On the evolution of elastic properties during laboratory stick-slip experiments spanning the transition from slow slip to dynamic rupture

The physical mechanisms governing slow earthquakes remain unknown, as does the relationship between slow and regular earthquakes. To investigate the mechanism(s) of slow earthquakes and related quasi-dynamic modes of fault slip we performed laboratory experiments on simulated fault gouge in the double direct shear configuration. We reproduced the full spectrum of slip behavior, from slow to fast stick slip, by altering the elastic stiffness of the loading apparatus (k) to match the critical rheologic stiffness of fault gouge (kc). Our experiments show an evolution from stable sliding, when k>kc, to quasi-dynamic transients when k ~ kc, to dynamic instabilities when k<kc. To evaluate the microphysical processes of fault weakening we monitored variations of elastic properties. We find systematic changes in P wave velocity (Vp) for laboratory seismic cycles. During the coseismic stress drop, seismic velocity drops abruptly, consistent with observations on natural faults. In the preparatory phase preceding failure, we find that accelerated fault creep causes a Vp reduction for the complete spectrum of slip behaviors. Our results suggest that the mechanics of slow and fast ruptures share key features and that they can occur on same faults, depending on frictional properties. In agreement with seismic surveys on tectonic faults our data show that their state of stress can be monitored by Vp changes during the seismic cycle. The observed reduction in Vp during the earthquake preparatory phase suggests that if similar mechanisms are confirmed in nature high-resolution monitoring of fault zone properties may be a promising avenue for reliable detection of earthquake precursors

The role of fault rock fabric in the dynamics of laboratory faults

Fault stability is inherently linked to the frictional and healing properties of fault rocks and associated fabrics. Their complex interaction controls how the stored elastic energy is dissipated, that is, through creep or seismic motion. In this work, we focus on the relevance of fault fabrics in controlling the reactivation and slip behavior of dolomite-anhydrite analog faults. We designed a set of laboratory experiments where we first develop fault rocks characterized by different grain size reduction and localization at normal stresses of σN = 15, 35, 60, and 100 MPa and second, we reload and reactivate these fault rocks at the frictional stability transition, achieved at σN = 35 MPa by reducing the machine stiffness. If normal stress is lowered this way, reactivation occurs with relatively large stress drops and large peak-slip velocities. Subsequent unstable behavior produces slow stick-slip events with low stress drop and with either asymmetric or Gaussian slip velocity function depending on the inherited fault fabric. If normal stress is raised, deformation is accommodated within angular cataclasites promoting stable slip. The integration of microstructural data (showing brittle reworking of preexisting textures) with mechanical data (documenting restrengthening and dilation upon reactivation) suggests that frictional and chemically assisted healing, which is common in natural faults during the interseismic phase, can be a relevant process in developing large instabilities. We also conclude that fault rock heterogeneity (fault fabric) modulates the slip velocity function and thus the dynamics of repeating stick-slip cycles

Modeling the dynamic rupture propagation on heterogeneous faults with rate- and state-dependent friction

We investigate the effects of non-uniform distribution of constitutive parameters on the dynamic propagation of an earthquake rupture. We use a 2D finite difference numerical method and we assume that the dynamic rupture propagation is governed by a rate- and state-dependent constitutive law. We first discuss the results of several numerical experiments performed with different values of the constitutive parameters a (to account for the direct effect of friction), b (controlling the friction evolution) and L (the characteristic length-scale parameter) to simulate the dynamic rupture propagation on homogeneous faults. Spontaneous dynamic ruptures can be simulated on velocity weakening (a < b) fault patches: our results point out the dependence of the traction and slip velocity evolution on the adopted constitutive parameters. We therefore model the dynamic rupture propagation on heterogeneous faults. We use in this study the characterization of different frictional regimes proposed by Boatwright and Cocco (1996) based on different values of the constitutive parameters a, b and L. Our numerical simulations show that the heterogeneities of the L parameter affect the dynamic rupture propagation, control the peak slip velocity and weakly modify the dynamic stress drop and the rupture velocity. Moreover, a barrier can be simulated through a large contrast of L parameter. The heterogeneity of a and b parameters affects the dynamic rupture propagation in a more complex way. A velocity strengthening area (a > b) can arrest a dynamic rupture, but can be driven to an instability if suddenly loaded by the dynamic rupture front. Our simulations provide a picture of the complex interactions between fault patches having different frictional properties and illustrate how the traction and slip velocity evolutions are modified during the propagation on heterogeneous faults. These results involve interesting implications for slip duration and fracture energy

