Geology of Tindfjallajökull volcano, Iceland

The geology of Tindfjallajökull volcano, southern Iceland, is presented as a 1:50,000 scale map. Field mapping was carried out with a focus on indicators of past environments. A broad stratocone of interbedded fragmental rocks and lavas was constructed during Tindfjallajökull’s early development. This stratocone has been dissected by glacial erosion and overlain by a variety of mafic to silicic volcanic landforms. Eruption of silicic magma, which probably occurred subglacially, constructed a thick pile of breccia and lava lobes in the summit area. Mafic to intermediate flank eruptions continued through to the end of the last glacial period, producing lavas, hyaloclastite-dominated units and tuyas that preserve evidence of volcano-ice interactions. The Thórsmörk Ignimbrite, a regionally important chronostratigraphic marker, is present on the SE flank of the volcano. The geological mapping of Tindfjallajökull gives insights into the evolution of stratovolcanoes in glaciated regions and the influence of ice in their development

The photoinduced transition in magnetoresistive manganites: a comprehensive view

We use femtosecond x-ray diffraction to study the structural response of charge and orbitally ordered Pr$_{1-x}$Ca$_x$MnO$_3$ thin films across a phase transition induced by 800 nm laser pulses. By investigating the dynamics of both superlattice reflections and regular Bragg peaks, we disentangle the different structural contributions and analyze their relevant time-scales. The dynamics of the structural and charge order response are qualitatively different when excited above and below a critical fluence $f_c$. For excitations below $f_c$ the charge order and the superlattice is only partially suppressed and the ground state recovers within a few tens of nanosecond via diffusive cooling. When exciting above the critical fluence the superlattice vanishes within approximately half a picosecond followed by a change of the unit cell parameters on a 10 picoseconds time-scale. At this point all memory from the symmetry breaking is lost and the recovery time increases by many order of magnitudes due to the first order character of the structural phase transition

Changes in skeletal muscle and tendon structure and function following genetic inactivation of myostatin in rats

Myostatin is a negative regulator of skeletal muscle and tendon mass. Myostatin deficiency has been well studied in mice, but limited data are available on how myostatin regulates the structure and function of muscles and tendons of larger animals. We hypothesized that, in comparison to wild‐type (MSTN+/+) rats, rats in which zinc finger nucleases were used to genetically inactivate myostatin (MSTNΔ/Δ) would exhibit an increase in muscle mass and total force production, a reduction in specific force, an accumulation of type II fibres and a decrease and stiffening of connective tissue. Overall, the muscle and tendon phenotype of myostatin‐deficient rats was markedly different from that of myostatin‐deficient mice, which have impaired contractility and pathological changes to fibres and their extracellular matrix. Extensor digitorum longus and soleus muscles of MSTNΔ/Δ rats demonstrated 20–33% increases in mass, 35–45% increases in fibre number, 20–57% increases in isometric force and no differences in specific force. The insulin‐like growth factor‐1 pathway was activated to a greater extent in MSTNΔ/Δ muscles, but no substantial differences in atrophy‐related genes were observed. Tendons of MSTNΔ/Δ rats had a 20% reduction in peak strain, with no differences in mass, peak stress or stiffness. The general morphology and gene expression patterns were similar between tendons of both genotypes. This large rodent model of myostatin deficiency did not have the negative consequences to muscle fibres and extracellular matrix observed in mouse models, and suggests that the greatest impact of myostatin in the regulation of muscle mass may not be to induce atrophy directly, but rather to block hypertrophy signalling.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/111244/1/tjp6572.pd

Neurophysiological signatures of Alzheimer's disease and frontotemporal lobar degeneration : pathology versus phenotype

