Dynamic triggering of creep events in the Salton Trough, Southern California by regional M≥5.4M≥5.4 earthquakes constrained by geodetic observations and numerical simulations

Author Posting. © The Author(s), 2015. This is the author's version of the work. It is posted here by permission of Elsevier for personal use, not for redistribution. The definitive version was published in Earth and Planetary Science Letters 427 (2015): 1-10, doi:10.1016/j.epsl.2015.06.044.Since a regional earthquake in 1951, shallow creep events on strike-slip faults within the Salton Trough, Southern California have been triggered at least 10 times by M ≥ 5.4 earthquakes within 200 km. The high earthquake and creep activity and the long history of digital recording within the Salton Trough region provide a unique opportunity to study the mechanism of creep event triggering by nearby earthquakes. Here, we document the history of fault creep events on the Superstition Hills Fault based on data from creepmeters, InSAR, and field surveys since 1988. We focus on a subset of these creep events that were triggered by significant nearby earthquakes. We model these events by adding realistic static and dynamic perturbations to a theoretical fault model based on rate- and state-dependent friction. We find that the static stress changes from the causal earthquakes are less than 0.1 MPa and too small to instantaneously trigger creep events. In contrast, we can reproduce the characteristics of triggered slip with dynamic perturbations alone. The instantaneous triggering of creep events depends on the peak and the time-integrated amplitudes of the dynamic Coulomb stress change. Based on observations and simulations, the stress change amplitude required to trigger a creep event of 0.01 mm surface slip is about 0.6 MPa. This threshold is at least an order of magnitude larger than the reported triggering threshold of non-volcanic tremors (2-60 KPa) and earthquakes in geothermal fields (5 KPa) and near shale gas production sites (0.2-0.4 kPa), which may result from differences in effective normal stress, fault friction, the density of nucleation sites in these systems, or triggering mechanisms. We conclude that shallow frictional heterogeneity can explain both the spontaneous and dynamically triggered creep events on the Superstition Hills Fault.This work was supported by NSF EAR awards 1246966 and 1411704 (M. Wei) and a Canada NSERC Discovery grant (Y. Liu)

Pre-treatment Resting-State Functional MR Imaging Predicts the Long-Term Clinical Outcome After Short-Term Paroxtine Treatment in Post-traumatic Stress Disorder

Background: The chronic phase of post-traumatic stress disorder (PTSD) and the limited effectiveness of existing treatments creates the need for the development of potential biomarkers to predict response to antidepressant medication at an early stage. However, findings at present focus on acute therapeutic effect without following-up the long-term clinical outcome of PTSD. So far, studies predicting the long-term clinical outcome of short-term treatment based on both pre-treatment and post-treatment functional MRI in PTSD remains limited.Methods: Twenty-two PTSD patients were scanned using resting-state functional MRI (rs-fMRI) before and after 12 weeks of treatment with paroxetine. Twenty patients were followed up using the same psychopathological assessments 2 years after they underwent the second MRI scan. Based on clinical outcome, the follow-up patients were divided into those with remitted PTSD or persistent PTSD. Amplitude of low-frequency fluctuations (ALFF) and degree centrality (DC) derived from pre-treatment and post-treatment rs-fMRI were used as classification features in a support vector machine (SVM) classifier.Results: Prediction of long-term clinical outcome by combined ALFF and DC features derived from pre-treatment rs-fMRI yielded an accuracy rate of 72.5% (p < 0.005). The most informative voxels for outcome prediction were mainly located in the precuneus, superior temporal area, insula, dorsal medial prefrontal cortex, frontal orbital cortex, supplementary motor area, lingual gyrus, and cerebellum. Long-term outcome could not be successfully classified by post-treatment imaging features with accuracy rates <50%.Conclusions: Combined information from ALFF and DC from rs-fMRI data before treatment could predict the long-term clinical outcome of PTSD, which is critical for defining potential biomarkers to customize PTSD treatment and improve the prognosis

Ameliorative patterns of grey matter in patients with first-episode and treatment-naïve schizophrenia

