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Thesis
Peer Reviewed

Magnetic Assembly Route to Colloidal Responsive Photonic Nanostructures

He, Le
Advisor(s): Yin, Yadong

UC Riverside Electronic Theses and Dissertations (2013)

Responsive photonic bandgap materials, more commonly known as responsive photonic crystals, which can remotely change their structural colors in response to the external stimuli, have important applications in areas such as color displays, biological and chemical sensors, inks and paints, or many optically active components. Despite the development of different types of colloidal responsive photonic systems, wide use of these systems in practical applications is hampered by low fabrication efficiency, limited tunability of the band gap, a slow response to the external stimuli, and difficulty of integration into existing photonic systems.

Through the magnetic assembly route, we attempted to develop new types of responsive photonic nanostructures with improved fabrication efficiency, rapid response, and wide tunability of the band gap. We have demonstrated the rapid assembly of superparamagnetic colloidal particles into various photonic nanostructures. We have also demonstrated that an external magnetic field can be used as an effective stimulus to manipulate the photonic properties of the self-assembled nanostructures by affecting the lattice constant, the orientation, or the crystal structures.

As there are many more choices for nonmagnetic colloidal particles with uniform size and optimal refractive index, it would be advantageous to extend this magnetic assembly strategy to nonmagnetic particles. We have demonstrated the use of nanocrystal-based ferrofluids to direct the assembly of nonmagnetic colloidal particles into photonic crystal structures. The process is general, efficient, convenient, and scalable and thus represents a new and practical platform for the fabrication of colloidal crystal-based photonic devices.

We have also developed a universal strategy that allows convenient magnetically-driven assembly of general objects in defined locations with high spatial resolution. The process involves immersing a polymer relief pattern in a uniformly magnetized ferrofluid, which modulates the local magnetic fields around the pattern. Nonmagnetic target objects dispersed in the same ferrofluid can then be magnetically assembled at positions defined by the polymer pattern. As the nonmagnetic polymer patterns can be conveniently fabricated at low cost, our method provides a general yet very effective means to assemble a wide range of nanoscale objects, paving the way towards patterning functional microstructures.

Cover page: Magnetic Assembly Route to Colloidal Responsive Photonic Nanostructures

Article
Peer Reviewed

Editorial: Recent Advances in Responsive Optical Nanomaterials

UC Riverside Previously Published Works (2021)

Peer Reviewed

Flame Synthesis of Nanomaterials

UC Riverside Previously Published Works (2019)

Article
Peer Reviewed

Defects in the C. elegans acyl-CoA synthase, acs-3, and nuclear hormone receptor, nhr-25, cause sensitivity to distinct, but overlapping stresses.

UC San Francisco Previously Published Works (2014)

Metazoan transcription factors control distinct networks of genes in specific tissues, yet understanding how these networks are integrated into physiology, development, and homeostasis remains challenging. Inactivation of the nuclear hormone receptor nhr-25 ameliorates developmental and metabolic phenotypes associated with loss of function of an acyl-CoA synthetase gene, acs-3. ACS-3 activity prevents aberrantly high NHR-25 activity. Here, we investigated this relationship further by examining gene expression patterns following acs-3 and nhr-25 inactivation. Unexpectedly, we found that the acs-3 mutation or nhr-25 RNAi resulted in similar transcriptomes with enrichment in innate immunity and stress response gene expression. Mutants of either gene exhibited distinct sensitivities to pathogens and environmental stresses. Only nhr-25 was required for wild-type levels of resistance to the bacterial pathogen P. aeruginosa and only acs-3 was required for wild-type levels of resistance to osmotic stress and the oxidative stress generator, juglone. Inactivation of either acs-3 or nhr-25 compromised lifespan and resistance to the fungal pathogen D. coniospora. Double mutants exhibited more severe defects in the lifespan and P. aeruginosa assays, but were similar to the single mutants in other assays. Finally, acs-3 mutants displayed defects in their epidermal surface barrier, potentially accounting for the observed sensitivities. Together, these data indicate that inactivation of either acs-3 or nhr-25 causes stress sensitivity and increased expression of innate immunity/stress genes, most likely by different mechanisms. Elevated expression of these immune/stress genes appears to abrogate the transcriptional signatures relevant to metabolism and development.

Cover page: Defects in the C. elegans acyl-CoA synthase, acs-3, and nuclear hormone receptor, nhr-25, cause sensitivity to distinct, but overlapping stresses.

Article
Peer Reviewed

Defects in the C. elegans acyl-CoA Synthase, acs-3, and Nuclear Hormone Receptor, nhr-25, Cause Sensitivity to Distinct, but Overlapping Stresses

UC Santa Cruz Previously Published Works (2014)

Metazoan transcription factors control distinct networks of genes in specific tissues, yet understanding how these networks are integrated into physiology, development, and homeostasis remains challenging. Inactivation of the nuclear hormone receptor nhr-25 ameliorates developmental and metabolic phenotypes associated with loss of function of an acyl-CoA synthetase gene, acs-3. ACS-3 activity prevents aberrantly high NHR-25 activity. Here, we investigated this relationship further by examining gene expression patterns following acs-3 and nhr-25 inactivation. Unexpectedly, we found that the acs-3 mutation or nhr-25 RNAi resulted in similar transcriptomes with enrichment in innate immunity and stress response gene expression. Mutants of either gene exhibited distinct sensitivities to pathogens and environmental stresses. Only nhr-25 was required for wild-type levels of resistance to the bacterial pathogen P. aeruginosa and only acs-3 was required for wild-type levels of resistance to osmotic stress and the oxidative stress generator, juglone. Inactivation of either acs-3 or nhr-25 compromised lifespan and resistance to the fungal pathogen D. coniospora. Double mutants exhibited more severe defects in the lifespan and P. aeruginosa assays, but were similar to the single mutants in other assays. Finally, acs-3 mutants displayed defects in their epidermal surface barrier, potentially accounting for the observed sensitivities. Together, these data indicate that inactivation of either acs-3 or nhr-25 causes stress sensitivity and increased expression of innate immunity/stress genes, most likely by different mechanisms. Elevated expression of these immune/stress genes appears to abrogate the transcriptional signatures relevant to metabolism and development.