A new analytical approach to optimize a generation schedule

Identification of the optimum generation schedule by various methods of coordinating incremental generation costs and incremental transmission losses has been described previously in the literature. This paper presents an analytical approach which reduces the time-consuming iterative procedure into a mere positive-root determination of a third-order polynomial in λ. This approach includes the effect of transmission losses and is suitable for systems with any number of plants. The validity and effectiveness of this method are demonstrated by analysing a sample system.

Exergy analysis of a Gifford-McMahon cycle cryorefrigerator

Exergy analysis of a Gifford-McMahon cycle refrigerator is presented. Exergy losses occurring in various components are considered and the exergy balance is shown in tabular form. It is observed that the major losses occur in the compressor and at the cold end.

Performance of an Al-Si-graphite particle composite piston in a diesel engine

Al-Si-graphite particle composite alloy pistons containing different percentages of about 80 μm uncoated graphite particles were successfully cast by foundry techniques. Tests with a 5 hp single-cylinder diesel engine show that Al-Si-graphite particle composite pistons can withstand an endurance test of 500 h without any apparent deterioration and do not seize during the running-in period. The use of the Al-Si-3% graphite particle composite piston also results in (a) up to 3% reduction in the specific fuel consumption, (b) considerable reduction in the wear of all four piston rings, (c) a reduction in piston wear, (d) a 9% reduction in the frictional horsepower losses of the engine as determined by the motoring test and (e) a slight increase in the exhaust gas temperature. These reductions (a)–(d) appear to be due to increased lubrication from the graphite particles which are smeared on the bearing surface, the higher damping capacity of the composite pistons and the reduced coefficient of thermal expansion of the composite pistons. Preliminary results indicate that aluminum-graphite particle composite alloy is a promising material for automotive pistons.

Developing and communicating strategies for controlling virus diseases in vegetable cucurbit crops

Virus diseases cause serious yield and quality losses in field grown cucurbit crops worldwide. In Australia, the main viruses of cucurbits are Papaya ringspot virus (PRSV), Squash mosaic virus (SqMV), Watermelon mosaic virus (WMV) and Zucchini yellow mosaic virus (ZYMV). Plants infected early have severely distorted fruit. High infection incidences, of ZYMV and PRSV in crops cause losses of marketable fruit of up to 100% and infected crops are often abandoned. Two new alternative hosts of ZYMV were identified, the native cucurbit Cucumis maderaspatanus and wild legume Rhyncosia minima. No new alternative hosts of PRSV, SqMV or WMV were found in Western Australia or Queensland. Seed transmission of ZYMV (0.7%) was found in seedlings grown from ZYMV-infected fruit of zucchini but not of pumpkin. None was detected with PRSV or SqMV in zucchini or pumpkin seedlings, respectively. ZYMV spread to pumpkins by aphids was greater downwind than upwind of a virus source. Delaying sowing by 2 weeks decreased ZYMV spread. Millet non-host barriers between pumpkin plantings slowed ZYMV infection. Host resistance gene (zym) in cucumber cultivars was effective against ZYMV. Pumpkin cultivars with resistance gene (Zym) became infected under high virus pressure but leaf symptoms were milder and infected plants higher yielding with more market-acceptable fruit than those without Zym. Most zucchini cultivars with Zym developed severe leaf and fruit symptoms. ZYMV, PRSV, WMV and SqMV spread readily from infected to healthy cucurbit plants by direct leaf contact. ZYMV survives and remains infective on diverse surfaces for up to 6 hours but can be inactivated by some disinfectants. Phylogenetic analysis indicates at least three separate introductions of ZYMV into Australia, with new introductions rarely occurring. ZYMV isolates clustered into three groups according to collection location i) Kununurra, ii) Northern Territory and iii) Carnarvon, Qld and Vic. A multiplex Real-Time PCR was developed which distinguished between the three groups of Australian isolates. Integrated disease management (IDM) strategies for virus diseases of vegetable cucurbit crops grown in the field were improved incorporating the new information gathered. These strategies are aimed at causing using minimal extra expense, labour demands and disruption to normal practices.

