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Characteristics of CAD patients with and without diastolic dysfunction. QT dispersion (QTD) was used to evaluate the variation in ventricular repolarization. In patients with diastolic dysfunction, QTD duration was significantly longer than in control group (174 ± 23 ms vs 132 ± 20 ms, p < 0.001). The increase in heart rate in patients with diastolic dysfunction was not found to be related to an increase in QTc dispersion duration. The QTD duration was significantly related to left atrial (LA) volume and right ventricular (RV) wall thickness (r = 0.51, p < 0.001 and r = 0.41, p < 0.001, respectively). Increased LA and RV volumes were not related to the increase in QTD duration. Considering that there was a relationship between QT dispersion and both left atrial and right ventricular volumes, we hypothesized that myocardial fibrosis leads to a structural alteration of the atrium and ventricles, which enhances the dispersion of ventricular repolarization. In conclusion, patients with diastolic dysfunction may have increased ventricular repolarization dispersion and heart rate-independent dispersion in the QT interval, which may be related to diastolic dysfunction, and we think that this can be a new surrogate of using noninvasive parameters to detect CAD patients at higher risk for atrial fibrillation (AF). ⁶⁶

Inhibitors of TLR4 are widely used to determine the LPS activity of microbial pathogens in vitro and in vivo. However, cellular response to LPS in this process is likely mediated by more than one TLR and requires LPS to activate multiple TLR4 heterodimers, which lead to sequential recruitment of other TLR family members, such as TLR2 or TLR1, and then nucleotide-binding oligomerization domain-containing protein 2 (NOD2), TLR5, TLR6, and TLR3. ¹⁷⁸

The Notch ligand Delta-like 4 (Dll4) is expressed exclusively in ECs. 246 The EC-specific deletion of Notch2 results in embryonic death at day E10.5 due to hemorrhagic diathesis in the aorta and capillary plexus. Conditional-knockout of Dll4 (Dll4-CKO) in ECs in adult mice causes a progressive aneurysmal dilatation, leading to rupture of the aorta, resulting in severe hemorrhage and death. 247 Inhibition of Notch signaling in ECs leads to the morphological remodeling of the aorta and disturbed vascular homeostasis, including modulation of vasoconstriction and vasodilation, and leukocyte adhesion and transmigration. Notch signaling promotes the EMT of EC, and regulates EC apoptosis and proliferation in response to vascular injury.
The Notch pathway is considered an important target in cancer therapy. For example, Delta-like 4 (DLL4) expression is suppressed in several types of human cancers, including lung cancer, ovarian cancer, prostate cancer, head and neck cancer, and basal cell carcinoma. 248 The loss of DLL4 is associated with the higher tumor cell proliferation and/or increased migration, invasion and metastasis of tumor cells. 249
Notch activation through overexpression of DLL4 or RBPJκ-activated NICD induces cell apoptosis in carcinoma cells, including lung cancer A549 and breast cancer MDA-MB-231 cells. 250, 251 Reversal of DLL4/Notch signaling rescues the sensitivity of breast cancer cell line MCF-7 to cisplatin. 253
MD2 directly binds to LPS and is essential for TLR4-mediated LPS recognition. 174 It also associates with the TLR4 cytoplasmic domain and enhances the recruitment of adaptor proteins, like myeloid differentiation primary response gene 88 (MyD88) and TRIF, which play crucial roles in TLR4 signaling cascade via transducing LPS signals to downstream kinases, such as NF-κB and MAP kinases. 175, 176
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