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This paper provides a comprehensive characterisation of HVOF- and HVAF-sprayed Cr3C2–25 wt.% NiCr hardmetal coatings. One commercial powder composition with two different particle size distributions was processed using five HVOF and HVAF thermal spray systems.All coatings contain less Cr3C2 than the feedstock powder, possibly due to the rebound of some Cr3C2-rich particles during high-velocity impact onto the substrate.Dry sand-rubber wheel abrasive wear testing causes both grooving and pull-out of splat fragments. Mass losses depend on inter- and intra-lamellar cohesion, being higher (≥70 mg after a wear distance of 5904 m) for the coatings deposited with the coarser feedstock powder or with one type of HVAF torch.Sliding wear at room temperature against alumina involves shallower abrasive grooving, small-scale delamination and carbide pull-outs, and it is controlled by intra-lamellar cohesion. The coatings obtained from the fine feedstock powder exhibit the lowest wear rates (≈5x10−6 mm3/(Nm)). At 400 °C, abrasive grooving dominates the sliding wear behaviour; wear rates increase by one order of magnitude but friction coefficients decrease from ≈0.7 to ≈0.5. The thermal expansion coefficient of the coatings (11.08x10−6 °C−1 in the 30–400 °C range) is sufficiently close to that of the steel substrate (14.23x10−6 °C−1) to avoid macro-cracking

his paper provides a comprehensive assessment of the sliding and abrasive wear behaviour of WC–10Co4Cr hardmetal coatings, representative of the existing state-of-the-art. A commercial feedstock powder with two different particle size distributions was sprayed onto carbon steel substrates using two HVOF and two HVAF spray processes.Mild wear rates of < 10-7 mm3/(Nm) and friction coefficients of ≈ 0.5 were obtained for all samples in ball-on-disk sliding wear tests at room temperature against Al2O3 counterparts. WC–10Co4Cr coatings definitely outperform a reference electrolytic hard chromium coating under these test conditions. Their wear mechanisms include extrusion and removal of the binder matrix, with the formation of a wavy surface morphology, and brittle cracking. The balance of such phenomena is closely related to intra-lamellar features, and rather independent of those properties (e.g. indentation fracture toughness, elastic modulus) which mainly reflect large-scale inter-lamellar cohesion, as quantitatively confirmed by a principal component analysis. Intra-lamellar dissolution of WC into the matrix indeed increases the incidence of brittle cracking, resulting in slightly higher wear rates. At 400 °C, some of the hardmetal coatings fail because of the superposition between tensile residual stresses and thermal expansion mismatch stresses (due to the difference between the thermal expansion coefficients of the steel substrate and of the hardmetal coating). Those which do not fail, on account of lower residual stresses, exhibit higher wear rates than at room temperature, due to oxidation of the WC grains.The resistance of the coatings against abrasive wear, assessed by dry sand–rubber wheel testing, is related to inter-lamellar cohesion, as proven by a principal component analysis of the collected dataset. Therefore, coatings deposited from coarse feedstock powders suffer higher wear loss than those obtained from fine powders, as brittle inter-lamellar deta