Controlling Pythium and associated pests in ginger

This project is to identify treatments that ginger growers can use to control two serious soil-borne pathogens that have emerged and threaten the viability of the ginger industry. Pythium myriotylum, responsible for a severe rhizome rot, is the more serious of the two. It was first identified by ginger growers in the 2007/08 growing season, with some producers reporting total crop losses in some blocks. Symphylids are wingless soil-inhabiting arthropods that feed on the ginger plant's root tips and impair the plants´ ability to absorb nutrients, seriously restricting plant growth and development. Damage caused by symphylids to ginger roots is also expected to facilitate entry of Pythium into the plant.

Gifford-McMahon cycle- a theoretical analysis

A theoretical analysis of the Gifford-McMahon cycle is presented. Expressions for the ideal refrigeration produced and the figure of merit are developed. Various losses occurring in a real machine are considered and equations to account for these losses are derived. Results are presented in graphical form.

Heat balance analysis of single stage Gifford-McMahon cycle cryorefrigerator

A heat balance analysis of single stage Gifford-McMahon cycle cryorefrigerator is presented. Ideal refrigeration, actual refrigeration, net refrigeration and the various losses are tabulated. It is observed that pressure-volume losses account for a major fraction of the total losses.

Better integration of crop-legume sequencing under limited water

It is proposed that over 4-5 years of study period, multiple collaborative sites will be established with on-farm cooperators to demonstrate better integration of crop-legume sequencing for improved root growth and functioning under limited water, leading to improved productivity and carbon sequestration, and reduced runoff and deep drainage losses.

Array Comparative Genomic Hybridization in Sarcomas

Over the past years, much research on sarcomas based on low-resolution cytogenetic and molecular cytogenetic methods has been published, leading to the identification of genetic abnormalities partially underlying the tumourigenesis. Continued progress in the identification of genetic events such as copy number aberrations relies upon adapting the rapidly evolving high-resolution microarray technology, which will eventually provide novel insights into sarcoma biology, and targets for both diagnostics and drug development. The aim of this Thesis was to characterize DNA copy number changes that are involved in the pathogenesis of soft tissue leiomyosarcoma (LMS), dermatofibrosarcoma protuberans (DFSP), osteosarcoma (OS), malignant fibrous histiocytoma (MFH), and uterine leiomyosarcoma (ULMS) by applying fine resolution array comparative genomic hybridization (aCGH) technology. Both low- and high-grade LMS tumours showed distinct copy number patterns, in addition to sharing two minimal common regions of gains and losses. Small aberrations were detected by aCGH, which were beyond the resolution of chromosomal comparative genomic hybridization (cCGH). DFSP tumours analysed by aCGH showed gains in 17q, 22q, and 21 additional gained regions, but only one region (22q) with copy number loss. Recurrent amplicons identified in OS by aCGH were 12q11-q15, 8q, 6p12-p21, and 17p. Amplicons 12q and 17p were further characterized in detail. The amplicon at 17p was characterized by aCGH in low- and high-grade LMS, OS, and MFH. In all but one case this amplicon, with minimal common regions of gains at 17p11-p12, started with the distal loss of 17p13-pter. OS and high-grade LMS were grouped together as they showed a complex pattern of copy number gains and amplifications at 17p, whereas MFH and low-grade LMS showed a continuous pattern of copy number gains and amplification at 17p. In addition to the commonly gained and lost regions identified in ULMS by aCGH, various biological processes affected by these copy number changes were also indicated by pathway analysis. The three novel findings obtained in this work were: characterization of amplicon 17p in low- and high-grade LMS and MFH, profiles of DNA copy number changes in LMS, and detection of various pathways affected by copy number changes in ULMS. These studies have not been undertaken previously by aCGH technology, thus this Thesis adds new information regarding DNA copy number changes in sarcomas. In conclusion, the aCGH technique used in this Thesis has provided new insights into the genetics of sarcomas by detecting the precise regions affected by copy number changes and some potential candidate target genes within those regions, which had not been uncovered by previously applied low resolution techniques.

