Regional noise source location based on the time delays between station pairs from ambient noise interferometry.

Identifying the location of a potential noise source assists in understanding the characteristics of the seismic or volcanic activity and provides valuable information for hazard assessment. Unlike the conventional waveform-based techniques that rebuild the source energy into the possible source region, we apply a simplified method to determine the absolute location of the noise source based on the station-pair time-delays from ambient noise interferometry. Synthetic tests demonstrate the robustness of the method and the locating precision is mainly influenced by the signal-to-noise ratio of the synthetic waveforms, and the higher frequency bandwidth source signals are more likely to result in accurate detection of the source. An application at the Central Tien Shan indicates that our method is capable of locating the known virtual source from the empirical Green's functions. Furthermore, assuming a surface wave velocity, the depth of the source can be generally recovered from ambient noise interferometry in a simplified 3-D homogeneous model. The new method sheds light on applications of ambient noise interferometry for locating potential sources, making it suitable for detecting time-dependent behavior.

Seismic structure of the 2015 Mw7.8 Gorkha earthquake revealed by ambient seismic noise and teleseismic surface wave tomography.

The destructive 2015 Mw7.8 Gorkha earthquake occurred in the Main Himalayan Thrust due to the collision of the Indian and Asian plates, which provides a unique opportunity to understand the deep dynamic processes and seismogenic mechanisms of strong earthquakes. We construct a regional-scale shear-wave velocity model of the crust and uppermost mantle using ambient seismic noise and teleseismic surface wave at periods of 5-100 s around the Gorkha earthquake region. The new shear-wave velocity model exhibits prominently lateral heterogeneities in the Gorkha earthquake areas. We observe a high-velocity (high-V) zone around the Gorkha main shock in the Main Himalayan Thrust, indicating the existence of a high-strength asperity that sustains the stress accumulating. The aftershocks are primarily located in the low-velocity (low-V) anomalies and enclosed by two high-V anomalies, which appear to act as structural barriers that influence the spread of the aftershocks. Prominent low-Vanomalies from the lower crust to the mantle lithosphere are observed along the north-south trending rifts, suggesting the hot materials upwelling due to the tearing of the northward subducting Indian lithosphere. These observations may indicate that seismic velocity heterogeneity could play an essential role in earthquake initiation and the rupture process.

Fault-scale crustal structure across the Dunhua-Mishan fault (Tanlu northern segment) constrained from teleseismic P-wave receiver functions.

The Dunhua-Mishan fault, located in the northern segment of the Tanlu fault zone, experienced multiple tectonic processes associated with the effects of the Pacific Plate subduction and the Indo-Asia collision. The high-resolution fault-scale structure is critical for understanding the fault evolution and potential fault damage. However, the well-defined deep structure of the Dunhua-Mishan fault is still unclear due to the lack of the dense seismic array. In this study, we construct a high-resolution P-wave receiver function imaging based on linear dense seismic array across the fault. Our results reveal the strong Moho depth variation across the Dunhua-Mishan fault zone. The slightly higher Vp/Vs ratio values within the fault zone indicate the presence of a small amount of mafic crust composition. Interestingly, the significant double positive Ps converted phases are observed within the fault zone, which may represent double Moho discontinuities. The double Moho structure may be related to multiple significant tectonic activities in the Tanlu northern segment. These newly observed structures provide new seismic constraints on the formation and evolution of the Tanlu fault zone and probably reflect that the lithospheric structure of the Dunhua-Mishan fault has been modified by a series of tectonic processes.

Integrated analysis of single-cell and bulk RNA sequencing data identifies the characteristics of ferroptosis in lumbar disc herniation.

Lumbar disc herniation (LDH) is the most common condition associated with low back pain, and it adversely impacts individuals' health. Ferroptosis has recently emerged as a novel factor in the pathogenesis of LDH; however, the specific impacts of ferroptosis on LDH have not been fully elucidated. Ferroptosis-related differentially expressed genes (FRDEGs) were identified from the transcriptomic datasets of LDH. Gene set enrichment analysis (GSEA) was conducted to identify biological mechanism and related pathways. LASSO and SVM-RFE algorithms were applied to detect signature genes. Function of the signature gene was confirmed by RT-qPCR. The CIBERSORT algorithm was used to compare immune infiltration between LDH and normal samples. Correlation analysis between MYB and immune cells was analyzed using the Pearson method. Additionally, we used scRNA-seq to dissect cell clusters and cellular interactions. AUCell scoring was used to analyze the ferroptosis scores of different cell types. We found that MYB, a highly expressed ferroptosis-related gene, was associated with LDH By leveraging bioinformatics analysis. In immune infiltration analysis, the abundance of monocytes and macrophages varied significantly between the LDH group and disc spondylolisthesis (DS) group. MYB was correlated with most immune cells. GSEA revealed MYB was significantly enriched in immune-related pathways. Furthermore, scRNA-seq analysis revealed the presence of eight distinct cell types. AUCell analysis showed that macrophages had a high ferroptosis score. Cell trajectory analysis revealed that chondrocyte 1 was at the beginning of the trajectory, while calcification inhibiting chondrocytes and fibrochondrocytes accumulated along the middle and tail end of the trajectory, respectively. Cell-cell communication analysis identified chondrocyte 1 had an extensive communication network with other clusters and interacted with nucleus pulposus through collagen signaling pathway. Our analysis demonstrated that MYB may be a potential therapeutic target for LDH. This study provides a resource for the orthopedics community that will facilitate additional discoveries directedly toward understanding the pathogenesis process of LDH.

