Building icelandic igneous crust by repeated melt injections

Observations of microseismicity provide a powerful tool for mapping the movement of melt in the crust. Here we record remarkable sequences of earthquakes 20 km below the surface in the normally ductile crust in the vicinity of Askja volcano, in north-east Iceland. The earthquakes occur in swarms consisting of identical waveforms repeating as frequently as every 8 s for up to 3 hours. We use template waveforms from each swarm to detect and locate earthquakes with an automated cross-correlation technique. Events are located in the lower crust and are inferred to be the result of melt being injected into the crust. During melt intrusion high strain rates are produced in conjunction with high pore-fluid pressures from the melt or exsolved carbon dioxide. These cause brittle failure on high angle fault planes located at the tips of sills. Moment tensor solutions show that most of the earthquakes are opening cracks accompanied by volumetric increases. This is consistent with the failure causing the earthquakes by melt injection opening new tensile cracks. Analysis of the magnitude distribution of earthquakes within a swarm reveals a complicated relationship between the imposed strain rates and the fluids that cause brittle failure. The magnitude of the earthquakes is controlled by the distance fluids can migrate along a fault, whereas the frequency of the events is controlled by the strain rate. Faults at the tips of sills act to focus melt transport between sills and so must be an important method of transporting melt through the lower crust.Seismometers were borrowed from the Natural Environment Research Council (NERC) SEIS-UK facility (loans 914 and 968), and the work funded by a research grant from the NERC and by studentship funding for TG from Shell.This is the author accepted manuscript. The final version is available from Wiley via http://dx.doi.org/10.1002/2015JB01200

Motion in the north Iceland volcanic rift zone accommodated by bookshelf faulting

Along mid-ocean ridges the extending crust is segmented on length scales of 10–1,000 km. Where rift segments are offset from one another, motion between segments is accommodated by transform faults that are oriented orthogonally to the main rift axis. Where segments overlap, non-transform offsets with a variety of geometries accommodate shear motions. Here we use micro-seismic data to analyse the geometries of faults at two overlapping rift segments exposed on land in north Iceland. Between the rift segments, we identify a series of faults that are aligned sub-parallel to the orientation of the main rift. These faults slip through left-lateral strike-slip motion. Yet, movement between the overlapping rift segments is through right-lateral motion. Together, these motions induce a clockwise rotation of the faults and intervening crustal blocks in a motion that is consistent with a bookshelf-faulting mechanism, named after its resemblance to a tilting row of books on a shelf. The faults probably reactivated existing crustal weaknesses, such as dyke intrusions, that were originally oriented parallel to the main rift and have since rotated about 15° clockwise. Reactivation of pre-existing, rift-parallel weaknesses contrasts with typical mid-ocean ridge transform faults and is an important illustration of a non-transform offset accommodating shear motion between overlapping rift segments.This work was funded by a research grant and studentships from the NERC and Shell.This is the Accepted Version of the article. The final published version is available from the Nature Geoscience website at http://www.nature.com/ngeo/journal/v7/n1/full/ngeo2012.html

Seismicity of the Askja and Bárðarbunga volcanic systems of Iceland, 2009-2015

A large seismic network deployed in the Icelandic highlands recorded more than 100,000 earthquakes from 2009 to 2015. We develop a local magnitude scale, appropriate for use in central Iceland, which is similar to the scale used by the Iceland Meteorological Office. Using this large catalogue of earthquakes, we analyze the spatial and temporal changes in seismicity rates and b-values. In microearthquakes recorded from the usually ductile lower crust we find that b-values are high, reflecting the presence of high thermal gradients and low stresses driving seismicity associated with the movement of melt. In contrast, b-values in the upper crust are variable. Low b-values, indicative of a high stress environment, are observed during seismic swarms such as those around Mt. Herðubreið and around Bárðarbunga caldera. A persistently seismically active area around a geothermal area within Askja caldera has a b-value around 1 but has a strong annual cycle of seismicity. We attribute the annual cycle to varying load from the snow cover modulating the seismicity. Seismicity driven by the intrusion of a large dyke has a b-value well above 1, driven by the high pore fluid pressures and thermal gradients around the dyke.NERC, Shel

The magmatic plumbing system of the Askja central volcano, Iceland, as imaged by seismic tomography

