thromboplastin and Severe-Acute-Respiratory-Syndrome

Coronavirus disease 2019 (COVID-19) is a newly emerging human infectious disease that has quickly become a worldwide threat to health, mainly causing severe acute respiratory syndrome. In addition to the widely described respiratory syndrome, COVID-19 may cause life-treating complications directly or indirectly related to this infection. Among these, thrombotic complications have emerged as an important issue in patients with COVID-19 infection, particularly in patients in intensive care units. Thrombotic complications due to COVID-19 are likely to occur due to a pro-coagulant pattern encountered in some of these patients or to a progressive endothelial thrombo-inflammatory syndrome causing microvascular disease. In the present authors' experience, from five different hospitals in Italy and the UK, imaging has proved its utility in identifying these COVID-19-related thrombotic complications, with translational clinical relevance. The aim of this review is to illustrate thromboembolic complications directly or indirectly related to COVID-19 disease. Specifically, this review will show complications related to thromboembolism due to a pro-coagulant pattern from those likely related to an endothelial thrombo-inflammatory syndrome.

Topics: Adult; Aged; Anticoagulants; Brain Ischemia; Cause of Death; Communicable Diseases, Emerging; Coronavirus Infections; COVID-19; Female; Humans; Italy; Male; Middle Aged; Pandemics; Pneumonia, Viral; Pulmonary Embolism; Radiography, Thoracic; Severe Acute Respiratory Syndrome; Survival Analysis; Thromboembolism; Thromboplastin; Tomography, X-Ray Computed

Topics: Biomarkers; Dehydroepiandrosterone; Humans; Hydrocortisone; Inflammation; Respiration, Artificial; Sepsis; Severe Acute Respiratory Syndrome; Thromboplastin; United Kingdom

SARS coronavirus (SARS-CoV) is the etiologic agent of severe acute respiratory syndrome. The aim of this study was to construct Sars-CoV membrane (M), nucleocapsid (N) and spike 2 (S2) gene eukaryotic expression plasmids, and identify their expression in vitro. Gene fragments encoding N protein, M protein and S2 protein of SARS-CoV were amplified by PCR using cDNA obtained from lung samples of SARS patients as template, and subcloned into pcDNA3.1 vector to form eukaryotic expression plasmids. SARS-CoV protein eukaryotic expression plasmids were transfected respectively into CHO cells. Immunohistochemistry was employed to detect the expression of the structural proteins of SARS-CoV in transfected cells. SARS-CoV protein eukaryotic expression plasmids were successfully constructed by identification with digestion of restriction enzymes and sequencing. M, N and S2 proteins of SARS-CoV were detected in the cytoplasm of transfected CHO cells. It was concluded that these recombinant eukaryotic expression plasmids were constructed successfully, and SARS-CoV encoding proteins could activate transcription and expression of hfgl2 gene.

Topics: Animals; CHO Cells; Coronavirus M Proteins; Coronavirus Nucleocapsid Proteins; Cricetinae; Cricetulus; Fibrinogen; Genetic Vectors; Humans; Membrane Glycoproteins; Nucleocapsid Proteins; Plasmids; Recombinant Proteins; Severe Acute Respiratory Syndrome; Severe acute respiratory syndrome-related coronavirus; Spike Glycoprotein, Coronavirus; Thromboplastin; Transcription, Genetic; Transfection; Viral Envelope Proteins; Viral Matrix Proteins

Topics: Animals; Fibrinogen; Hepatitis B; Humans; Mice; Severe Acute Respiratory Syndrome; Thromboplastin