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https://www.selleckchem.com/products/TW-37.html Objective To investigate the underlying molecular mechanisms of brain injury in rats after cardiac arrest and cardiopulmonary resuscitation (CPR) by observing necroptosis of brain cells and changes of 90 cytokines in brain tissue. Methods Sprague-Dawley (SD) rats were divided into Sham group (n = 10) and cardiac arrest group (n = 10) according to random number table method. The model of asphyxia cardiac arrest for 6 minutes followed by CPR model was established. Tracheal intubation in Sham rats were routinely performed without inducing cardiac arrest. Neurological deficit score (NDS) was evaluated, blood samples were collected and rats were sacrificed, then serum S100B level was measured by enzyme linked immunosorbent assay (ELISA) on the third day after CPR. Necroptotic cells in brain were detected by immunofluorescence staining. The levels of 90 cytokines expression in brain were measured by antibody array. The relative ratio of the two groups of protein expression ≥ 1.5 or ≤ 0.5 and P less then 0.05 repr nerve cells.Objective To observe the value of heart-type fatty acid-binding protein (H-FABP) and echocardiographic indexes in the diagnosis of cardiac insufficiency in sepsis. Methods A prospective observational study was conducted. Eighty patients with sepsis admitted to the department of critical care medicine of the First Affiliated Hospital of Medical College of Shihezi University from October 2016 to January 2018 were enrolled. General clinical data such as gender, age, acute physiology and chronic health evaluation II (APACHE II), sequential organ failure assessment (SOFA) score, hospitalization time and 28-day mortality were recorded. Echocardiographic indexes at 1, 3, 7, 10 days after diagnosis, and white blood cell (WBC), neutrophilic granulocyte percentage (N%), N-terminal pro-brain natriuretic peptide (NT-proBNP), serum H-FABP level were recorded. Sepsis patients were divided into normal cardiac function

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