The Survival of Mafic Magmatic Enclaves and the Timing of Magma Recharge

Many intermediate to felsic intrusive and extrusive rocks contain mafic magmatic enclaves that are evidence for magma recharge and mixing. Whether enclaves represent records of prolonged mixing  or syn‐eruptive recharge depends on their preservation potential in their intermediate to felsic host magmas. We present a model for enclave consumption where an initial stage of diffusive equilibration loosens the crystal framework in the enclave followed by advective erosion and disaggregation of the loose crystal layer. Using experimental data to constrain the propagation rate of the loosening front leads to enclave “erosion” rates of 10−5–10−8 cm/s for subvolcanic magma systems. These rates suggest that under some circumstances, enclave records are restricted to syn‐eruptive processes, while in most cases, enclave populations represent the recharge history over centuries to millennia. On these timescales, mafic magmatic enclaves may be unique recorders that can be compared to societal and written records of volcano activity.Plain Language SummaryTwo major questions in volcano research are how magma chambers are built through time and how they are disrupted to cause volcanic eruptions. One piece of evidence that chambers are assembled by episodic magma addition from below (called “recharge”) comes from mingled magmas, where mingling is expressed by the presence of two or more chemically distinct magmas. In particular, the more primitive magma in such mingled magmas is commonly present as discrete blobs, called mafic magmatic enclaves. These enclaves are often interpreted as evidence for recharge‐triggered volcanic eruptions. However, they may also form during recharge episodes that are not associated with volcanic eruptions and instead only feed and sustain the magma chamber. Here, we develop a model that estimates how long mafic magmatic enclaves survive in a chemically distinct magma chamber to better understand how information drawn from enclaves informs the two major questions above. We find that under most common conditions, they survive for centuries to millennia. Therefore, the presence of enclaves is not explicitly evidence for a recharge‐triggered eruption without studying them in greater detail. That detail can then potentially provide information regarding both the run up to eruption as well as magma assembly over centuries and millennia.Key PointsCommon survival times for mafic enclaves in felsic volcanic systems are centuries to millennia extending timescale records from mineralsMafic enclaves record only syn‐eruptive processes in hot magmatic systemsMafic enclaves in plutonic systems may represent recharge histories of 10,000–100,000 yearsPeer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/156204/3/grl60839-sup-0002-2020GL087274-ds01.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156204/2/grl60868_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156204/1/grl60868.pd

NanoSIMS results from olivine-hosted melt embayments: Magma ascent rate during explosive basaltic eruptions

The explosivity of volcanic eruptions is governed in part by the rate at which magma ascends and degasses. Because the time scales of eruptive processes can be exceptionally fast relative to standard geochronometers, magma ascent rate remains difficult to quantify. Here we use as a chronometer concentration gradients of volatile species along open melt embayments within olivine crystals. Continuous degassing of the external melt during magma ascent results in diffusion of volatile species from embayment interiors to the bubble located at their outlets. The novel aspect of this study is the measurement of concentration gradients in five volatile elements (CO2, H2O, S, Cl, F) at fine-scale (5–10 μm) using the NanoSIMS. The wide range in diffusivity and solubility of these different volatiles provides multiple constraints on ascent timescales over a range of depths. We focus on four 100–200 μm, olivine-hosted embayments erupted on October 17, 1974 during the sub-Plinian eruption of Volcán de Fuego. H2O, CO2, and S all decrease toward the embayment outlet bubble, while F and Cl increase or remain roughly constant. Compared to an extensive melt inclusion suite from the same day of the eruption, the embayments have lost both H2O and CO2 throughout the entire length of the embayment. We fit the profiles with a 1-D numerical diffusion model that allows varying diffusivities and external melt concentrations as a function of pressure. Assuming a constant decompression rate from the magma storage region at approximately 220 MPa to the surface, H2O, CO2 and S profiles for all embayments can be fit with a relatively narrow range in decompression rates of 0.3–0.5 MPa/s, equivalent to 11–17 m/s ascent velocity and an 8 to 12 minute duration of magma ascent from ~ 10 km depth. A two stage decompression model takes advantage of the different depth ranges over which CO2 and H2O degas, and produces good fits given an initial stage of slow decompression (0.05–0.3 MPa/s) at high pressure (< 145 MPa), with similar decompression rates to the single-stage model for the shallower stage. The magma ascent rates reported here are among the first for explosive basaltic eruptions and demonstrate the potential of the embayment method for quantifying magmatic timescales associated with eruptions of different vigor