Molecular basis of colorectal cancer predisposition

Colorectal cancer (CRC) is one of the most frequent malignancies in Western countries. Inherited factors have been suggested to be involved in 35% of CRCs. The hereditary CRC syndromes explain only ~6% of all CRCs, indicating that a large proportion of the inherited susceptibility is still unexplained. Much of the remaining genetic predisposition for CRC is probably due to undiscovered low-penetrance variations. This study was conducted to identify germline and somatic changes that contribute to CRC predisposition and tumorigenesis. MLH1 and MSH2, that underlie Hereditary non-polyposis colorectal cancer (HNPCC) are considered to be tumor suppressor genes; the first hit is inherited in the germline and somatic inactivation of the wild type allele is required for tumor initiation. In a recent study, frequent loss of the mutant allele in HNPCC tumors was detected and a new model, arguing against the two-hit hypothesis, was proposed for somatic HNPCC tumorigenesis. We tested this hypothesis by conducting LOH analysis on 25 colorectal HNPCC tumors with a known germline mutation in the MLH1 or MSH2 genes. LOH was detected in 56% of the tumors. All the losses targeted the wild type allele supporting the classical two-hit model for HNPCC tumorigenesis. The variants 3020insC, R702W and G908R in NOD2 predispose to Crohn s disease. Contribution of NOD2 to CRC predisposition has been examined in several case-control series, with conflicting results. We have previously shown that 3020insC does not predispose to CRC in Finnish CRC patients. To expand our previous study the variants R702W and G908R were genotyped in a population-based series of 1042 Finnish CRC patients and 508 healthy controls. Association analyses did not show significant evidence for association of the variants with CRC. Single nucleotide polymorphism (SNP) rs6983267 at chromosome 8q24 was the first CRC susceptibility variant identified through genome-wide association studies. To characterize the role of rs6983267 in CRC predisposition in the Finnish population, we genotyped the SNP in the case-control material of 1042 cases and 1012 controls and showed that G allele of rs6983267 is associated with the increased risk of CRC (OR 1.22; P=0.0018). Examination of allelic imbalance in the tumors heterozygous for rs6983267 revealed that copy number increase affected 22% of the tumors and interestingly, it favored the G allele. By utilizing a computer algorithm, Enhancer Element Locator (EEL), an evolutionary conserved regulatory motif containing rs6983267 was identified. The SNP affected the binding site of TCF4, a transcription factor that mediates Wnt signaling in cells, and has proven to be crucial in colorectal neoplasia. The preferential binding of TCF4 to the risk allele G was showed in vitro and in vivo. The element drove lacZ marker gene expression in mouse embryos in a pattern that is consistent with genes regulated by the Wnt signaling pathway. These results suggest that rs6983267 at 8q24 exerts its effect in CRC predisposition by regulating gene expression. The most obvious target gene for the enhancer element is MYC, residing ~335 kb downstream, however further studies are required to establish the transcriptional target(s) of the predicted enhancer element.

Improved understanding of the damage, ecology, and management of mirids and stinkbugs in Bollgard II