In dieser Dissertation wurde eine isolierte Brachydaktylie vom Typ E (BDE) untersucht. Grundlage war eine Familie mit autosomal-dominanten Erbgang BDE. Der genetische Hintergrund ist eine balancierte Translokation t(8;12)(q13;p11.2). Der Bruchpunkt auf derivativem Chromosom der(8) liegt 86 kb strangaufwärts des chondrogenetisch essentiellen Kandidatengens PTHLH (Parathyroid hormone like hormone). PTHLH ist für die Differenzierungsrate von proliferativen Chondrozyten verantwortlich. Positiv oder negativ reguliertes Pthlh führen zu einer Dysbalance mit Brachydaktylie-ähnlichen Phänotypen in murinen Tiermodellen. Der Leserahmen des Kaliumkanals KCNB2 auf Chromosom 8 wurde durch die Translokation in Intron 2 getrennt. Chrondrogenetische KCNB2 Funktionen konnten durch in situ Hybridisierungen ausgeschlossen werden. Der Translokationsbruchpunkt auf der(8) liegt in einer in Mammalia hochkonservierten Region und beeinhaltet ein Bindungsmotiv für AP1 Transkriptionsfaktoren. Durch die Translokation befindet sich in unmittelbarer Nähe eine Kernkonsensussequenz für ETS Transkriptionsfaktoren. AP1 und ETS Transkriptionsfaktoren interagieren und wurden auf eine potentielle PTHLH Regulation untersucht. Epigenetische Histonmodifizierungen, charakteristisch für cis-regulatorische Elemente, sowie Reportergenassays mit AP1 und ETS1 Bindungsmotiven zeigten einen Bezug zur PTHLH Regulation. Bindungsassays mit AP1 und ETS1 Transkriptionsfaktoren an den Bruchpunktsequenzen, sowie funktionelle in vitro Experimente mit Chondrozyten verifizierten die Hypothese, dass der Translokationsbruchpunkt strangaufwärts von PTHLH regulatorische Eigenschaften besitzt. Die AP1 und ETS1 Transkriptionsfaktoren regulierten PTHLH positiv in ATDC5 und C28/I2 Chondrozyten. In chondrogeninduzierten Patientenfibroblasten war die PTHLH Expression inhibiert. Die molekulare Pathogenese der BDE wurde durch die bisher unbekannte chondrogene PTHLH Fehlregulation dargestellt., We studied a 3-generation family with Brachydactyly Type E (BDE) and identified a t(8;12)(q13;p11.2) translocation. We identified PTHLH (Parathyroid hormone like hormone) on chromosome 12p11.2 and the ionchannel KCNB2 on chromosome 8q13 as candidate genes. KCNB2 was disrupted in intron 2, while the chromosome 12 breakpoint is localized 86 kb upstream of PTHLH; only the latter gene is involved in chondrogenesis. The 12p11.2 breakpoint is conserved and features an AP1 binding site 86 kb upstream of PTHLH. Due to the translocation, an ETS binding site from 8q13 resided near the AP1 site. Since both transcription factors interact, we tested if AP1 and ETS1 can activate PTHLH in ATDC5 and C28/I2 chondrocytes. We used the breakpoint sequences of the derivative chromosomes 8 and 12 and the nonaffected chromosome 8 and 12 allele sequences in reporter-gene assays. Reporter-gene constructs containing the der(8) breakpoint revealed activation in murine and human chondrocytes. The enrichment of histone modifications, implicating cis-regulatory effects were investigated in the breakpoint area. We found the enriched histone H3K4me1 modification at the chromosome 12 breakpoint position in murine and human chondrocytes, while affected fibroblasts showed higher H3K4me1 enrichment at the der(8) breakpoint compared to wt(12) allele. Furthermore, the breakpoint sequence bound to AP1 and C-ets-1 in EMSA. Western blotting after PMA-stimulated AP1 and ETS1 activation and overexpression of different AP1 and ETS1 combinations showed activated PTHrP expression in chondrocytes. In chondrogenic induced BDE fibroblasts PTHLH was inhibited, while IHH was upregulated. We suggest that PTHLH was dysregulated by the translocation in BDE chondrocytes. This could lead to BDE. We highlight the impact to characterize genomic breakpoints in detail and demonstrate a novel AP1- and ETS1-directed chondrogenic PTHLH regulation in wild-type chondrocytes and dysregulation in the pathogenesis of BDE.

Udgivelsesdato: March 2005, We investigated the intestinal uptake and adverse effects of microcystins ingested with Microcystis on Daphnia galeata. The gut structure, blood microcystin concentration, appearance, and movements of Daphnia fed Microcystis PCC 7806 or a microcystin-deficient PCC 7806 mutant were monitored over time. Microcystins were rapidly taken up from the digestive cavity into the blood. This process apparently required a preceding disruption of the gut epithelium by an as-yet-unknown Microcystis factor. Once microcystins entered the blood, they affected the neuromuscular communication or another life function that influences major muscle systems. Consequently, the beat rates of the thoracic legs, mandibles, and second antennae as well as the activity of the foregut decreased, whereas the midgut muscles were stimulated. Finally, the animals exhibited symptoms of exhaustion and died. The present results suggest that an ingestion of between 10.2 ng and 18.3 ng of microcystin per 1 mg of Daphnia body fresh weight is sufficient to kill D. galeata within 2 d.

The influence of cell-bound microcystins on the survival time and feeding rates of six Daphnia clones belonging to five common species was studied. To do this, the effects of the microcystin-producing Microcystis strain PCC7806 and its mutant, which has been genetically engineered to knock out microcystin synthesis, were compared. Additionally, the relationship between microcystin ingestion rate by the Daphnia clones and Daphnia survival time was analyzed. Microcystins ingested with Microcystis cells were poisonous to all Daphnia clones tested. The median survival time of the animals was closely correlated to their microcystin ingestion rate. It was therefore suggested that differences in survival among Daphnia clones were due to variations in microcystin intake rather than due to differences in susceptibility to the toxins. The correlation between median survival time and microcystin ingestion rate could be described by a reciprocal power function. Feeding experiments showed that, independent of the occurrence of microcystins, cells of wild-type PCC7806 and its mutant are able to inhibit the feeding activity of Daphnia. Both variants of PCC7806 were thus ingested at low rates. In summary, our findings strongly suggest that (i) sensitivity to the toxic effect of cell-bound microcystins is typical for Daphnia spp., (ii) Daphnia spp. and clones may have a comparable sensitivity to microcystins ingested with food particles, (iii) Daphnia spp. may be unable to distinguish between microcystin-producing and -lacking cells, and (iv) the strength of the toxic effect can be predicted from the microcystin ingestion rate of the animals.