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Equitable romantic relationships are relationships in which partners perceive that they are giving benefits to their partner that equal the benefits they receive from their partner (e.g., Walster, Traupmann, & Walster, 1978), and such relationships promote commitment (Rusbult, 1980). But do equity considerations influence observers’ impressions of a romantic couple? In the present study, I tested this possibility by examining observers’ impressions of romantic partners who were mismatched in physical attractiveness (i.e., one partner will be more physically attractive than the other). In this situation, heterosexual observers instinctually categorize the opposite-sex member of the couple as a potential mate and the same-sex member of the couple as a competitor for the potential mate’s affection (e.g., Buss & Dedden, 1990; Fisher & Cox, 2009). Furthermore, observers also conclude that a potential mate who is more attractive than his or her current partner (i.e., the competitor) is not committed to his or her current relationship (Stinson & Reddoch, unpublished data). Thus, when evaluating a romantic couple, I hypothesize that observers’ will demonstrate mating-motivated biased perceptions of potential mates and competitors when the mate is more attractive than the competitor, because such more-attractive potential mates will be perceived as romantically “available.” Participants viewed photos of dating couples who matched in attractiveness, or viewed photos of dating couples where the mate was more attractive or less attractive than the competitor. Participants then rated the potential mates’ and competitors’ status-resources (SR; Fletcher et al., 1999). Results supported my theory of mating-motivated person-perception: Observers derogated the SRs of competitors who were paired with a more attractive (and romantically available) potential mate. / Graduate / 0623 / 0451 / c.joordens@gmail.com

Das menschliche MHS2 Gen ist eine sehr gut charakterisierte Komponente des Mismatch-Reparatur-Systems (MMR) und häufig mit der HNPCC Erkrankung assoziiert. Der Mechanismus über den MSH2 an der Karzinomentwicklung beteiligt ist, sind Defekte in der DNA-Reparatur. Es konnte gezeigt werden, dass Mutationen in den kodierenden Regionen dieses Gens direkt in die Mikrosatelliteninstabilität involviert sind. Generell ist MSH2 ein Teil des postreplikativen Reparatursystems der Zellen, und schützt so vor der Akkumulation von Mutationen. Dadurch wird die genetische Stabilität und Integrität gewährleistet. Ein anderer Teil der zellulären Krebsabwehr ist das p53 Tumorsuppressorgen. Ein möglicher DNA Schaden, der in der Lage ist, p53 zu aktivieren, ist UV-Licht. Eine weitere gut charakterisierte Komponente der zellulären UV Reaktion ist der Transkriptionsfaktor c-Jun. Ziel der Arbeit war es die Regulation und Signalfunktion von MSH2 näher zu charakterisieren. Dazu wurde der Promotor des Gens in ein Luziferase Promotorgenkonstrukt kloniert. Dieses Konstrukt wurde in menschliche Keratinozyten transfiziert, die nachfolgend mit UV bestrahlt wurden. Es konnte eine zeit- und dosisabhängige Hochregulation von MSH2 gezeigt werden. Diese Transkriptionserhöhung wurde von p53 initiiert, denn durch eine gezielte Mutation der p53-Bindungsstelle im MSH2 Promotor war dieser Effekt vollkommen aufgehoben. Interessanterweise war dieser Effekt von einem zusätzlichen Faktor abhängig, ohne den keine Hochregulation erkennbar war. Verantwortlich hierfür war der Transkriptionsfaktor c-Jun. Dadurch konnte eine funktionelle Interaktion von p53 und c-Jun in der transkriptionellen Aktivierung von hMSH2 gezeigt werden. Dieser zeit- und dosisabhängige Effekt war sowohl auf RNA als auch auf Proteinebene nachvollziehbar. Der größte Anstieg war bei 50 J/m2 zu verzeichnen, wohin gegen bei Verwendung von 75 J/m2 die Transkriptmenge geringer wurde, um bei 100 J/m2 erneut anzusteigen. Um diesen erneuten Anstieg des Proteins näher zu beschreiben wurden bei den stark bestrahlten Zellen TUNEL-Untersuchungen durchgeführt. Hierbei zeigte sich eine positive Korrelation zwischen der Menge