ABSTRACT
OBJECTIVE@#To evaluate the clinical effect of bridge combined internal fixation system in the treatment of periprosthesis fracture of femur after hip replacement.@*METHODS@#From October 2016 to June 2018, 5 patients of periprosthesis fractures of femur classified type B1 and type C in Vancouver were treated by open reduction and bridging combined with internal fixation, including 2 males and 3 females, with ages of 68, 70, 74, 75, 79 years;type B1 fractures in 4 and type C fractures in 1. Causes of injury:1 case of traffic injury, 4 cases of fall. After the operation, the patients were followed up for complications and fracture healing time by clinical and imaging examination, and Parker activity score was performed.@*RESULTS@#The wounds of 5 patients healed without infection. One case of DVT was confirmed by venography. Five patients were followed up, and the durations were 2, 8, 9, 10, 15 months. One patient died of myocardial infarction 2 months after operation. The average healing time was 12.5 weeks. No loss of reduction or failure of internal fixation was found. Two patients could walk without protection and 1 patient needed to rely on single crutch. One case of periprosthetic fracture had to walk with a single crutch before operation and move indoors with two crutches after operation. The average Parker activity score was 51.8% before operation.@*CONCLUSION@#The bridge combined internal fixation system can be used to fix the fracture after hip replacement with stable femoral prosthesis.
Subject(s)
Aged , Female , Humans , Male , Arthroplasty, Replacement, Hip , Bone Plates , Femoral Fractures , General Surgery , Fracture Fixation, Internal , Fracture Healing , Periprosthetic Fractures , General Surgery , Radiography , Reoperation , Retrospective Studies , Treatment OutcomeABSTRACT
AIM:To explore the therapeutic effect of a novel Rho kinase inhibitor FSD-C10 onβ-amyloid pro-tein precursor (APP)/presenilin-1 (PS1) double transgenic mice.METHODS: The transgenic mice overexpressing hu-man APP with the Swedish mutation (695) and human PS1 with ΔE9 mutation at the age of 8 months were used in this study.The mice were randomly divided into model group and FSD-C10 intervention group, and wild-type mice at the same age served as normal controls .The mice in FSD-C10 intervention group were treated with FSD-C10 (25 mg· kg-1 · d-1 ) for 2 months by intraperitoneal injection .The mice in model group and the wild-type mice were injected with saline in the similar manner.Morris water maze (MWM) test was applied to examine the capacity of learning and memory .The Aβ1-42 deposition, Tau protein phosphorylation , and the expression of β-site APP-cleaving enzyme ( BACE) as well as inflammato-ry molecules, such as TLR-4 and NF-Κb, and M1/M2 microglial markers, such as Inos and Arg-1, were determined by the methods of immunohistochemistry and Western blot .RESULTS: Compared with model group , FSD-C10 significantly improved the learning and memory abilities of APP/PS1 double transgenic mice , accompanied by reduced Aβ1-42 deposi-tion, Tau protein phosphorylation and BACE expression in the hippocampus .The intervention of FSD-C10 decreased the protein levels of TLR-4 and p-NF-Κb, reduced the expression of Inos and increased the expression of Arg-1 in the brain tissues.CONCLUSION:The novel Rho kinase inhibitor FSD-C10 improves the capacity of spatial learning and memory in APP/PS1 double transgenic mice , which may be related to the inhibition of TLRs/NF-Κb signaling pathway , the reduction of the secretion of inflammatory molecules and the polarization of anti-inflammatory M2 microglia, thus improving the in-flammatory microenvironment of the brain in APP/PS1 double transgenic mice .
ABSTRACT
AIM:To explore the therapeutic effect of a novel Rho kinase inhibitor FSD-C10 onβ-amyloid pro-tein precursor (APP)/presenilin-1 (PS1) double transgenic mice.METHODS: The transgenic mice overexpressing hu-man APP with the Swedish mutation (695) and human PS1 with ΔE9 mutation at the age of 8 months were used in this study.The mice were randomly divided into model group and FSD-C10 intervention group, and wild-type mice at the same age served as normal controls .The mice in FSD-C10 intervention group were treated with FSD-C10 (25 mg· kg-1 · d-1 ) for 2 months by intraperitoneal injection .The mice in model group and the wild-type mice were injected with saline in the similar manner.Morris water maze (MWM) test was applied to examine the capacity of learning and memory .The Aβ1-42 deposition, Tau protein phosphorylation , and the expression of β-site APP-cleaving enzyme ( BACE) as well as inflammato-ry molecules, such as TLR-4 and NF-Κb, and M1/M2 microglial markers, such as Inos and Arg-1, were determined by the methods of immunohistochemistry and Western blot .RESULTS: Compared with model group , FSD-C10 significantly improved the learning and memory abilities of APP/PS1 double transgenic mice , accompanied by reduced Aβ1-42 deposi-tion, Tau protein phosphorylation and BACE expression in the hippocampus .The intervention of FSD-C10 decreased the protein levels of TLR-4 and p-NF-Κb, reduced the expression of Inos and increased the expression of Arg-1 in the brain tissues.CONCLUSION:The novel Rho kinase inhibitor FSD-C10 improves the capacity of spatial learning and memory in APP/PS1 double transgenic mice , which may be related to the inhibition of TLRs/NF-Κb signaling pathway , the reduction of the secretion of inflammatory molecules and the polarization of anti-inflammatory M2 microglia, thus improving the in-flammatory microenvironment of the brain in APP/PS1 double transgenic mice .