In recent years mirids and stinkbugs have emerged as important sucking pests in cotton. While stinkbugs are causing damage to bolls, mirids are causing damage to seedlings, squares and bolls. With the increasing adoption of Bollgard II and IPM approaches the use of broad-spectrum chemicals to kill Helicoverpa has been reduced and as a result mirids and stinkbugs are building to levels causing damage to bolls later in crop growth stages. Studies on stinkbugs by Dr Moazzem Khan revealed that green vegetable bug (GVB) caused significant boll damage and yield loss. A preliminary study by Dr Khan on mirids revealed that high mirid numbers at later growth stages also caused significant boll damage and that damage caused by mirids and GVB were similar. Mirids and stinkbugs therefore demand greater attention in order to minimise losses caused by these pests and to develop IPM strategies against these pests to enhance gains in IPM that have been made with Bt-transgenic cotton. Progress in this area of research will maintain sustainability and profitability of the Australian cotton industry. Mirid damage at early growth stages of cotton (up to squaring stage) has been studied in detail by Dr Khan. He found that all ages of mirids cause damage to young plants and damage by mirid nymphs is cumulative. Maximum damage occurs when the insect reaches the 4th and 5th nymphal stages. He also found that mirid feeding causes shedding of small and medium squares, and damaged large squares develop as ‘parrot beak’ bolls. Detailed studies at the boll stage, such as which stage of mirids is most damaging or which age boll is most vulnerable to feeding, is lacking. This information is a prerequisite to developing an IPM strategy for the pest in later crop growth stages. Understanding population change of the pest over time in relation to crop development is an important aspect for developing management strategies for the pest which is lacking for mirids in BollgardII. Predators and parasitoids are integral components of any IPM system and play an important part in regulating pest populations. Some generalist predators such as ants, spiders, damsel bugs and assassin bugs are known to predate on mirids. Nothing is known about parasitoids of mirids. Since green mirid (GM), Creontiades dilutus, is indigenous to Australia it is likely that we have one or more parasitoids of this mirid in Australia, but that possibility has not been investigated yet. The impact of the GVB adult parasitoid, Trichopoda giacomelli, has been studied by Dr Khan who found that the fly is established in the released areas and continues to spread. However, to get wider and greater impact, the fly should be released in new locations across the valleys. The insecticides registered for mirids and stinkbugs are mostly non-selective and are extremely disruptive to a wide range of beneficial insects. Use of these insecticides at stage I and II will minimise the impact of existing IPM programs. Therefore less disruptive control tactics including soft chemicals for mirids and stinkbugs are necessary. As with soft chemicals, salt mixtures, biopesticides based on fungal pathogens and attractants based on plant volatiles may be useful tools in managing mirids and stinkbugs with less or no disruption. Dr Khan has investigated salt mixture against mirids and GVB. While salt mixtures are quite effective and less disruptive, they are quite chemical specific. Not all chemicals mixed with salt will give the desired benefit. Therefore further investigation is needed to identify those chemicals that are effective with salt mixture against mirids and 3 of 37 GVB. Dr Caroline Hauxwell of DPI&F is working on fungal pathogen-based biopesticides against mirids and GVB and Drs Peter Gregg and Alice Del Socorro of Australian Cotton CRC are working on plant volatile-based attractants against mirids. Depending on their findings, inclusion of fungal-based biopestcides and plant volatile-based attractants in developing a management system against mirids and stinkbugs in cotton could be an important component of an IPM approach.

Molecular Genetic Background of Tumours in Hereditary Leiomyomatosis and Renal Cell Cancer Syndrome

