Objective To investigate the changes of composition and level of serum free fatty acid (FFA)of children with critical illness.Methods The serum FFAs were measured by gas chromatography in 61 children(27 critically ill eases and 34 healthy controls).The changes in serum FFA was compared between healthy children and critically ill cases.We also evaluated the difference between the data before treatment and those after recovery in children with critical illness.Results Levels of palmitic acid,palmitoleic acid.oleic acid,docosanoic acid.arachidonic acid(AA)and eicosapentaenoic acid(EPA)were evidently higher in the critically ill children than those of healthy control(P＜0.05);children underthe recovery stage showed higher levels of myristic acid,palmitic acid,palmitoleic acid,oleic acid,arechidic acid as compared with healthy controis(P＜0.05).Conclusion Compexed with healthy children,the profile of serum FFA was quite different in critically ill and recovery ones.Critical illness may influence the profile of serum FFA.

Objective To evaluate the clinical results of a combination of lateral buttress plate and medical antiglide plate internal fixation for biocondylar tibia plateau fractures. Methods A total of 26 biocondylar tibia plateau fractures belonged to type Ⅴ and type Ⅵ according to Schatzker classification and treated with open reduction. Lateral buttress plate and medical antiglide plate were applied for limited internal fixation. The follow up continued till fracture healing to observe if there existed bone dislocation and determine the range of knee motion and Iowa knee score. Results No obvious shift of fragment was found in 26 cases with mean range of knee motion for 92? and mean Iowa knee score for 93 points. Conclusion Combination of lateral buttress plate and medical antiglide plate is a good method for internal fixation of biocondylar tibia plateau fractures,but the conclusion needs large number of clinical verifications.

Objective:To perform a prospective cohort study to identify individual susceptibility of glucocorticoid (GC) -associated osteonecrosis of the femoral head (GA-ONFH) and their clinical and genetic risk factors. Methods:The present prospective cohort study enrolled patients who received their first GC therapy between July 2015 and January 2018 at Zhongshan Hospital. All patients did not receive any GC treatment before enrollment. Further, they planned to start GC treatment with the dose (equivalent prednisone) of ≥30 mg/d, lasted ≥3 weeks, or pulse dose ≥200 mg/d, lasted ≥3 d. Blood samples were collected before GC treatment to evaluate bone metabolism and its released factors. Hip MRI was performed at the 1st, 3rd, 6th, 12th and 24th month to diagnose GA-ONFH. All patients were followed-up for ≥2 years. The endpoint was regarded as diagnosis of GA-ONFH or completion of 2 years follow-up. Lasso regression was performed to determine which clinical features were associated with GA-ONFH. A nested case-control sub-cohort (A, n=12) was established prospectively based on the main cohort by 1∶1 matching. Whole exome sequencing was performed to screen differential and functional candidate single nucleotide polymorphisms and insertion-deletions (SNP/InDels). Another sub-cohort (B, n=50) was constructed retrospectively in patients with GA-ONFH and non-ONFH patients received standard high dose GC treatment for more than two years. The candidate SNP/InDels were verified by Sanger sequencing based on the patients from sub-cohort B. Results:A total of 96 patients were enrolled of which 88 of them (32 males and 56 females, mean age 42.30 years) completed follow-up. Eight cases (9.1%) were diagnosed with GA-ONFH. The median time from the start of GC therapy to the diagnosis of ONFH was 53.00(34.00,13.50) days. The baseline characteristics, such as age, sex and body mass index, indicated no significant difference between the ONFH group and the non-ONFH group. The cumulative GC dose of the ONFH patients in the first month was higher than that of non-ONFH [32.74(29.55, 47.05) mg/kg vs. 24.00(21.10, 29.45) mg/kg, Z=-2.410, P=0.016]. However, there was no significant difference of patients who underwent pulse therapy (37.5% vs. 10.0%, adjusted χ 2=2.829, P=0.093). The ratio of serum apolipoprotein B/apolipoprotein A1 (ApoB/ApoA1) in patients with ONFH was higher than that in non-ONFH group before GC use [0.95(0.80, 1.50) vs. 0.70(0.60, 0.80), Z=-2.875, P=0.000]. Due to the multicollinearity, Lasso regression model was performed to reduce overfitting. All variables were included in the model. The results suggested that higher ApoB/ApoA1 ratio, lower serum β-c-terminal telopeptide (β-CTX) and higher cumulative GC dose in the first month were the top three risk factors of GA-ONFH. This model had an accuracy of 0.982 in internal validation. Seven differential candidate SNP/InDels were found by whole exome sequencing of sub-cohort A. We further verified these SNP/InDels in sub-cohort B. The patients with COLEC12 mutation (rs2305027, G1816A) were at risk of GA-ONFH ( OR=6.00, 95% CI: 1.17, 30.73). Conclusion:Higher first-month GC dose, lower serum β-CTX level before treatment, higher ApoB/ApoA1 ratio and COLEC12 mutation (rs2305027, G1816A) could increase the risk of GA-ONFH.