Increase in newly diagnosed type 1 diabetes and serological evidence of recent SARS-CoV-2 infection: Is there a connection?

Several studies have investigated the correlation between the COVID-19 pandemic and the onset of type 1 diabetes (T1D) in children, reporting an increased incidence of T1D and severe diabetic ketoacidosis (DKA). This study aimed to investigate the infection by SARS-CoV-2 in children with newly-diagnosed T1D to explore a possible link between SARS-CoV-2 infection, T1D and DKA. Thirty-nine children with a T1D new onset between October 15, 2020, and April 15, 2021, were enrolled. SARS-CoV-2 infection was investigated through a polymerase chain reaction on the nasal swab, dosage of specific antibodies, and an anamnestic question form. Nine (23%) of them had antibodies directed toward SARS-CoV-2, and five (12%) had a history of recent SARS-CoV-2 infection in themselves or in their family. No molecular swabs were positive. Compared to the general pediatric population, the overall incidence of COVID-19 was 5.6 times higher in the T1D patients' group (p < 0.00001). Referring only to the cases in the metropolitan area, we find a net increase in the incidence of T1D compared to the 5 years preceding our study, by 50% compared to the same months in 2016/2017 and 2017/2018, by 69% compared to 2018/2019 and by 77% compared to 2019/2020. The same trend was observed regarding DKA cases. The attributable risk of the pandemic cohort compared to the previous year is 44%. The abnormal disproportion of SARS-CoV-2 infection between children with T1D and the pediatric reference population, with a ratio of 5.6, appears to support the causative role of SARS-CoV-2 in triggering the immune response underlying diabetes, as often described for other viral infections. The difficulty accessing care services during the pandemic, with a consequent diagnosis delay, does not justify the increase in observed T1D cases, which could to be directly linked to the pandemic. The acceleration of the immune process provoked by SARS-CoV-2 may play a suggestive role in the development of T1D with DKA. Multicenter studies are needed to deepen and fully understand the pathophysiological link between SARS-CoV-2 and the onset of T1D in children

Anadara kagoshimensis (Mollusca: Bivalvia: Arcidae) in Adriatic Sea: morphological analysis, molecular taxonomy, spatial distribution, and prediction

Morphological analysis, molecular characterization, and information on distribution and density of Anadara kagoshimensis (Tokunaga, 1906) specimens collected in the Adriatic Sea were here carried out as based on various material and data from five surveys conducted from 2010 to 2014, for a total of 329 bottom trawl hauls. The morphological and molecular analyses allowed to clarify the confused taxonomy regarding the biggest ark clam alien species invading the Italian waters and the Mediterranean Sea. The analysis on distribution and density revealed that A. kagoshimensis mostly occurs along the Italian coast at depths from 8 to 50 m, with a catch frequency of more than 98% in all hauls performed on silty-clay sediment at 8-30 m depth. The hotspot map clearly shows a reduction of its distribution area from 2010 to 2012

HCV cirrhotic patients treated with direct acting antivirals: detection of tubular dysfunction and resolution after viral clearance

