Acute myocardial infarction after inactivated COVID-19 vaccination: a case report and literature review.

A number of vaccines have been developed and deployed globally to restrain the spreading of the coronavirus disease 2019 (COVID-19). The adverse effect following vaccination is an important consideration. Acute myocardial infarction (AMI) is a kind of rare adverse event after COVID-19 vaccination. Herein, we present a case of an 83-year-old male who suffered cold sweat ten minutes after the first inactivated COVID-19 vaccination and AMI one day later. The emergency coronary angiography showed coronary thrombosis and underlying stenosis in his coronary artery. Type II Kounis syndrome might be a potential mechanism, which is manifested as coronary thrombosis secondary to allergic reactions in patients with underlying asymptomatic coronary heart disease. We also summarize the reported AMI cases post COVID-19 vaccination, as well as overview and discuss the proposed mechanisms of AMI after COVID-19 vaccination, thus providing insights for clinicians to be aware of the possibility of AMI following COVID-19 vaccination and potential underlying mechanisms.

Case Report: A balloon-based technique to remove a pearl-like embolus out of the coronary artery.

Coronary embolism is considered a rare non-atherosclerotic etiology of acute myocardial infarction, whereas atrial fibrillation is the main etiology of coronary embolism. We report a rare case of a patient with coronary embolism with a specific pearl-like embolus attributed to atrial fibrillation. For this patient, we used a balloon-based technique to successfully remove the embolus from the coronary artery.

Is compromised intestinal barrier integrity responsible for the poor prognosis in critically ill patients with pre-existing hyperglycemia?

BACKGROUND: Compromised intestinal barrier integrity can be independently driven by hyperglycemia, and both hyperglycemia and intestinal barrier injury are associated with poor prognosis in critical illness. This study investigated the intestinal barrier biomarkers in critically ill patients, to explore the role of compromised intestinal barrier integrity on the prognosis of critically ill patients with pre-existing hyperglycemia. METHODS: This was a retrospective observational study. The relationships between intestinal barrier biomarkers and glycated hemoglobin A1c (HbA1c), fasting blood glucose (FBG), indicators of clinical characteristics, disease severity, and prognosis in critically ill patients were investigated. Then the metrics mentioned above were compared between survivors and non-survivors, the risk factors of 90-day mortality were investigated by logistic regression analysis. Further, patients were divided into HbA1c < 6.5% Group and HbA1c ≥ 6.5% Group, metrics mentioned above were compared between these two groups. RESULTS: A total of 109 patients with critical illness were included in the study. D-lactate and lipopolysaccharide (LPS) were associated with sequential organ failure assessment (SOFA) score and 90-day mortality. LPS was an independent risk factor of 90-day mortality. DAO, NEU (neutrophil) proportion, temperature, lactate were lower in HbA1c ≥ 6.5% Group while D-lactate, LPS, indicators of disease severity and prognosis showed no statistical difference between HbA1c < 6.5% Group and HbA1c ≥ 6.5% Group. CONCLUSIONS: Intestinal barrier integrity is associated with the disease severity and prognosis in critical illness. Compromised intestinal barrier integrity might be responsible for the poor prognosis in critically ill patients with pre-existing hyperglycemia.

Transcription factor McWRKY71 induced by ozone stress regulates anthocyanin and proanthocyanidin biosynthesis in Malus crabapple.

In plants, anthocyanins and proanthocyanidins (PAs) play important roles in plant resistance to abiotic stress. In this study, ozone (O3) treatments caused the up-regulation of Malus crabapple structural genes McANS, McCHI, McANR and McF3H, which promoted anthocyanin and PA accumulation. We identified the WRKY transcription factor (TF) McWRKY71 by screening differentially expressed genes (DEGs) that were highly expressed in response to O3 stress from an RNA sequencing (RNA-seq) analysis. Overexpressing McWRKY71 increased the resistance of 'Orin' apple calli to O3 stress and promoted the accumulation of anthocyanins and PAs, which facilitated reactive oxygen species scavenging to further enhance O3 tolerance. Biochemical and molecular analyses showed that McWRKY71 interacted with McMYB12 and directly bound the McANR promoter to participate in the regulation of PA biosynthesis. These findings provide new insights into the WRKY TFs mechanisms that regulate the biosynthesis of secondary metabolites, which respond to O3 stress, in Malus crabapple.

FXYD domain containing ion transport regulator 5 (FXYD5) silencing promotes cell viability and alleviates inflammatory response in cerulein-induced AR42J cells by blocking JAK2/STAT3 signaling pathway.