an MSH2 Protein und an TUNEL-positiven apoptotischen Zellen. Um weiter zu zeigen, dass der zweite Anstieg des Proteins nicht mit einer Reparaturfunktion verbunden ist, wurde ein biochemisch basierter Test durchgeführt, welcher die Reparaturkapazität semiquantitativ beschreibt. Dabei konnte klar gezeigt werden, dass die mit 100 J/m2 bestrahlten Zellen keine Reparaturfunktion mehr erfüllen. FACS-Analysen und Zellfärbungen gegen Annexin V und mit Propidiumiodid bestätigten die stattfindende Apoptose in den Zellen. Eine weitere Komponente des MMR-Systems ist MSH6. MSH6 bildet mit MSH2 ein Dimer, welches den Fehler in der DNA erkennt und das weitere Reparaturprogramm einleitet. Die Expression dieses Proteins konnte nur bis zu einer Dosis von 50-75 J/m2 UV nachgewiesen werden. Im Gegensatz zu MSH2 war MSH6 nicht in 100 J/m2 bestrahlten Keratinozyten detektierbar. Um über die Lokalisation dieser Proteine mehr zu erfahren wurden Immunfärbungen gegen MSH2 durchgeführt. Es zeigte sich eine Translokation des Proteins vom Kern in das Zytoplasma in Korrelation zum zunehmenden DNA-Schaden durch höhere Dosen an UV-Licht. Dies stellt eine mögliche Verbindung zwischen dem Mismatch-Reparatursystem und apoptotischen Signalwegen dar. / MSH2 is a well-characterized component of the DNA mismatch repair system (MMR) frequently associated with Hereditary Nonpolyposis Colorectal Cancer (HNPCC). The mechanism of MSH2-induced cancer is via defects in DNA mismatch repair. Mutations in the coding region of the human gene (hMSH2) have been shown to be directly involved in microsatellite instability in HNPCC. The MSH2 gene is part of the post-replicative mismatch repair system that prevents the accumulation of spontaneous mutations, and thereby ensures the integrity and stability of the genome. Another component of the cancer prevention machinery is the p53 tumor suppressor. A relevant stress that activates p53 is UV-light. Another well known component of the mammalian UV response is the transcription factor c-Jun. To study the stress regulation and signaling function of hMSH2, we cloned the promoter region of hMSH2 in a luciferase reportergene construct. This construct was transfected in human keratinocytes. The cells were then irradiated with UV light. A time and dosage dependent upregulation of hMSH2 was seen. The transcription of the human mismatch repair gene was activated by p53. This activation was lost upon mutation of the p53 binding site. Interestingly this upregulation critically depends on functional interaction of p53 with c-Jun in the transcriptional control of the hMSH2 promoter. The same effect was seen in analyses of the endogenous hMSH2 gene on the RNA level as well as on the protein level. The highest hMSH2-expression was seen at 50 J/m2. At 75 J/m2 the hMSH2 expression level decreased. Surprisingly, at 100 J /m2 hMSH2 expression increased again. The same dosage dependent function was seen on the protein level. To address the question of a second function of hMSH2 in cells irradiated at high dose, TUNEL-assays were performed. A positive correlation between the level of hMSH2 protein and the number of apoptotic cells was found. To study the repair function of hMSH2 in highly irradiated cells, we used a biochemical mismatch repair assay system. Cells treated with high dosage of UV showed no repair activity in contrast to non-irradiated cells. Annexin V staining and FACS analysis confirmed the apoptotic status of these cells. It is well-known that hMSH6 is necessary for dimer formation with hMSH2 (MutSa) to detect DNA mismatches. So far there are little data on a possible involvement of hMSH6 in apoptosis. Therefore was performed an analysis of hMSH6 protein levels in irradiated cells, revealed that hMSH6 was expressed at doses up to 50 – 75 J/m2. In contrast no hMSH6 was detectable in UV-irradiated cells treated with 100 J/m2. In addition fluorescence immuno labelling of MSH2 revealed the subcellular translocation of the protein from the nucleus to the cytoplasm in apoptotic cells. This effect may indicate a possible link between the mismatch repair system and apoptotic pathways.

