Objective To explore the treatment of laterognathism of the mandible.Methods Nineteen cases of laterognathism of the mandible were treated by Lefort Ⅰ osteotomy,sagittal split ramus osteotomy,genioplasty,anterior mandibular subapical osteotomy and prosthesis implantation,respectively,and their efficacy was evaluated and clinical experience summarized.Results The nineteen cases were followed up for average 12 months after the treatments and all the patients were satisfied with the surgical effects.All osteotomy lines healed well and there were no complications,such as root damage or neurotrosis.Conclusions The orthognathic procedure for laterognathism of the mandible should be selected according to the types and locations of asymmetry deformities.Anterior mandibular subapical osteotomy combined with mandibular cosmetic surgery for slight laterognathism of the mandible could achieve satisfactory results.

Objective To investigate the application of the frontal branch of superficial temporal vessels pedicled flap in repairing lower eyelid ectropion.Methods Eight cases were collected from patients diagnosed with lower eyelid ectropion in our hospital from April 2012 to April 2015.In phase 1 of operation,the dilators were implanted into the frontal branch of superficial temporal vessels and fully expanded by normal saline injection;In phase 2,the scar of lower eyelid was incised,and the expanded forehead flaps were transferred to cover the wound after the lower eyelid released back to normal anatomy location;In phase 3,the flap delay operation was manipulated 3 weeks after phase 2,and the left wound after scar excision was finished by pedicle division 1 week later.Results All patients in the study showed a good appearance and function of lower eyelid.There were no complications such as flap congestion and necrosis occurred.Meantime there were no relapses observed according to the follow-ups ranging from 6 months to 1 year.Conclusions The application of the frontal branch of superficial temporal vessels pedicled flap shows a promising procedure in treatment of lower eyelid ectropion.

Objective: To analyze the association of cytogenetic abnormalities with the prognosis of chronic myeloid leukemia (CML) patients in tyrosine kinase inhibitors (TKI) era. Methods: Karyotype analysis of chromosome G-banding was carried out in 387 newly diagnosed CML patients by short-term culture of bone marrow cells. The correlation of cytogenetic abnormalities and CML progression was explored in combination with ABL tyrosine point mutations. Result: Of 387 patients with positive BCR-ABL fusion gene assayed by fluorescence in situ hybridization (FISH) technique, 94.1% (364/387) patients were Ph positive and 5.9% (23/387) Ph negative; 320 patients (87.9%) had a translocation t (9;22) (q34;q11) and 5 (1.4%) a variant translocation t (v;22) . Additional cytogenetic aberrations (ACA) at diagnosis were found in 10.7% (39/387) Ph⁺ patients, major route ACA in 22 (56.4%) cases and minor route ACA in 15 (38.5%) cases and 2 patients (5.1%) lacked the Y chromosome (−Y) ; 23.4% (71/303) patients occurred ACA during TKI treatment and the most frequent abnormalities were abnormal chromosome numbersd, which were likely associated with high proportion of disease progression (χ²=168.21, P<0.001) and ABL tyrosine point mutations (χ²=29.04, P<0.001) . Newly diagnosed CML-CP patients with t (9;22) (q34;q11) had a longer event-free survival (EFS) and disease-free survival (DFS) rates than that of patients with ACA (P=0.037; P=0.003) , while the overall survival (OS) had no significant differences (P=0.209) . As for CML-CP patients that occurred ACA during TKI therapy would have a marked low OS, EFS and DFS (all P<0.001) compared with no ACA occurred patients. Survival of advanced patients that occurred ACA were dramatically reduced. Conclusion ACA often emerged during the disease progress in CML patients, regular and timely detection of chromosomes karyotype and ABL tyrosine point mutations during TKI treatment was important for therapeutic evaluation, progress and prognosis of CML.