The microstructure infl uence on the chip formation process of Al-Cu alloy cast conventionally and in semi solid state

For many metal alloys, the process of metal cutting is accompanied by extensive plastic deformation and fracture. To study this process, quick stop sectional samples of hypoeutectic Al-Cu alloy chip formation, either as conventionally cast alloy or as “semi solid metal” are used. The type of chip formation is classifi ed according to crack formation mechanism and propagation. During cutting, in all specimens used, quasi-continuous chips with built-up edge (BUE) are obtained. The formation of BUE is undesirable since it is a highly deformed body with a semi stable top which periodically breaks away giving rise to poor workpiece surface quality

Utjecaj mikrostrukture na proces nastajanja strugotine za konvencionalnu i polutekuću lijevanu Al-Cu leguru

For many metal alloys, the process of metal cutting is accompanied by extensive plastic deformation and fracture. To study this process, quick stop sectional samples of hypoeutectic Al-Cu alloy chip formation, either as conventionally cast alloy or as “semi solid metal” are used. The type of chip formation is classified according to crack formation mechanism and propagation. During cutting, in all specimens used, quasi-continuous chips with built-up edge (BUE) are obtained. The formation of BUE is undesirable since it is a highly deformed body with a semi stable top which periodically breaks away giving rise to poor workpiece surface quality.Za mnoge metalne legure, proces rezanja je praćen intenzivnom plastičnom deformacijom i lomom. Za istraživanje tog procesa u radu je korištena metoda brzog zaustavljanja procesa rezanja. Materijal uzorka je podeutektička Al-Cu legura, lijevana konvencionalno i kao „polu čvrsti metal“ (semi solid metal-SSM). Vrsta strugotine koja je obrazovana klasifi cirana je prema mehanizmu nastajanja i širenja pukotina. Tokom rezanja, u svim uzorcima nastajala je, kvazi-kontinuirano strugotina sa naslagama (BUE). Stvaranje BUE je nepoželjan proces, jer je to jako deformirani volumen sa polu stabilnim oblikom, koji povremeno raste i odvaja se, što dovodi do lošeg kvaliteta obrađene površine

Cloning of Canine Galactokinase (\u3cem\u3eGALK1\u3c/em\u3e) and Evaluation as a Candidate Gene for Hereditary Cataracts in Labrador Retrievers

We identified a pedigree of Labrador retrievers (LR) that develop hereditary cataracts between 6 and 18 months of age. In humans, galactokinase deficiency is an autosomal recessive disorder characterized by juvenile onset of cataracts.1 In order to evaluate GALK1 as a candidate gene, we cloned and sequenced the canine GALK1 gene and tested a single nucleotide polymorphism (SNP) in the gene for segregation with cataracts in the LR pedigree

Cloning and Characterization of Canine \u3cem\u3ePAX6\u3c/em\u3e and Evaluation as a Candidate Gene in a Canine Model of Aniridia

Purpose: Mutations in PAX6 cause human aniridia. The small eye (sey) mouse represents an animal model for aniridia. However, no large animal model currently exists. We cloned and characterized canine PAX6, and evaluated PAX6 for causal associations with inherited aniridia in dogs. Methods: Canine PAX6 was cloned from a canine retinal cDNA library using primers designed from human and mouse PAX6 consensus sequences. An RH3000 radiation hybrid panel was used to localize PAX6 within the canine genome. Genomic DNA was extracted from whole blood of dogs with inherited aniridia, and association testing was performed using markers on CFA18. Fourteen PAX6 exons were sequenced and scanned for mutations, and a Southern blot was used to test for large deletions. Results: Like the human gene, canine PAX6 has 13 exons and 12 introns, plus an alternatively spliced exon (5a). PAX6 nucleotide and amino acid sequences were highly conserved between dog, human, and mouse. The canine PAX6 cDNA sequence determined in this study spans 2 large gaps present in the current canine genomic sequence. Radiation hybrid mapping placed canine PAX6 on CFA18 in a region with synteny to HSA11p13. Exon-scanning revealed single nucleotide polymorphisms, but no pathological mutations, and Southern blot analysis revealed no differences between normal and affected animals. Conclusions: Canine PAX6 was cloned and characterized, and results provide sequence information for gaps in the current canine genome sequence. Canine PAX6 nucleotide and amino acid sequences, as well as gene organization and map location, were highly homologous with that of the human gene. PAX6 was evaluated in dogs with an inherited form of aniridia, and sequence analysis indicated no pathological mutations in the coding regions or splice sites of aniridia-affected dogs, and Southern blot analysis showed no large deletions