College mismatch occurs when a student enrolls in a college with a selectivity level that is above (overmatch) or below (undermatch) his or her academic qualifications. A primary concern regarding college mismatch is that it could lead to social stratification. However, studies on mismatch provide mixed results and fail to articulate the determinants of college mismatch and the effects of college mismatch on degree attainment. My dissertation comprises two studies. The first study examines the role of social capital in college mismatch. Using data from ELS:2002, I find students from families with a lower level of social capital are more likely to apply to and enroll in an undermatched college, and less likely to apply to and enroll in an overmatched college. I further find intergenerational alignment of educational goal is associated with both college undermatch and overmatch. Results suggest that enhancing family social capital may help low-SES students to engage in broader college searches and find a college with a better academic fit. The second study examines the association between college mismatch and degree attainment within a timely manner. I find students who enrolled in a matched college are less likely to graduate within 6 years than those who enrolled in an overmatched college, but have a higher probability of obtaining a bachelor’s degree than those who enrolled in an undermatched college. Furthermore, I find there is no significant difference in obtaining a bachelor’s degree between matched and mismatched students as far as institutional characteristics are concerned. Results suggest that scholars need to be cautious before claiming systemic mismatch penalty or match advantage.

This thesis is an empirical investigation of the concentration of employment in Australian cities since 1976. In 1976, Australians shared the same access to employment irrespective of where they lived. However, by 1991 the employment–population ratios varied systematically by socio-economic status. The purpose of this thesis is to use a variety of basic statistical techniques to discern whether it matters where one lives.¶ A panel of 9384 small urban areas is constructed from the last four censuses to enable us to fully document the increasing spatial employment inequality in urban areas and to analyse the possible causes and effects of this increase. The first two chapters describe the overall changes in employment inequality in the urban panel using several summary indexes. Group averages from deciles ranked by socio-economic status are used to illustrate the nature of the problem.¶ The more formal analysis of the causes of increasing inequality commences with a shift share analysis of the changes in employment levels. The results show that national changes in industry structure play an important role in determining the intra-urban distribution of employment. The index of sectoral change also varies systematically within Australian cities, with sectoral change being concentrated in low status areas. The apparent importance of industry structure in determining the geographic dispersion of employment points to employment demand being a significant part of the story.¶ Basic regression techniques and principal component analysis are also used to shed light on several possible inter-related causes and effects of the increasing inequality of employment–population ratios including: increased concentrations of personal characteristics, spatial mismatch, neighbourhood effects and the development of an underclass.¶ There are three main findings about the causes and effects of neighbourhood employment inequality. Firstly, spatial mismatch within or between Australian cities is not an important explanation of the changes in the geographic dispersion of employment. Outside Sydney the location of workers vis-à-vis firms does not influence neighbourhood employment–population ratios. However, even in Sydney, spatial mismatch provides a very limited explanation of neighbourhood inequality.¶ Secondly, substantial neighbourhood-specific effects on employment–population ratios are apparent in the bottom decile(s) of urban neighbourhoods ranked by socio-economic status. These neighbourhood effects explain between one and two-thirds of the differential between the top and bottom decile. The rest of the differential can be explained by differences in endowments of personal characteristics such as human capital variables.¶ Finally, there is convincing evidence that class, and perhaps even an Australian underclass, are important determinants of the distribution of employment outcomes. The underclass in Australia, as measured using techniques similar to US studies, is still very small but is increasing at an alarming rate. However, the sensitivity analysis shows that the underclass, so measured, is closely related to a more general concept of class captured in standard socio-economic status indexes.¶ The scope of this thesis is limited by the regional aggregates supplied in all four censuses. Regional aggregates prevent us from asking subtle questions about who is being affected by the observed changes. The lack of adequate individual-level migration data for neighbourhoods means that it is not possible to directly test any hypothesis about social mobility. This thesis is merely a preliminary analysis of whether the local social environment is important.

