| 1. |
- Pemmasani, S. P., et al.
(författare)
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Effect of microstructure and phase constitution on mechanical properties of Ti1-xAlxN coatings
- 2014
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Ingår i: Applied Surface Science. - : Elsevier. - 0169-4332 .- 1873-5584. ; 313, s. 936-946
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Tidskriftsartikel (refereegranskat)abstract
- Monolithic TiAlN coatings with varying Al content in the range 0-65 at.% were deposited by cathodic arc evaporation. The variation in mechanical properties was studied by nanoindentation and scratch testing, and correlated with the phase constitution, grain size and residual stress. The hardness was found to be nearly stable up to Al content of 53% followed by a large drop at 65%. Depending on the stoichiometry, phase constitution and microstructure of the Ti1-xAlxN coatings, the mechanical property measurements were observed to reveal distinct trends at particular Al contents-ranging from a large scatter to clustering of data around specific values. Focused Ion Beam milling and Transmission Electron Microscopy studies showed a gradual change in microstructure, from large columnar grains in TiN to finer columns at intermediate Al content and near equiaxed, ultrafine grains with a nanocomposite structure in case of Ti0.35Al0.65N. Scratch studies revealed the deformation modes to vary with Al content, with the ductile failure modes at low Al content giving way to brittle failure at the highest Al content. Toughness studies showed a gradual increase in toughness with Al%, with the maximum seen at 53% and a moderate drop seen at 65%. The toughness shows a close dependence on the mechanical properties, phase constitution and microstructure. The study outlines the role of Al content on the microstructure of PVD TiAlN coatings and highlights the advantage of a cubic, nanocomposite structure for enhancing the toughness of these coatings. © 2014 Elsevier B.V. All rights reserved.
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| 2. |
- Buckley, Patrick G., et al.
(författare)
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Identification of genetic aberrations on chromosome 22 outside the NF2 locus in schwannomatosis and neurofibromatosis type 2
- 2005
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Ingår i: Human Mutation. - : Hindawi Limited. - 1059-7794 .- 1098-1004. ; 26:6, s. 540-9
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Tidskriftsartikel (refereegranskat)abstract
- Schwannomatosis is characterized by multiple peripheral and cranial nerve schwannomas that occur in the absence of bilateral 8th cranial nerve schwannomas. The latter is the main diagnostic criterion of neurofibromatosis type 2 (NF2), which is a related but distinct disorder. The genetic factors underlying the differences between schwannomatosis and NF2 are poorly understood, although available evidence implicates chromosome 22 as the primary location of the gene(s) of interest. To investigate this, we comprehensively profiled the DNA copy number in samples from sporadic and familial schwannomatosis, NF2, and a large cohort of normal controls. Using a tiling-path chromosome 22 genomic array, we identified two candidate regions of copy number variation, which were further characterized by a PCR-based array with higher resolution. The latter approach allows the detection of minute alterations in total genomic DNA, with as little as 1.5 kb per measurement point of nonredundant sequence on the array. In DNA derived from peripheral blood from a schwannomatosis patient and a sporadic schwannoma sample, we detected rearrangements of the immunoglobulin lambda (IGL) locus, which is unlikely to be due to a B-cell specific somatic recombination of IGL. Analysis of normal controls indicated that these IGL rearrangements were restricted to schwannomatosis/schwannoma samples. In the second candidate region spanning GSTT1 and CABIN1 genes, we observed a frequent copy number polymorphism at the GSTT1 locus. We further describe missense mutations in the CABIN1 gene that are specific to samples from schwannomatosis and NF2 and make this gene a plausible candidate for contributing to the pathogenesis of these disorders.
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| 3. |
- Hansson, Caisa M., et al.
