Novel 3D printed lattice structure titanium cages evaluated in an ovine model of interbody fusion.

Background: The use of intervertebral cages within the interbody fusion setting is ubiquitous. Synthetic cages are predominantly manufactured using materials such as Ti and PEEK. With the advent of additive manufacturing techniques, it is now possible to spatially vary complex 3D geometric features within interbody devices, enabling the devices to match the stiffness of native tissue and better promote bony integration.

Beyond Placement of Pedicle Screws - New Applications for Robotics in Spine Surgery: A Multi-Surgeon, Single-Institution Experience.

Interest in robotic-assisted spine surgery has grown as surgeon comfort and technology has evolved to maximize benefits of time saving and precision. However, the Food and Drug Administration (FDA) has currently only approved robotics to assist in determining the ideal trajectory for pedicle screw placement after extensive research supporting its efficacy and efficiency. To be considered a durable and effective option, robotics need to expand beyond the indication of just placing pedicle screws.

A Novel Radiographic Indicator of Developmental Cervical Stenosis.

Background: Developmental cervical stenosis of the spinal canal predisposes patients to neural compression and loss of function. The Torg-Pavlov ratio has been shown to provide high sensitivity but low specificity for identifying developmental cervical stenosis. A more sensitive and specific radiographic index has not been reported to our knowledge.

Unique CD8+ T Cell-Mediated Immune Responses Primed in the Liver.

Background: The liver immune environment is tightly regulated to balance immune activation with immune tolerance. Understanding the dominant immune pathways initiated in the liver is important because the liver is a site for cell transplantation, such as for islet and hepatocyte transplantation. The purpose of this study is to examine the consequences of alloimmune stimulation when allogeneic cells are transplanted to the liver in comparison to a different immune locale, such as the kidney.

Low incidence of symptomatic thromboembolic events after total ankle arthroplasty without routine use of chemoprophylaxis.

Background: There is little evidence regarding the incidence of symptomatic venous thromboembolism (VTE) following total ankle arthroplasty (TAA) to allow formulation of treatment recommendations. The purpose of this study was to determine the incidence of symptomatic VTE events after TAA without use of chemoprophylaxis and to identify risk factors contributing to the occurrence of VTEs.

Methods: We conducted a retrospective chart review of 637 patients (664 ankles) who received a TAA between May 2007 and January 2014 and had a minimum follow-up of 3 months.

Targeting pro-inflammatory cytokines following joint injury: acute intra-articular inhibition of interleukin-1 following knee injury prevents post-traumatic arthritis.

Introduction: Post-traumatic arthritis (PTA) is a progressive, degenerative response to joint injury, such as articular fracture. The pro-inflammatory cytokines, interleukin 1(IL-1) and tumor necrosis factor alpha (TNF-α), are acutely elevated following joint injury and remain elevated for prolonged periods post-injury. To investigate the role of local and systemic inflammation in the development of post-traumatic arthritis, we targeted both the initial acute local inflammatory response and a prolonged 4 week systemic inflammatory response by inhibiting IL-1 or TNF-α following articular fracture in the mouse knee.

The role of cytokines in posttraumatic arthritis.

The development of arthritis after joint injury is commonly known as posttraumatic arthritis (PTA). The inciting traumatic event may range from cartilage contusion and bone bruise combined with meniscus or ligament tear, to intra-articular fracture. End-stage PTA is often indistinguishable from primary osteoarthritis.

Cytotoxic effector function of CD4-independent, CD8(+) T cells is mediated by TNF-α/TNFR.

Background: Liver parenchymal cell allografts initiate both CD4-dependent and CD4-independent, CD8(+) T cell-mediated acute rejection pathways. The magnitude of allospecific CD8(+) T cell in vivo cytotoxic effector function is maximal when primed in the presence of CD4(+) T cells. The current studies were conducted to determine if and how CD4(+) T cells might influence cytotoxic effector mechanisms.

