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Will be Epicardial Adipose Tissues Associated with Atrial Fibrillation Right after Heart failure Surgery? A deliberate Review as well as Meta-Analysis.
Cardiac arrest is the leading cause of death among patients receiving hemodialysis. Despite guidelines recommending CPR training and AED presence in dialysis clinics, rates of CPR and AED use by dialysis staff are suboptimal. Given that racial disparities exist in bystander CPR administration in non-healthcare settings, we examined the relationship between patient race/ethnicity and staff-initiated CPR and AED application within dialysis clinics.

We analyzed data prospectively collected in the Cardiac Arrest Registry to Enhance Survival across the U.S. from 2013 to 2017 and the Centers for Medicare & Medicaid Services dialysis facility database to identify outpatient dialysis clinic cardiac arrest events. Using multivariable logistic regression models, we examined relationships between patient race/ethnicity and dialysis staff-initiated CPR and AED application.

We identified 1568 cardiac arrests occurring in 809 hemodialysis clinics. The racial/ethnic composition of patients was 31.3% white, 32.9% Bon practices.
Black and Asian patients are significantly less likely than white patients to receive CPR from dialysis staff. Further understanding of practices in dialysis clinics and increased awareness of this disparity are necessary to improve resuscitation practices.Epidermal growth factor receptor (EGFR) amplification and EGFRvIII mutation drive glioblastoma (GBM) pathogenesis, but their regulation remains elusive. Here we characterized the EGFR/EGFRvIII "interactome" in GBM and identified thyroid receptor-interacting protein 13 (TRIP13), an AAA + ATPase, as an EGFR/EGFRvIII-associated protein independent of its ATPase activity. Functionally, TRIP13 augmented EGFR pathway activation and contributed to EGFR/EGFRvIII-driven GBM growth in GBM spheroids and orthotopic GBM xenograft models. Mechanistically, TRIP13 enhanced EGFR protein abundance in part by preventing Cbl-mediated ubiquitination and proteasomal degradation. Reciprocally, TRIP13 was phosphorylated at tyrosine(Y) 56 by EGFRvIII and EGF-activated EGFR. Abrogating TRIP13 Y56 phosphorylation dramatically attenuated TRIP13 expression-enhanced EGFR signaling and GBM cell growth. Clinically, TRIP13 expression was upregulated in GBM specimens and associated with poor patient outcome. In GBM, TRIP13 localized to cell membrane and cytoplasma and exhibited oncogenic effects in vitro and in vivo, depending on EGFR signaling but not the TRIP13 ATPase activity. Collectively, our findings uncover that TRIP13 and EGFR form a feedforward loop to potentiate EGFR signaling in GBM growth and identify a previously unrecognized ATPase activity-independent mode of action of TRIP13 in GBM biology.The blood vessel growth inhibitor bevacizumab targets vascular endothelial growth factor (VEGF), a crucial regulator of angiogenesis. Recently, small extracellular vesicles (sEVs) have been demonstrated to be important vehicles in the transport of growth factors to target cells. In this study, we isolated primary carcinoma-associated fibroblasts (CAFs) from four human oral squamous cell carcinoma (OSCC) specimens. PIN1 inhibitor API-1 Compared with other non-extracellular vesicle components, CAF-derived sEVs were found to be the main regulators of angiogenesis. The ability of CAF sEVs to activate VEGF receptor 2 (VEGFR2) signaling in human umbilical vein endothelial cells (HUVEC) was dependent on the association between sEVs and VEGF. In addition, sEV-bound VEGF secreted by CAFs further activated VEGFR2 signaling in HUVEC in a bevacizumab-resistant manner. VEGF was found to interact with heparan sulfate proteoglycans on the CAF sEV surface and could be released by heparinase I/III. The bioactivity of the dissociated VEGF was retained in vitro and in vivo and could be neutralized by bevacizumab. These findings suggest that the combined use of heparinase and bevacizumab might inhibit angiogenesis in patients with high levels of sEV-bound VEGF.Arsenic and benzo[α]pyrene (BaP) are widespread carcinogens and important etiology factors for lung cancer. Moreover, arsenic and BaP co-exposure displays a significantly stronger effect in inducing lung cancer than arsenic or BaP exposure alone. This study was performed to investigate the basic mechanism of the synergistic carcinogenic effect of arsenic and BaP co-exposure. It was found that integrin α4 (ITGA4) expression levels are significantly up-regulated and the Hedgehog pathway is highly activated in arsenic plus BaP co-exposure-transformed human bronchial epithelial cells. Either ITGA4 downregulation or Hedgehog pathway inhibition in the co-exposure-transformed cells significantly reduced their cancer stem cell (CSC)-like property and tumorigenicity. It was determined that ITGA4 downregulation leads to the inhibition of the Hedgehog pathway activation, which is achieved by increasing suppressor of fused (SUFU) protein stability through reducing the PI3K/Akt signaling. Moreover, stably overexpressing SUFU in the co-exposure-transformed cells significantly reduces their CSC-like property and tumorigenicity. These findings indicate that ITGA4 up-regulation activates the Hedgehog pathway to enhance the CSC-like property and tumorigenicity of arsenic and BaP co-exposure-transformed cells, offering new mechanistic insight for the synergistic carcinogenic effect of arsenic and BaP co-exposure.The majority of ovarian cancer (OC) patients recur with a platinum-resistant disease. OC cells activate adaptive resistance mechanisms that are only partially described. Here we show that OC cells can adapt to chemotherapy through a positive-feedback loop that favors chemoresistance. In platinum-resistant OC cells we document that the endothelin-1 (ET-1)/endothelin A receptor axis intercepts the YAP pathway. This cross-talk occurs through the LATS/RhoA/actin-dependent pathway and contributes to prevent the chemotherapy-induced apoptosis. Mechanistically, β-arrestin1 (β-arr1) and YAP form a complex shaping TEAD-dependent transcriptional activity on the promoters of YAP target genes, including EDN1, which fuels a feed-forward signaling circuit that sustains a platinum-tolerant state. The FDA approved dual ET-1 receptor antagonist macitentan in co-therapy with cisplatin sensitizes resistant cells to the platinum-based therapy, reducing their metastatic potential. Furthermore, high ETAR/YAP gene expression signature is associated with a poor platinum-response in OC patients.
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