Volatile loss from melt inclusions in pyroclasts of differing sizes

We have investigated the loss of H2O from olivine-hosted melt inclusions (MIs) by designing an experiment using tephra samples that cooled at different rates owing to their different sizes: ash, lapilli, and bomb samples that were deposited on the same day (10/17/74) of the sub-Plinian eruption of Volcán de Fuego in Guatemala. Ion microprobe, laser ablation-ICPMS, and electron probe analyses show that MIs from ash and lapilli record the highest H2O contents, up to 4.4 wt%. On the other hand, MIs from bombs indicate up to 30 % lower H2O contents (loss of ~1 wt% H2O) and 10 % post-entrapment crystallization of olivine. This evidence is consistent with the longer cooling time available for a bomb-sized clast, up to 10 min for a 3–4-cm radius bomb, assuming conductive cooling and the fastest H diffusivities measured in olivine (D~10−9 to 10−10 m2/s). On the other hand, several lines of evidence point to some water loss prior to eruption, during magma ascent and degassing in the conduit. Thus, results point to both slower post-eruptive cooling and slower magma ascent affecting MIs from bombs, leading to H2O loss over the timescale of minutes to hours. The important implication of this study is that a significant portion of the published data on H2O concentrations in olivine-hosted MIs may reflect unrecognized H2O loss via diffusion. This work highlights the importance of reporting clast and MI sizes in order to assess diffusive effects and the potential benefit of using water loss as a chronometer of magma ascent

SIGLEC1 (CD169): a marker of active neuroinflammation in the brain but not in the blood of multiple sclerosis patients

We aimed to evaluate SIGLEC1 (CD169) as a biomarker in multiple sclerosis (MS) and Neuromyelitis optica spectrum disorder (NMOSD) and to evaluate the presence of SIGLEC1(+) myeloid cells in demyelinating diseases. We performed flow cytometry-based measurements of SIGLEC1 expression on monocytes in 86 MS patients, 41 NMOSD patients and 31 healthy controls. Additionally, we histologically evaluated the presence of SIGLEC1(+) myeloid cells in acute and chronic MS brain lesions as well as other neurological diseases. We found elevated SIGLEC1 expression in 16/86 (18.6%) MS patients and 4/41 (9.8%) NMOSD patients. Almost all MS patients with high SIGLEC1 levels received exogenous interferon beta as an immunomodulatory treatment and only a small fraction of MS patients without interferon treatment had increased SIGLEC1 expression. In our cohort, SIGLEC1 expression on monocytes was-apart from those patients receiving interferon treatment-not significantly increased in patients with MS and NMOSD, nor were levels associated with more severe disease. SIGLEC1(+) myeloid cells were abundantly present in active MS lesions as well as in a range of acute infectious and malignant diseases of the central nervous system, but not chronic MS lesions. The presence of SIGLEC1(+) myeloid cells in brain lesions could be used to investigate the activity in an inflammatory CNS lesion

A pre-ribosomal RNA interaction network involving snoRNAs and the Rok1 helicase

Ribosome biogenesis in yeast requires 75 small nucleolar RNAs (snoRNAs) and a myriad of cofactors for processing, modification, and folding of the ribosomal RNAs (rRNAs). For the 19 RNA helicases implicated in ribosome synthesis, their sites of action and molecular functions have largely remained unknown. Here, we have used UV cross-linking and analysis of cDNA (CRAC) to reveal the pre-rRNA binding sites of the RNA helicase Rok1, which is involved in early small subunit biogenesis. Several contact sites were identified in the 18S rRNA sequence, which interestingly all cluster in the “foot” region of the small ribosomal subunit. These include a major binding site in the eukaryotic expansion segment ES6, where Rok1 is required for release of the snR30 snoRNA. Rok1 directly contacts snR30 and other snoRNAs required for pre-rRNA processing. Using cross-linking, ligation and sequencing of hybrids (CLASH) we identified several novel pre-rRNA base-pairing sites for the snoRNAs snR30, snR10, U3, and U14, which cluster in the expansion segments of the 18S rRNA. Our data suggest that these snoRNAs bridge interactions between the expansion segments, thereby forming an extensive interaction network that likely promotes pre-rRNA maturation and folding in early pre-ribosomal complexes and establishes long-range rRNA interactions during ribosome synthesis

Loss of aquaporin-4 expression and putative function in non-small cell lung cancer

