Long noncoding RNAs (lncRNAs) play important roles in the development of vascular diseases. However, the effect of lncRNA NORAD on atherosclerosis remains unknown. This study aimed to investigate the effect NORAD on endothelial cell injury and atherosclerosis. Ox-LDL-treated human umbilical vein endothelial cells (HUVECs) and high-fat-diet (HFD)-fed ApoE −/− mice were used as in vitro and in vivo models. Results showed that NORAD-knockdown induced cell cycle arrest in G0/G1 phase, aggravated ox-LDL-induced cell viability reduction, cell apoptosis, and cell senescence along with the increased expression of Bax, P53, P21 and cleaved caspase-3 and the decreased expression of Bcl-2. The effect of NORAD on cell viability was further verified via NORAD-overexpression. NORAD-knockdown increased ox-LDL-induced reactive oxygen species, malondialdehyde, p-IKBα expression levels and NF-κB nuclear translocation. Proinflammatory molecules ICAM, VCAM, and IL-8 were also increased by NORAD-knockdown. Additionally, we identified the strong interaction of NORAD and IL-8 transcription repressor SFPQ in HUVECs. In ApoE −/− mice, NORAD-knockdown increased the lipid disorder and atherosclerotic lesions. The results have suggested that lncRNA NORAD attenuates endothelial cell senescence, endothelial cell apoptosis, and atherosclerosis via NF-κB and p53-p21 signaling pathways and IL-8, in which NORAD-mediated effect on IL-8 might through the direct interaction with SFPQ.

The Global Precipitation Measurement (GPM) mission is a constellation-based satellite mission designed to unify and advance precipitation measurements using both research and operational microwave sensors. This requires consistency in the input brightness temperatures (Tb), which is accomplished by intercalibrating the constellation radiometers using the GPM Microwave Imager (GMI) as the calibration reference. The first step in intercalibrating the sensors involves prescreening the sensor Tb to identify and correct for calibration biases across the scan or along the orbit path. Next, multiple techniques developed by teams within the GPM Intersatellite Calibration Working Group (XCAL) are used to adjust the calibrations of the constellation radiometers to be consistent with GMI. Comparing results from multiple approaches helps identify flaws or limitations of a given technique, increase confidence in the results, and provide a measure of the residual uncertainty. The original calibration differences relative to GMI are generally within 2–3 K for channels below 92 GHz, although AMSR2 exhibits larger differences that vary with scene temperature. SSMIS calibration differences also vary with scene temperature but to a lesser degree. For SSMIS channels above 150 GHz, the differences are generally within ~2 K with the exception of SSMIS on board DMSP F19, which ranges from 7 to 11 K colder than GMI depending on frequency. The calibrations of the cross-track radiometers agree very well with GMI with values mostly within 0.5 K for the Sondeur Atmosphérique du Profil d’Humidité Intertropicale par Radiométrie (SAPHIR) and the Microwave Humidity Sounder (MHS) sensors, and within 1 K for the Advanced Technology Microwave Sounder (ATMS).

Acute myocardial ischaemia/reperfusion (MI/R) injury causes severe arrhythmias with a high rate of lethality. Extensive research focus on endoplasmic reticulum (ER) stress and its dysfunction which leads to cardiac injury in MI/R Our study evaluated the effects of sulodexide (SDX) on MI/R by establishing MI/R mice models and in vitro oxidative stress models in H9C2 cells. We found that SDX decreases cardiac injury during ischaemia reperfusion and decreased myocardial apoptosis and infarct area, which was paralleled by increased superoxide dismutase and reduced malondialdehyde in mice plasm, increased Bcl‐2 expression, decreased BAX expression in a mouse model of MI/R. In vitro, SDX exerted a protective effect by the suppression of the ER stress which induced by tert‐butyl hydroperoxide (TBHP) treatment. Both of the in vivo and in vitro effects were involved in the phosphatidylinositol 3‐kinase (PI3K)/Akt signalling pathway. Inhibition of PI3K/Akt pathway by specific inhibitor, LY294002, partially reduced the protective effect of SDX. In short, our results suggested that the cardioprotective role of SDX was related to the suppression of ER stress in mice MI/R models and TBHP‐induced H9C2 cell injury which was through the PI3K/Akt signalling pathway.

Kawasaki disease (KD) is an acute, self-limited vasculitis that predominantly affects medium-sized arteries, particularly the coronary arteries. Recent studies have indicated that microRNAs are involved in many diseases, including KD. However, the detailed mechanism remains unclear. The aim of the present study was to explore the role of miR-186 in KD and potentially discover a new target for KD treatment. The results demonstrated that miR-186 was upregulated in serum from patients with KD and KD serum could increase miR-186 transcript levels in endothelial cells (HUVECs). Overexpression of miR-186 mimic induced HUVEC apoptosis through mitogen-activated protein kinase (MAPK) activation by targeting and inhibiting SMAD family member 6 (SMAD6). Furthermore, KD serum induced HUVEC apoptosis through miR-186. In conclusion, the present results suggested that KD serum-associated miR-186 has an essential role in endothelial cell apoptosis by activating the MAPK pathway through targeting the SMAD6 gene.

As the prevalence of systemic fungal infections caused by Candida albicans gradually increases, it is necessary to explore potential and effective antifungals. Carvacrol is reported to be lethally toxic to C. albicans, involving several potential mechanisms. However, the form and specific mechanism of cell death caused by this compound has not been delineated. In this study, we found that carvacrol could significantly decrease C. albicans survival rates, consistent with previous researches. Further examination proved that carvacrol treatment caused cell membrane permeability and depolarization. To elucidate the association between cell death and apoptosis, DNA fragmentation and metacaspase activation were determined; as expected, these two apoptosis-related markers were clearly observed. Moreover, total and mitochondrial reactive oxygen species (ROS) levels were elevated, and both mitochondrial transmembrane potential and morphology were disrupted. Additionally, cytosolic and mitochondrial calcium levels were also increased by carvacrol. Calcineurin inhibition experiments revealed cyclosporine A (CsA) addition notably rescued cell growth and inhibited metacaspase activation, indicating that carvacrol triggered C. albicans apoptosis through inducing calcineurin activation. Carvacrol was demonstrated to both have low toxicity and be effective in alleviating systemic infections with C. albicans, which might be via its antifungal and immunomodulation activities. This study suggests that carvacrol has excellent potential as a natural protective compound against C. albicans infections.