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1.
China Journal of Orthopaedics and Traumatology ; (12): 454-461, 2015.
Article in Chinese | WPRIM | ID: wpr-241018

ABSTRACT

<p><b>OBJECTIVE</b>TFo compare the efficacy and complications rate of intramedullary (IM) nailing or K-wire versus plating fixation for clavicular fractures.</p><p><b>METHODS</b>Pubmed, Embase, Cochrane Library databases, CNKI, VIP and Wangfang databases were searched to find all randomized or quasi-randomized controlled trials of clavicle fractures using plating versus IM nailing or K-wire. The methodologic quality of the studies was assessed. After independent study selection by 2 authors ,data were collected and extracted independently. Outcomes of postoperative shoulder functional measurement, the efficacy and information of the operation and complications rate were meta-analyzed using RevMan 5 software.</p><p><b>RESULTS</b>Nine hundreds and seventy-six patients in 10 randomized controlled trials (RCTs) and 3 quasi-RCTs were involved in the meta-analysis,of which 5 studies compared the K-wire and the plating fixations and 8 studies compared the IM nailing and the plating fixations. The overall odds ratio(OR) (with 95% CI) of the operation efficacy for K-wire versus the plating was 3.79 (1.93, 7.46). The overall weighted mean difference (with 95% CI) of Constant Shoulder score for plating versus IM fixation was -1.39 (-3.43, 0.65) in 6 studies. The overall OR of the plating versus IM nailing was 9.34(2.70, 32.32) for the overall major complications in 5 studies and 5.04 (1.52,16.77) for the revision rate in 5 studies.</p><p><b>CONCLUSION</b>The current limited evidences suggested that the IM fixation could reduce the incidences of the overall major complications and the revision surgery, while the post-operative efficacy of the plating was superior to the K-wire. More high quality RCTs are still needed in the future.</p>


Subject(s)
Humans , Bone Nails , Bone Wires , Clavicle , Wounds and Injuries , General Surgery , Fracture Fixation, Intramedullary , Methods , Fractures, Bone , General Surgery , Randomized Controlled Trials as Topic
2.
Journal of Applied Clinical Pediatrics ; (24)2006.
Article in Chinese | WPRIM | ID: wpr-640320

ABSTRACT

Objective To screen the mutation of certain gene of a 10-years-old boy with multiple xanthomas and very high level of cholesterol who could be diagnosed as homozygous familial hypercholesterolemia (FH),to explore the relationship between the genotype and phenotype,and to discuss the molecular pathologic mechanism.Methods The basic information of life styles were asked from the boy and his familial members.The blood was drown to examine the lipid and genes.The boy was examined with electrocardiogram examination,ultrasonography and coronary CT angiography (CTA) to evaluate the degree of atherosclerosis.Peripheral blood DNA of the boy and his parents were extracted by phenol-chloroform method and investigated for mutations of promoter and all 18 exons of low density lipoprotein receptor(LDLR) gene.Screening was carried out by using Touch-down polymerase chain reaction (PCR) and single strand conformation polymorphism(PCR-SSCP),combined with DNA sequence analysis.In addition,the apolipoprotein B100 gene(apoB100) for known mutations (R3500Q) which caused familial defective apoB100 was screened by PCR-DNA sequence analysis.Results 1.The level of cholesterol of his parents were higher than the normal.2.Several clinical manifestations of atherosclerosis were detected from that boy.Increased intima-media thickness and plaques were detected in the common carotid artery.Mitral valve regurgitation was found by echocardiography.Coronary stenosis was confirmed by CTA.3.No mutations R3500Q of apoB100 was observed.4.A homozygous mutation in exon13 of the LDLR gene (D601Y) were identified in the boy and his parents harbour D601Y heterozygous mutation due to a single base pair substitution of G for T in the codon for residue 1864.Conclusions The final diagnosis of the boy with multiple xanthomas was homozygous FH.His disease was caused by D601Y homozygous mutation in exon13 of the LDLR gene inherited from his heterozygous parents.

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