Acute pancreatitis (AP), which causes severe morbidity and mortality, is a heavy burden for people clinically and financially. This study was designed to explore the mechanism of AP and try to find effective therapies against AP. The expression of FXYD5 was interfered by performing transfection. RT-qPCR and Western blot were utilized to measure FXYD5 expression. In addition, the viability, apoptosis and inflammatory response were evaluated using CCK-8, TUNEL and ELISA, respectively. Moreover, Western blot was employed to measure the expressions of apoptosis-, inflammation- and signaling pathway-related proteins. FXYD5 was found to be overexpressed in AP patients and AP cell model. The results showed that in cerulein-induced AR42J cells, cell viability was remarkably increased, and apoptosis was inhibited compared to the normal FXYD5-expressing group because FXYD5 was downregulated. Similarly, in such cells, interference with FXYD5 significantly suppressed the inflammatory response. In addition, Western blot analysis revealed that JAK2/STAT3 signaling was also strongly inhibited by FXYD5 interference. However, the effect of FXYD5 downregulation was reversed upon simultaneous activation of JAK2/STAT3 signaling. In conclusion, downregulation of FXYD5 could promote cell viability and alleviate inflammatory response in cerulein-induced AP via blocking JAK2/STAT3 signaling pathway.

LncRNA AZIN1-AS1 ameliorates myocardial ischemia-reperfusion injury by targeting miR-6838-5p/WNT3A axis to activate Wnt-ß/catenin signaling pathway.

Myocardial reperfusion, the effective therapy for acute myocardial infarction (AMI), commonly leads to myocardial ischemia/reperfusion (I/R) injury. The effects and functional mechanisms of LncRNA AZIN1-AS1 on myocardial I/R injury in vivo and vitro are not uncovered. In our present study, we established myocardial I/R injury model of mice and H/R injury model of cardiomyocytes and we discovered AZIN1-AS1 was decreased but miR-6838-5p was increased significantly in myocardial tissues injured by I/R treatment and H9c2 cells injured by hypoxia/reoxygenation (H/R) treatment. Silencing AZIN1-AS1 down-regulated cell viability but up-regulated apoptosis rate and CK-MB in addition LDH release of cardiomyocyte under H/R injury. However, overexpression of AZIN1-AS1 recovered abovementioned effects. Additionally, miR-6838-5p was found to be the direct target of AZIN1-AS1 and exhibited negative correlation with AZIN1-AS1. Moreover, miR-6838-5p inhibitor effectively eliminated the effects of AZIN1-AS1 knockdown on H/R-injured myocardial cells. Further experiments showed that WNT3A was the target of miR-6838-5p axis and overexpression of WNT3A also counteracted the roles of AZIN1-AS1 knockdown. Furthermore, knockdown of AZIN1-AS1 dramatically inhibited the activity of WNT-ß/catenin signaling pathway, which was recovered effectively by plasmid with overexpressing WNT3A. Therefore, this study firstly revealed that LncRNA AZIN1-AS1/miR-6838 axis inhibited apoptosis by activating WNT/ß-catenin pathway to protect mice or H9c2 cell from I/R-induced or H/R-induced injury respectively, which advised that AZIN1-AS1 could be regarded as a potential target for treating patients with AMI.

Intestinal fatty acid-binding protein, a biomarker of intestinal barrier dysfunction, increases with the progression of type 2 diabetes.

OBJECTIVE: To investigate serum intestinal fatty acid-binding protein (I-FABP) in two groups of patients with different duration of hyperglycemia in a cross-sectional study. MATERIALS AND METHODS: In the present study, a total of 280 individuals (158 outpatients and 122 inpatients) suffering from hyperglycemia were recruited between May and September 2019. The clinical information of all participants was collected from the hospital information system, including the duration of hyperglycemia, age, gender, hemoglobin A1c (HbA1c), 75-g oral glucose tolerance test including fasting plasma glucose (FPG), 2-hour plasma glucose (2hPG), fasting C-peptide (FC-pep), 2-hour C-peptide (2hC-pep), fasting insulin (FIns), and 2-hour insulin (2hIns). In addition, the morbidity of diabetic complications (retinopathy, neuropathy, and nephropathy) in the inpatient group was determined. Furthermore, the difference between 2hPG and FPG (ΔPG), the difference between 2hC-pep and FC-pep (ΔC-pep), and the difference between 2hIns and FIns (ΔIns) were calculated. The level of serum I-FABP, a biomarker of intestinal barrier (IB) dysfunction, was estimated by an enzyme-linked immunosorbent assay. RESULTS: For the outpatient group, the median duration of hyperglycemia was less than a year; the serum I-FABP level was positively correlated with age (R = 0.299, P < 0.001). For the inpatient group, the median duration of hyperglycemia was ten years; correlation analysis showed that the serum I-FABP level was positively associated with age and ΔPG (R = 0.286, P = 0.001; R = 0.250, P = 0.006, respectively) while negatively associated with FC-pep and 2hC-pep (R =  - 0.304, P = 0.001; R =  - 0.241, P = 0.008, respectively); multiple linear regression analysis showed that the serum I-FABP level was positively associated with the duration of hyperglycemia (ß = 0.362, P < 0.001); moreover, patients with retinopathy had a significantly higher I-FABP level than those without retinopathy (P = 0.001). CONCLUSIONS: In the outpatients whose duration of hyperglycemia was less than a year, the serum I-FABP level was positively associated with age. In the inpatients with different courses of diabetes, the serum I-FABP level was positively associated with the duration of hyperglycemia and glycemic variability but negatively associated with islet beta-cell function; moreover, the serum I-FABP level was higher in patients with retinopathy than in those without retinopathy, suggesting that the IB dysfunction got worse with the progression of diabetes.