Hereditary Leiomyomatosis and Renal Cell Cancer (HLRCC) is a hereditary tumour predisposition syndrome. Its phenotype includes benign cutaneous and uterine leiomyomas (CLM, ULM) with high penetrance and rarer renal cell cancer (RCC), most commonly of papillary type 2 subtype. Over 130 HLRCC families have been identified world-wide but the RCC phenotype seems to concentrate in families from Finland and North America for unknown reasons. HLRCC is caused by heterozygous germline mutations in the fumarate hydratase (FH) gene. FH encodes the enzyme fumarase from mitochondrial citric acid cycle. Fumarase enzyme activity or type or site of the FH mutation are unassociated with disease phenotype. The strongest evidence for tumourigenesis mechanism in HLRCC supports a hypoxia inducible factor driven process called pseudohypoxia resulting from accumulation of the fumarase substrate fumarate. In this study, to assess the importance of gene- or exon-level deletions or amplifications of FH in patients with HLRCC-associated phenotypes, multiplex ligation-dependent probe amplification (MLPA) method was used. One novel FH mutation, deletion of exon 1, was found in a Swedish male patient with an evident HLRCC phenotype with CLM, RCC, and a family history of ULM and RCC. Six other patients with CLM and 12 patients with only RCC or uterine leiomyosarcoma (ULMS) remained FH mutation-negative. These results suggest that copy number aberrations of FH or its exons are an infrequent cause of HLRCC and that only co-occurrence of benign tumour types justifies FH-mutation screening in RCC or ULMS patients. Determination of the genomic profile of 11 HLRCC-associated RCCs from Finnish patients was performed by array comparative genomic hybridization. The most common copy number aberrations were gains of 2, 7, and 17 and losses of 13q12.3-q21.1, 14, 18, and X. When compared to aberrations of sporadic papillary RCCs, HLRCC-associated RCCs harboured a distinct DNA copy number profile and lacked many of the changes characterizing the sporadic RCCs. The findings suggest a divergent molecular pathway for tumourigenesis of papillary RCCs in HLRCC. In order to find a genetic modifier of RCC risk in HLRCC, genome-wide linkage and identical by descent (IBD) analysis studies were performed in Finnish HLRCC families with microsatellite marker mapping and SNP-array platforms. The linkage analysis identified only one locus of interest, the FH gene locus in 1q43, but no mutations were found in the genes of the region. IBD analysis yielded no convincing haplotypes shared by RCC patients. Although these results do not exclude the existence of a genetic modifier for RCC risk in HLRCC, they emphasize the role of FH mutations in the malignant tumourigenesis of HLRCC. To study the benign tumours in HLRCC, genome-wide DNA copy number and gene expression profiles of sporadic and HLRCC ULMs were defined with modern SNP- and gene-expression array platforms. The gene expression array suggests novel genes involved in FH-deficient ULM tumourigenesis and novel genes with putative roles in propagation of sporadic ULM. Both the gene expression and copy number profiles of HLRCC ULMs differed from those of sporadic ULMs indicating distinct molecular basis of the FH-deficient HLRCC tumours.

GM solutions to root diseases of cereals - A situation analysis and business case

Root disease causes about $503 million in losses annually to Australia's wheat and barley industries. Because of these large losses and in many cases the difficulty in reducing these losses through breeding or management, root diseases are candidates for solutions through genetic modification (GM). Through an extensive review of the scientific literature and patents, a range of approaches to GM solutions to root diseases are critically discussed. Given the high cost of regulatory approval for GM crops and a complex intellectual property (IP) landscape, it is likely that research in this area will be done in collaboration with international partners.

Herbicide tolerance of barley and wheat cultivars in NR (phase III)

During the past 10 years, this project tested 23 barley and 51 wheat varieties with 19 and 34 registered herbicides, respectively. It concentrated on new varieties and herbicides. The research highlighted that Northern Region (NR) wheat and barley varieties differed considerably in their sensitivity to these herbicides. Overall, 9 per cent of wheat variety x herbicide combinations and 6 per cent of barley variety x herbicide combinations had significant yield losses (3 to 38%) from herbicides at recommended rates and crop stages. In addition, 21 to 23 per cent had significant yield losses from herbicides at double rates, indicating a narrow margin of crop safety.

Genetic approaches to resistance to Fusarium and Bipolaris in wheat and barley

This project provided information on the genetics of crown rot (CR) resistance to help breeding work, located new parent lines in wheat and barley, and provided an insight into yield losses that occur in commercial varieties with increasing levels of CR for risk management. Genetic experiments found some highly resistant lines were poor parents, and CR resistance was complex. Best parent lines and many specific crosses were identified for further work. New potential parent lines were identified in wheat and barley, some now used in breeding programs. Yield loss can be severe even with low levels of CR when combined with drought stress. CR can reduce yield even with a wet finish.