Background/aims: Hepatitis C virus (HCV) has been identified in tubular epithelial cells of infected patients, however the presence of tubular dysfunction, which is a risk factor for chronic kidney disease, has never been examined in vivo. The present prospective longitudinal study aimed to estimate the prevalence of tubular dysfunction alone or with glomerular damage and its evolution after HCV clearance in cirrhotic patients. Methods: One-hundred-thirty-five consecutive Child-Pugh-A cirrhotic patients were evaluated before antiviral treatment and six months after the end of therapy. Tubular dysfunction was evaluated by urinary-alpha1-microglobulin-to-creatinine-ratio (α1-MCR), glomerular damage was assessed by urinary-albumin-to-creatinine-ratio (ACR). Results: Almost all the patients (93.3%) showed a normal or mildly decreased e-GFR (KDIGO-G1/G2-categories). Tubular dysfunction was found in 23.7% (32/135) of patients, co-occurring with glomerular damage in 37.5% (12/32) of cases, while glomerular damage was found in 16.3% (22/135) of patients. In multiple logistic regression, glomerular damage and the concomitant presence of diabetes and hypertension were the only predictors significantly associated with tubular dysfunction. After HCV-clearance, patients experienced a significant reduction of α1-MCR levels (21.0 vs 10.5 μg/mg, p=0.009) and tubular dysfunction resolved in 57.1% of subjects. Conclusions: Tubular dysfunction is an unrecognized feature of HCV-related kidney disease in cirrhotic patients and its presence should be primarily investigated in subjects with glomerular damage, diabetes and hypertension, despite normal e-GFR. Tubular dysfunction resolves in the majority of cases after HCV clearance, however, it may persist after antiviral treatment and further studies should evaluate its long term impact on kidney function

PAK6 phosphorylates 14-3-3γ to regulate steady state phosphorylation of LRRK2

Mutations in Leucine-rich repeat kinase 2 (LRRK2) are associated with Parkinson's disease (PD) and, as such, LRRK2 is considered a promising therapeutic target for age-related neurodegeneration. Although the cellular functions of LRRK2 in health and disease are incompletely understood, robust evidence indicates that PD-associated mutations alter LRRK2 kinase and GTPase activities with consequent deregulation of the downstream signaling pathways. We have previously demonstrated that one LRRK2 binding partner is P21 (RAC1) Activated Kinase 6 (PAK6). Here, we interrogate the PAK6 interactome and find that PAK6 binds a subset of 14-3-3 proteins in a kinase dependent manner. Furthermore, PAK6 efficiently phosphorylates 14-3-3γ at Ser59 and this phosphorylation serves as a switch to dissociate the chaperone from client proteins including LRRK2, a well-established 14-3-3 binding partner. We found that 14-3-3γ phosphorylated by PAK6 is no longer competent to bind LRRK2 at phospho-Ser935, causing LRRK2 dephosphorylation. To address whether these interactions are relevant in a neuronal context, we demonstrate that a constitutively active form of PAK6 rescues the G2019S LRRK2-associated neurite shortening through phosphorylation of 14-3-3γ. Our results identify PAK6 as the kinase for 14-3-3γ and reveal a novel regulatory mechanism of 14-3-3/LRRK2 complex in the brain

