BACKGROUND Management of incessant electrical storm is poorly defined. These 2 case studies demonstrate a simplified percutaneous approach to achieve stellate ganglion ablation (SGA) and to promptly control malignant ventricular arrhythmias. CASE REPORT This report describes 2 patients with deteriorating hemodynamics, progressive ventricular arrhythmias, and worsening heart failure, managed with emergent percutaneous fluoroscopically-guided bilateral SGA to achieve bilateral cardiac sympathetic denervation. While supine and intubated, the left and then right stellate ganglion were identified guided by anatomic landmarks. Using a 22-guage, 3.5-inch spinal needle, contrast dye was injected with appropriate outline of the stellate ganglion at the uncinate process of the C6 vertebra. Bupivacaine 0.5% was injected, followed by phenol 6%. Successful SGA was confirmed by intentional Horner’s syndrome with bilateral eye lag. The procedures were completed in about 30 min without complications and there was a dramatic reduction in ventricular arrhythmias. CONCLUSIONS Emergent percutaneous bilateral SGA can be accomplished with a brief procedure resulting in management of electrical storm.BACKGROUND Freshly isolated mouse embryonic fibroblasts (MEFs) have great proliferation capacity but quickly enter senescent state after several rounds of cell cycle, a process called premature senescence. Cellular senescence can be induced by various stresses such as telomere erosion, DNA damage, and oncogenic signaling. But the contribution of other molecules, such as growth factors, to cellular senescence is incompletely understood. This study aimed to compare the gene expression difference between non-senescent and senescent MEFs to identify the key molecule(s) involved in the spontaneous senescence of MEFs. MATERIAL AND METHODS Primary MEFs were isolated from E12.5 pregnant C57/BL6 mice. The cells were continuously cultured in Dulbecco’s Modified Eagle Medium for 9 passages. SA-ß-Gal staining was used as an indicator of cell senescence. The supernatant from primary MEFs (P1 medium) or Passage 6 MEFs (P6 medium) were used to culture freshly isolated MEFs to observe the effects on cell senescence state. Gene expression profiles of primary and senescent MEFs were investigated by RNA-Seq to find the key genes involved in cell senescence. Adipocyte differentiation assay was used to evaluate the stemness of MEFs cultured in FGF2-stimulated medium. RESULTS The senescence of MEFs cultured in the P1 medium was alleviated when compared to the P6 medium. Downregulation of FGF2 expression was revealed by RNA-Seq and further confirmed by real-time quantitative polymerase chain reaction and western blot. FGF2-stimulated medium also had anti-senescence function and could maintain the differentiation ability of MEFs. CONCLUSIONS The premature senescence of MEFs was at least partially caused by FGF2 deficiency. Exogenous FGF2 could alleviate the senescent phenotype.High fat diet (HFD) treated mouse is widely used as experimental animal model for hyperlipidemia and hyperglycemia study. Many factors contribute to establish animal model that meant to simulate high fat and glucose diet induced phenotypes. In the present study, four strains of experiment mouse treated by HFD were used to explore the impact of mouse strain on lipid profile, glucose level, and major inflammation cytokines. HFD fed Kunming and ICR mouse gained significantly higher body weight than control which was not shown by C57BL/6 and BALB/c mouse. All four strains fed by HFD has heavier liver and adipose tissue than control ones. Obvious fat droplets and enlarged adipose cells were observed in obese mouse of four strains. Birinapant datasheet Additionally, obese mouse showed typical response to glucose and insulin load in OGTT and ITT. Serum TC, LDL-c, and TC/HDL-c ratio, but not TG, increased in all four strains. Major inflammatory cytokines and insulin level showed little changes in obese mouse as well (P less then 0.05) The present study could provide basic information for diet induced obesity developed by four commonly used experimental mouse strains.BACKGROUND Prompt and potent antiplatelet effects are important aspects of management of ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI). We evaluated the association between platelet-derived thrombogenicity during PPCI and enzymatic infarct size in STEMI patients.Methods and ResultsPlatelet-derived thrombogenicity was assessed in 127 STEMI patients undergoing PPCI by (1) the area under the flow-pressure curve for the PL-chip (PL18-AUC10) using the total thrombus-formation analysis system (T-TAS); and (2) P2Y12reaction units (PRU) using the VerifyNow system. Patients were divided into 2 groups (High and Low) based on median PL18-AUC10during PPCI. PRU levels during PPCI were suboptimal in both the High and Low PL18-AUC10groups (median [interquartile range] 266 [231-311] vs. 272 [217-317], respectively; P=0.95). The percentage of final Thrombolysis in Myocardial Infarction (TIMI) 3 flow was lower in the High PL18-AUC10group (75% vs. 90%; P=0.021), whereas corrected TIMI frame count (31.3±2.5 vs. 21.0±2.6; P=0.005) and the incidence of slow-flow/no-reflow phenomenon (31% vs. 11%, P=0.0055) were higher. The area under the curve for creatine kinase (AUCCK) was greater in the High PL18-AUC10group (95,231±7,275 IU/L h vs. 62,239±7,333 IU/L h; P=0.0018). Multivariate regression analysis identified high PL18-AUC10during PPCI (β=0.29, P=0.0006) and poor initial TIMI flow (β=0.37, P less then 0.0001) as independent determinants of AUCCK. CONCLUSIONS T-TAS-based high platelet-derived thrombogenicity during PPCI was associated with enzymatic infarct size in patients with STEMI.BACKGROUND To take full advantage of transesophageal echocardiography (TEE) during cardiopulmonary resuscitation (CPR), we propose a flowchart derived from representative cases.Methods and ResultsTEE was used in patients requiring CPR to obtain information potentially helpful for rescue. TEE navigated the CPR procedures (navigation TEE), identified the possible cause of arrest (focus TEE), and optimized treatment while checking for pitfalls (secure TEE). In addition, TEE corrected prehospital misdiagnoses and detected new complications caused by CPR. CONCLUSIONS TEE provides valuable information without interrupting CPR procedures. It is hoped that our flowchart may facilitate goal-directed, efficient assessment.