DNA is the central storage molecule for genetic information in the cell. Therefore, the DNA must be protected from damage that will otherwise be passed on to future generations as deleterious mutations. Although many different pathways have evolved for repairing different classes of damage there are certain features that are common to all repair pathways. Generically, for DNA damage to be repaired it must first be recognized, then excised and replaced with undamaged DNA. DNA damage recognition is highly varied since specific interactions are required between the protein and the damaged DNA. DNA damage repair, paradoxically, requires the action of highly processive nucleases. The nucleases may digest hundreds if not thousands of nucleotides, sometimes for the repair of a single mutant nucleotide. We have chosen to focus on Exonuclease VII (ExoVII), one of the processive nucleases that have been implicated in the process of Mismatch Repair (MMR). ExoVII is a hetero-pentameric enzyme composed of one large subunit (XseA) and four small subunits (XseB). It has been previously characterized as a processive, single-strand specific nuclease able to digest DNA in either the 5'->3' or 3'->5' direction by a metalindependent mechanism. Early studies have shown that although ExoVII is a hydrolytic nuclease it was completely active in the presence of large amounts of EDTA and was strongly stimulated by phosphate. This feature is unusual because hydrolytic DNA nucleases typically function by a mechanism that requires coordination of a divalent cation. To further our understanding of the mechanism ExoVII we have identified and characterized the ExoVII homolog from Thermotoga maritima (T. maritima, Tm), a hyperthermophilic bacterium. The genes responsible for Tm ExoVII (TM1768 and TM1769) were cloned into an overexpression construct and the resulting proteins were overexpressed, co-purified and characterized. Consistent with previous studies, we found that Tm ExoVII is a processive, single-strand specific nuclease. Surprisingly, unlike Ec ExoVII, the T. maritima homolog was found to have an absolute requirement for the divalent cation magnesium and was strongly inhibited by the presence of either phosphate or sulfate in the reaction buffer. Using multiple sequence alignments of the large subunit we have identified a conserved core present within the C-terminal ExoVII_Large domain. This conserved core, RGGGx27GHx2Dx4Dx9P, although unique among nucleases, is reminiscent of a metal-coordinating hydrolytic active site. We have tested this putative active site using site-directed mutagenesis to create the TmD235A/TmD240A double mutant. This mutant protein was purified and the resulting protein was found to be inactive. We propose that this conserved core represents the metal-coordinating active site of all ExoVII homologs and that the group of E. coli-like homologs are unique in their EDTA resistance and anion (phosphate and sulfate) stimulation. Since ExoVII is a bi-directional nuclease (both 5'->3' and 3'->5' activity), and MMR is a bi-directional process, our model was that ExoVII was the primary nuclease associated with MMR. To test this model and determine if, in fact, a minimal conserved MMR pathway can be defined, we performed an analysis of the genomic occurrence profiles for the genes involved in MMR. To do this we have developed a bioinformatic application, Magma, which assists in the creation of a searchable relational database. Using Magma we have found that MutH, the enzyme responsible for generating a nick that directs MMR to excise the newly synthesized DNA strand including a DNA mispair, is only present in E. coli and a subset of gamma-proteobacteria, suggesting that MutH is not a core component of MMR. Instead, most organisms employ a nicking activity found in the MutL subunit. We also show that, although four nucleases have been implicated as having "redundant" roles in bacterial mismatch repair, RecJ is the primary nuclease responsible for degrading the mutated DNA strand and that 5'->3' single-strand exonuclease activity is a core MMR component. From this analysis, it appears that prokaryotic mismatch repair is more similar to eukaryotic mismatch repair than was previously thought, from the genetic and biochemical work done in E. coli. We offer a model for a universal minimal MMR system.

