B-O-O-B Impurity Induces Ultralong Room-Temperature Phosphorescence of Boric Acid.

Organic materials that can emit ultralong room-temperature phosphorescence (RTP) have attracted a great deal of interest. Whether the pure boric acid (BA) solid can emit RTP and the origin of the RTP in BA caused a debate recently. Herein, our first-principles calculations and experimental measurements suggest that RTP of BA originates from the B-O-O-B group in a (H2BO3)2 species, which can be formed by polymerization of two dehydrogenated BA molecules under light irradiation. The calculated absorption, fluorescence, and phosphorescence spectra of B-O-O-B match well with the experiments. Experimental X-ray photoelectron and X-ray absorption spectra evidence the existence of B-O-O-B in BA. The O-O bond in B-O-O-B can break upon optical excitation, creating two B-O radicals. Radiative transition from localized dangling orbitals of the B-O radicals to the delocalized orbitals of the crystal bulk leads to the observed RTP. Our calculated phosphorescence lifetime is ∼1 s, which agrees well with the experiment.

Crucial Role of Defect States in the Ultralong Phosphorescence of Organic Molecular Crystals.

Ultralong organic phosphorescence (UOP) in pure organic molecular crystals has attracted a lot of interest recently. There is much debate on the emission mechanism of this UOP. Two recent experimental works published in Nat. Photonics 2019, 13, 406-411 and Nat. Mater. 2021, 20, 175-180 attribute UOP in the 2,4,6-trimethoxy-1,3,5-triazine (TMOT) crystals and the carbazole crystals to H-aggregation of the TMOT molecules or the formation of charge-transfer excitons between the carbazole and impurity molecules. Our first-principles many-body Green's function theory calculations show that the lowest triplet states of these two crystals are in fact the localized defect states originating from the twisted TMOT molecules and the impurities, respectively. Energies of the H-aggregation-induced exciton and the charge-transfer exciton are too high to account for UOP. UOP should be mainly due to the little orbital overlap between the localized defect state and the delocalized band edges of the crystal. Strong intermolecular interactions suppress nonradiative decay of the triplet exciton localized on the defect.

Valsartan Regulates PI3K/AKT Pathways through lncRNA GASL1 to Improve Isoproterenol-Induced Heart Failure.

OBJECTIVE: This study is aimed at determining the expression and function of the GASL1 and PI3K/AKT pathways in isoproterenol- (ISO-) induced heart failure (HF). To determine the moderating effect of valsartan (VAL) on the progression of ISO-induced HF and to elucidate the related mechanism. MATERIALS AND METHODS: First, in in vivo experiment, we examined the effect of VAL on cardiac function in rats with ISO-induced HF. Similarly, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to detect the effect of VAL on ISO-treated rat primary cardiomyocytes. Then, si-GASL1-transfected primary cardiomyocytes were constructed and Ad-si-GASL1 was injected through rat tail vein to achieve the effect of lowering GASL1 expression, so as to investigate the role of GASL1 in VAL's treatment of ISO-induced HF. RESULTS: In ISO-induced HF rat models, the GASL1 decreased while PI3K and p-AKT expressions were abnormally elevated and cardiac function deteriorated, and VAL was able to reverse these changes. In primary cardiomyocytes, ISO induces apoptosis of cardiomyocytes, and expression of GASL1 decreased while PI3K and p-AKT were abnormally elevated, which can be reversed by VAL. The transfection of primary cardiomyocytes with si-GASL1 confirmed that GASL1 affected the expression of PI3K, p-AKT, and the apoptosis of primary cardiomyocytes. Rat myocardium injected with Ad-si-GASL1 was found to aggravate the cardiac function improved by VAL. CONCLUSIONS: This study was the first to confirm that VAL improves ISO-induced HF by regulating the PI3K/AKT pathway through GASL1. And this study demonstrated a significant correlation between HF, VAL, GASL1, and the PI3K/AKT pathway.

miRNA-19b-3p Stimulates Cardiomyocyte Apoptosis Induced by Myocardial Ischemia Reperfusion via Downregulating PTEN.