Inhibition of recall responses through complementary therapies targeting CD8+ T-cell- and alloantibody-dependent allocytotoxicity in sensitized transplant recipients.

Allospecific T memory cell responses in transplant recipients arise from environmental exposure to previous transplantation or cross-reactive heterologous immunity. Unfortunately, these memory responses pose a significant barrier to the survival of transplanted tissue. We have previously reported that concurrent inhibition of CD154 and LFA-1 suppresses primary CD8-dependent rejection responses that are not controlled by conventional immunosuppressive strategies.

Direct anterior approach for total hip arthroplasty using the fracture table.

Total hip arthroplasty is a successful procedure for treatment of painful hip arthritides. A large volume of literature is devoted to the patient outcomes and complication profiles of the commonly used surgical approaches to help refine the technique, enhance patient function, and limit cost and patient morbidity. The direct anterior approach has been reported using a fracture table to promote surgical exposure to the proximal femur.

Recipient immune repertoire and engraftment site influence the immune pathway effecting acute hepatocellular allograft rejection.

As novel acute allograft rejection mechanisms are being discovered, determining the conditions that promote or subvert these distinct rejection pathways is important to interpret the clinical relevance of these pathways for specific recipient groups as well as specific tissue and organ transplants. We have employed a versatile hepatocellular allograft model to analyze how the host immune repertoire and immune locale influences the phenotype of the rejection pathway. In addition, we investigated how peripheral monitoring of cellular and humoral immune parameters correlates with the activity of a specific rejection pathway.

Critical role of effector macrophages in mediating CD4-dependent alloimmune injury of transplanted liver parenchymal cells.

Despite the recognition that humoral rejection is an important cause of allograft injury, the mechanism of Ab-mediated injury to allograft parenchyma is not well understood. We used a well-characterized murine hepatocellular allograft model to determine the mechanism of Ab-mediated destruction of transplanted liver parenchymal cells. In this model, allogeneic hepatocytes are transplanted into CD8-deficient hosts to focus on CD4-dependent, alloantibody-mediated rejection.

Disparate primary and secondary allospecific CD8+ T cell cytolytic effector function in the presence or absence of host CD4+ T cells.

The role of CD4+ T cells in promoting CD8+ T cell effector activity in response to transplant Ags in vivo has not been reported. We used a hepatocellular allograft model known to initiate both CD4-dependent and CD4-independent rejection responses to investigate the contribution of CD4+ T cells to the development, function, and persistence of allospecific CD8+ T cell effectors in vivo. Complete MHC-mismatched hepatocellular allografts were transplanted into C57BL/6 (CD4-sufficient) or CD4 knockout (CD4-deficient) hosts.

Targeting LFA-1 and cd154 suppresses the in vivo activation and development of cytolytic (cd4-Independent) CD8+ T cells.

Short-term immunotherapy targeting both LFA-1 and CD40/CD154 costimulation produces synergistic effects such that long-term allograft survival is achieved in the majority of recipients. This immunotherapeutic strategy has been reported to induce the development of CD4+ regulatory T cells. In the current study, the mechanisms by which this immunotherapeutic strategy prevents CD8+ T cell-dependent hepatocyte rejection in CD4 knockout mice were examined.

CD4+ T-cell-dependent immune damage of liver parenchymal cells is mediated by alloantibody.

Background: Allogeneic hepatocytes initiate both CD4- and CD8-dependent rejection responses. The current studies address the hypothesis that acute damage of allogeneic liver parenchymal cells by the CD4-dependent pathway is alloantibody-mediated and examines immune conditions which promote activation of this pathway.

Methods: The role of alloantibody in CD4-dependent hepatocyte rejection was evaluated by assessing hepatocyte (FVB/N, H-2q) survival in CD8-depleted B-cell knockout (KO) (H-2b) recipients and by monitoring hepatocyte survival in C57BL/6.