Black market exchange rate versus official exchange rate : which one better reflects economic fundamentals? An examination of the Balassa-Samuelson effect in China

Imperial Users onl

THE FUNCTION OF Socs GENES IN DROSOPHILA DEVELOPMENT AND SIGNALING PATHWAYS

The duration and intensity of the JAK/stat signaling must be tightly regulated to prevent excessive transcriptional response and to reset the pathway to receive additional signals. Socs are the largest class of these regulators in mammals. Eight Socs genes have been found in mammals. CIS, and SOCS1-3, the canonical Socs, are transcriptionally activated by and down-regulate the JAK signaling. Socs4-7, the non-canonical Socs, are less studied and their relationship with the JAK/STAT pathway has not been well established. The Drosophila genome encodes three non-canonical Socs homologues, Socs16D, Socs36E, and Socs44A. Expression of Socs36E is controlled by the JAK pathway and misexpression causes phenotypes similar to that from reduction of JAK in both ovary and wing, which may make it functionally more similar to the canonical Socs. Expression of Socs44A is not controlled by the JAK pathway and misexpression causes JAK mutant phenotypes in wing but not in ovary. Imprecise excision mutants of the three Socs genes have been generated by us and have no visible phenotypes. The mutants of Socs36E and Socs44A significantly enhance the tumor formation in hopTum-l mutant, a gain-of-function mutation of the JAK/STAT pathway. The function of Drosophila Socs will be further studied with different strategies

Doctor of Philosophy

dissertationThe mitochondrion is an essential organelle in eukaryotic cells and organisms. This compartment is responsible for many important cellular activities. In many cell types, healthy mitochondria are branched and form tubular networks that spread evenly throughout the cytoplasm. The balance of mitochondrial fission, fusion and movement is required to maintain this morphology and proper mitochondrial functions. Recent studies suggest that disruption of mitochondria dynamics is associated with metabolic and neurodegenerative diseases. This dissertation interrogates the function of mitochondrial fission adaptors using Saccharomyces cerevisiae as a model system and research tool. Mitochondrial fission is mediated by protein complexes that encircle and divide mitochondrial tubules. In budding yeast, fission requires the membrane-anchored protein Fis1 and the dynamin-related GTPase Dnm1. Dnm1 is recruited to mitochondria via interactions with the adaptor proteins Caf4 and Mdv1, which bind directly to the mitochondrial outer membrane protein Fis1. Unlike Mdv1, a function for Caf4 in fission has not been established. In Chapter 2, I demonstrate that Caf4 is a bona fide adaptor that assembles at mitochondrial division sites. Fission complexes may contain Caf4 alone or both Caf4 and Mdv1 without compromising fission function. Furthermore, despite correspondence between Caf4 and Mdv1 expression levels, functional and phylogenetic analyses indicate that Caf4 mitochondrial fission activity has diverged from that of Mdv1. In mammals, mitochondrial fission is mediated by the dynamin-related GTPase Drp1, which is recruited to mitochondrial surface by additional membrane-associated adaptor proteins (hFis1, Mff and MiDs). In Chapter 3, a yeast strain lacking all fission proteins is used to identify whether these adaptors is able to participate in both membrane scission and GTPase recruitment. While hFis1 is dispensable for fission, membrane-anchored Mff or MiDs paired with Drp1 are sufficient to divide mitochondria. In addition, Drp1 coassembled with MiDs in vitro forms a heteropolymer that alters Drp1 homopolymer structure with a narrower diameter. It is the first demonstration that an adaptor protein alters the architecture of a mitochondrial dynamin GTPase polymer in a manner that could facilitate membrane constriction and severing activity. Altogether, these studies advance our understanding of the multiple adaptors that function in yeast and mammalian mitochondrial fission complexes

A Test of the Balassa-Samuelson Effect Applied to Chinese Regional Data

In this paper, we investigate the relevance of the Balassa-Samuelson effect to the determination of regional inflation in China, for the period 1985 – 2000. To do this, we first construct annual measures of Chinese inflation and industry input on regional and sectoral basis. Then we generalise the Asea and Mendoza (1994) settings to consider asymmetric productivity shocks across sectors. Testing this model on Chinese Regional Data aid of non-stationary panel data techniques, it shows that our extended theoretical model is a good empirical representation of the Chinese data that supports the Balassa-Samuelson effect. Moreover, we are able to test the Asea and Mendoza (1994) version of our general model and find that the restrictions are rejected.Balassa-Samuelson effect, productivity shocks, panel data

A Test of the Balassa-Samuelson Effect Applied to Chinese Regional Data

In this paper we investigate the relevance of the Balassa-Samuelson effect to the determination of regional inflation in China, for the period 1985 – 2000. To do this, we first construct annual measures of Chinese inflation and industry input on regional and sectoral basis. Then we generalize the Asea and Mendoza (1994) settings to consider asymmetric productivity shocks across sectors. Testing this model on Chinese Regional Data aid of non-stationary panel data techniques, it shows that our extended theoretical model is a good empirical representation of the Chinese data which supports the Balassa- Samuelson effect. Moreover, we are able to test the Asea and Mendoza (1994) version of our general model and find that the restrictions are rejected.

Corrections to the Forward Limit Dispersion Relations for γZ\gamma Z-Exchange Contributions

In the past fifteen years, dispersion relations (DRs) in the forward limit have been widely accepted as a model-independent method for estimating the $\gamma Z$-exchange contributions to the parity asymmetry $A_{\textrm{PV}}$ in elastic $ep$ scattering. In this work, for the first time, we estimate the corrections to these DRs. Firstly, we analyze the properties of $A_{\textrm{PV}}$ based on a general formalism, and discuss the possibility of the DRs breaking down due to two kinematic poles in $A_{\textrm{PV}}$. Then, we use point-like interactions as an example to illustrate the exact breakdown of these DRs at the experimental energy regions. Furthermore, by using the effective low-energy interactions, we estimate the $\gamma Z$-exchange contributions for the upcoming P2 experiment, and the results indicate that the correction to the forward limit DR for $\Box_{\gamma Z}^{V}$ is abot 47\%, which is significantly larger than the naive expectation prior to this study.Comment: 4 figure