Source Mechanism and Rupture Directivity of the 18 May 2009 M_W 4.6 Inglewood, California, Earthquake

On 18 May 2009, an M_w 4.6 earthquake occurred beneath Inglewood, California, and was widely felt. Though source mechanism and its location suggest that the Newport–Inglewood fault (NIF) may be involved in generating the earthquake, rupture directivity must be modeled to establish the connection between the fault and the earthquake. We first invert for the event’s source mechanism and depth with the cut-and-paste method in the long-period band (>5 s). Because of the low velocity shallow sediments in the Los Angeles (LA) basin, we use two velocity models in the inversion for stations inside and outside the LA basin. However, little difference is observed in the resolved source mechanism (M_w 4.6, strike 246°/145°, dip 50°/77°, rake 17°/138°) and depth (7 to ~9 km), compared to an inversion using the standard southern Calfornia model. With the resolved source parameters, we calibrate the amplitude anomaly of the short-period (0.5–2 Hz) P waves with amplitude adjustment factors (AAF). These AAFs are used as corrections when retrieving source mechanisms of the smaller aftershocks using short-period P waves alone. Most of the aftershocks show similar source mechanisms as that of the mainshock, providing ideal empirical Green’s functions (EGFs) for studying its rupture process. We use a forward modeling approach to retrieve rupture directivity of the mainshock, consistent with movement on the NIF with rupture toward the southeast. Although we focus on P waves for analyzing rupture directivity, the resolved unilateral pattern is also confirmed with the azimuthal variation of the duration of SH waves observed in the basin. The high rupture velocity near the shear velocity and relatively low stress drop are consistent with the hypothesis of rupture on a mature fault

The differential interaction effect of mastery and performance climate on athletes’ emotional and physical exhaustion:The role of athletes’ gratitude.

Motivational climate (i.e., mastery and performance climate) has been found to shape athletes’ emotional and physical exhaustion, the core dimension of burnout. However, the interactional effect between mastery and performance climate on emotional and physical exhaustion has been rarely examined. In this study, we proposed that athletes’ gratitude will determine the interaction effect of mastery climate and performance climate on emotional and physical exhaustion. Specifically, we hypothesized that among athletes high in gratitude, mastery climate can mitigate the association between performance climate and emotional and physical exhaustion; among those low in gratitude, mastery climate can intensify the association between performance climate and emotional and physical exhaustion. Using a time-lagged survey, data from 293 athletes revealed a three-way interaction effect among mastery climate, performance climate, and gratitude. We did not find that mastery climate can mitigate the association between performance climate and emotional and physical exhaustion for those high in gratitude but found that among athletes low in gratitude, the positive association between performance climate and emotional and physical exhaustion was stronger in a higher mastery climate than in a lower mastery climate. Our study offers an interactionist perspective to help further understand the joint effect of mastery and performance climates on emotional and physical exhaustion by taking the role of individual differences into account.</p

Screening immune-related blood biomarkers for DKD-related HCC using machine learning

BackgroundDiabetes mellitus is a significant health problem worldwide, often leading to diabetic kidney disease (DKD), which may also influence the occurrence of hepatocellular carcinoma (HCC). However, the relationship and diagnostic biomarkers between DKD and HCC are unclear.MethodsUsing public database data, we screened DKD secretory RNAs and HCC essential genes by limma and WGCNA. Potential mechanisms, drugs, and biomarkers for DKD-associated HCC were identified using PPI, functional enrichment, cMAP, and machine learning algorithms, and a diagnostic nomogram was constructed. Then, ROC, calibration, and decision curves were used to evaluate the diagnostic performance of the nomograms. In addition, immune cell infiltration in HCC was explored using CIBERSORT. Finally, the detectability of critical genes in blood was verified by qPCR.Results104 DEGs associated with HCC using WGCNA were identified. 101 DEGs from DKD were predicated on secreting into the bloodstream with Exorbase datasets. PPI analysis identified three critical modules considered causative genes for DKD-associated HCC, primarily involved in inflammation and immune regulation. Using lasso and RM, four hub genes associated with DKD-associated HCC were identified, and a diagnostic nomogram confirmed by DCA curves was established. The results of immune cell infiltration showed immune dysregulation in HCC, which was associated with the expression of four essential genes. PLVAP was validated by qPCR as a possible blood-based diagnostic marker for DKD-related HCC.ConclusionWe revealed the inflammatory immune pathways of DKD-related HCC and developed a diagnostic nomogram for HCC based on PLVAP, C7, COL15A1, and MS4A6A. We confirmed with qPCR that PLVAP can be used as a blood marker to assess the risk of HCC in DKD patients

GABA, progesterone and zona pellucida activation of PLA2 and regulation by MEK-ERK1/2 during acrosomal exocytosis in guinea pig spermatozoa

AbstractWe investigated whether GABA activates phospholipase A2 (PLA2) during acrosomal exocytosis, and if the MEK-ERK1/2 pathway modulates PLA2 activation initiated by GABA, progesterone or zona pellucida (ZP). In guinea pig spermatozoa prelabelled with [14C]arachidonic acid or [14C]choline chloride, GABA stimulated a decrease in phosphatidylcholine (PC), and release of arachidonic acid and lysoPC, during exocytosis. These lipid changes are indicative of PLA2 activation and appear essential for exocytosis since inclusion of aristolochic acid (a PLA2 inhibitor) abrogated them, along with exocytosis. GABA activation of PLA2 seems to be mediated, at least in part, by diacylglycerol (DAG) and protein kinase C since inclusion of the DAG kinase inhibitor R59022 enhanced PLA2 activity and exocytosis stimulated by GABA, whereas exposure to staurosporine decreased both. GABA-, progesterone- and ZP-induced release of arachidonic acid and exocytosis were prevented by U0126 and PD98059 (MEK inhibitors). Taken together, our results suggest that PLA2 plays a fundamental role in agonist-stimulated exocytosis and that MEK-ERK1/2 are involved in PLA2 regulation during this process