scispace - formally typeset
J

Jonathan G. Schoenecker

Researcher at Vanderbilt University Medical Center

Publications -  132
Citations -  2221

Jonathan G. Schoenecker is an academic researcher from Vanderbilt University Medical Center. The author has contributed to research in topics: Medicine & Thrombin. The author has an hindex of 24, co-authored 114 publications receiving 1618 citations. Previous affiliations of Jonathan G. Schoenecker include Boston Children's Hospital & Monroe Carell Jr. Children's Hospital at Vanderbilt.

Papers
More filters
Journal ArticleDOI

The multifaceted role of fibrinogen in tissue injury and inflammation

TL;DR: There remains a critical need to define the precise temporal and spatial mechanisms by which fibrinogen-directed inflammatory events may dictate the severity of tissue injury and coordinate the remodeling and repair events essential to restore normal organ function.
Journal ArticleDOI

Complications and outcomes of diaphyseal forearm fracture intramedullary nailing: a comparison of pediatric and adolescent age groups.

TL;DR: Flexible intramedullary nailing is an effective technique for pediatric forearm fractures with good to excellent outcomes in 91%.
Journal ArticleDOI

Micro-computed tomography assessment of the progression of fracture healing in mice

TL;DR: Sample size estimates indicate that utilization of μCT requires fewer animals than biomechanics and thus is more practical for evaluating the healing femur in the mouse fracture model.
Journal ArticleDOI

Protease-activated receptor-2 signaling triggers dendritic cell development.

TL;DR: It is shown that a serine protease acting via protease-activated receptor-2 (PAR-2) stimulates the development of DC from bone marrow progenitor cells cultured in granulocyte-macrophage colony-stimulating factor and IL-4.
Journal ArticleDOI

Bisphosphonates Inhibit Osteosarcoma-Mediated Osteolysis Via Attenuation of Tumor Expression of MCP-1 and RANKL

TL;DR: It is established that osteosarcoma growth directly correlates with tumor‐induced osteolysis and activation of osteoclasts in vivo, and ZOL administration directly attenuates osteosARcoma production of RANKL/MCP‐1, reducing tumor‐ induced bone destruction.