The disruption of brain networks is characteristic of neurodegenerative dementias. However, it is controversial whether changes in connectivity reflect only the functional anatomy of disease, with selective vulnerability of brain networks, or the specific neurophysiological consequences of different neuropathologies within brain networks. We proposed that the oscillatory dynamics of cortical circuits reflect the tuning of local neural interactions, such that different pathologies are selective in their impact on the frequency spectrum of oscillations, whereas clinical syndromes reflect the anatomical distribution of pathology and physiological change. To test this hypothesis, we used magnetoencephalography from five patient groups, representing dissociated pathological subtypes and distributions across frontal, parietal and temporal lobes: amnestic Alzheimer's disease, posterior cortical atrophy, and three syndromes associated with frontotemporal lobar degeneration. We measured effective connectivity with graph theory-based measures of local efficiency, using partial directed coherence between sensors. As expected, each disease caused large-scale changes of neurophysiological brain networks, with reductions in local efficiency compared to controls. Critically however, the frequency range of altered connectivity was consistent across clinical syndromes that shared a likely underlying pathology, whilst the localization of changes differed between clinical syndromes. Multivariate pattern analysis of the frequency-specific topographies of local efficiency separated the disorders from each other and from controls (accuracy 62% to 100%, according to the groups' differences in likely pathology and clinical syndrome). The data indicate that magnetoencephalography has the potential to reveal specific changes in neurophysiology resulting from neurodegenerative disease. Our findings confirm that while clinical syndromes have characteristic anatomical patterns of abnormal connectivity that may be identified with other methods like structural brain imaging, the different mechanisms of neurodegeneration also cause characteristic spectral signatures of physiological coupling that are not accessible with structural imaging nor confounded by the neurovascular signalling of functional MRI. We suggest that these spectral characteristics of altered connectivity are the result of differential disruption of neuronal microstructure and synaptic physiology by Alzheimer's disease versus frontotemporal lobar degeneration.Peer reviewe

Watching mesoporous metal films grow during templated electrodeposition with in situ SAXS

In this paper, we monitor the real-time growth of mesoporous platinum during electrodeposition using small-angle X-ray scattering (SAXS). Previously, we have demonstrated that platinum films featuring the ‘single diamond’ (Fd3m) morphology can be produced from ‘double diamond’ (Pn3m) lipid cubic phase templates; the difference in symmetry provides additional scattering signals unique to the metal. Taking advantage of this, we present simultaneous in situ SAXS/electrochemical measurement as the platinum nanostructures grow within the lipid template. This measurement allows us to correlate the nanostructure appearance with the deposition current density and to monitor the evolution of the orientational and lateral ordering of the lipid and platinum during deposition and after template removal. In other periodic metal nanomaterials deposited within any of the normal topology liquid crystal, mesoporous silica or block copolymer templates previously published, the template and emerging metal have the same symmetry, so such a study has not been possible previously

In vivo rate-determining steps of tau seed accumulation in Alzheimer's disease.

[Figure: see text].We acknowledge funding from Sidney Sussex College Cambridge (GM) and the European Research Council Grant Number 669237 (to D.K.) and the Royal Society (to D.K.). The Cambridge Brain Bank is supported by the NIHR Cambridge Biomedical Research Centre

Nitrous Oxide Abatement Coupled with Biopolymer Production As a Model GHG Biorefinery for Cost-Effective Climate Change Mitigation

Producción CientíficaN2O represents ∼6% of the global greenhouse gas emission inventory and the most important O3-depleting substance emitted in this 21st century. Despite its environmental relevance, little attention has been given to cost-effective and environmentally friendly N2O abatement methods. Here we examined, the potential of a bubble column (BCR) and an internal loop airlift (ALR) bioreactors of 2.3 L for the abatement of N2O from a nitric acid plant emission. The process was based on the biological reduction of N2O by Paracoccus denitrificans using methanol as a carbon/electron source. Two nitrogen limiting strategies were also tested for the coproduction of poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) coupled with N2O reduction. High N2O removal efficiencies (REs) (≈87%) together with a low PHBV cell accumulation were observed in both bioreactors in excess of nitrogen. However, PHBV contents of 38–64% were recorded under N limiting conditions along with N2O-REs of ≈57% and ≈84% in the ALR and BCR, respectively. Fluorescence in situ hybridization analyses showed that P. denitrificans was dominant (>50%) after 6 months of experimentation. The successful abatement of N2O concomitant with PHBV accumulation confirmed the potential of integrating biorefinery concepts into biological gas treatment for a cost-effective GHG mitigation.Ministerio de Economía, Industria y Competitividad (Proyect CTM2015-70442-R and Red NOVEDAR CTQ2014-51693-REDC