OBJECTIVE: To clarify the function of miRNA-19b-3p in accelerating myocardial ischemia-reperfusion injury- (MIRI-) induced cardiomyocyte apoptosis by downregulating gene of phosphate and tension homology deleted on chromsome ten (PTEN), thus influencing the progression of acute myocardial infarction. MATERIALS AND METHODS: miRNA-19b-3p and PTEN levels in HCM cells undergoing hypoxia/reoxygenation (H/R) were determined. Meanwhile, activities of myocardium injury markers [lactate dehydrogenase (LDH), malondialdehyde; malonic dialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX)] in H/R-induced HCM cells were tested. Through dual-luciferase reporter gene assay, the binding between miRNA-19b-3p and PTEN was verified. Regulatory effects of miRNA-19b-3p and PTEN on apoptotic rate and apoptosis-associated gene expressions (proapoptotic protein Bcl-2 associated X protein (Bax), antiapoptotic protein B-cell lymphoma-2 (Bcl-2), and cytochrome C) in H/R-induced human cardiac myocytes (HCM) cells were examined. RESULTS: miRNA-19b-3p was upregulated, while PTEN was downregulated in H/R-induced HCM cells. Knockdown of miRNA-19b-3p decreased activities of LDH, MDA, and GSH-PX, but increased SOD level in H/R-induced HCM cells. The binding between miRNA-19b-3p and PTEN was confirmed. More importantly, knockdown of miRNA-19b-3p reduced apoptotic rate, downregulated proapoptosis gene expressions (Bax and cytochrome C), and upregulated antiapoptosis gene expression (Bcl-2), which were reversed by silence of PTEN. CONCLUSIONS: miRNA-19b-3p is upregulated in HCM cells undergoing hypoxia and reoxygenation, which accelerates MIRI-induced cardiomyocyte apoptosis through downregulating PTEN.

Regulatory Mechanism of LINC00152 on Aggravating Heart Failure through Triggering Fibrosis in an Infarcted Myocardium.

OBJECTIVE: To elucidate the role of LINC00152 in the progression of heart failure following myocardial infarction. Patients and Methods. Serum levels of LINC00152 in acute myocardial infarction (AMI) patients were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Receiver operating characteristic (ROC) curves were depicted for assessing the diagnostic value of LINC00152 in AMI. Subsequently, an in vivo AMI model was generated in mice. LINC00152 level in a mouse infarcted myocardium was detected. Echocardiogram was conducted to evaluate the influence of LINC00152 on cardiac function in AMI mice. Primary cardiac fibroblasts were isolated from neonatal mice. After knockdown of LINC00152, proliferative and migratory changes in primary cardiac fibroblasts were assessed by cell counting kit-8 (CCK-8) and transwell assay, respectively. The regulatory effect of LINC00152 on Smad7 level was determined by qRT-PCR. Finally, the involvement of Smad7 in LINC00152-regulated proliferative and migratory abilities in primary cardiac fibroblasts was explored by rescue experiments. RESULTS: Serum level of LINC00152 was elevated in AMI patients. ROC curves demonstrated the diagnostic potential of LINC00152 in AMI (95% CI: 0.806-0.940, p = 0.034). In myocardial tissues collected from AMI mice, LINC00152 level was higher than those collected from mice of the sham group. LVEF and FS markedly decreased in AMI mice overexpressing LINC00152 on the 4th week of AMI modeling. After knockdown of LINC00152 in primary cardiac fibroblasts, proliferative and migratory abilities were declined, which were abolished by Smad7 intervention. CONCLUSIONS: By downregulating Smad7, LINC00152 aggravates heart failure following AMI via promoting the proliferative and migratory abilities in cardiac fibroblasts.

Relationship between Expression of Plasma lncRNA-HEIH and Prognosis in Patients with Coronary Artery Disease.

OBJECTIVE: We aimed to investigate the expression of long noncoding RNA- (lncRNA-) HEIH in patients with coronary artery disease (CAD) and its impact on patients' prognosis. Patients and Methods. From July 2015 to December 2018, 250 patients who underwent coronary angiography, including 50 in the control group and 150 in the CAD group, were collected for detection of the expression of lncRNA-HEIH by real-time quantitative polymerase chain reaction (qPCR). The severity of CAD was evaluated through SYNTAX scoring system. In addition, these patients with CAD were followed up for 3 years, and the major cardiac adverse events such as myocardial infarction and revascularization were recorded. RESULTS: The expression of lncRNA-HEIH in plasma of patients with CAD was remarkably higher than that in the control subjects and was verified to be relevant to the severity of CAD. Meanwhile, it was found that CAD patients with high expression of lncRNA-HEIH had higher rates of dyslipidemia as well as CAD family history and higher overall incidence of major cardiac adverse events than those with low expression of lncRNA-HEIH. CONCLUSIONS: lncRNA-HEIH expression is upregulated in the plasma of CAD patients, which is capable of affecting the prognosis of patients.