An austempering study of ductile iron alloyed with copper

Austempered ductile iron (ADI) has proved to be an excellent material as it possesses attractive properties: high strength, ductility and toughness are combined with good wear resistance and machinability. These properties can be achieved upon adequate heat treatment which yields the optimum microstructure for a given chemical composition. In this paper the results of an investigation the austempering of ADI alloyed with 0.45 % Cu for a range of times and temperatures are reported. The microstructure and fracture mode developed throughout these treatments have been identified by means of light and scanning electron microscopy and X-ray diffraction analysis. It was shown that the strength, elongation and impact energy strongly depend on the amounts of bainitic ferrite and retained austenite. Based on these results, and optimal processing window was established

Radiation Hybrid Mapping of Cataract Genes in the Dog

Purpose: To facilitate the molecular characterization of naturally occurring cataracts in dogs by providing the radiation hybrid location of 21 cataract-associated genes along with their closely associated polymorphic markers. These can be used for segregation testing of the candidate genes in canine cataract pedigrees. Methods: Twenty-one genes with known mutations causing hereditary cataracts in man and/or mouse were selected and mapped to canine chromosomes using a canine:hamster radiation hybrid RH5000 panel. Each cataract gene ortholog was mapped in relation to over 3,000 markers including microsatellites, ESTs, genes, and BAC clones. The resulting independently determined RH-map locations were compared with the corresponding gene locations from the draft sequence of the canine genome. Results: Twenty-one cataract orthologs were mapped to canine chromosomes. The genetic locations and nearest polymorphic markers were determined for 20 of these orthologs. In addition, the resulting cataract gene locations, as determined experimentally by this study, were compared with those determined by the canine genome project. All genes mapped within or near chromosomal locations with previously established homology to the corresponding human gene locations based on canine:human chromosomal synteny. Conclusions: The location of selected cataract gene orthologs in the dog, along with their nearest polymorphic markers, serves as a resource for association and linkage testing in canine pedigrees segregating inherited cataracts. The recent development of canine genomic resources make canine models a practical and valuable resource for the study of human hereditary cataracts. Canine models can serve as large animal models intermediate between mouse and man for both gene discovery and the development of novel cataract therapies

MIP/Aquaporin 0 Represents a Direct Transcriptional Target of PITX3 in the Developing Lens

The PITX3 bicoid-type homeodomain transcription factor plays an important role in lens development in vertebrates. PITX3 deficiency results in a spectrum of phenotypes from isolated cataracts to microphthalmia in humans, and lens degeneration in mice and zebrafish. While identification of downstream targets of PITX3 is vital for understanding the mechanisms of normal ocular development and human disease, these targets remain largely unknown. To isolate genes that are directly regulated by PITX3, we performed a search for genomic sequences that contain evolutionarily conserved bicoid/PITX3 binding sites and are located in the proximity of known genes. Two bicoid sites that are conserved from zebrafish to human were identified within the human promoter of the major intrinsic protein of lens fiber, MIP/AQP0. MIP/AQP0 deficiency was previously shown to be associated with lens defects in humans and mice. We demonstrate by both chromatin immunoprecipitation and electrophoretic mobility shift assay that PITX3 binds to MIP/AQP0 promoter region in vivo and is able to interact with both bicoid sites in vitro. In addition, we show that wild-type PITX3 is able to activate the MIP/AQP0 promoter via interaction with the proximal bicoid site in cotransfection experiments and that the introduction of mutations disrupting binding to this site abolishes this activation. Furthermore, mutant forms of PITX3 fail to produce the same levels of transactivation as wild-type when cotransfected with the MIP/AQP0 reporter. Finally, knockdown of pitx3 in zebrafish affects formation of a DNA-protein complex associated with mip1 promoter sequences; and examination of expression in pitx3 morphant and control zebrafish revealed a delay in and reduction of mip1 expression in pitx3-deficient embryos. Therefore, our data suggest that PITX3 is involved in direct regulation of MIP/AQP0 expression and that the alteration of MIP/AQP0 expression is likely to contribute to the lens phenotype in cataract patients with PITX3 mutations