Background Grey matter (GM) reduction is a consistent observation in established late stages of schizophrenia, but patients in the untreated early stages of illness display an increase as well as a decrease in GM distribution relative to healthy controls (HC). The relative excess of GM may indicate putative compensatory responses, though to date its relevance is unclear. Methods 343 first-episode treatment-naïve patients with schizophrenia (FES) and 342 HC were recruited. Multivariate source-based morphometry was performed to identify covarying \u27networks\u27 of grey matter concentration (GMC). Neurocognitive scores using the Cambridge Neuropsychological Test Automated Battery (CANTAB) and symptom burden using the Positive and Negative Symptoms Scale (PANSS) were obtained. Bivariate linear relationships between GMC and cognition/symptoms were studied. Results Compared to healthy subjects, FES had prominently lower GMC in two components; the first consists of the anterior insula, inferior frontal gyrus, anterior cingulate and the second component with the superior temporal gyrus, precuneus, inferior/superior parietal lobule, cuneus, and lingual gyrus. Higher GMC was seen in adjacent areas of the middle and superior temporal gyrus, middle frontal gyrus, inferior parietal cortex and putamen. Greater GMC of this component was associated with lower duration of untreated psychosis, less severe positive symptoms and better performance on cognitive tests. Conclusions In untreated stages of schizophrenia, both a distributed lower and higher GMC is observable. While the higher GMC is relatively modest, it occurs across frontoparietal, temporal and subcortical regions in association with reduced illness burden suggesting a compensatory role for higher GMC in the early stages of schizophrenia

Efficient current-induced spin torques and field-free magnetization switching in a room-temperature van der Waals magnet

The discovery of magnetism in van der Waals (vdW) materials has established unique building blocks for the research of emergent spintronic phenomena. In particular, owing to their intrinsically clean surface without dangling bonds, the vdW magnets hold the potential to construct a superior interface that allows for efficient electrical manipulation of magnetism. Despite several attempts in this direction, it usually requires a cryogenic condition and the assistance of external magnetic fields, which is detrimental to the real application. Here, we fabricate heterostructures based on Fe3GaTe2 flakes that possess room-temperature ferromagnetism with excellent perpendicular magnetic anisotropy. The current-driven non-reciprocal modulation of coercive fields reveals a high spin-torque efficiency in the Fe3GaTe2/Pt heterostructures, which further leads to a full magnetization switching by current. Moreover, we demonstrate the field-free magnetization switching resulting from out-of-plane polarized spin currents by asymmetric geometry design. Our work could expedite the development of efficient vdW spintronic logic, memory and neuromorphic computing devices

Mapping current trends and hotspots in myasthenia gravis from 2003 to 2022: a bibliometric analysis

IntroductionResearch on myasthenia gravis (MG) has undergone rapid development in recent years. This article aimed to elucidate the characteristics of MG publications over the past 20 years and analyze emerging trends using bibliometric methods.MethodsInformation on MG articles was obtained from the Web of Science Core Collection and stored in Excel for quantitative analyses. Bibliometric analyses were performed using CiteSpace and VOSviewer to visualize publications according to countries/regions, institutions, journals, and authors.ResultsA total of 3,610 publications were included in the analysis. The USA had the highest number of publications (NP) and H-index. Among the institutions, the University of Oxford had the highest NP, followed by the University of Toronto and Duke University. Close cooperation was observed among countries and institutions. The most productive author was Renato Mantegazza, followed by Jan J. Verschuuren, and Amelia Evoli. Muscle & Nerve published the most articles on MG, followed by the Journal of Neuroimmunology and Neuromuscular Disorders. The keyword with the highest strength is “neuromuscular transmission,” followed by “safety” and “rituximab.” Co-citation analysis includes 103 publications cited at least 65 times, categorized into four clusters. Additionally, 123 keywords cited more than 40 times were analyzed and divided into five clusters.ConclusionThis bibliometric analysis shows the framework of research over the past 20 years by mapping the scholarly contributions of various countries or regions, institutions, journals, and authors in MG. The analysis also explores future trends and prospective directions, emphasizing individualized treatment based on subtypes, novel immunotherapeutic approaches, and thymectomy

