Search

Economic understandings of prospective business education teachers did not differ from a group of high-school students who had completed a one-semester course in secondary-level economics. (DM)

A casual glance at the bankruptcy statistics of recent years is enough to make one aware that many American individuals and families are having severe financial problems. Looking deeper, one will find that financial problems are not confined to just the few. people filing for bankruptcy. by David C. Myhre ... [et al.]

Modules designed to fill the need for learning materials in the field of family financial counseling.

Adequate financial plans and records can help families become more responsible consumers and help protect against financial problems. Reprint

This module presents information designed to assist you in becoming more effective in helping clients solve financial problems related to: How to decrease living expenses How to increase income How to adjust debt payments by David C. Myhre ... [et al.]

In this module, a number of techniques and methods are presented which will help a financial counselor to identify the problems of clients. More specifically, this module will present skills that a counselor can use to find out what problems clients have that they want to be assisted with. by David C. Myhre ... [et al.]

An annotated listing of works of both specific and general topics that may be useful to professionals and lay persons seeking information on these topics.

Consumer Education and Financial Management Project sponsored by Virginia Cooperative Extension, Extension Division, Virginia Polytechnic Institute and State University in cooperation with Title I Higher Education Act of 1965, Blacksburg, Virginia ; developed by Sarah D. Monroe, E. Thomas Garman, and Nancy A. Barclay. MW 28

Not available

Malaria, caused by the Plasmodium parasite, is responsible for the deaths of close to half a million people a year. During the course of infection, the parasite invades and remodels the host red blood cell, often requiring the export of a number of proteins to the erythrocyte surface. These include the RIFIN family of Plasmodium falciparum, which have been shown to directly modulate the host immune response through interactions with inhibitory immune receptors such as LILRB1 and LAIR1. Additionally, the PIR family of a number of human- and rodent-infective Plasmodium species have been implicated in the determination of parasite virulence and the outcome of infection, along with cytoadhesion of infected erythrocytes to the vasculature. Here, I present the structure of the variable region of a RIFIN in complex with LILRB1. This is the first structure of any member of the RIFIN family and reveals that the RIFIN utilises a conserved mode of binding, which can be blocked through a single mutation in all RIFINs tested, and which mimics the interaction of MHC class I, the native ligand of LILRB1. The RIFIN is also able to mimic the effect of MHC binding both on signalling through LILRB1, and on inhibition of NK cell activation at the immunological synapse. I also present the structure of the extracellular domain of a PIR protein from Plasmodium chabaudi, the first for a member of this family, revealing a novel α-helical fold. Sequence analysis and homology modelling show conservation of this fold across PIRs from 4 human- and 3 rodent-infective Plasmodium species, as well as excluding the RIFINs and STEVORs from membership of the PIR family. These findings provide both a molecular mechanism for RIFIN function, along with a structural definition of the PIRs, giving valuable insight into 2 major families of Plasmodium variant surface antigens.

The Amino acid/Polyamine/Cationic transporter superfamily is among the largest of the sec-ondary active transporters. APC family members use either a proton or sodium gradient to drive substrate translocation across the membrane. Members of the APC superfamily are responsible for the uptake of amino acids and are found in all kingdoms of life. Amino acids, and their derivatives, are crucial for both prokaryotic and eukaryotic cell biology, being the building blocks of a variety of macromolecules and play important roles in metabolism and cell signalling. Therefore, the systems responsible for their transport are important targets of further study, in particular to gain greater insight into how these proteins recognise and discriminate between different types of amino acids. The transport mechanism of several APC members has been elucidated using a variety of structural, biophysical and functional approaches. However, these studies have focussed on sodium coupled transporters due to their function as neurotransmitter transporters. Here, the crystal structure of the first pro-ton-coupled amino acid transporter of the APC superfamily, from Geobacillus kaustophilus, GkApcT, is presented. GkApcT closely related to the mammalian cationic amino acid trans-porters (CATs) of the SLC7 family, responsible for the transport arginine and lysine into the cell. The mechanism of transport was further investigated using liposome-based functional assays to characterise the substrate specificity and kinetics. The crystal structure was used to guide a detailed site-directed mutagenesis study, which identified several conserved res-idues involved in substrate binding and proton-coupling. The current structure serves as a template to further understand proton coupled amino acid transport in bacteria and to un-derstand mammalian amino acid transport via the SLC7 and SLC36 families.

Macromolecular X-ray crystallography (MX) is currently the dominant technique for the structural eluci- dation of macromolecules at near atomic resolution. However, the progression and deleterious effects of radiation damage remains a major limiting factor in the success of diffraction data collection and subsequent structural solution at modern third generation synchrotron facilities. For experiments conducted at 100 K, protein specific damage to particular amino acids has been widely reported at doses of just several MGy, before any observable decay in average diffraction intensities. When undetected, such artefacts of X-ray irradiation can lead to significant modelling errors in protein structures, and ultimately the failure to derive the correct biological function from a model. It is thus vital to develop tools to help MX experimenters to detect and correct for such damage events. This thesis presents the development of an automated program, RIDL, which is designed to objectively quantify radiation-induced changes to electron density at individual atoms, based on Fobs,n − Fobs,1 Fourier difference maps between different dose states for a single crystal. The high-throughput RIDL program developed in this work provides the ability to systematically investigate a wide range of macromolecular systems. To date, damage to the broad class of nucleic acids and nucleoprotein complexes has remained largely uncharacterised, and it is unclear how radiation damage will disrupt the validity of such models derived from MX experiments. This thesis presents the first systematic investigations on a range of nucleic acid, protein-RNA and protein-DNA complex case studies. In general, it is concluded that nucleic acids are highly robust to radiation damage effects at 100K, relative to control protein counterparts across the tested systems. For protein crystals at 100K, cleavage of the phenolic C–O bond in tyrosine has disseminated through the MX radiation damage literature as a dominant specific damage event at 100K, despite the absence of any energetically favourable cleavage mechanism. To clarify the radiation susceptibility of tyrosine, this thesis presents a systematic investigation on radiation damage to tyrosine in a wide range of MX protein radiation damage series retrieved from the Protein Data Bank. It is concluded that the tyrosine C – O bond remains intact following X-ray irradiation, however the aromatic side-group can undergo radiation-induced displacement. This thesis also presents further applications of the RIDL program. A protocol is introduced to calculate explicit half-dose values for the electron density at individual atoms to decay to half of their initial value at zero absorbed dose. In addition, a methodology is developed to detect radiation-induced changes to electron density occurring over the course of the collection of a single MX dataset of diffraction images, all of which are required for structural solution. These protocols aim to advise experimenters of when previously-undetected site-specific damage effects may have corrupted the quality of their macromolecular model. Overall, the work in this thesis is highly applicable to both the future understanding of radiation damage in macromolecular structures, as well as of interest to the wider crystallographic community.