Objective To valuate the effect of high energy ultrapulse CO2 laser on congenital melanocytic nevi of the orbit. Methods 46 patient with congenital melanocytic nevi of eyelid, 58 le-sions were vaporized with high energy ultrapulse CO2 laser. The area of the largest one was 3.0 cm×6.0 cm, and the smallest one was 0.3 cm×0.3 cm, with average of 1.3 cm×2.0 cm. The depth of the vaporizing reached the layer of lowest skin, even the orbicularis, aponeurosis and conjunctiva of tarsus, till no melanin on the wound in view, tried the best to reserve the normal follicle of eyelash. There was no eschar and bleeding on the wound during the procedure. Followed up lasted for 1 - 56 months, with average 12.9 months. Results 44 of 46 patients were satisfactory to the effect of the laser. The most of scars resulted from the vaporizing with the laser became evenness and smooth (50/58). The edge of eyelid looked normal after the laser. The excellent result was observed in 84.5 % (49/58) lesions, good in 10.3 % (6/58), and improved in 5.2 % (3/58). The overall effect was 94.8 % (55/58). And eyelashes were getting growth. Conclusion The treatment of con-genital melanocytic nevus of eyelid with high energy ultrapulse CO2 is a good method. But to be careful in selecting the lesions that may not he too large.

Chronic myeloid leukemia (CML) is a slowly progressing hematopoietic cell disorder. Sphingosine kinase 1 (SPHK1) plays established roles in tumor initiation, progression, and chemotherapy resistance in a wide range of cancers, including leukemia.However, small-molecule inhibitors targeting SPHK1 in CML still need to be developed. This study revealed the role of SPHK1 in CML and investigated the potential anti-leukemic activity of hirsuteine (HST), an indole alkaloid obtained from the oriental plant Uncaria rhynchophylla, in CML cells. These results suggest that SPHK1 is highly expressed in CML cells and that overexpression of SPHK1 represents poor clinical outcomes in CML patients. HST exposure led to G2/M phase arrest, cellular apoptosis, and downregulation of Cyclin B1 and CDC2 and cleavage of Caspase 3 and PARP in CML cells. HST shifted sphingolipid rheostat from sphingosine 1-phosphate (S1P) towards the ceramide coupled with a marked inhibition of SPHK1. Mechanistically, HST significantly blocked SPHK1/S1P/S1PR1 and BCR-ABL/PI3K/Akt pathways. In addition, HST can be docked with residues of SPHK1 and shifts the SPHK1 melting curve, indicating the potential protein-ligand interactions between SPHK1 and HST in both CML cells. SPHK1 overexpression impaired apoptosis and proliferation of CML cells induced by HST alone. These results suggest that HST, which may serve as a novel and specific SPHK1 inhibitor, exerts anti-leukemic activity by inhibiting the SPHK1/S1P/ S1PR1 and BCR-ABL/PI3K/Akt pathways in CML cells, thus conferring HST as a promising anti-leukemic drug for CML therapy in the future.