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In this paper, the short-circuit robustness of 1200 V silicon carbide (SiC) trench MOSFETs with different gate structures has been investigated. The MOSFETs exhibited different failure modes under different DC bus voltages. For double trench SiC MOSFETs, failure modes are gate failure at lower dc bus voltages and thermal runaway at higher dc bus voltages, while failure modes for asymmetric trench SiC MOSFETs are soft failure and thermal runaway, respectively. The shortcircuit withstanding time (SCWT) of the asymmetric trench MOSFET is higher than that of the double trench MOSFETs. The thermal and mechanical stresses inside the devices during the short-circuit tests have been simulated to probe into the failure mechanisms and reveal the impact of the device structures on the device reliability. Finally, post-failure analysis has been carried out to verify the root causes of the device failure.
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Objective: To observe the effects of dynamic pressure monitoring on the lifespan of the extracorporeal circuit and the efficiency of solute removal during continuous renal replacement therapy (CRRT). Materials and Methods: A prospective observational study was performed at the West China Hospital of Sichuan University in the ICU. Analyses of the downloaded pressure data recorded by CRRT machines and the solute removal efficiencies, calculated by 2*Ce/(Cpre+Cpost), where Ce, Cpre, and Cpost are the concentrations of the effluent, pre-filter blood, and post-filter blood, respectively, were performed. Samples were collected at 0, 2, 6, 12, and 24 h when continuous veno-venous hemodiafiltration (CVVHDF) was used after the initiation of CRRT. Measurements in concentrations of creatinine, blood urea nitrogen, and ß2-microglobulin in the plasma and effluent were recorded. Results: Extracorporeal circuits characterized by moderate-to-severe (M-S) access outflow dysfunction (AOD) events, defined as access outflow pressure less than or equal to -200 mmHg for more than 5 min, had shorter median lifespans with no anticoagulation (32.3 vs. 10.90 h, P = 0.001) compared with the no M-S AOD events group. The significant outcome also existed in regional citrate anticoagulation (RCA) (72 vs. 42.47 h, P = 0.02). Moreover, Cox regression analysis revealed that the lack of M-S AOD events, RCA, or CVVHDF independently prolonged the circuit lifespan. All tested solutes removal efficiencies started to decline at 12 h. Furthermore, efficiencies of all solutes removal dropped obviously at 24 h when TMP ≥ 150 mmHg. Conclusion: RCA and CVVHDF predicted a longer circuit lifespan. M-S AOD events were associated with a shorter circuit lifespan when RCA or no anticoagulant was used. Replacement of extracorporeal circuit could be considered when running time of filter lasted up to 24 h with TMP ≥ 150 mmHg.
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The coronavirus disease 2019 (COVID-19) pandemic has a serious impact on health and economics worldwide. Even though the majority of patients present with moderate and mild symptoms, yet a considerable portion of patients need to be treated in the intensive care unit. Aside from dexamethasone, there is no established pharmacological therapy. Moreover, some of the currently tested drugs are contraindicated for special patient populations like remdesivir for patients with severely impaired renal function. On this background, several extracorporeal treatments are currently explored concerning their potential to improve the clinical course and outcome of critically ill patients with COVID-19. Here, we report the use of the Seraph 100 Microbind Affinity filter, which is licensed in the European Union for the removal of pathogens. Authorization for emergency use in patients with COVID-19 admitted to the intensive care unit with confirmed or imminent respiratory failure was granted by the U.S. Food and Drug Administration on April 17, 2020. A 53-year-old Caucasian male with a severe COVID-19 infection was treated with a Seraph Microbind Affinity filter hemoperfusion after clinical deterioration and commencement of mechanical ventilation. The 70-minute treatment at a blood flow of 200 mL/minute was well tolerated, and the patient was hemodynamically stable. The hemoperfusion reduced D-dimers dramatically. This case report suggests that the use of Seraph 100 Microbind Affinity filter hemoperfusion might have positive effects on the clinical course of critically ill patients with COVID-19. However, future prospective collection of data ideally in randomized trials will have to confirm whether the use of Seraph 100 Microbind Affinity filter hemoperfusion is an option of the treatment for COVID-19.
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OBJECTIVE: It is difficult to indicate whether the limitation in a failing Fontan circulation lies within the pulmonary vasculature or the heart. Such differentiation is crucial to direct adequate therapy. This study was set out to determine if a volume challenge could identify the limiting factor. METHODS AND STUDY POPULATION: Thirty-two catheterizations in 28 patients with a Fontan circulation were included. Pressures and oxygen saturations were measured before and after volume challenge (NaCl 0.9%; 15 cc/Kg). The changes in data were grouped based on the location of the major pressure increase. Ventricular function was measured in the resting state. RESULTS: The majority of the patients showed an increase in aortic oxygen saturation, mixed venous oxygen saturation, systolic, pulmonary and systemic venous pressures. The arterio-venous oxygen gradient decreased, suggesting an increase in cardiac output. Different patterns in pressure changes were observed. Most (n=17) showed a similar increase of ventricular end-diastolic pressure and mean venous pressure (MVP); some (n=7) showed a lower increase of MVP, suggesting pulmonary reserve and recruitment; others (n=8) showed a significant higher increase in MVP, suggesting increased pulmonary vascular resistance. All volume challenge was well tolerated. CONCLUSION: Most patients were preload-responsive. The pressure changes following volume load showed patterns with a potential of differentiating between patients with a major pulmonary or cardiac limiting factor.