13 research outputs found
A case report of nivolumab-induced myasthenia gravis and myositis in a metastatic renal cell carcinoma patient
We present a 78-year-old male with renal cell carcinoma who developed myasthenia gravis complicated by myositis after nivolumab administration, which was verified by the presence of antibodies against the acetylcholine receptor. The initial symptom was posterior neck pain, and biochemical examination of blood showed elevated levels of hepatic enzymes and creatine phosphokinase. The level of antibody against the acetylcholine receptor increased 4.1-fold. His condition progressed rapidly resulting in respiratory failure 15 days after conservative therapy
A case report of nivolumab-induced myasthenia gravis and myositis in a metastatic renal cell carcinoma patient
TNF Receptor-Associated Factor 1 Expressed in Resident Lung Cells Is Required for the Development of Allergic Lung Inflammation
Tetraspanin CD9 Negatively Regulates Lipopolysaccharide-Induced Macrophage Activation and Lung Inflammation
4-Hydroxy-2-nonenal induces endothelial cell injury via PKCdelta and biphasic JNK activation
4-Hydroxy-2-nonenal (4-HNE), a major product generated during oxidative stress, exhibits
cytotoxic effects; however, the mechanisms of 4-HNE-induced endothelial cell injury are not
well defined. To explore this issue, we examined how 4-HNE damages human umbilical vein
endothelial cells (HUVECs) and found that 4-HNE induced biphasic activation of c-Jun
N-terminal kinase (JNK). Both pre- and post-treatment of HUVECs with SP600125, a specific
JNK inhibitor, significantly suppressed the cytotoxic effects of 4-HNE. Inhibition of
protein kinase Cd (PKCd), which was also phosphorylated by 4-HNE, reduced endothelial
cell injury as well as late-phase JNK phosphorylation elicited by 4-HNE. Inversely,
pre-treatment of HUVECs with SP600125 suppressed PKCd activation. Taken together, these
results support the concept that 4-HNE induces vascular endothelial cell injury by the interaction
between biphasic JNK activation and the PKCd pathway