The magmatic plumbing system beneath Askja, a volcano in the central Icelandic highlands, is imaged using local earthquake tomography. We use a catalog of more than 1300 earthquakes widely distributed in location and depth to invert for the $P$ wave velocity ($V_p$) and the $V_p$/$V_s$ ratio. Extensive synthetic tests show that the minimum size of any velocity anomaly recovered by the model is ~4 km in the upper crust (depth < 8 km below sea level (bsl)), increasing to ~10 km in the lower crust at a depth of 20 km bsl. The plumbing system of Askja is revealed as a series of high-$V_p$/$V_s$ ratio bodies situated at discrete depths throughout the crust to depths of over 20 km. We interpret these to be regions of the crust which currently store melt with melt fractions of ~10%. The lower crustal bodies are all seismically active, suggesting that melt is being actively transported in these regions. The main melt storage regions lie beneath Askja volcano, concentrated at depths of 5 km bsl with a smaller region at 9 km bsl. Their total volume is ~100 km$^3$. Using the recorded waveforms, we show that there is also likely to be a small, highly attenuating magmatic body at a shallower depth of about 2 km bsl.Seismometers were provided by the Natural Environment Research Council SEIS-UK under loans 968 and 1022, and the Icelandic Meteorological Office kindly provided data from the seismometers which they operate around Askja. Funding was provided to T.G. from a Shell UK studentship and to R.S.W. by a Natural Environment Research Council grant NE/H025006/1. T.G. and R.S.W. would also like to acknowledge funding from the European Community’s Seventh Framework Programme grant 308377 (Project FUTUREVOLC)

Glucose-6-phosphate dehydrogenase contributes to the regulation of glucose uptake in skeletal muscle

The development of skeletal muscle insulin resistance is an early physiological defect, yet the intracellular mechanisms accounting for this metabolic defect remained unresolved. Here, we have examined the role of glucose-6-phosphate dehydrogenase (G6PDH) activity in the pathogenesis of insulin resistance in skeletal muscle. Methods Multiple mouse disease states exhibiting insulin resistance and glucose intolerance, as well as obese humans defined as insulin-sensitive, insulin-resistant, or pre-diabetic, were examined. Results We identified increased glucose-6-phosphate dehydrogenase (G6PDH) activity as a common intracellular adaptation that occurs in parallel with the induction of insulin resistance in skeletal muscle and is present across animal and human disease states with an underlying pathology of insulin resistance and glucose intolerance. We observed an inverse association between G6PDH activity and nitric oxide synthase (NOS) activity and show that increasing NOS activity via the skeletal muscle specific neuronal (n)NOS&mu; partially suppresses G6PDH activity in skeletal muscle cells. Furthermore, attenuation of G6PDH activity in skeletal muscle cells via (a) increased nNOS&mu;/NOS activity, (b) pharmacological G6PDH inhibition, or (c) genetic G6PDH inhibition increases insulin-independent glucose uptake. Conclusions We have identified a novel, previously unrecognized role for G6PDH in the regulation of skeletal muscle glucose metabolism. <br /

Retrospective Review of Positive Newborn Screening Results for Isovaleric Acidemia and Development of a Strategy to Improve the Efficacy of Newborn Screening in the UK

\ua9 2024 by the authors.Since the UK commenced newborn screening for isovaleric acidemia in 2015, changes in prescribing have increased the incidence of false positive (FP) results due to pivaloylcarnitine. A review of screening results between 2015 and 2022 identified 24 true positive (TP) and 84 FP cases, with pivalate interference confirmed in 76/84. Initial C5 carnitine (C5C) did not discriminate between FP and TP with median (range) C5C of 2.9 (2.0–9.6) and 4.0 (1.8–&gt;70) \ub5mol/L, respectively, and neither did Precision Newborn Screening via Collaborative Laboratory Integrated Reports (CLIR), which identified only 1/47 FP cases. However, among the TP cases, disease severity showed a correlation with initial C5C in ‘asymptomatic’ individuals (n = 17), demonstrating a median (range) C5C of 3.0 (1.8–7.1) whilst ‘clinically affected’ patients (n = 7), showed a median (range) C5C of 13.9 (7.7–70) \ub5mol/L. These findings allowed the introduction of dual cut-off values into the screening algorithm to reduce the incidence of FPs, with initial C5C results ≥ 5 \ub5mol/L triggering urgent referral, and those &gt;2.0 and &lt;5.0 \ub5mol/L prompting second-tier C5-isobar testing. This will avoid delayed referral in babies at particular risk whilst reducing the FP rate for the remainder

Functional interface micromechanics of 11 en-bloc retrieved cemented femoral hip replacements

