NF-κB pathway play a role in SCD1 deficiency-induced ceramide de novo synthesis.

Stearoyl-CoA-desaturase 1 (SCD1) deficiency mediates apoptosis in colorectal cancer cells by promoting ceramide de novo synthesis. The mechanisms underlying the cross-talk between SCD1 and ceramide synthesis have not been explored. We treated colorectal cancer cells with an SCD1 inhibitor and examined the effects on gene expression, cell growth, and cellular lipid contents. The main effect of SCD1 inhibition on the fatty acid contents of colorectal cancer cells was a decrease in monounsaturated fatty acids (MUFAs). RNA sequencing (RNA-seq) showed that the most intense alteration of gene expression after SCD1 inhibition occurred in the NF-κB signaling pathway. Further experiments revealed that SCD1 inhibition resulted in increased levels of phosphorylated NF-κB p65 and increased nuclear translocation of NF-κB p65. Treatment with an NF-κB inhibitor eliminated several effects of SCD1 inhibition, mainly including overexpression of serine palmitoyltransferase1 (SPT1), elevation of dihydroceramide contents, and suppression of cell growth. Furthermore, treatment with supplemental oleate counteracted the SCD1-induced NF-κB activation and downstream effects. In summary, our data demonstrate that the NF-κB pathway plays a role in SCD1 deficiency-induced ceramide de novo synthesis in colorectal cancer cells, and that reduced MUFA levels contribute to the course.

The anatomic basis and the clinical treatment of the elbow joint stiffness after electric injury / 中华烧伤杂志

<p><b>OBJECTIVE</b>To explore the optimal method for the treatment of the elbow joint stiffness accompanied with neural injury after electrical injury.</p><p><b>METHODS</b>Thirty adult cadaver elbows were fixed and dissected to observe the attachments of the ligaments and the muscles around the joint, and its relationship with the major nerves. Ten patients with electric burns with stiffness of the elbow joint were treated by means of loosening the anterior and posterior fascicles of radial and ulnar collateral ligaments, at the same time down shifting the insertion of flexor muscles, replacing the ulnar nerve anteriorly, in order to reconstruct flexor and extension functions of the elbow. The effect was evaluated with biomechanics criteria.</p><p><b>RESULTS</b>Through anatomical study, it was revealed that contracture of the posterior fascicles of the radial and ulnar collateral ligaments and triceps brachii muscle would result in stiffness of the elbow joint, and contracture due to disuse of the two anterior fascicles of the radial and ulnar collateral ligaments and M.biceps brachii would produce flexion deformity of the elbow joint. Postoperatively, the functions of the elbow joints of all the 10 patients recovered satisfactorily. Follow-up from 1 to 3 years showed no change in the range of flexion and extension movements of the elbows, and on the contrary, mobility of the elbow joints was improved.</p><p><b>CONCLUSION</b>Loosening of the anterior and posterior fascicles of the two collateral ligaments and replacement of insertions of biceps and triceps are pivotal in the treatment of stiffness of the elbow joint. Meanwhile lowering the origins of forearm flexor muscles on epicondylus and replacing anteriorly the ulnar nerve can further improve the flexion, function of the joint and relieve compression of the nerve.</p>