CNPase, a 2',3'-Cyclic-nucleotide 3'-phosphodiesterase, as a Therapeutic Target to Attenuate Cardiac Hypertrophy by Enhancing Mitochondrial Energy Production.

Heart failure is the end-stage of all cardiovascular diseases with a ~25% 5-year survival rate, and insufficient mitochondrial energy production to meet myocardial demand is the hallmark of heart failure. Mitochondrial components involved in the regulation of ATP production remain to be fully elucidated. Recently, roles of 2',3'-cyclic nucleotide-3'-phosphodiesterase (CNPase) in the pathophysiological processes of heart diseases have emerged, implicated by evidence that mitochondrial CNPase proteins are associated with mitochondrial integrity under metabolic stress. In this study, a zebrafish heart failure model was established, by employing antisense morpholino oligonucleotides and the CRISPR-Cas9 gene-editing system, which recapitulates heart failure phenotypes including heart dysfunction, pericardial edema, ventricular enlargement, bradycardia, and premature death. The translational implications of CNPase in the pathophysiological process of heart failure were tested in a pressure overload-induced heart hypertrophy model, which was carried out in rats through transverse abdominal aorta constriction (TAAC). AAV9-mediated myocardial delivery of CNPase mitigated the hypertrophic response through the specific hydrolysis of 2'-3'-cyclic nucleotides, supported by the decrease of cardiac hypertrophy and fibrosis, the integrity of mitochondrial ultrastructure, and indicators of heart contractility in the AAV9-TAAC group. Finally, the biometrics of a mitochondrial respiration assay carried out on a Seahorse cellular energy analyzer demonstrated that CNPase protects mitochondrial respiration and ATP production from AngII-induced metabolic stress. In summary, this study provides mechanistic insights into CNPase-2',3'-cyclic nucleotide metabolism that protects the heart from energy starvation and suggests novel therapeutic approaches to treat heart failure by targeting CNPase activity.

Therapeutic evaluation and metabolic reprograming of isosteviol sodium in a rat model of ischemic cardiomyopathy.

Ischemia heart disease, one of the lethal cardiovascular diseases, irreversibly impairs cardiac function and is recognized as the primary risk factor for mortality in industrialized countries. The myocardial ischemia treatment still faces a considerable degree of increasing unmet needs. Isosteviol sodium (STVNa) and its derivatives have been proven to effectively alleviate metabolic diseases, hypertension, and heart hypertrophy. Little is known about how STVNa confers the cardioprotective effect during acute myocardial ischemia (AMI). In the present study, a rat model of acute ST-segment-elevation myocardial ischemia by left anterior descending (LAD) ligation was established. Compared to the AMI model group, STVNa administration (4 mg/kg, twice a day) well preserved left ventricle function by ejection fraction (45.10 ± 10.39 vs. 73.64 ± 13.15, p = 0.0013) and fractional shortening (22.94 ± 6.28 vs. 44.00 ± 11.05, p = 0.0017). Further analysis shows that high-dose STVNa (4 mg/kg) significantly improved the hemodynamics in AMI rats, with LVSP (88.25 ± 12.78 vs 99.75 ± 5.10, p = 0.018), max dP/dt (2978.45 ± 832.46 vs 4048.56 ± 827.23, p = 0.096), LVEDP (19.88 ± 2.00 vs 22.26 ± 3.21, p = 0.04) and left ventricular relaxation time constant (Tau) (0.030 ± 0.006 vs 0.021 ± 0.004, p = 0.021). Mechanically, STVNa administration retained the myocardial levels of phosphorylated AMPK, and CPT1b. Moreover, STVNa significantly increased the total energy expenditure, and reduced fatty acid accumulation through mitochondrial oxidative phosphorylation, which was supported by the indirect calorimetry and cellular energy analysis. Taken together, these findings suggest that STVNa is a potential cardioprotection agent for ischemic cardiomyopathy, likely through improving energy homeostasis, left ventricular hemodynamics, and heart function.

Poly[bis-[µ-1,4-bis-(1H-imidazol-5-yl)benzene-κN:N]diformatomanganese(II)].

In the title compound, [Mn(CHO(2))(2)(C(12)H(10)N(4))(2)](n), the Mn(II) atom and the benzene ring of the ligand lie on an inversion centers. The Mn(II) atom has an octa-hedral coordination environment composed of four N atoms from two different symmetry-related N-heterocyclic ligands forming the basal plane, and two O atoms from symmetry-related formate anions occupying the apical positions. The title compound forms a two-dimensional (4,4) net parallel to (100) with all the Mn(II) atoms lying on a plane. The crystal structure is consolidated by inter-molecular N-H⋯O hydrogen bonds..