Modifiable risk factors for dementia and dementia risk profiling. A user manual for Brain Health Services-part 2 of 6

We envisage the development of new Brain Health Services to achieve primary and secondary dementia prevention. These services will complement existing memory clinics by targeting cognitively unimpaired individuals, where the focus is on risk profiling and personalized risk reduction interventions rather than diagnosing and treating late-stage disease. In this article, we review key potentially modifiable risk factors and genetic risk factors and discuss assessment of risk factors as well as additional fluid and imaging biomarkers that may enhance risk profiling. We then outline multidomain measures and risk profiling and provide practical guidelines for Brain Health Services, with consideration of outstanding uncertainties and challenges. Users of Brain Health Services should undergo risk profiling tailored to their age, level of risk, and availability of local resources. Initial risk assessment should incorporate a multidomain risk profiling measure. For users aged 39-64, we recommend the Cardiovascular Risk Factors, Aging, and Incidence of Dementia (CAIDE) Dementia Risk Score, whereas for users aged 65 and older, we recommend the Brief Dementia Screening Indicator (BDSI) and the Australian National University Alzheimer's Disease Risk Index (ANU-ADRI). The initial assessment should also include potentially modifiable risk factors including sociodemographic, lifestyle, and health factors. If resources allow, apolipoprotein E ɛ4 status testing and structural magnetic resonance imaging should be conducted. If this initial assessment indicates a low dementia risk, then low intensity interventions can be implemented. If the user has a high dementia risk, additional investigations should be considered if local resources allow. Common variant polygenic risk of late-onset AD can be tested in middle-aged or older adults. Rare variants should only be investigated in users with a family history of early-onset dementia in a first degree relative. Advanced imaging with 18-fluorodeoxyglucose positron emission tomography (FDG-PET) or amyloid PET may be informative in high risk users to clarify the nature and burden of their underlying pathologies. Cerebrospinal fluid biomarkers are not recommended for this setting, and blood-based biomarkers need further validation before clinical use. As new technologies become available, advances in artificial intelligence are likely to improve our ability to combine diverse data to further enhance risk profiling. Ultimately, Brain Health Services have the potential to reduce the future burden of dementia through risk profiling, risk communication, personalized risk reduction, and cognitive enhancement interventions

Apathy in presymptomatic genetic frontotemporal dementia predicts cognitive decline and is driven by structural brain changes

INTRODUCTION: Apathy adversely affects prognosis and survival of patients with frontotemporal dementia (FTD). We test whether apathy develops in presymptomatic genetic FTD, and is associated with cognitive decline and brain atrophy. METHODS: Presymptomatic carriers of MAPT, GRN or C9orf72 mutations (N = 304), and relatives without mutations (N = 296) underwent clinical assessments and MRI at baseline, and annually for 2 years. Longitudinal changes in apathy, cognition, gray matter volumes, and their relationships were analyzed with latent growth curve modeling. RESULTS: Apathy severity increased over time in presymptomatic carriers, but not in non-carriers. In presymptomatic carriers, baseline apathy predicted cognitive decline over two years, but not vice versa. Apathy progression was associated with baseline low gray matter volume in frontal and cingulate regions. DISCUSSION: Apathy is an early marker of FTD-related changes and predicts a subsequent subclinical deterioration of cognition before dementia onset. Apathy may be a modifiable factor in those at risk of FTD