Orbit in a Box: A Simplified Technique for Patient-Specific Virtually Planned Orbital Floor Reconstruction.

Purpose: Possibilities for the reconstruction of orbital floor fractures have been extensive for years with regard to materials, methods and differential indications and are inconsistent worldwide. With the spread of CAD/CAM techniques, new and mostly time-consuming possibilities for orbital floor reconstructions have been added.

Methods: The simple and time-efficient CT-to-patient-specific implant workflow presented here shows that a "form-box" can be created from a patient's computer tomography data set using planning software and a 3D printer.

Caspase-1 is hepatoprotective during trauma and hemorrhagic shock by reducing liver injury and inflammation.

Adaptive immune responses are induced in liver after major stresses such as hemorrhagic shock (HS) and trauma. There is emerging evidence that the inflammasome, the multiprotein platform that induces caspase-1 activation and promotes interleukin (IL)-1β and IL-18 processing, is activated in response to cellular oxidative stress, such as after hypoxia, ischemia and HS. Additionally, damage-associated molecular patterns, such as those released after injury, have been shown to activate the inflammasome and caspase-1 through the NOD-like receptor (NLR) NLRP3.

Models of lower extremity damage in mice: time course of organ damage and immune response.

Background: Post-traumatic inflammatory changes have been identified as major causes of altered organ function and failure. Both hemorrhage and soft tissue damage induce these inflammatory changes. Exposure to heterologous bone in animal models has recently been shown to mimic this inflammatory response in a stable and reproducible fashion.

Complement factor 3 deficiency attenuates hemorrhagic shock-related hepatic injury and systemic inflammatory response syndrome.

Although complement activation is known to occur in the setting of severe hemorrhagic shock and tissue trauma (HS/T), the extent to which complement drives the initial inflammatory response and end-organ damage is uncertain. In this study, complement factor 3-deficient (C3(-/-)) mice and wild-type control mice were subjected to 1.5-h hemorrhagic shock, bilateral femur fracture, and soft tissue injury, followed by 4.

Systemic inflammation and liver injury following hemorrhagic shock and peripheral tissue trauma involve functional TLR9 signaling on bone marrow-derived cells and parenchymal cells.

Hemorrhagic shock due to trauma (HS/T) induces an inflammatory response that can contribute to end-organ injury. The pathways involved in the initiation and propagation of HS/T-induced inflammation are incompletely understood. Here, we hypothesized that the DNA sensor TLR9 would have a role in inflammatory signaling after HS/T.