C1q complement/tumor necrosis factor-associated proteins in cardiovascular disease and covid-19

With continually improving treatment strategies and patient care, the overall mortality of cardiovascular disease (CVD) has been significantly reduced. However, this success is a double-edged sword, as many patients who survive cardiovascular complications will progress towards a chronic disorder over time. A family of adiponectin paralogs designated as C1q complement/tumor necrosis factor (TNF)-associated proteins (CTRPs) has been found to play a role in the development of CVD. CTRPs, which are comprised of 15 members, CTRP1 to CTRP15, are secreted from different organs/tissues and exhibit diverse functions, have attracted increasing attention because of their roles in maintaining inner homeostasis by regulating metabolism, inflammation, and immune surveillance. In particular, studies indicate that CTRPs participate in the progression of CVD, influencing its prognosis. This review aims to improve understanding of the role of CTRPs in the cardiovascular system by analyzing current knowledge. In particular, we examine the association of CTRPs with endothelial cell dysfunction, inflammation, and diabetes, which are the basis for development of CVD. Additionally, the recently emerged novel coronavirus (COVID-19), officially known as severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), has been found to trigger severe cardiovascular injury in some patients, and evidence indicates that the mortality of COVID-19 is much higher in patients with CVD than without CVD. Understanding the relationship of CTRPs and the SARS-CoV-2-related damage to the cardiovascular system, as well as the potential mechanisms, will achieve a profound insight into a therapeutic strategy to effectively control CVD and reduce the mortality rate

Community Code Verification Exercise for Simulating Sequences of Earthquakes and Aseismic Slip (SEAS)

Numerical simulations of sequences of earthquakes and aseismic slip (SEAS) have made great progress over past decades to address important questions in earthquake physics. However, significant challenges in SEAS modeling remain in resolving multiscale interactions between earthquake nucleation, dynamic rupture, and aseismic slip, and understanding physical factors controlling observables such as seismicity and ground deformation. The increasing complexity of SEAS modeling calls for extensive efforts to verify codes and advance these simulations with rigor, reproducibility, and broadened impact. In 2018, we initiated a community code‐verification exercise for SEAS simulations, supported by the Southern California Earthquake Center. Here, we report the findings from our first two benchmark problems (BP1 and BP2), designed to verify different computational methods in solving a mathematically well‐defined, basic faulting problem. We consider a 2D antiplane problem, with a 1D planar vertical strike‐slip fault obeying rate‐and‐state friction, embedded in a 2D homogeneous, linear elastic half‐space. Sequences of quasi‐dynamic earthquakes with periodic occurrences (BP1) or bimodal sizes (BP2) and their interactions with aseismic slip are simulated. The comparison of results from 11 groups using different numerical methods show excellent agreements in long‐term and coseismic fault behavior. In BP1, we found that truncated domain boundaries influence interseismic stressing, earthquake recurrence, and coseismic rupture, and that model agreement is only achieved with sufficiently large domain sizes. In BP2, we found that complexity of fault behavior depends on how well physical length scales related to spontaneous nucleation and rupture propagation are resolved. Poor numerical resolution can result in artificial complexity, impacting simulation results that are of potential interest for characterizing seismic hazard such as earthquake size distributions, moment release, and recurrence times. These results inform the development of more advanced SEAS models, contributing to our further understanding of earthquake system dynamics

MicroRNA100 Inhibits Self-Renewal of Breast Cancer Stem–like Cells and Breast Tumor Development

miRNAs are essential for self-renewal and differentiation of normal and malignant stem cells by regulating the expression of key stem cell regulatory genes. Here, we report evidence implicating the miR100 in self-renewal of cancer stem-like cells (CSC). We found that miR100 expression levels relate to the cellular differentiation state, with lowest expression in cells displaying stem cell markers. Utilizing a tetracycline-inducible lentivirus to elevate expression of miR100 in human cells, we found that increasing miR100 levels decreased the production of breast CSCs. This effect was correlated with an inhibition of cancer cell proliferation in vitro and in mouse tumor xenografts due to attenuated expression of the CSC regulatory genes SMARCA5, SMARCD1, and BMPR2. Furthermore, miR100 induction in breast CSCs immediately upon their orthotopic implantation or intracardiac injection completely blocked tumor growth and metastasis formation. Clinically, we observed a significant association between miR100 expression in breast cancer specimens and patient survival. Our results suggest that miR100 is required to direct CSC self-renewal and differentiation

