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To investigate the effects of ultrasound-assisted immersion freezing on the osmotic mass transfer characteristics of blueberries, air freezing, immersion freezing and ultrasound-assisted immersion freezing were applied to blueberries. The freezing rate, water distribution, calcium content, anthocyanin content, cell membrane permeability and malondialde-hyde content were measured and analyzed. The results showed that compared with air freezing and immersion freezing, ultrasonic-assisted immersion freezing significantly shortened the freezing time of blueberries, and the drip loss after thawing was the lowest, 8.26%, and the water distribution was more similar to that of fresh blueberries. Ultrasonic promoted the permeation migration of exogenous calcium, and the calcium content in whole fruit and pulp increased significantly (P < 0.05); the hardness was better preserved, but the retention rate of anthocyanin decreased, and the cell membrane permeability and malondialdehyde content decreased significantly (P<0.05), which were 54.65% and 9.15 nmol/g FW, respectively. In conclusion, ultrasound-assisted immersion freezing can not only improve freezing rate, reduce lipid membrane peroxidation and maintain the integrity of cell membrane, but also promote the infiltration of solution solute into food. [ABSTRACT FROM AUTHOR]

Autoantibodies against the second extracellular loop of β1-adrenergic receptor (β1-AA) have been shown to be involved in the development of cardiovascular diseases. Recently, there has been considerable interest in strategies to remove these autoantibodies, particularly therapeutic peptides to neutralize β1-AA. Researchers are investigating the roles of cyclic peptides that mimic the structure of relevant epitopes on the β1-AR-ECII in a number of immune-mediated diseases. Here, we used a cyclic peptide, namely, RD808, to neutralize β1-AA, consequently alleviating β1-AA-induced myocardial injury. We investigated the protective effects of RD808 on the myocardium both in vitro and in vivo. RD808 was found to increase the survival rate of cardiomyocytes; furthermore, it decreased myocardial necrosis and apoptosis and improved the cardiac function of BalB/c mice in a β1-AA transfer model. In vitro and in vivo experiments showed that myocardial autophagy was increased in the presence of RD808, which might contribute to its cardioprotective effects. Our findings indicate that RD808 reduced myocardial injury induced by β1-AA. [ABSTRACT FROM AUTHOR]

Hypoxic pulmonary vascular remodelling (PVR) is the major pathological basis of aging-related chronic obstructive pulmonary disease and obstructive sleep apnea syndrome. The pulmonary artery endothelial cell (PAEC) inflammation, and pulmonary artery smooth muscle cell (PASMC) proliferation, hypertrophy and collagen remodelling are the important pathophysiological components of PVR. Endogenous sulfur dioxide (SO 2 ) was found to be a novel gasotransmitter in the cardiovascular system with its unique biological properties. The study was aimed to investigate the role of endothelial cell- (EC-) derived SO 2 in the progression of PAEC inflammation, PASMC proliferation, hypertrophy and collagen remodelling in PVR and the possible mechanisms. EC-specific aspartic aminotransferase 1 transgenic (EC-AAT1-Tg) mice were constructed in vivo . Pulmonary hypertension was induced by hypoxia. Right heart catheterization and echocardiography were used to detect mouse hemodynamic changes. Pathologic analysis was performed in the pulmonary arteries. High-performance liquid chromatography was employed to detect the SO 2 content. Human PAECs (HPAECs) with lentiviruses containing AAT1 cDNA or shRNA and cocultured human PASMCs (HPASMCs) were applied in vitro . SO 2 probe and enzyme-linked immunosorbent assay were used to detect the SO 2 content and determine p50 activity, respectively. Hypoxia caused a significant reduction in SO 2 content in the mouse lung and HPAECs and increases in right ventricular systolic pressure, pulmonary artery wall thickness, muscularization, and the expression of PAEC ICAM-1 and MCP-1 and of PASMC Ki-67, collagen I, and α -SMA ( p < 0.05). However, EC-AAT1-Tg with sufficient SO 2 content prevented the above increases induced by hypoxia ( p < 0.05). Mechanistically, EC-derived SO 2 deficiency promoted HPAEC ICAM-1 and MCP-1 and the cocultured HPASMC Ki-67 and collagen I expression, which was abolished by andrographolide, an inhibitor of p50 ( p < 0.05). Meanwhile, EC-derived SO 2 deficiency increased the expression of cocultured HPASMC α -SMA ( p < 0.05). Taken together, these findings revealed that EC-derived SO 2 inhibited p50 activation to control PAEC inflammation in an autocrine manner and PASMC proliferation, hypertrophy, and collagen synthesis in a paracrine manner, thereby inhibiting hypoxic PVR., Competing Interests: The authors declare that there is no conflict of interest regarding the publication of this paper., (Copyright © 2021 Xin Liu et al.)

Sp1-CSE-H 2 S pathway plays an important role in homocysteine-metabolism, whose disorder can result in hyperhomocysteinemia. H 2 S deficiency in hyperhomocysteinemia has been reported, while the underlying mechanism and whether it in turn affects the progress of hyperhomocysteinemia are unclear. This study focused on the post-translational modification of Sp1/CSE and revealed four major findings: (1) Homocysteine-accumulation augmented CSE's nitration, inhibited its bio-activity, thus caused H 2 S deficiency. (2) H 2 S deficiency inhibited the S-sulfhydration of Sp1, down-regulated CSE and decreased H 2 S further, which in turn weakened CSE's own S-sulfhydration. (3) CSE was S-sulfhydrated at Cys84, Cys109, Cys172, Cys229, Cys252, Cys307 and Cys310, among which the S-sulfhydration of Cys172 and Cys310 didn't affect its enzymatic activity, while the S-sulfhydration of Cys84, Cys109, Cys229, Cys252 and Cys307 was necessary for its bio-activity. (4) H 2 S deficiency trapped homocysteine-metabolism into a vicious cycle, which could be broken by either blocking nitration or restoring S-sulfhydration. This study detected a new mechanism that caused severe hyperhomocysteinemia, thereby provided new therapeutic strategies for hyperhomocysteinemia., (Copyright © 2020 Elsevier Inc. All rights reserved.)