A rare case of severe pulmonary embolism revealed by consciousness disorders.

Over the several years, only few cases of consciousness was diagnosed as pulmonary embolism in the world. The obstruction of the pulmonary arterial tree is viewed as the source of pulmonary embolism, and eventually trigger the severe cardiopulmonary failure. Diagnosis of pulmonary embolism is dependent on the imaging data, such as the computed tomographic detection. Above 50% of patients with pulmonary embolism are normotensive and they have neither echocardiographic nor laboratory signs of right heart dysfunction. Therefore, the precise prognosis of acute pulmonary embolism presented with rare characteristic is important to improve risk management. In some circumstance, the diagnosis of pulmonary embolism remains a challenge with atypical characterization presented in this case. A case report of this is given to accumulate the diagnostic experience for further analysis. Herein, we report a case of a severe pulmonary embolism that revealed by consciousness disorders. This report highlights the extracorporeal membrane oxygenation (ECMO) could be the only life-sustaining and the possibility of the solution treatment of acute pulmonary embolism.

Arsenic trioxide induces gasdermin E mediated pyroptosis in astroglioma cells.

BACKGROUND: Arsenic trioxide (ATO) has been proved useful for the treatment of acute promyelocytic leukemia (APL). Apoptosis is the result of the cytotoxic effect of ATO, apoptotic mediated cell death confirmed by DNA fragmentation and Annexin V staining. Although signaling associated with ATO-induced apoptosis has been well defined, it is still unknown whether other forms of cell death are involved in ATO-induced cell death. METHODS: Western blotting, cytotoxicity assay, transmission electron microscopy were used to evaluate other forms of cell death in U251 cells. RESULTS: We found that pyroptotic mediated cell death was observed in U251 cells after ATO treatment, which was confirmed by observing the increased gasdermin E (GSDME) cleavage, lactate dehydrogenase (LDH) release and transmission electron microscopy imaging. Consistent with previous results, caspase-3 was activated by ATO, which was also important for GSDME cleavage and subsequent pyroptosis. CONCLUSIONS: We reported that GSDME mediated pyroptosis involved in ATO induced cell death in astroglioma cells.

Carfilzomib Inhibits Constitutive NF-κB Activation in Mantle Cell Lymphoma B Cells and Leads to the Induction of Apoptosis.

Mantle cell lymphoma (MCL) remains incurable and new treatments are needed, especially in the relapsed/refractory setting. We therefore investigated the effects of carfilzomib, a novel, long-acting, second-generation proteasome inhibitor, in MCL cells. Eight established MCL cell lines and freshly isolated primary MCL cells were treated with carfilzomib. Cell proliferation was assessed by a 3H-thymidine incorporation assay. Cell apoptosis was evaluated by flow cytometry with annexin V and propidium iodide. Electrophoresis mobility shift (EMSA), Western blot, and luciferase assays were used to analyze NF-κB activation and related signaling proteins. Carfilzomib inhibited growth and induced apoptosis in both established MCL cell lines and freshly isolated primary MCL cells in a dose-dependent manner. In contrast, carfilzomib was less toxic to normal peripheral blood mononuclear cells from healthy individuals. The carfilzomib-induced apoptosis of MCL cells occurred in a caspase-dependent manner through both intrinsic and extrinsic caspase pathways. In addition, carfilzomib inhibited constitutive activation of the NF-κB signaling cascade, both in MCL cell lines and primary MCL cells, by completely blocking the phosphorylation of IκBα. Our results demonstrate that carfilzomib can induce growth arrest and apoptosis in MCL cells and that the mechanism may involve the NF-κB signaling pathway.