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Your search keyword '"Rodriguez, Maria J."' showing total 35 results
Start Over Author "Rodriguez, Maria J." Language english Publisher elsevier b.v.
35 results on '"Rodriguez, Maria J."'

27. 3D freeform printing of silk fibroin.

Author

Rodriguez, Maria J., Dixon, Thomas A., Cohen, Eliad, Huang, Wenwen, Omenetto, Fiorenzo G., and Kaplan, David L.

Subjects
RAPID prototyping, THREE-dimensional printing, SILK fibroin, CROSSLINKING (Polymerization), BIOPRINTING, EQUIPMENT & supplies
Abstract

Freeform fabrication has emerged as a key direction in printing biologically-relevant materials and structures. With this emerging technology, complex structures with microscale resolution can be created in arbitrary geometries and without the limitations found in traditional bottom-up or top-down additive manufacturing methods. Recent advances in freeform printing have used the physical properties of microparticle-based granular gels as a medium for the submerged extrusion of bioinks. However, most of these techniques require post-processing or crosslinking for the removal of the printed structures (Miller et al., 2015; Jin et al., 2016) [1,2] . In this communication, we introduce a novel method for the one-step gelation of silk fibroin within a suspension of synthetic nanoclay (Laponite) and polyethylene glycol (PEG). Silk fibroin has been used as a biopolymer for bioprinting in several contexts, but chemical or enzymatic additives or bulking agents are needed to stabilize 3D structures. Our method requires no post-processing of printed structures and allows for in situ physical crosslinking of pure aqueous silk fibroin into arbitrary geometries produced through freeform 3D printing. Statement of Significance 3D bioprinting has emerged as a technology that can produce biologically relevant structures in defined geometries with microscale resolution. Techniques for fabrication of free-standing structures by printing into granular gel media has been demonstrated previously, however, these methods require crosslinking agents and post-processing steps on printed structures. Our method utilizes one-step gelation of silk fibroin within a suspension of synthetic nanoclay (Laponite), with no need for additional crosslinking compounds or post processing of the material. This new method allows for in situ physical crosslinking of pure aqueous silk fibroin into defined geometries produced through freeform 3D printing. [ABSTRACT FROM AUTHOR]

Published
2018
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30. Single Balloon Enteroscopy: Latin America Experience.

Author

Sanseverino, José Inácio V., Landaeta, Jorge L., Safatle-Ribeiro, Adriana V., Blancas Valencia, Juan M., Rollan, Antonio, Dias, Carla, Azevedo, Andrea P., Sakai, Paulo, Galiano De Sanchez, Maria T., Rodriguez, Maria J., Zepeda-Gómez, Sergio, and Ospina, John

Published
2009
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35. A missense point mutation in nerve growth factor (NGFR100W) results in selective peripheral sensory neuropathy.

Author

Yang, Wanlin, Sung, Kijung, Xu, Wei, Rodriguez, Maria J, Wu, Andrew C., Santos, Sarai A., Fang, Savannah, Uber, Rebecca K., Dong, Stephanie X., Guillory, Brandon C., Orain, Xavier, Raus, Jordan, Jolivalt, Corrine, Calcutt, Nigel, Rissman, Robert A., Ding, Jianqing, and Wu, Chengbiao

Subjects
*NERVE growth factor, *DORSAL root ganglia, *MISSENSE mutation, *PERIPHERAL neuropathy, *SPINAL nerve roots, *NERVE fibers, *SEPTUM (Brain)
Abstract

• A NGFR100W knockin mouse model of Hereditary Sensory Autonomic Neuropathy V (HSAN V). • Homozygous mutant mice showed severe,deficits in peripheral sensory structure and function. • Heterozygous mutant mice developed progressive degeneration of small sensory fibers. • Heterozygous mutant mice showed no apparent structural/functional changes in the brain. • HSAN V is likely resulted from reduced secretion of NGF. The R100W mutation in nerve growth factor is associated with hereditary sensory autonomic neuropathy V in a Swedish family. These patients develop severe loss of perception to deep pain but with apparently normal cognitive functions. To better understand the disease mechanism, we examined a knockin mouse model of HSAN V. The homozygous mice showed significant structural deficits in intra-epidermal nerve fibers (IENFs) at birth. These mice had a total loss of pain perception at ∼2 months of age and often failed to survive to adulthood. Heterozygous mutant mice developed a progressive degeneration of small sensory fibers both behaviorally and functionally: they showed a progressive loss of IENFs starting at the age of 9 months accompanied with progressive loss of perception to painful stimuli such as noxious temperature. Quantitative analysis of lumbar 4/5 dorsal root ganglia revealed a significant reduction in small size neurons, while analysis of sciatic nerve fibers revealed the heterozygous mutant mice had no reduction in myelinated nerve fibers. Significantly, the amount of NGF secreted from mouse embryonic fibroblasts were reduced from both heterozygous and homozygous mice compared to their wild-type littermates. Interestingly, the heterozygous mice showed no apparent structural alteration in the brain: neither the anterior cingulate cortex nor the medial septum including NGF-dependent basal forebrain cholinergic neurons. Accordingly, these animals did not develop appreciable deficits in tests for brain function. Our study has thus demonstrated that the NGFR100W mutation likely affects the structure and function of peripheral sensory neurons. [ABSTRACT FROM AUTHOR]

Published
2020
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