A methodology of designing a novel sliding surface for a class of large-scale systems with matched and mismatched perturbations is proposed in this thesis. The main idea is that some adaptive mechanisms are embedded both in the sliding surface function and in the controllers, so that not only the mismatched perturbations are suppressed during the sliding mode, but also the information of upper bound of perturbation is not required except the upper bound of perturbation from input channel. The proposed controller of each subsystem contains two parts. The first part is measurable feedback signals, and the second part is an adaptive control mechanism, which is used for overcoming the perturbation of each subsystem as well as interconnections among subsystems. The dynamics of the controlled system can be driven into the sliding surface in a finite time, and the property of asymptotical stability of each subsystem is guaranteed. Two numerical examples are given to demonstrate the feasibility of the proposed methodology.

By using Lyapunov stability theorem, a quasi-optimal model reference adaptive control (QOMRAC) scheme is presented in this thesis to stabilize a class of uncertain systems with input nonlinearity. This control scheme contains two main types of controllers. The first type is a linear feedback controller, which is an optimal controller if the controlled systems do not have any perturbations. The second type is an adaptive controller, which is used for adapting the unknown upper bound of perturbation or perturbation estimation error. The property of uniformly ultimately boundness is guaranteed when employing the proposed control scheme, and the effects of each design parameter on the dynamic performance are also analyzed. An example is demonstrated for showing the feasibility of the proposed control scheme.

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Water is a constantly changing resource by way of the hydrological cycle. It is unevenly distributed and crosses boundaries of all kinds i.e. political, social, cultural and natural. Samoa is a small developing state in the Pacific Region that is facing rapid pressure with its water resource availability. Consequently, access to and use of water resources has created tensions between water resources regulators, water utilities and villages. Therefore, managing and governing of water becomes a challenging process that has to take into account the complexity of both nature and society. With the emergence of the Integrated Water Resources Management (IWRM) framework, a greater social acceptance and importance has been given to catchment scale management and governance. Nowadays, many countries including Samoa, have embraced this appealing concept where catchments are seen as natural units for water governance and management. This study used a social qualitative approach, aimed to investigate the implementation of catchment management and examine local community perceptions of catchment management, using Apia Catchment as case study. It is based on a conceptual framework of the concept of scale i.e. set out in recent debates and ideas in the arena of catchment scale water governance and management. The primary data was collected from community focus groups within two villages of Apia Catchment, and semi-structured interviews with government agencies involved in the Water and Sanitation Sector programmes. The findings revealed a shift in water resources management and governance and a spatial scale mismatch in Apia Catchment management. According to government officials, the catchment approach is a ‘management tool’ adopted to improve the coordination between water users and to promote local ownership of catchment activities amongst individual villages. However, several challenges arose around land ownership, monetary cost, community resistance and issues outside of catchment areas when implementing catchment management. Despite the challenges that government officials encountered and the concerns raised by the communities, catchment scale management is still being adopted in Samoa. With the adoption of catchment management, many individual villages within Apia Catchment are expected to make decisions collectively. However, some local groups have concerns about the use of the term ‘boundary’, the possibility of the government taking over their land and the proposed catchment-based authority taking precedence over pre-existing cultural hierarchy. Overall, this research reveals that catchment management is often viewed or seen by government as a ‘one size fits all’ notion that ignores the range of the socio-ecological realities on the ground. This study shows that in order to design better water resources policies and strategies that are fully applicable and workable for Samoa, it is very important to identify these mismatches in scales (e.g. spatial and administrative) and levels (e.g. national and local). Understanding scales and associated levels is critical to understanding the whole system and can reduce possible consequences of mismatches due to lack of interaction and collaboration between levels and scales. Local villages have expressed their opinions on how to enhance catchment management and this could perhaps be useful for government in terms of implementation. Based on the results, recommendations are made for water resources managers to assess the importance of different levels and their interactions but, more importantly, to consider how local communities perceive catchment management.