls, presymptomatic mutation carriers (split into early and late groups) and symptomatic mutation carriers. Groups were compared using a linear regression model with bootstrapping, adjusting for age, sex, education, and for the FP recognition test, language. Neural correlates of social cognition deficits were explored using a voxel-based morphometry (VBM) study. All three of the symptomatic genetic groups were impaired on both tasks with no significant difference between them. However, prior to onset, only the late presymptomatic C9orf72 mutation carriers on the FER test were impaired compared to the control group, with a subanalysis showing differences particularly in fear and sadness. The VBM analysis revealed that impaired social cognition was mainly associated with a left hemisphere predominant network of regions involving particularly the striatum, orbitofrontal cortex and insula, and to a lesser extent the inferomedial temporal lobe and other areas of the frontal lobe. In conclusion, theory of mind and emotion processing abilities are impaired in familial FTD, with early changes occurring prior to symptom onset in C9orf72 presymptomatic mutation carriers. Future work should investigate how performance changes over time, in order to gain a clearer insight into social cognitive impairment over the course of the disease
FDG-PET underscores the key role of the thalamus in frontotemporal lobar degeneration caused by C9ORF72 mutations
C9ORF72 mutations are the most common cause of familial frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). MRI studies have investigated structural changes in C9ORF72-associated FTLD (C9FTLD) and provided first insights about a prominent involvement of the thalamus and the cerebellum. Our multicenter, F-18-fluorodeoxyglucose positron-emission tomography study of 22 mutation carriers with FTLD, 22 matched non-carriers with FTLD, and 23 cognitively healthy controls provided valuable insights into functional changes in C9FTLD: compared to non-carriers, mutation carriers showed a significant reduction of glucose metabolism in both thalami, underscoring the key role of the thalamus in C9FTLD. Thalamic metabolism did not correlate with disease severity, duration of disease, or the presence of psychotic symptoms. Against our expectations we could not demonstrate a cerebellar hypometabolism in carriers or non-carriers. Future imaging and neuropathological studies in large patient cohorts are required to further elucidate the central role of the thalamus in C9FTLD
Characterizing the Clinical Features and Atrophy Patterns of MAPT-Related Frontotemporal Dementia With Disease Progression Modeling.
BACKGROUND AND OBJECTIVE: Mutations in the MAPT gene cause frontotemporal dementia (FTD). Most previous studies investigating the neuroanatomical signature of MAPT mutations have grouped all different mutations together and shown an association with focal atrophy of the temporal lobe. The variability in atrophy patterns between each particular MAPT mutation is less well-characterized. We aimed to investigate whether there were distinct groups of MAPT mutation carriers based on their neuroanatomical signature. METHODS: We applied Subtype and Stage Inference (SuStaIn), an unsupervised machine learning technique that identifies groups of individuals with distinct progression patterns, to characterize patterns of regional atrophy in MAPT-associated FTD within the Genetic FTD Initiative (GENFI) cohort study. RESULTS: Eighty-two MAPT mutation carriers were analyzed, the majority of whom had P301L, IVS10+16, or R406W mutations, along with 48 healthy noncarriers. SuStaIn identified 2 groups of MAPT mutation carriers with distinct atrophy patterns: a temporal subtype, in which atrophy was most prominent in the hippocampus, amygdala, temporal cortex, and insula; and a frontotemporal subtype, in which atrophy was more localized to the lateral temporal lobe and anterior insula, as well as the orbitofrontal and ventromedial prefrontal cortex and anterior cingulate. There was one-to-one mapping between IVS10+16 and R406W mutations and the temporal subtype and near one-to-one mapping between P301L mutations and the frontotemporal subtype. There were differences in clinical symptoms and neuropsychological test scores between subtypes: the temporal subtype was associated with amnestic symptoms, whereas the frontotemporal subtype was associated with executive dysfunction. CONCLUSION: Our results demonstrate that different MAPT mutations give rise to distinct atrophy patterns and clinical phenotype, providing insights into the underlying disease biology and potential utility for patient stratification in therapeutic trials.National Institute for Health Research Cambridge Biomedical
Research Centre
Medical Research Counci
A data-driven disease progression model of fluid biomarkers in genetic frontotemporal dementia
Several CSF and blood biomarkers for genetic frontotemporal dementia (FTD) have been proposed, including those reflecting neuroaxonal loss (neurofilament light chain (NfL) and phosphorylated neurofilament heavy chain (pNfH)), synapse dysfunction (neuronal pentraxin 2 (NPTX2)), astrogliosis (glial fibrillary acidic protein (GFAP)), and complement activation (C1q, C3b). Determining the sequence in which biomarkers become abnormal over the course of disease could facilitate disease staging and help identify mutation carriers with prodromal or early-stage FTD, which is especially important as pharmaceutical trials emerge. We aimed to model the sequence of biomarker abnormalities in presymptomatic and symptomatic genetic FTD using cross-sectional data from the Genetic Frontotemporal dementia Initiative (GENFI), a longitudinal cohort study. 275 presymptomatic and 127 symptomatic carriers of mutations in GRN, C9orf72 or MAPT, as well as 247 non-carriers, were selected from the GENFI cohort based on availability of one or more of the aforementioned biomarkers. Nine presymptomatic carriers developed symptoms within 18 months of sample collection ('converters'). Sequences of biomarker abnormalities were modelled for the entire group using discriminative event-based modelling (DEBM) and for each genetic subgroup using co-initialised DEBM. These models estimate probabilistic biomarker abnormalities in a data-driven way and do not rely on prior diagnostic information or biomarker cut-off points. Using cross-validation, subjects were subsequently assigned a disease stage based on their position along the disease progression timeline. CSF NPTX2 was the first biomarker to become abnormal, followed by blood and CSF NfL, blood pNfH, blood GFAP, and finally CSF C3b and C1q. Biomarker orderings did not differ significantly between genetic subgroups, but more uncertainty was noted in the C9orf72 and MAPT groups than for GRN. Estimated disease stages could distinguish symptomatic from presymptomatic carriers and non-carriers with areas under the curve (AUC) of 0.84 (95% confidence interval 0.80-0.89) and 0.90 (0.86-0.94) respectively. The AUC to distinguish converters from non-converting presymptomatic carriers was 0.85 (0.75-0.95). Our data-driven model of genetic FTD revealed that NPTX2 and NfL are the earliest to change among the selected biomarkers. Further research should investigate their utility as candidate selection tools for pharmaceutical trials. The model's ability to accurately estimate individual disease stages could improve patient stratification and track the efficacy of therapeutic interventions
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