Magnetic Resonance Imaging–Guided Microdialysis Cannula Implantation in a Spontaneous High-Grade Glioma Murine Model

Elmeliegy, Mohamed; Carcaboso, Ángel M.; Chow, Lionel M.L.; Zhang, Ziwei M.; Calabrese, Christopher; Throm, Stacy L.; Wang, Fan; Baker, Suzanne J.; Stewart, Clinton F.

doi:10.1002/jps.22723

Cited by 13 publications

(6 citation statements)

References 16 publications

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“…During DBS surgery, the site of catheter placement may be confirmed with fluoroscopy. Probes have also been implanted in gliomas under CT, MRI or three-dimensional ultrasonography guidance (49,50). On the other hand, during standard clinical microdialysis, a suture is used to hold the catheter in order to make measurements in the same location throughout the procedure.…”

Section: Insertionmentioning

confidence: 99%

Optimizing microdialysis for deep brain stimulation

Martinez¹

2016

Front Biosci

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Cerebral microdialysis is a chemical detection method capable of identifying and simultaneously sampling a wide range of substances in the micromilieu of the monitoring probe. The interstitial space of biological tissues and fluids is sampled through a thin fenestrated dialysis catheter inserted into the brain. The technique has been reported in patients with Parkinson's disease. However, the procedure is not widely used by neurosurgeons, possibly owing to unclear indications and poor effective benefits, mostly secondary to significant pitfalls. In spite of the feasibility of microdialysis in humans, many factors can affect the quality of the process. Possible pitfalls include improperly designed probe, probe insertion effects, ineffective perfusion rate, issues to optimize stabilization period, and insufficient volume sample. This article reviews those key technical features necessary for performing microdialysis in humans during deep brain stimulation for Parkinson's Disease.

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Section: Insertionmentioning

confidence: 99%

Optimizing microdialysis for deep brain stimulation

Martinez¹

2016

Front Biosci

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“…Nevertheless, the fast development of novel imaging techniques [23] allows following tumor growth and assessing its exact location, facilitate the use of genetically engineered models in the preclinical testing of translational therapeutics.…”

Section: Experimental Glioblastoma Modelsmentioning

confidence: 99%

Gene therapy for brain tumors: Basic developments and clinical implementation

Assi

Candolfi

Baker

et al. 2012

Neuroscience Letters

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Glioblastoma multiforme (GBM) is the most common and deadliest of adult primary brain tumors. Due to its invasive nature and sensitive location, complete resection remains virtually impossible. The resistance of GBM against chemotherapy and radiotherapy necessitate the development of novel therapies. Gene therapy is proposed for the treatment of brain tumors and has demonstrated pre-clinical efficacy in animal models. Here we review the various experimental therapies that have been developed for GBM including both cytotoxic and immune stimulatory approaches. We also review the combined conditional cytotoxic immune stimulatory therapy that our lab has developed which is dependent on the adenovirus mediated expression of the conditional cytotoxic gene, Herpes Simplex Type 1 Thymidine Kinase (TK) and the powerful DC growth factor Fms-like tyrosine kinase 3 ligand (Flt3L). Combined delivery of these vectors elicits tumor cell death and an anti-tumor adaptive immune response that requires TLR2 activation. The implications of our studies indicate that the combined cytotoxic and immunotherapeutic strategies are effective strategies to combat deadly brain tumors and warrant their implementation in human Phase I clinical trials for GBM.

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“…The binding of the surface subunit gp120 to the CD4 receptor on host cells triggers conformational changes of Env that allow gp120 binding to the chemokine receptor CCR5 or CXCR4. After that, the hydrophobic fusion peptide at N-terminal region of transmembrane subunit gp41 inserts into cell membrane and the pre-hairpin intermediate forms [1–4]. Subsequently, three C-terminal heptad-repeat region (HR2) helices refold and package in the grooves of coiled-coil core assembled by N-terminal heptad-repeat region (HR1) in an antiparallel manner and a thermostable six-helix bundle (6HB) forms [5, 6].…”

Section: Introductionmentioning

confidence: 99%

Mutations of Glu560 within HIV-1 Envelope Glycoprotein N-terminal heptad repeat region contribute to resistance to peptide inhibitors of virus entry

et al. 2019

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BackgroundPeptides corresponding to N- and C-terminal heptad repeat regions (HR1 and HR2, respectively) of gp41 can inhibit HIV-1 infection in a dominant negative manner by interfering with refolding of the viral HR1 and HR2 to form a six-helix bundle (6HB) that induces fusion between viral and host cell membranes. Previously, we found that HIV-1 acquired the mutations of Glu560 (E560) in HR1 of envelope (Env) to escape peptide inhibitors. The present study aimed to elucidate the critical role of position 560 in the virus entry and potential resistance mechanisms.ResultsThe Glu560Lys/Asp/Gly (E560K/D/G) mutations in HR1 of gp41 that are selected under the pressure of N- and C-peptide inhibitors modified its molecular interactions with HR2 to change 6HB stability and peptide inhibitor binding. E560K mutation increased 6HB thermostability and resulted in resistance to N peptide inhibitors, but E560G or E560D as compensatory mutations destabilized the 6HB to reduce inhibitor binding and resulted in increased resistance to C peptide inhibitor, T20. Significantly, the neutralizing activities of all mutants to soluble CD4 and broadly neutralizing antibodies targeting membrane proximal external region, 2F5 and 4E10 were improved, indicating the mutations of E560 could regulate Env conformations through cross interactions with gp120 or gp41. The molecular modeling analysis of E560K/D/G mutants suggested that position 560 might interact with the residues within two potentially flexible topological layer 1 and layer 2 in the gp120 inner domain to apparently affect the CD4 utilization. The E560K/D/G mutations changed its interactions with Gln650 (Q650) in HR2 to contribute to the resistance of peptide inhibitors.ConclusionsThese findings identify the contributions of mutations of E560K/D/G in the highly conserved gp41 and highlight Env’s high degree of plasticity for virus entry and inhibitor design.

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Magnetic Resonance Imaging–Guided Microdialysis Cannula Implantation in a Spontaneous High-Grade Glioma Murine Model

Cited by 13 publications

References 16 publications

Optimizing microdialysis for deep brain stimulation

Optimizing microdialysis for deep brain stimulation

Gene therapy for brain tumors: Basic developments and clinical implementation

Mutations of Glu560 within HIV-1 Envelope Glycoprotein N-terminal heptad repeat region contribute to resistance to peptide inhibitors of virus entry

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