<p>Abstract</p> <p>Background</p> <p>Aquaporins (AQPs) have been recognized to promote tumor progression, invasion, and metastasis and are therefore recognized as promising targets for novel anti-cancer therapies. Potentially relevant AQPs in distinct cancer entities can be determined by a comprehensive expression analysis of the 13 human AQPs.</p> <p>Methods</p> <p>We analyzed the presence of all AQP transcripts in 576 different normal lung and non-small cell lung cancer (NSCLC) samples using microarray data and validated our findings by qRT-PCR and immunohistochemistry.</p> <p>Results</p> <p>Variable expression of several AQPs (AQP1, -3, -4, and -5) was found in NSCLC and normal lung tissues. Furthermore, we identified remarkable differences between NSCLC subtypes in regard to AQP1, -3 and -4 expression. Higher transcript and protein levels of AQP4 in well-differentiated lung adenocarcinomas suggested an association with a more favourable prognosis. Beyond water transport, data mining of co-expressed genes indicated an involvement of AQP4 in cell-cell signalling, cellular movement and lipid metabolism, and underlined the association of AQP4 to important physiological functions in benign lung tissue.</p> <p>Conclusions</p> <p>Our findings accentuate the need to identify functional differences and redundancies of active AQPs in normal and tumor cells in order to assess their value as promising drug targets.</p

Interleukin-6 receptor blockade in treatment-refractory MOG-IgG–associated disease and neuromyelitis optica spectrum disorders

BACKGROUND AND OBJECTIVES: To evaluate the long-term safety and efficacy of tocilizumab (TCZ), a humanized anti–interleukin-6 receptor antibody in myelin oligodendrocyte glycoprotein–IgG–associated disease (MOGAD) and neuromyelitis optica spectrum disorders (NMOSD). METHODS: Annualized relapse rate (ARR), Expanded Disability Status Scale score, MRI, autoantibody titers, pain, and adverse events were retrospectively evaluated in 57 patients with MOGAD (n = 14), aquaporin-4 (AQP4)-IgG seropositive (n = 36), and seronegative NMOSD (n = 7; 12%), switched to TCZ from previous immunotherapies, particularly rituximab. RESULTS: Patients received TCZ for 23.8 months (median; interquartile range 13.0–51.1 months), with an IV dose of 8.0 mg/kg (median; range 6–12 mg/kg) every 31.6 days (mean; range 26–44 days). For MOGAD, the median ARR decreased from 1.75 (range 0.5–5) to 0 (range 0–0.9; p = 0.0011) under TCZ. A similar effect was seen for AQP4-IgG+ (ARR reduction from 1.5 [range 0–5] to 0 [range 0–4.2]; p < 0.001) and for seronegative NMOSD (from 3.0 [range 1.0–3.0] to 0.2 [range 0–2.0]; p = 0.031). During TCZ, 60% of all patients were relapse free (79% for MOGAD, 56% for AQP4-IgG+, and 43% for seronegative NMOSD). Disability follow-up indicated stabilization. MRI inflammatory activity decreased in MOGAD (p = 0.04; for the brain) and in AQP4-IgG+ NMOSD (p < 0.001; for the spinal cord). Chronic pain was unchanged. Regarding only patients treated with TCZ for at least 12 months (n = 44), ARR reductions were confirmed, including the subgroups of MOGAD (n = 11) and AQP4-IgG+ patients (n = 28). Similarly, in the group of patients treated with TCZ for at least 12 months, 59% of them were relapse free, with 73% for MOGAD, 57% for AQP4-IgG+, and 40% for patients with seronegative NMOSD. No severe or unexpected safety signals were observed. Add-on therapy showed no advantage compared with TCZ monotherapy. DISCUSSION: This study provides Class III evidence that long-term TCZ therapy is safe and reduces relapse probability in MOGAD and AQP4-IgG+ NMOSD

Friction forces position the neural anlage

During embryonic development, mechanical forces are essential for cellular rearrangements driving tissue morphogenesis. Here, we show that in the early zebrafish embryo, friction forces are generated at the interface between anterior axial mesoderm (prechordal plate, ppl) progenitors migrating towards the animal pole and neurectoderm progenitors moving in the opposite direction towards the vegetal pole of the embryo. These friction forces lead to global rearrangement of cells within the neurectoderm and determine the position of the neural anlage. Using a combination of experiments and simulations, we show that this process depends on hydrodynamic coupling between neurectoderm and ppl as a result of E-cadherin-mediated adhesion between those tissues. Our data thus establish the emergence of friction forces at the interface between moving tissues as a critical force-generating process shaping the embryo