THE MECHANICS OF SEISMIC SOURCE: DYNAMICALLY CONSISTENT MODELS OF EARTHQUAKE RUPTURE

In the first chapter we review the theoretical modeling of a dynamic rupture propagation governed by friction processes. We introduce two of the most commonly used constitutive laws in the literature: slip weakening law and rate and state law. We present the analytical expressions of these frictions laws and we discuss the different competing physical mechanisms which contribute to dynamic fault weakening during earthquakes. In particular, we describe the dynamic traction and the slip velocity evolution within the cohesive zone during a 2-D inplane dynamic rupture using rate and state dependent constitutive laws. In the second chapter we show how the rate and state constitutive laws allow a quantitative description of the dynamic rupture growth. These modeling results help understanding the physical interpretation of the breakdown process and the weakening mechanisms. We compare the time histories of slip velocity, state variable and total dynamic traction to investigate the temporal evolution of slip acceleration and stress drop during the breakdown time. Because the adopted analytical expression for the state variable evolution controls the slip velocity time histories, we test different evolution laws to investigate slip duration and the healing mechanisms. We will discuss how the direct effect of friction and the friction behavior at high slip rates affect the weakening and healing mechanisms. In the third chapter we investigate the effects of non-uniform distribution of constitutive parameters of rate and state laws on the 2D dynamic rupture propagations. We use the characterization of different frictional regimes proposed by Boatwright and Cocco (1996), which is based on different values of the constitutive parameters a, b and L (these are the parameters defining rate and state constitutive laws). The results involve interesting implications for slip duration and fracture energy. In the fourth chapter we check the possibility to constrain and to estimate the critical slip weakening distance from slip velocity functions, following a recent idea of Mikumo et al.(2003). Because of the poor knowledge of the scaling relation between dynamic parameters inferred from laboratory experiments and from real faults, it is still open to debate the actual dimensions of physical parameters characterizing the seismic source. Particularly, the range of real Dc values is still unknown. We model the dynamic propagation of a 2-D in-plane crack obeying to either slip weakening (SW) or rate- and state-dependent friction laws (R&S). Therefore we compare the value of slip weakening distance (Dc), adopted or estimated from the traction versus slip curves, with the critical slip distance measured as the slip at the time of peak slip velocity (D' c). In the fifth chapter we compute the temporal evolution of traction by solving the elasto-dynamic equation and by using the slip velocity history as aboundary condition on the fault plane. We employ a 3D finite difference algorithm. In this chapter we do not consider a fully dynamic model because we do not assume any constitutive law, but we infer the dynamic parameters and the traction evolution from kinematic models. We use different source time functions to derive a suite of kinematic source models to image the spatial distribution of dynamic and breakdown stress drop, strength excess and critical slip weakening distance (Dc). Therefore we compare the inferred dynamic parameters trying to answer the following questions: Can we constrain the actual values of fundamental dynamic parameters from kinematic models? If the kinematic slip velocity histories affect the inferred dynamic parameters, is it still possible to constrain the dynamic source parameters of real earthquakes? We suggest that source time functions compatible with earthquake dynamics have to be used to infer the traction time history. For this reason, we propose a new source time function to be used in kinematic modelling of ground motion time histories, which is consistent with dynamic propagation of earthquake ruptures and makes feasible the dynamic interpretation of kinematic slip models. This function is derived from a source time function first proposed by Yoffe (1951), which yields a traction evolution showing a slip-weakening behavior. In order to remove its singularity we apply a convolution with a triangular function and obtain a regularized source time function called “regularized Yoffe'' function. Using this analytical function we examine the relation between kinematic parameters, such as peak slip velocities and slip duration, and dynamic parameters, such as slip weakening distance and breakdown stress drop. In the sixth chapter we estimate fracture energy on extended faults for several recent earthquakes (having moment magnitudes between 5.6 and 7.2) by retrieving dynamic traction evolution at each point on the fault plane from slip history imaged by inverting ground motion waveforms. We define the breakdown work (Wb) as the excess of work over some minimum traction level achieved during slip. Wb is equivalent to "seismological" fracture energy (G) in previous investigations. We employ a 3-D finite difference algorithm to compute the dynamic traction evolution in the time domain during the earthquake rupture. We estimate Wb by calculating the scalar product between dynamic traction and slip velocity vectors. Finally we compare our inferred values with geologic surface energies.Istituto Nazionale di Geofisica e VulcanologiaUnpublished3.1. Fisica dei terremotiope

The first month of the 2016 central Italy seismic sequence: fast determination of time domain moment tensors and finite fault model analysis of the ML 5.4 aftershock

We present the revised Time Domain Moment Tensor (TDMT) catalogue for earthquakes with M_L larger than 3.6 of the first month of the ongoing Amatrice seismic sequence (August 24th - September 25th). Most of the retrieved focal mechanisms show NNW–SSE striking normal faults in agreement with the main NE-SW extensional deformation of Central Apennines. We also report a preliminary finite fault model analysis performed on the larger aftershock of this period of the sequence (M_w 5.4) and discuss the obtained results in the framework of aftershocks distribution