Publications by authors named "Jason Taub"

Object: Infections following spine surgery negatively affect patient quality of life (QOL) and impose a significant financial burden on the health care system. Postoperative wound infections occur at higher rates following dorsal cervical procedures than ventral procedures. Quantifying the health outcomes and costs associated with infections following dorsal cervical procedures may help to guide treatment strategies to minimize the deleterious consequences of these infections.

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Background: No United States-based clinical trials have attempted delivery of biological therapies directly to the spinal cord for treatment of amyotrophic lateral sclerosis (ALS) because of the lack of a meaningful US Food and Drug Administration-authorized cell candidate and a validated delivery approach.

Objective: To assess safety of delivery of a neural stem cell-based treatment into the upper lumbar segments of the ALS spinal cord in the first US Food and Drug Administration-authorized phase I trial.

Methods: Each microinjection series comprised 5 injections (10 μL/injection) separated by 4 mm.

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Background: Only recently have data been published attempting to validate a technology and technique suitable for targeted delivery of biological payloads to the human spinal cord.

Objective: To characterize the development and evolution of a spine-stabilized microinjection platform as a vehicle for biologics delivery to the cervical and thoracolumbar spine on the basis of preclinical experience in both non-Good Laboratory Practice (GLP) experimental series and GLP studies.

Methods: Our laboratory completed > 100 cervical and lumbar porcine microinjection procedures between July 2004 and June 2010.

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Study Design: Assessment of long-term surgical risks from multiple intraspinal cell injections.

Objective: To prove that multilevel-targeted cell injection to the spinal cord can be a feasible and safe procedure.

Summary Of Background Data: Neural cell transplantation has been proposed as a treatment for a variety of neurologic disorders, including degenerative, ischemic, autoimmune, and traumatic etiologies.

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Objective: Patients with acute to subacute neurologic decline undergo a battery of imaging and laboratory tests to determine a diagnosis and treatment plan. Often, after an extensive evaluation, a brain biopsy is recommended as yet another tool to assist in determining the diagnosis. The goal of this retrospective cohort analysis is to measure the sensitivity of open brain biopsy in this patient population, compare these results with the preoperative presumed diagnosis, and evaluate if the biopsy result significantly alters treatment.

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Background: The post-ischemic gut may serve to prime and activate neutrophils which may lead to the subsequent development of the systemic inflammatory response syndrome (SIRS) and multiple organ failure. However, the initiating event which may trigger this immunoinflammatory cascade from the gut is unknown. Recent studies have indicated that intestinal epithelial cells (IEC) play an integral role in generating and transmitting signals between luminal bacteria and the host cells in the underlying gut tissues.

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Kinins exert multiple pathophysiological functions, including vascular permeability and mitogenesis, by activating their cognate receptors, bradykinin subtype 1 receptor (B1R) and bradykinin subtype 2 receptor (B2R), which belong to the superfamily of G protein-coupled receptors. Tissue-specific expression pattern or contribution of the individual kinin receptors to pathological prostate cell growth is not known. We report here the differential expression of B1R and B2R in human benign and malignant prostate specimens.

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Advanced and recurrent prostate tumors contain elevated levels of activated extracellular signal-regulated kinases 1 and 2 (ERK) in comparison to early-stage or benign specimens, and inhibition of ERK activation attenuates growth factor-dependent proliferation of prostate cells, suggesting a potential regulatory role for ERK in prostate tumorigenesis. Factors responsible for ERK activation in prostate cells are not well defined. Here, we show positive cooperative interaction between the G protein-coupled lysophosphatidic acid (LPA) and tyrosine kinase epidermal growth factor (EGF) receptors in androgen-insensitive prostate cancer PC-3 cells.

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