(författare)
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Comprehensive genetic and epigenetic analysis of sporadic meningioma for macro-mutations on 22q and micro-mutations within the NF2 locus
- 2007
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Ingår i: BMC Genomics. - : Springer Science and Business Media LLC. - 1471-2164. ; 8, s. 16-
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Tidskriftsartikel (refereegranskat)abstract
- Background: Meningiomas are the most common intracranial neoplasias, representing a clinically and histopathologically heterogeneous group of tumors. The neurofibromatosis type 2 (NF2) tumor suppressor is the only gene known to be frequently involved in early development of meningiomas. The objective of this study was to identify genetic and/or epigenetic factors contributing to the development of these tumors. A large set of sporadic meningiomas were analyzed for presence of 22q macro-mutations using array-CGH in order to identify tumors carrying gene dosage aberrations not encompassing NF2. The NF2 locus was also comprehensively studied for point mutations within coding and conserved non-coding sequences. Furthermore, CpG methylation within the NF2 promoter region was thoroughly analyzed. Results: Monosomy 22 was the predominant finding, detected in 47% of meningiomas. Thirteen percent of the tumors contained interstitial/ terminal deletions and gains, present singly or in combinations. We defined at least two minimal overlapping regions outside the NF2 locus that are small enough (∼550 kb and ∼250 kb) to allow analysis of a limited number of candidate genes. Bialleinactivationo the NF2 gne was detected in 36% of meningiomas. Among the monosomy 22 cases, no additional NF2 mutations could be identified in 35% (17 out of 49) of tumors. Furthermore, the majority of tumors (9 out of 12) with interstitial/terminal deletions did not have any detectable NF2 mutations. Methylation within the NF2 promoter region was only identified at a single CpG site in one tumor sample. Conclusion: We confirmed previous findings of pronounced differences in mutation frequency between different histopathological subtypes. There is a higher frequency of biallelic NF2 inactivation in fibroblastic (52%) compared to meningothelial (18%) tumors. The presence of macro-mutations on 22q also shows marked differences between fibroblastic (86%) and meningothelial (39%) subtypes. Thus, inactivation of NF2, often combined with the presence of macro-mutation on 22q, is likely not as important for the development of the meningothelial subtype, as opposed to the fibroblastic form. Analysis of 40 CpG sites distributed within 750 bp of the promoter region suggests that NF2 promoter methylation does not play a major role in meningioma development.
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| 4. |
- Koppoju, S., et al.
(författare)
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Evolution of texture during laser surface treatment of an austenitic manganese steel
- 2015
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Ingår i: Materials Characterization. - 1044-5803 .- 1873-4189. ; 102, s. 29-34
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Tidskriftsartikel (refereegranskat)abstract
- This work describes the evolution of microstructure and texture of an austenitic manganese steel (1.34C-13.6Mn-0.45Si-Fe, wt.%) during surface modification using a high power diode laser. Strong (002) texture has been observed on the surface of the steel with increase in interaction time. It has been found that columnar type dendrites are responsible for the strong texture which is favorably grown in the < 001 > direction perpendicular to the substrate plane. The growth of dendrites with specific crystallographic direction is governed by the interfacial energy anisotropy and thermal gradient direction. (C) 2015 Elsevier Inc. All rights reserved.
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| 5. |
- Mantripragada, K K, et al.
(författare)
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Identification of novel deletion breakpoints bordered by segmental duplications in the NF1 locus using high resolution array-CGH.
- 2006
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Ingår i: Journal of medical genetics. - : BMJ. - 1468-6244 .- 0022-2593. ; 43:1, s. 28-38
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Segmental duplications flanking the neurofibromatosis type 1 (NF1) gene locus on 17q11 mediate most gene deletions in NF1 patients. However, the large size of the gene and the complexity of the locus architecture pose difficulties in deletion analysis. We report the construction and application of the first NF1 locus specific microarray, covering 2.24 Mb of 17q11, using a non-redundant approach for array design. The average resolution of analysis for the array is approximately 12 kb per measurement point with an increased average resolution of 6.4 kb for the NF1 gene. METHODS: We performed a comprehensive array-CGH analysis of 161 NF1 derived samples and identified heterozygous deletions of various sizes in 39 cases. The typical deletion was identified in 26 cases, whereas 13 samples showed atypical deletion profiles. RESULTS: The size of the atypical deletions, contained within the segment covered by the array, ranged from 6 kb to 1.6 Mb and their breakpoints could be accurately determined. Moreover, 10 atypical deletions were observed to share a common breakpoint either on the proximal or distal end of the deletion. The deletions identified by array-CGH were independently confirmed using multiplex ligation-dependent probe amplification. Bioinformatic analysis of the entire locus identified 33 segmental duplications. CONCLUSIONS: We show that at least one of these segmental duplications, which borders the proximal breakpoint located within the NF1 intron 1 in five atypical deletions, might represent a novel hot spot for deletions. Our array constitutes a novel and reliable tool offering significantly improved diagnostics for this common disorder.
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