Rim plate in the treatment of hyperextension tibial plateau fracture: surgical technique and a series of cases

Abstract Background The existence of a “bare area” at the anterior plateau has been observed in cases where anteromedial and/or anterolateral proximal tibial locking plates are used for fixation in the treatment of hyperextension tibial plateau fractures (HTPF). The objective of this study is to introduce the rim plate fixation technique and evaluate its clinical efficacy. Methods A retrospective analysis was conducted on HTPF patients who underwent treatment with a combination of rim plate and proximal tibial locking plate at our hospital between April 2015 and December 2019. All patients were followed up for a minimum of one year. Open reduction and internal fixation were performed using anteromedial/posteromedial and/or anterolateral approaches for all cases. The surgical strategies employed for rim plate fixation were introduced, and both radiographic and clinical outcomes were assessed. Results Thirteen patients were enrolled in the study, with an average follow-up time of 4.3 years. Satisfactory reduction was achieved and radiographically maintained in all cases. Additionally, all patients exhibited satisfactory clinical functions, as evidenced by a mean hospital for special surgery (HSS) knee score of 96.2 ± 2.0 (range: 90–98). Furthermore, no wound complications or implant breakage were observed in this series. Conclusion The combination of the rim plate and proximal tibial plate proved to be an effective fixation configuration, resulting in satisfactory clinical outcomes

A Stromal Cell-Derived Factor 1α Analogue Improves Endothelial Cell Function in Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome

Abstract Endothelial cell (EC) dysfunction is a critical mediator of the acute respiratory distress syndrome (ARDS). Recent studies have demonstrated that stromal cell-derived factor 1α (SDF-1α) promotes EC barrier integrity. Our previous studies used a SDF-1α analogue CTCE-0214 (CTCE) in experimental sepsis and demonstrated that it attenuated vascular leak and modulated microRNA (miR) levels. We examined the hypothesis that CTCE improves EC function in lipopolysaccharide (LPS)-induced ARDS through increasing miR-126 expression. Human microvascular endothelial cells (HMVECs) were treated with thrombin to disrupt the EC integrity followed by incubation with CTCE or SDF-1α. Barrier function was determined by trans-endothelial electrical resistance assay. CTCE-induced alterations in miRNA expression and signaling pathways involved in barrier function were determined. Thrombin-induced vascular leak was abrogated by both CTCE and SDF-1α. CTCE also prevented thrombin-induced decreases of vascular endothelial (VE)-cadherin cell surface expression and expansion of the intercellular space. CTCE increased miR-126 levels and induced activation of AKT/Rac 1 signaling. Cotreatment with a miR-126 inhibitor blocked the protective effects of CTCE on AKT activation and endothelial permeability. In subsequent in vivo studies, ARDS was induced by intratracheal instillation of LPS. Intravenous injection of CTCE diminished the injury severity as evidenced by significant reductions in protein, immune cells, inflammatory cytokines and chemokines in the bronchoalveolar lavage fluid, increased miR-126 expression and decreased pulmonary vascular leak and alveolar edema. Taken together, our data show that CTCE improves endothelial barrier integrity through increased expression of miR-126 and activation of Rac 1 signaling and represents an important potential therapeutic strategy in ARDS

Coating Urchinlike Gold Nanoparticles with Polypyrrole Thin Shells To Produce Photothermal Agents with High Stability and Photothermal Transduction Efficiency

Photothermal therapy using inorganic nanoparticles (NPs) is a promising technique for the selective treatment of tumor cells because of their capability to convert the absorbed radiation into heat energy. Although anisotropic gold (Au) NPs present an excellent photothermal effect, the poor structural stability during storage and/or upon laser irradiation still limits their practical application as efficient photothermal agents. With the aim of improving the stability, in this work we adopted biocompatible polypyrrole (PPy) as the shell material for coating urchinlike Au NPs. The experimental results indicate that a several nanometer PPy shell is enough to maintain the structural stability of NPs. In comparison to the bare NPs, PPy-coated NPs exhibit improved structural stability toward storage, heat, pH, and laser irradiation. In addition, the thin shell of PPy also enhances the photothermal transduction efficiency (η) of PPy-coated Au NPs, resulting from the absorption of PPy in the red and near-infrared (NIR) regions. For example, the PPy-coated Au NPs with an Au core diameter of 120 nm and a PPy shell of 6.0 nm exhibit an η of 24.0% at 808 nm, which is much higher than that of bare Au NPs (η = 11.0%). As a primary attempt at photothermal therapy, the PPy-coated Au NPs with a 6.0 nm PPy shell exhibit an 80% death rate of Hela cells under 808 nm NIR laser irradiation

Polypyrrole-Coated Chainlike Gold Nanoparticle Architectures with the 808 nm Photothermal Transduction Efficiency up to 70%

Aqueous Au nanoparticles (NPs) are employed as the building blocks to construct chainlike self-assembly architectures, which greatly enhance the photothermal performance at 808 nm. Biocompatible polypyrrole (PPy) is further adopted as the package material to coat Au NP chains, producing stable photothermal agents. As a result of contributions from chainlike Au, the PPy shell, as well as the Au–PPy composite structures, the capability of photothermal transduction at 808 nm is greatly enhanced, represented by the high photothermal transduction efficiency up to 70%. Primary animal experiment proves that the current composite photothermal agents are efficient in inhibiting tumor growth under an 808 nm irradiation, showing the potentials for in vivo photothermal therapy

Hesperidin Prevents Retinal and Plasma Abnormalities in Streptozotocin-Induced Diabetic Rats

Diabetic retinopathy is a complex disease that potentially involves increased production of advanced glycosylation end products (AGEs) and elevated aldose reductase (AR) activity, which are related with oxidative stress and inflammation. The aim of this study was to investigate the effects of hesperidin on retinal and plasma abnormalities in streptozotocin-induced diabetic rats. Hesperidin (100, 200 mg/kg daily) was given to diabetic rats for 12 weeks. The blood-retina breakdown (BRB) was determined after 2 weeks of treatment followed by the measurement of related physiological parameters with ELISA kits and immunohistochemistry staining at the end of the study. Elevated AR activity and blood glucose, increased retinal levels of vascular endothelial growth factor (VEGF), ICAM-1, TNF-α, IL-1β and AGEs as well as reduced retina thickness were observed in diabetic rats. Hesperidin treatment significantly suppressed BRB breakdown and increased retina thickness, reduced blood glucose, AR activity and retinal TNF-α, ICAM-1, VEGF, IL-1β and AGEs levels. Furthermore, treatment with hesperidin significantly reduced plasma malondialdehyde (MDA) levels and increased SOD activity in diabetic rats. These data demonstrated that hesperidin attenuates retina and plasma abnormalities via anti-angiogenic, anti-inflammatory and antioxidative effects, as well as the inhibitory effect on polyol pathway and AGEs accumulation