Higher Energy Gap Control of Fluorescence in Conjugated Polymers

Chemo- and biosensors based on fluorescent conjugated polymer benefit from greater detection sensitivity due to amplification of the electronic perturbations produced by analyte binding. This amplification stems from the exciton-transporting properties of conjugated polymers. A conventional design paradigm relies on the analyte binding events which generate sites of lower energy relative to the polymer energy: either fluorescence quenching sites (turn-off sensors) or bathochromically shifted fluorophores (turn-on sensors). In both type sensors, the excitons migrate to the lower-energy site created by analyte binding. This dissertation primarily focused the investigation of an alternative paradigm when analyte binding creates higher energy gap sites in the polymer backbone. Such higher-energy gap sites act as “roadblocks” for excitons to reduce their migration length. Decreasing exciton migration length is accompanied by increasing fluorescence intensity, thus generating an amplified turn-on fluorescent response. The new paradigm expands the generality and universality of the signal amplification concept in conjugated polymers, and can be used to design amplifying turn- on fluorescent sensors for various practically useful analytes such as hydrogen sulfide and cysteine. In the last part of this dissertation, we present a series of poly(p-phenylene ethynylene) thin films prepared by stepwise surface-initiated polymerization. In addition to experimental simplicity and reproducibility of the preparation, and broad variety of compatible building blocks, this method requires low material consumption and no purification for the final bulk thin films. The stepwise surface-initiated polymerization yields dense films of covalently immobilized polymer chains with precisely controlled molecular structure and organization

System modeling and vibration reduction of a flexible beam under rotary motion

The objective of this thesis work is to reduce the end-point vibration of a flexible beam using the feedback control of the partial state variables. The dynamic model is derived from the assumed-modes method. The new feature of this model is that it is applicable to control system analysis and synthesis. A practical example is presented to illustrate the use of control law to improve the transient response --Abstract, page ii

Development of sustainable esterification reactions and the transformation of carbohydrates into applicable building blocks

This thesis showcases some developments in chemical processes and synthesis leading to products of commercial interest. The thesis includes studies on esterification reactions to improve the catalysis of these reactions. In addition, deoxydehydration (DODH) reactions of alkyl glycosides are studied and illustrated. DODH reactions were performed to convert alkyl glycosides into diols, by eliminating a cis-diol moiety in pyranosides to result in alkenes and alkanes. Furthermore, this thesis presents the transformation of some common alkyl glycosides into their rare counterparts (C3-epimers) by sequential C3-oxidation and heterogeneous hydrogenation. Finally, the development of novel fructose-based surfactants from fructose and its derived saccharides is studied and discussed

Cloud Computing

Cloud computing was a cloud technology pioneered by Amazon for a long time due to its software technology that is based on the online shopping platform. After Google, Microsoft also follow up, and this technology, in fact, already exists in our lives, and applications continue to expand, become an integral part of life. With the rapid development of the Internet and the demand for high-speed computing of mobile devices, the simplest cloud computing technology has been widely used in online services, such as “search engine, webmail,” and so on. Users can get a lot of information by simply entering a simple instruction. Further cloud computing is not only for data search and analysis function, but also can be used in the biological sciences, such as: analysis of cancer cells, analysis of DNA structure, gene mapping sequencing; in the future more Smart phone, GPS and other mobile devices through the cloud computing to develop more application service

Battle between influenza A virus and a newly identified ZAPL antiviral activity

Influenza A virus infection causes a highly contagious annual respiratory disease in humans as well as periodic pandemics with higher mortality rates. The Krug laboratory has shown that one of the major ways that the influenza virus NS1 protein counteracts host antiviral responses is to bind the 30 kDa subunit of the cleavage and polyadenylation specificity factor (CPSF30). As a consequence, 3’ end processing of cellular pre-mRNAis is inhibited, leading to reduced production of cellular mRNAs, including interferon mRNAs. I showed that NS1-CPSF30 complexes contain an array of cellular proteins. I purified the NS1-CPSF30 complexes from virus infected cells by affinity selection of CPSF30 and the NS1 protein. I identified the associated cellular proteins by mass spectrometry. Two cellular RNA helicases, DDX21 and DHX30, were identified. SiRNA knockdown of either RNA helicase enhanced virus replication, indicating that DDX21 and DHX30 inhibit influenza A virus replication. Further study demonstrated that DDX21 RNA helicase inhibits viral RNA synthesis, and is countered by the NS1 protein. The cellular ZAPL antiviral protein was also identified in the NS1-CPSF30 complexes. Previous studies have shown that ZAPL antiviral activity is mediated by its N-terminal zinc-fingers, which targets viral mRNA of several viruses for degradation. Little is known about the antiviral role of the ZAPL C-terminal PARP domain. Here I discovered the antiviral role of ZAPL C-terminal PARP domain against influenza A virus. I showed that the ZAPL PARP domain targets the viral polymerase PA and PB2 proteins. These two viral polymerases are poly(ADP-ribosylated), presumably by other PARP protein(s). The ZAPL-associated, poly(ADP-ribosylated) PA and PB2 are then ubiquitinated and proteasomally degraded. This ZAPL antiviral activity is counteracted by the binding of polymerase PB1 protein to the WWE region adjacent to the PARP domain, and causes PA and PB2 to dissociate from ZAPL and thus escape degradation. Because PB1 displaces PA and PB2 and protects them from ZAPL-mediated degradation, endogenous ZAPL only moderately inhibits influenza A virus replication (20-30-fold), as determined by siRNA knockdown experiment. These results suggest that influenza A virus has partially won the battle against the newly identified ZAPL antiviral activity.Microbiolog