Contains fulltext : 88556.pdf (publisher's version ) (Open Access)BACKGROUND AND PURPOSE: Despite the longstanding use of micromotion as a measure of implant stability, direct measurement of the micromechanics of implant/bone interfaces from en bloc human retrievals has not been performed. The purpose of this study was to determine the stem-cement and cement-bone micromechanics of functionally loaded, en-bloc retrieved, cemented femoral hip components. METHODS: 11 fresh frozen proximal femurs with cemented implants were retrieved at autopsy. Specimens were sectioned transversely into 10-mm slabs and fixed to a loading device where functional torsional loads were applied to the stem. A digital image correlation technique was used to document micromotions at stem-cement and cement-bone interfaces during loading. RESULTS: There was a wide range of responses with stem-cement micromotions ranging from 0.0006 mm to 0.83 mm (mean 0.17 mm, SD 0.29) and cement-bone micromotions ranging from 0.0022 mm to 0.73 mm (mean 0.092 mm, SD 0.22). There was a strong (linear-log) inverse correlation between apposition fraction and micromotion at the stem-cement interface (r(2) = 0.71, p < 0.001). There was a strong inverse log-log correlation between apposition fraction at the cement-bone interface and micromotion (r(2) = 0.85, p < 0.001). Components that were radiographically well-fixed had a relatively narrow range of micromotions at the stem-cement (0.0006-0.057 mm) and cement-bone (0.0022-0.029 mm) interfaces. INTERPRETATION: Minimizing gaps at the stem-cement interface and encouraging bony apposition at the cement-bone interface would be clinically desirable. The cement-bone interface does not act as a bonded interface in actual use, even in radiographically well-fixed components. Rather, the interface is quite compliant, with sliding and opening motions between the cement and bone surfaces.1 juni 201

Upregulation of α7 Nicotinic Receptors by Acetylcholinesterase C-Terminal Peptides

BACKGROUND: The alpha-7 nicotinic acetylcholine receptor (alpha7-nAChR) is well known as a potent calcium ionophore that, in the brain, has been implicated in excitotoxicity and hence in the underlying mechanisms of neurodegenerative disorders such as Alzheimer's disease. Previous research implied that the activity of this receptor may be modified by exposure to a peptide fragment derived from the C-terminal region of the enzyme acetylcholinesterase. This investigation was undertaken to determine if the functional changes observed could be attributed to peptide binding interaction with the alpha7-nAChR, or peptide modulation of receptor expression. METHODOLOGY/PRINCIPAL FINDINGS: This study provides evidence that two peptides derived from the C-terminus of acetylcholinesterase, not only selectively displace specific bungarotoxin binding at the alpha7-nAChR, but also alter receptor binding properties for its familiar ligands, including the alternative endogenous agonist choline. Of more long-term significance, these peptides also induce upregulation of alpha7-nAChR mRNA and protein expression, as well as enhancing receptor trafficking to the plasma membrane. CONCLUSIONS/SIGNIFICANCE: The results reported here demonstrate a hitherto unknown relationship between the alpha7-nAChR and the non-enzymatic functions of acetylcholinesterase, mediated independently by its C-terminal domain. Such an interaction may prove valuable as a pharmacological tool, prompting new approaches for understanding, and combating, the process of neurodegeneration

Upregulation of α7 Nicotinic Receptors by Acetylcholinesterase C-Terminal Peptides

BACKGROUND: The alpha-7 nicotinic acetylcholine receptor (alpha7-nAChR) is well known as a potent calcium ionophore that, in the brain, has been implicated in excitotoxicity and hence in the underlying mechanisms of neurodegenerative disorders such as Alzheimer's disease. Previous research implied that the activity of this receptor may be modified by exposure to a peptide fragment derived from the C-terminal region of the enzyme acetylcholinesterase. This investigation was undertaken to determine if the functional changes observed could be attributed to peptide binding interaction with the alpha7-nAChR, or peptide modulation of receptor expression. METHODOLOGY/PRINCIPAL FINDINGS: This study provides evidence that two peptides derived from the C-terminus of acetylcholinesterase, not only selectively displace specific bungarotoxin binding at the alpha7-nAChR, but also alter receptor binding properties for its familiar ligands, including the alternative endogenous agonist choline. Of more long-term significance, these peptides also induce upregulation of alpha7-nAChR mRNA and protein expression, as well as enhancing receptor trafficking to the plasma membrane. CONCLUSIONS/SIGNIFICANCE: The results reported here demonstrate a hitherto unknown relationship between the alpha7-nAChR and the non-enzymatic functions of acetylcholinesterase, mediated independently by its C-terminal domain. Such an interaction may prove valuable as a pharmacological tool, prompting new approaches for understanding, and combating, the process of neurodegeneration