Pulsed focused ultrasound treatment of muscle mitigates paralysis-induced bone loss in the adjacent bone: A study in a mouse model

2013 ◽  
Vol 134 (5) ◽  
pp. 4181-4181
Author(s):  
Sandra L. Poliachik ◽  
Tatiana D. Khokhlova ◽  
Yak-Nam Wang ◽  
Julianna C. Simon ◽  
Ted S. Gross ◽  
...  
2014 ◽  
Vol 40 (9) ◽  
pp. 2113-2124 ◽  
Author(s):  
Sandra L. Poliachik ◽  
Tatiana D. Khokhlova ◽  
Yak-Nam Wang ◽  
Julianna C. Simon ◽  
Michael R. Bailey

2018 ◽  
Author(s):  
Pierre D. Mourad

Multiple sclerosis is a debilitating disease whose symptoms arise from de-myelination of axons within brain tissue with an attendant loss of central and peripheral function. We among others have shown that transcranial delivery of pulsed focused ultrasound (pFU) can non-destructively activate central neural circuits. Others have shown enhanced myelin remodeling of axons activated by laser light in an optogenetic mouse model. We hypothesize that pFU activation of axons within MS lesions in a rodent model will decrease their de-myelination and increase their re-myelination. If successful, this non-invasive therapy may lead to rapid advancements in the treatment of MS and other de-myelinating neurological disorders.


2014 ◽  
Vol 41 (6Part1) ◽  
pp. 063301 ◽  
Author(s):  
Birgit Rieck ◽  
David Bates ◽  
Kunyan Zhang ◽  
Nicholas Escott ◽  
Charles Mougenot ◽  
...  

2018 ◽  
Vol 78 (1) ◽  
pp. 47-56 ◽  
Author(s):  
Xiaoming Yao ◽  
Matthew S Adams ◽  
Peter D Jones ◽  
Chris J Diederich ◽  
Alan S Verkman

Abstract Neuromyelitis optica spectrum disorders (herein called NMO) is an autoimmune disease of the CNS characterized by astrocyte injury, inflammation, and demyelination. In seropositive NMO, immunoglobulin G autoantibodies against aquaporin-4 (AQP4-IgG) cause primary astrocyte injury. A passive transfer model of NMO was developed in which spatially targeted access of AQP4-IgG into the CNS of seropositive rats was accomplished by pulsed focused ultrasound through intact skin. Following intravenous administration of microbubbles, pulsed ultrasound at 0.5 MPa peak acoustic pressure was applied using a 1 MHz transducer with 6-cm focal length. In brain, the transient opening of the blood-brain barrier (BBB) in an approximately prolate ellipsoidal volume of diameter ∼3.5 mm and length ∼44 mm allowed entry of IgG-size molecules for up to 3–6 hours. The ultrasound treatment did not cause erythrocyte extravasation or inflammation. Ultrasound treatment in AQP4-IgG seropositive rats produced localized NMO pathology in brain, with characteristic astrocyte injury, inflammation, and demyelination after 5 days. Pathology was not seen when complement was inhibited, when non-NMO human IgG was administered instead of AQP4-IgG, or in AQP4-IgG seropositive AQP4 knockout rats. NMO pathology was similarly created in cervical spinal cord in seropositive rats. These results establish a noninvasive, spatially targeted model of NMO in rats, and demonstrate that BBB permeabilization, without underlying injury or inflammation, is sufficient to create NMO pathology in AQP4-IgG seropositive rats.


PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e24730 ◽  
Author(s):  
Scott R. Burks ◽  
Ali Ziadloo ◽  
Hilary A. Hancock ◽  
Aneeka Chaudhry ◽  
Dana D. Dean ◽  
...  

2018 ◽  
Vol 6 (1) ◽  
Author(s):  
T. A. Olmstead ◽  
P. A. Chiarelli ◽  
D. J. Griggs ◽  
A. M. McClintic ◽  
A. N. Myroniv ◽  
...  

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