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There remains a lack of data on the epidemiological characteristics of surgical site infection (SSI) following the open reduction and internal fixation (ORIF) of intra‐articular fractures of distal femur, and the aim of this study was to solve this key clinical issue. The electronic medical records (EMRs) of patients who underwent ORIF for distal femoral fracture from January 2013 to December 2017 were reviewed to identify those who developed a SSI. Then, we conducted univariate Chi‐square analyses and used a multivariate logistic regression analysis model to determine the adjusted risk factors associated with SSI. A total of 724 patients who underwent ORIF of intra‐articular fractures of the distal femur were studied retrospectively, and 29 patients had postoperative SSIs. The overall incidence of SSIs was 4.0% (29/724), with deep SSIs being 1.5% (11/724), and superficial SSIs being 2.5% (18/724). Staphylococcus aureus was the most common causative pathogen (8, 42.1%), followed by mixed bacterial pathogens (5, 26.3%). Open fracture, obesity, smoking, and diabetes mellitus were identified as the adjusted risk factors associated with SSIs. Although modification of these risk factors may be difficult, patients and families should be counselled regarding their increased risk of SSI because these patients potentially benefit from focused perioperative medical optimisation.

Osteoarthritis (OA) is a major joint disease in which inflammatory cytokine interleukin-1β (IL-1β) and matrix metalloproteinases (MMPs) play a pivotal role. Isoliquiritigenin has been reported to have anti-inflammation activity. In this study, the effect of isoliquiritigenin on IL-1β-induced production of matrix metalloproteinase and nuclear factor κB (NF-κB) activation was analyzed. We treated primary cultured articular chondrocytes with isoliquiritigenin and the expressions of MMPs were analyzed on mRNA and protein level. The phosphorylation of IκBa and p65 was analyzed to detect NF-κB activation. We also used in vivo model by treating mice with isoliquiritigenin and detecting the level of MMPs. IL-1β induced NF-κB activation and MMP-1, MMP-3, MMP-9, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4 and ADAMTS-5 production on chondrocytes. A 10-μM isoliquiritigenin treatment significantly inhibited IL-1β-induced NF-κB activation and these MMPs production on chondrocytes. Injecting isoliquiritigenin into rat knee joint also inhibited IL-1β-induced NF-κB activation and MMPs production in articular cartilage. Isoliquiritigenin treatment inhibited IL-1β-induced MMPs production and NF-κB activation both in vitro and in vivo, suggesting a potential therapeutic role of isoliquiritigenin to treat osteoarthritis.

Patients involved with female, living in institutions, osteoporosis, low vision, dizziness, dementia, respiration diseases and cardiac diseases were at risk for a second contralateral hip fracture after the initial hip fracture.

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BackgroundBased on published data, we aimed to quantitatively elucidate the possible genetic influence of rs17561 and rs1800587 polymorphisms of the IL1A (interleukin 1 alpha) gene in the susceptibility to several autoimmune diseases.MethodsA series of meta-analyses were carried out. After database searching, we utilized our inclusion/exclusion criteria to screen and include the eligible studies. Passociation (P value of association test), Bonferroni-corrected Passociation value; false discovery rate (FDR)-corrected Passociation, ORs (odd ratios), and 95% CI (confidence interval) were generated to assess the magnitudes of genetic relationships.ResultsA total of 35 eligible articles were included. Pooled analysis data of both rs17561 and rs1800587 in the overall population indicated a negative association between cases of autoimmune diseases and negative controls (all Passociation>0.05, Bonferroni-corrected Passociation>0.05, FDR-corrected Passociation>0.05). Similar results were found in most subgroup analyses (all Passociation>0.05, Bonferroni-corrected Passociation>0.05, FDR-corrected Passociation>0.05), apart from the rs1800587 in the Graves’ disease subgroup, which showed an increased risk in some cases, compared with controls, under the models of allele vs. , carrier vs. , + vs. , and vs. (all Passociation<0.05, Bonferroni-corrected Passociation<0.05, FDR-corrected Passociation>0.05, OR>1).ConclusionBased on the available data, genotype of the rs1800587 polymorphism within IL1A gene may be associated with an increased Graves’ disease risk. We did not see evidence regarding a positive role for rs1800587 or rs17561 in the risk of other autoimmune diseases, such as systemic sclerosis or rheumatoid arthritis. These conclusions still merit further data support and molecular exploration.