C1q/TNF-Related Protein 3 Prevents Diabetic Retinopathy via AMPK-Dependent Stabilization of Blood–Retinal Barrier Tight Junctions

Background The impairment of the inner blood–retinal barrier (iBRB) increases the pathological development of diabetic retinopathy (DR), a severe complication in diabetic patients. Identifying approaches to preserving iBRB integrity and function is a significant challenge in DR. C1q/tumor necrosis factor-related protein-3 (CTRP3) is a newly discovered adipokine and a vital biomarker, predicting DR severity. We sought to determine whether and how CTRP3 affects the pathological development of non-proliferative diabetic retinopathy (NPDR). Methods To clarify the pathophysiologic progress of the blood–retinal barrier in NPDR and explore its potential mechanism, a mouse Type 2 diabetic model of diabetic retinopathy was used. The capillary leakage was assessed by confocal microscope with fluorescent-labeled protein in vivo. Furthermore, the effect of CTRP3 on the inner blood–retinal barrier (iBRB) and its molecular mechanism was clarified. Results The results demonstrated that CTRP3 protects iBRB integrity and resists the vascular permeability induced by DR. Mechanistically, the administration of CTRP3 activates the AMPK signaling pathway and enhances the expression of Occludin and Claudin-5 (tight junction protein) in vivo and in vitro. Meanwhile, CTRP3 improves the injury of human retinal endothelial cells (HRMECs) induced by high glucose/high lipids (HG/HL), and its protective effects are AMPK-dependent. Conclusions In summary, we report, for the first time, that CTRP3 prevents diabetes-induced retinal vascular permeability via stabilizing the tight junctions of the iBRB and through the AMPK-dependent Occludin/Claudin-5 signaling pathway, thus critically affecting the development of NPDR

Nicotine aggravates vascular adiponectin resistance via ubiquitin-mediated adiponectin receptor degradation in diabetic Apolipoprotein E knockout mouse

There is limited and discordant evidence on the role of nicotine in diabetic vascular disease. Exacerbated endothelial cell dysregulation in smokers with diabetes is associated with the disrupted adipose function. Adipokines possess vascular protective, anti-inflammatory, and anti-diabetic properties. However, whether and how nicotine primes and aggravates diabetic vascular disorders remain uncertain. In this study, we evaluated the alteration of adiponectin (APN) level in high-fat diet (HFD) mice with nicotine (NIC) administration. The vascular pathophysiological response was evaluated with vascular ring assay. Confocal and co-immunoprecipitation analysis were applied to identify the signal interaction and transduction. These results indicated that the circulating APN level in nicotine-administrated diabetic Apolipoprotein E-deficient (ApoE−/−) mice was elevated in advance of 2 weeks of diabetic ApoE−/− mice. NIC and NIC addition in HFD groups (NIC + HFD) reduced the vascular relaxation and signaling response to APN at 6 weeks. Mechanistically, APN receptor 1 (AdipoR1) level was decreased in NIC and further significantly reduced in NIC + HFD group at 6 weeks, while elevated suppressor of cytokine signaling 3 (SOCS3) expression was induced by NIC and further augmented in NIC + HFD group. Additionally, nicotine provoked SOCS3, degraded AdipoR1, and attenuated APN-activated ERK1/2 in the presence of high glucose and high lipid (HG/HL) in human umbilical vein endothelial cells (HUVECs). MG132 (proteasome inhibitor) administration manifested that AdipoR1 was ubiquitinated, while inhibited SOCS3 rescued the reduced AdipoR1. In summary, this study demonstrated for the first time that nicotine primed vascular APN resistance via SOCS3-mediated degradation of ubiquitinated AdipoR1, accelerating diabetic endothelial dysfunction. This discovery provides a potential therapeutic target for preventing nicotine-accelerated diabetic vascular dysfunction