RESUMEN
It is widely believed that perinatal cardiomyocyte terminal differentiation blocks cytokinesis, thereby causing binucleation and limiting regenerative repair after injury. This suggests that heart growth should occur entirely by cardiomyocyte hypertrophy during preadolescence when, in mice, cardiac mass increases many-fold over a few weeks. Here, we show that a thyroid hormone surge activates the IGF-1/IGF-1-R/Akt pathway on postnatal day 15 and initiates a brief but intense proliferative burst of predominantly binuclear cardiomyocytes. This proliferation increases cardiomyocyte numbers by ~40%, causing a major disparity between heart and cardiomyocyte growth. Also, the response to cardiac injury at postnatal day 15 is intermediate between that observed at postnatal days 2 and 21, further suggesting persistence of cardiomyocyte proliferative capacity beyond the perinatal period. If replicated in humans, this may allow novel regenerative therapies for heart diseases.
Asunto(s)
Diferenciación Celular , Proliferación Celular , Corazón/crecimiento & desarrollo , Miocitos Cardíacos/citología , Animales , Separación Celular , Masculino , Ratones , Ratones Endogámicos C57BL , Miocitos Cardíacos/fisiología , Triyodotironina/metabolismoRESUMEN
We describe a 37-year-old man complaining of right back pain and gait disturbance. He had a big soft tumor on his right back, hemihypertrophy of the right lower extremity, and right thoracic scoliosis. We diagnosed Klippel-Trenaunay-Weber syndrome based on the pathological findings of the soft tumor. Computed tomography (CT) scan revealed severe spinal stenosis due to a hypertrophic vertebral body and facet joint at T7. Treatment by decompression of hypertrophic bone led to complete neurological recovery. To our knowledge, no case has been reported of Klippel-Trenaunay-Weber syndrome with myelopathy which originated from thoracic scoliosis with a hypertrophic facet joint and vertebral body. We suggest that the cause of myelopathy in Klippel-Trenaunay-Weber syndrome originated not only from arteriovenous fistula, medullary angioma, and extradural hemangioma but also vertebral hypertrophy with scoliosis.
Asunto(s)
Síndrome de Klippel-Trenaunay-Weber/diagnóstico , Escoliosis/diagnóstico , Enfermedades de la Médula Espinal/diagnóstico , Vértebras Torácicas/patología , Adulto , Biopsia con Aguja , Estudios de Seguimiento , Humanos , Hipertrofia/complicaciones , Hipertrofia/diagnóstico , Síndrome de Klippel-Trenaunay-Weber/complicaciones , Laminectomía/métodos , Masculino , Escoliosis/complicaciones , Escoliosis/cirugía , Enfermedades de la Médula Espinal/complicaciones , Vértebras Torácicas/diagnóstico por imagen , Vértebras Torácicas/cirugía , Tomografía Computarizada por Rayos X , Resultado del TratamientoRESUMEN
INTRODUCTION: Type III fracture of the tibial tubercle by Watson-Jones, or type IIIa injury according to John Ogden's classification has been well described and its management is now well codified in standard orthopaedic textbooks. MATERIALS AND METHODS: The authors present a case of type III fracture of the tibial tubercle associated with an avulsion of the tibialis anterior muscle. RESULTS: We demonstrated the effectiveness of bioabsorbable material for fixing the fracture preventing the need for removal of metalware, and that the anterior tibialis muscle had been stripped by the injury. CONCLUSION: A displaced type III fracture of the tibial tubercle may have an associated with avulsion of the tibialis anterior muscle, particularly in adolescent athletes. Prompt recognition and appropriate surgical treatment can give an excellent outcome.