11 results match your criteria: "Texas Brain and Spine Institute[Affiliation]"
World Neurosurg
August 2023
Neurosurgery Simulation and Innovation Lab, Mayo Clinic, Phoenix, Arizona, USA; Precision Neuro-Therapeutics Innovation Lab, Mayo Clinic, Phoenix, Arizona, USA; Department of Neurological Surgery, Mayo Clinic, Phoenix, Arizona, USA; Department of Radiology, Mayo Clinic, Phoenix, Arizona, USA; Department of Otolaryngology-Head & Neck Surgery, Mayo Clinic, Phoenix, Arizona, USA. Electronic address:
Objective: A cerebrospinal fluid (CSF) venous fistula (CVF) is an aberrant connection between the subarachnoid space and a vein resulting in CSF loss. The presentation and management of CVF with cognitive decline is incompletely understood.
Methods: A systematic review was completed following the PRISMA guidelines.
Leptomeningeal carcinomatosis (LC) after metastasis of breast cancer is a rare occurrence with potentially devastating complications. Treatment options are limited, and there is a lack of literature on this topic. We report the case of a 38-year-old woman with estrogen/progesterone receptor negative (ER/PR-), human epidermal growth factor receptor 2 positive (HER2+) invasive ductal carcinoma of the left breast who underwent bilateral mastectomies with axillary lymph node dissection and chemotherapy treatment.
View Article and Find Full Text PDFBMJ Case Rep
July 2019
Baptist Neurological Institute, Lyerly Neurosurgery, Jacksonville, Florida, USA.
We report an unusual case of a dural arteriovenous fistula (dAVF) presenting as acute neck pain and quadripareis in a 55-year-old previously healthy man. Imaging was suspicious for cervicomedullary venous thrombosis and angiography failed to show evidence of arteriovenous malformation or dAVF. The patient was started on warfarin for a presumed cervicomedullary venous thrombosis and there was a significant clinical improvement.
View Article and Find Full Text PDFJ Neurosurg Spine
January 2019
3United Health Services, Johnson City, NY.
Curr Biol
December 2016
Department of Molecular and Cellular Medicine, Texas A&M Health Science Center, College Station, TX 77843-1114, USA; The Texas Brain and Spine Institute, Bryan, TX 77807, USA. Electronic address:
Although the role of NF-κB-inducing kinase (NIK) in immunity is well established, its relevance in cancer is just emerging. Here we describe novel functions for NIK in regulating mitochondrial dynamics and motility to promote cell invasion. We show that NIK is localized to mitochondria in cancer cell lines, ex vivo tumor tissue, and mouse embryonic fibroblasts (MEFs).
View Article and Find Full Text PDFBMC Neurol
November 2016
Department of Neurosurgery, Universitätsmedizin Göttingen, Robert-Koch-Straße 40, 37075, Göttingen, Germany.
Background: In accordance with German neurosurgical and neurological consensus recommendations, lead placements for deep brain stimulation (DBS) in patients with Parkinson's disease (PD) are usually performed with the patient awake and in "medication off" state. This allows for optimal lead position adjustment according to the clinical response to intraoperative test stimulation. However, exacerbation of Parkinsonian symptoms after withdrawal of dopaminergic medication may endanger the patient by inducing severe "off" state motor phenomena.
View Article and Find Full Text PDFOncogenesis
June 2016
Department of Molecular and Cellular Medicine, Texas A&M Health Science Center, College Station, TX, USA.
A growing body of evidence implicates the noncanonical NF-κB pathway as a key driver of glioma invasiveness and a major factor underlying poor patient prognoses. Here, we show that NF-κB-inducing kinase (NIK/MAP3K14), a critical upstream regulator of the noncanonical NF-κB pathway, is both necessary and sufficient for cell-intrinsic invasion, as well as invasion induced by the cytokine TWEAK, which is strongly associated with tumor pathogenicity. NIK promotes dramatic alterations in glioma cell morphology that are characterized by extensive membrane branching and elongated pseudopodial protrusions.
View Article and Find Full Text PDFAnticancer Res
June 2015
Department of Neuroscience and Experimental Therapeutics, Texas A&M University Health Science Center, Bryan, TX, U.S.A. The Texas Brain and Spine Institute, Bryan, TX, U.S.A.
Background/aim: Novel treatment strategies aiming to eliminate or attenuate the invasive phenotype of glioblastoma multiforme (GBM), the most common and aggressive primary brain tumor, could offer a profound therapeutic benefit to patients. We previously demonstrated one method to create invasive sub-populations of GBM cells (IM3 cells) and a positive regulatory role for the miR-143/-145 locus in enhancing the invasion of GBM cells. Herein, we investigated the correlation between miR-145 and srGAP1 (SLIT-ROBO Rho GTPase-activating protein1) that is purported to be a target of miR-145 and involved in migration and invasion.
View Article and Find Full Text PDFMol Cancer
January 2015
Department of Molecular and Cellular Medicine, Texas A&M University College of Medicine, College Station, TX, USA.
Background: High-grade gliomas are one of the most invasive and therapy-resistant cancers. We have recently shown that noncanonical NF-κB/RelB signaling is a potent driver of tumorigenesis and invasion in the aggressive, mesenchymal subtype of glioma. However, the relevant signals that induce activation of noncanonical NF-κB signaling in glioma and its function relative to the canonical NF-κB pathway remain elusive.
View Article and Find Full Text PDFCase Rep Neurol Med
April 2014
Department of Neurosurgery, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224, USA.
A 68-year-old female had a three-week history of severe low back pain radiating down the posterior left buttocks and left leg exacerbated by standing and walking. Lumbar spine MRI revealed cystic mass with similar intensity to cerebrospinal fluid located on dorsolateral left side of the sacral spinal canal inferior to the S1 pedicle. There was compression of left exiting S1 and traversing S2 nerve roots.
View Article and Find Full Text PDFBackground: High-grade gliomas, including glioblastomas (GBMs), are recalcitrant to local therapy in part because of their ability to invade the normal brain parenchyma surrounding these tumors. Animal models capable of recapitulating glioblastoma invasion may help identify mediators of this aggressive phenotype.
Methods: Patient-derived glioblastoma lines have been propagated in our laboratories and orthotopically xenografted into the brains of immunocompromized mice.