Intermittent hypobaric hypoxia improves postischemic recovery of myocardial contractile function via redox signaling during early reperfusion. Am J Physiol Heart Circ Physiol 301: H1695-H1705, 2011. First published August 5, 2011; doi:10.1152/ajpheart.00276.2011.-Intermittent hypobaric hypoxia (IHH) protects hearts against ischemiareperfusion (I/R) injury, but the underlying mechanisms are far from clear. ROS are paradoxically regarded as a major cause of myocardial I/R injury and a trigger of cardioprotection. In the present study, we investigated whether the ROS generated during early reperfusion contribute to IHH-induced cardioprotection. Using isolated perfused rat hearts, we found that IHH significantly improved the postischemic recovery of left ventricular (LV) contractile function with a concurrent reduction of lactate dehydrogenase release and myocardial infarct size (20.5 Ϯ 5.3% in IHH vs. 42.1 Ϯ 3.8% in the normoxic control, P Ͻ 0.01) after I/R. Meanwhile, IHH enhanced the production of protein carbonyls and malondialdehyde, respective products of protein oxidation and lipid peroxidation, in the reperfused myocardium and ROS generation in reperfused cardiomyocytes. Such effects were blocked by the mitochondrial ATP-sensitive K ϩ channel inhibitor 5-hydroxydecanoate. Moreover, the IHH-improved postischemic LV performance, enhanced phosphorylation of PKB (Akt), PKC-ε, and glycogen synthase kinase-3␤, as well as translocation of PKC-ε were not affected by applying H 2O2 (20 mol/l) during early reperfusion but were abolished by the ROS scavengers N-(2-mercaptopropionyl-)glycine (MPG) and manganese (III) tetrakis (1-methyl-4-pyridyl)porphyrin. Furthermore, IHH-reduced lactate dehydrogenase release and infarct size were reversed by MPG. Consistently, inhibition of Akt with wortmannin and PKC-ε with εV1-2 abrogated the IHH-improved postischemic LV performance. These findings suggest that IHHinduced cardioprotection depends on elevated ROS production during early reperfusion.reactive oxygen species; ischemia-reperfusion injury EARLY REPERFUSION during evolving myocardial infarction is essential for saving the myocardium, but lethal reperfusion injury can occur and limit the beneficial effects (49). A number of cardioprotective strategies have been developed to ameliorate or retard the irreversible injury. However, the clinical translation of these strategies has failed to achieve the anticipated results (13, 34). Intermittent hypobaric hypoxia (IHH) has been shown to protect the heart against ischemia-reperfusion (I/R) injury by improving the manifestations including contractile dysfunction (3, 33), arrhythmias (31, 52), and cell death (8,27). Recently, we (48) revealed a therapeutic effect of IHH on permanent coronary artery ligation-induced myocardial infarction by attenuating infarct size, myocardial fibrosis, and apoptosis and improving cardiac performance. Because IHH is a relatively simple intervention with a longer protection duration and fewer adverse effects and may offer profound benefit to patients ...

The findings reveal a novel role of Hsp27 in the protection of cTnI and cTnT from I/R-induced degradation by preventing their proteolytic cleavage via interacting with these proteins. Such protection may result in restored post-ischaemic myofilament response to Ca(2+) and improved post-ischaemic contractile function.

The outbreak of COVID-19, caused by 2019 novel coronavirus (2019-nCoV), has been a global public health threat and caught the worldwide concern. Scientists throughout the world are sparing all efforts to explore strategies for the determination of the 2019-nCoV virus and diagnosis of COVID-19 rapidly. Several assays are developed for COVID-19 test , including RT-PCR, coronavirus antigens-based immunoassays, and CRISPR-based strategies (Cas13a or Cas12a), etc. Different assays have their advantages and drawbacks, and people should choose the most suitable assay according to their demands. Here, we make a brief introduction about these assays and give a simple overview of them, hoping to help doctors and researchers to select the most suitable assay for the Coronavirus Disease 2019 test (COVID-19 test) .

Intermittent hypobaric hypoxia (IHH) is an effective protective strategy against myocardial ischaemia-reperfusion (I/R

COVID-19, a novel pathogenic coronavirus (2019-nCoV, now named SARS-CoV2) induced disease, emerged in China and spread globally rapidly. 2019-nCoV(SARS-CoV2) shares above 85% identity in genome with SARS-CoV. Patients infected by 2019-nCoV and SARS-CoV also reveal similar clinical characteristics. Here we compare the clinical and pathological features between patients of COVID-19 and SARS respectively. Conclusions:1. Older patients refer to a higher case fatality rate (CFR) than young. 2. Males show a higher CFR than females, and this difference may converge as age increase.3.COVID-19 may cause a kidney and testis damage. Combined with higher CFR in males, genitourinary system disorder caused by the COVID-19 needs to be cautioned.4. It is critical to control the cytokine release syndrome(CRS) in COVID-19. IL-6, IL-10 and their receptors may be the drugable target.5. Consistently to decrease of CD4+T and CD8+T cells, spleen damage, and lymphocyte depletion may exist inCOVID-19 patients. Approaches for T cell rescued may be considered. 6. Compared with SARS-CoV’s Spike protein, 2019-nCoV(SARS-CoV2) Spike protein present a higher binding affinity to ACE2, which suggests that soluble ACE2 might be a potential candidate for COVID-19 treatment. Other receptors, such as L-SIGN and DC-SIGN, need to be investigated in the future.

The vaccine helps to provoke the immune system and is an efficacious means for disease prevention and treatment. At this particular time of the COVID-19 outbreak, the vaccine for COVID-19 is urgently needed to save tens of thousands of people’s lives. Here we give some basic information on vaccine classification, generation, and application, and make a brief review on the current status of COVID-19 vaccine and tumor vaccine development both in the clinical trial stage and pre-clinical stage. vaccine

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Hopes for a COVID-19 vaccine are now a reality. The spike protein of SARS-CoV-2, which majorly binds to the host receptor ACE2 for cell entry, is used by most of the COVID-19 vaccine candidates as a choice of antigen. ACE2 is highly expressed in the heart and is known to be protective in multiple organs. Interaction of spike with ACE2 has been reported to reduce ACE2 expression and affect ACE2-mediated signal transduction in the heart. However, whether a spike-encoding vaccine will aggravate myocardial damage after a heart attack via affecting ACE2 remains unclear. Therefore, for patients with or at risk of heart diseases, questions arise around the safety of the spike-based vaccines. Here, we demonstrate that ACE2 is up-regulated and protective in the injured mouse heart after myocardial ischemia/reperfusion (I/R). Infecting human cardiomyocyte, smooth muscle cells, endothelial cells, and cardiac fibroblasts with a recombinant adenovirus type-5 vectored COVID-19 vaccine expressing the spike protein (AdSpike) does not affect cell survival and cardiomyocyte function, whether the cells are subjected to hypoxia-reoxygenation injury or not. This observation is further confirmed in human engineered heart tissues. Furthermore, AdSpike vaccination does not aggravate heart damage in wild-type or humanized ACE2 mice after I/R injury, even at a dose that is ten-fold higher as used in human. This study represents the first systematic evaluation of the safety of a leading COVID-19 vaccine under a disease context and may provide important information to ensure maximal protection from COVID-19 in patients with or at risk of heart diseases.