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1.
J Orthop Trauma ; 36(3): 152-156, 2022 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-34294667

RESUMEN

OBJECTIVES: To investigate patient demographics, injury characteristics, radiographic outcomes, and identify risk factors for developing posttraumatic arthritis in high-energy transsyndesmotic ankle fracture dislocations or "logsplitter" injuries. DESIGN: Retrospective cohort study. SETTING: Academic level one trauma center. PATIENTS/PARTICIPANTS: Twenty-seven adult patients with logsplitter injuries. INTERVENTION: All patients were treated with open reduction internal fixation, with possible addition of syndesmosis screw(s) and deltoid repair. MAIN OUTCOME MEASUREMENTS: The rate of posttraumatic arthritis at one year along with rate and reasons for reoperation. RESULTS: Twenty-seven patients were included with a mean follow-up of 14.5 ± 12.5 months. At one-year postoperative, 14 of the 20 patients (70%) demonstrated posttraumatic arthritis. Two patients (7.4%) went onto fusion. The reoperation rate was 51.9%. There was no significant difference in the arthritis rate with the number of syndesmosis screws used, quality of reduction, or addition of deltoid repair. CONCLUSIONS: The logsplitter injury is one with devastating outcomes and high rates of arthritis; it should be considered separately from conventional ankle fractures. The role of deltoid repair remains unclear. Further study of this injury pattern is required. LEVEL OF EVIDENCE: Prognostic Level IV. See Instructions for Authors for a complete description of levels of evidence.


Asunto(s)
Fracturas de Tobillo , Artritis , Fractura-Luxación , Adulto , Tobillo , Fracturas de Tobillo/diagnóstico por imagen , Fracturas de Tobillo/cirugía , Artritis/etiología , Artritis/cirugía , Fijación Interna de Fracturas , Humanos , Estudios Retrospectivos , Resultado del Tratamiento
2.
Am J Pathol ; 187(5): 1121-1133, 2017 May.
Artículo en Inglés | MEDLINE | ID: mdl-28320610

RESUMEN

Carbon monoxide-releasing molecules (CORMs) suppress inflammation by reducing polymorphonuclear leukocyte (PMN) recruitment to the affected organs. We investigated modulation of PMN-endothelial cell adhesive interactions by water-soluble CORM-401 using an experimental model of endotoxemia in vitro. Human umbilical vein endothelial cells (HUVEC) grown on laminar-flow perfusion channels were stimulated with 1 µg/mL lipopolysaccharide for 6 hours and perfused with 100 µmol/L CORM-401 (or inactive compound iCORM-401)-pretreated PMN for 5 minutes in the presence of 1.0 dyn/cm2 shear stress. HUVEC: PMN co-cultures were perfused for additional 15 minutes with PMN-free medium containing CORM-401/inactive CORM-401. The experiments were videorecorded (phase-contrast microscopy), and PMN adhesion/migration were assessed off-line. In parallel, CORM-401-dependent modulation of PMN chemotaxis, F-actin expression/distribution, and actin-regulating pathways [eg, p21-activated protein kinases (PAK1/2) and extracellular signal-regulated kinase (ERK)/C-Jun N-terminal kinase (JNK) mitogen-activated protein kinases (MAPK)] were assessed in response to N-formyl-methionyl-leucyl-phenylalanine (fMLP) stimulation. Pretreating PMN with CORM-401 did not suppress PMN adhesion to HUVEC, but significantly reduced PMN transendothelial migration (P < 0.0001) and fMLP-induced PMN chemotaxis (ie, migration directionality and velocity). These changes were associated with CORM-401-dependent suppression of F-actin levels/cellular distribution and fMLP-induced phosphorylation of PAK1/2 and ERK/JNK MAPK (P < 0.05). CORM-401 had no effect on p38 MAPK activation. In summary, this study demonstrates, for the first time, CORM-401-dependent suppression of neutrophil migratory potential associated with modulation of PAK1/2 and ERK/JNK MAPK signaling and F-actin dynamics.


Asunto(s)
Monóxido de Carbono/metabolismo , Movimiento Celular/fisiología , Neutrófilos/fisiología , Actinas/metabolismo , Antígenos CD18/metabolismo , Adhesión Celular/fisiología , Células Cultivadas , Células Endoteliales de la Vena Umbilical Humana , Humanos , MAP Quinasa Quinasa 4/metabolismo , Sistema de Señalización de MAP Quinasas/fisiología , Quinasas de Proteína Quinasa Activadas por Mitógenos/metabolismo , Fosforilación/fisiología , Molécula-1 de Adhesión Celular Endotelial de Plaqueta/metabolismo
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