[Analysis of the risk factors for delayed union of extra-articular fractures of the middle and lower third of the tibia treated by locking plate].

OBJECTIVE: To investigate the risk factors for delayed union of extra-articular fractures of the middle and lower third of the tibia treated by locking plate. METHODS: Total of 135 patients of extra-articular fractures of the middle and lower third of the tibia from January 2013 to December 2018 were retrospectively analyzed, including 85 males and 50 females, ranged from 19 to 80 years old. All cases were treated with locking plates. The patients were divided into union group and delayed union group according to the condition of fracture union. The risk factors of delayed healing were determined by univariate analysis of 14 factors that might affect fracture healing first, then the factors with significance were analyzed by binary Logistic regression. RESULTS: There were 13 patients of delayed union, and the rate of delayed union was 9.63%. Univariate analysis showed that delayed union was associated with age, smoking, reduction method, anemia and time of preoperative preparation. Regression analysis showed that age[OR=0.849, 95%CI（0.755, 0.954）, P=0.006], smoking[OR=0.020, 95%CI（0.002, 0.193）, P=0.001], reduction method[OR=23.924, 95%CI（2.210, 258.943）, P=0.009], anemia[OR=0.016, 95%CI（0.001, 0.289）, P=0.005] were the contributory factors for delayed union. CONCLUSION: Young age, smoking, closed reduction and anemia are the risk factors for delayed union of extra-articular fractures of the middle and lower third of the tibia treated by locking plate.

Glucosamine regulation of fibroblast growth factor 21 expression in liver and adipose tissues.

Obesity is associated with metabolic disorders. Fibroblast growth factor 21 (FGF21) has been recognized as important in metabolism. Glucosamine (GLN) has been demonstrated to perform diverse beneficial functions. This study aimed to reveal whether and how GLN would modulate FGF21 production in relation to metabolism. With in vivo model of normal diet (ND) and high-fat diet (HFD) mice receiving GLN injection and in vitro model of mouse AML12 liver cells and differentiated 3T3L1 adipocytes challenged with GLN, GLN appeared to improve the glucose metabolism in HFD and ND mice and to elevate FGF21 protein expression in HFD liver and to increase both FGF21 protein and mRNA levels in WAT from HFD and ND mice and it also upregulated FGF21 expression in both AML12 and differentiated 3T3L1 cells. By using inhibitors against various signaling pathways, p38, Akt, NF-κB, and PKA appeared potentially involved in GLN-mediated FGF21 production in AML12 cells; GLN was able to mediate activation of NF-κB, p38 or PKA/CREB signaling. Our accumulated findings suggest that GLN may potentially improve the metabolic performance by inducing FGF21 production in liver and adipose tissues and such induction in liver cells may act in part due to GLN induction of the NF-κB, p38 and PKA pathways.