RESUMEN
Tendinopathy is a leading cause of mobility issues. Currently, the cell-matrix interactions involved in the development of tendinopathy are not fully understood. In vitro tendon models provide a unique tool for addressing this knowledge gap as they permit fine control over biochemical, micromechanical, and structural aspects of the local environment to explore cell-matrix interactions. In this study, direct-write, near-field electrospinning of gelatin solution was implemented to fabricate micron-scale fibrous scaffolds that mimic native collagen fiber size and orientation. The stiffness of these fibrous scaffolds was found to be controllable between 1 MPa and 8 MPa using different crosslinking methods (EDC, DHT, DHT+EDC) or through altering the duration of crosslinking with EDC (1 h to 24 h). EDC crosslinking provided the greatest fiber stability, surviving up to 3 weeks in vitro. Differences in stiffness resulted in phenotypic changes for equine tenocytes with low stiffness fibers (â¼1 MPa) promoting an elongated nuclear aspect ratio while those on high stiffness fibers (â¼8 MPa) were rounded. High stiffness fibers resulted in the upregulation of matrix metalloproteinase (MMPs) and proteoglycans (possible indicators for tendinopathy) relative to low stiffness fibers. These results demonstrate the feasibility of direct-written gelatin scaffolds as tendon in vitro models and provide evidence that matrix mechanical properties may be crucial factors in cell-matrix interactions during tendinopathy formation.
Asunto(s)
Gelatina , Tenocitos , Andamios del Tejido , Gelatina/química , Animales , Caballos , Tenocitos/citología , Tenocitos/metabolismo , Andamios del Tejido/química , Fenómenos Mecánicos , Regulación de la Expresión Génica , Forma de la Célula , Fenómenos BiomecánicosRESUMEN
Sweet's syndrome (acute febrile neutrophilic dermatosis) is an uncommon inflammatory condition most often associated with painful skin lesions of the head, neck, and upper extremities. To the authors' knowledge, this case report is the only published record of the necrotizing clinical variant of Sweet's syndrome in the periorbital space. This case follows a 91-year-old female who presented with generalized cutaneous eruptions of tender erythematous plaques, including a necrotic plaque of the left upper eyelid, and pancytopenia. A biopsy of an inner thigh lesion was consistent with Sweet's syndrome. Initially diagnosed with preseptal cellulitis, the patient experienced marked clinical improvement with corticosteroids. This, coupled with the histopathologic findings of her thigh biopsy and the absence of eyelid margins, led to the diagnosis of periorbital necrotizing Sweet's syndrome. Although cases of Sweet's syndrome in the periorbital region are rare, these diagnoses should not be overlooked and may be critical to patient care.
Asunto(s)
Enfermedades de la Piel , Síndrome de Sweet , Humanos , Femenino , Anciano de 80 o más Años , Síndrome de Sweet/complicaciones , Síndrome de Sweet/diagnóstico , Síndrome de Sweet/tratamiento farmacológico , Celulitis (Flemón)/complicaciones , CaraRESUMEN
Quadriceps tendon ruptures are devastating injuries that impair the extensor mechanism of the knee. Complete tears require prompt surgical intervention in order to ensure optimal clinical outcomes. Chronic, neglected ruptures- marked by severe extensor lag, muscular atrophy, and tendon retraction- are difficult to treat. Further, severe patella baja complicates surgical planning. While there is no consensus on optimal treatment for these injuries, many different techniques have been proposed. Unlike many of these approaches, our technique focuses on restoration of patellar height via patellar tendon lengthening. Once patellar height is restored, quadriceps tendon repair can be performed using the native quadriceps tendon. Both the patellar tendon lengthening and the quadriceps tendon repair are augmented with bioinductive implants to ensure optimal healing environments, enabling us to reestablish native extensor mechanism function.