Residual stress measurements on a deep rolled aluminum specimen through X-Ray Diffraction and Hole-Drilling, validated on a calibration bench

Residual stress measurements are notably affected by a high sensitivity to errors in input data. Measurements should then be presented together with an estimation of their accuracy. A common strategy is to carry out more measurements and/or to compare the results of different techniques. However, error contributions due to biases could be dangerously left unseen. In a previous work, the authors presented a calibration bench which can impose a known bending stress distribution on a specimen while simultaneously performing X-Ray Diffraction (XRD) or Hole-Drilling Method (HDM) residual stress measurements. Since the external load can freely be applied and removed, the superposition principle can be exploited to simultaneously identify either the reference bending stress distribution or the actual residual stress distribution, with the same experimental setup. A deep rolling treatment was measured and analyzed on the calibration bench with both XRD and HDM. First, residual stresses on the surface were evaluated with XRD measurements, then electrochemical material removal was performed to investigate stresses at higher depths. After that, HDM measurements were carried out and compared with the results of XRD. Both methods were also used to identify the known bending stresses, providing an additional validation of the residual stress results

Exploring the performance of the spectrometer prisma in heavy zirconium and xenon mass regions

We present results from two recent runs which illustrate the performance of the PRISMA spectrometer in the proximity of the upper limit of its operational interval, namely 96Zr + 124Sn at Elab = 500 MeV and 136Xe + 208Pb at Elab = 930 MeV. In the latter run, the γ array CLARA also allowed us to identify previously unknown γ transitions in the nuclides 136Cs and 134I

An unusual mutation in RECQ4 gene leading to Rothmund-Thomson syndrome

Rothmund-Thomson syndrome (OMIM #268400) is a severe autosomal recessive genodermatosis: characterised by growth retardation, hyperpigmentation and frequently accompanied by congenital bone defects, brittle hair and hypogonadism. Mutations in helicase RECQ4 gene are responsible for a subset of cases of RTS. Only six mutations have been reported, thus, far and each affecting the coding sequence or the splice junctions. We report the first homozygous mutation in RECQ4 helicase: 2746-2756-delTGGGCTGAGGC in IVS8 responsible for the severe phenotype associated with RTS in a Malaysian pedigree. We report also a 5321 G-->A transition in exon 17 and the updated list of the RECQ4 gene mutations

Precise phylogenetic analysis of microbial isolates and genomes from metagenomes using PhyloPhlAn 3.0

Microbial genomes are available at an ever-increasing pace, as cultivation and sequencing become cheaper and obtaining metagenome-assembled genomes (MAGs) becomes more effective. Phylogenetic placement methods to contextualize hundreds of thousands of genomes must thus be efficiently scalable and sensitive from closely related strains to divergent phyla. We present PhyloPhlAn 3.0, an accurate, rapid, and easy-to-use method for large-scale microbial genome characterization and phylogenetic analysis at multiple levels of resolution. PhyloPhlAn 3.0 can assign genomes from isolate sequencing or MAGs to species-level genome bins built from >230,000 publically available sequences. For individual clades of interest, it reconstructs strain-level phylogenies from among the closest species using clade-specific maximally informative markers. At the other extreme of resolution, it scales to large phylogenies comprising >17,000 microbial species. Examples including Staphylococcus aureus isolates, gut metagenomes, and meta-analyses demonstrate the ability of PhyloPhlAn 3.0 to support genomic and metagenomic analyses

The Interaction of Failure Modes in the Compression Response and Failure of Laminated Composites

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/97075/1/AIAA2012-1895.pd

Dasatinib impairs long-term expansion of leukemic progenitors in a subset of acute myeloid leukemia cases

A number of signaling pathways might be frequently disrupted in acute myeloid leukemia (AML). We questioned whether the dual SRC/ABL kinase inhibitor dasatinib can affect AML cells and whether differences can be observed with normal CD34+ cells. First, we demonstrated that normal cord blood (CB) CD34+ cells were unaffected by dasatinib at a low concentration (0.5 nM) in the long-term culture on MS5 stromal cells. No changes were observed in proliferation, differentiation, and colony formation. In a subset of AML cases (3/15), a distinct reduction in cell proliferation was observed, ranging from 48% to 91% inhibition at 0.5 nM of dasatinib, in particular, those characterized by BCR–ABL or KIT mutations. Moreover, the inhibitory effects of dasatinib were cytokine specific. Stem cell factor-mediated proliferation was significantly impaired, associated with a reduced phosphorylation of ERK1/2 and STAT5, whereas no effect was observed on interleukin-3 and thrombopoietin-mediated signaling despite SRC activation. In conclusion, this study demonstrates that dasatinib is a potential inhibitor in a subgroup of AML, especially those that express BCR–ABL or KIT mutations

Systemic mastocytosis associated with t(8;21)(q22;q22) acute myeloid leukemia

Although KIT mutations are present in 20–25% of cases of t(8;21)(q22;q22) acute myeloid leukemia (AML), concurrent development of systemic mastocytosis (SM) is exceedingly rare. We examined the clinicopathologic features of SM associated with t(8;21)(q22;q22) AML in ten patients (six from our institutions and four from published literature) with t(8;21) AML and SM. In the majority of these cases, a definitive diagnosis of SM was made after chemotherapy, when the mast cell infiltrates were prominent. Deletion 9q was an additional cytogenetic abnormality in four cases. Four of the ten patients failed to achieve remission after standard chemotherapy and seven of the ten patients have died of AML. In the two patients who achieved durable remission after allogeneic hematopoietic stem cell transplant, recipient-derived neoplastic bone marrow mast cells persisted despite leukemic remission. SM associated with t(8;21) AML carries a dismal prognosis; therefore, detection of concurrent SM at diagnosis of t(8;21) AML has important prognostic implications

Molecular analysis of PDGFRA and PDGFRB genes by rapid single-strand conformation polymorfism (SSCP) in patients with core-binding factor leukaemias with KIT or FLT3 mutation

BACKGROUND: Mutations involving KIT and FLT3 genes, encoding tyrosine kinase (TK) membrane receptors, are detected in core-binding factor leukaemia (CBFL) patients. PDFGRA and PDGFRB encode class III TK receptors and are involved both in physiological processes and in the pathogenesis of haematological and solid tumours. The aim of this study was to investigate if PDGFR mutations are involved in CBFL. PATIENTS AND METHODS: In order to detect PDGFR mutations in CBFL, 35 patients without KIT or FLT3 mutations patients were screened by rapid and sensitive single-strand conformation polymorphism (SSCP) analysis. Sequence analysis was performed in polymerase chain reaction (PCR) products showing altered mobility in SSCP analysis in order to determine the nucleotide changes. RESULTS: Three types of single-nucleotide polymorphism (SNP) were detected in the PDGFRA gene (exon 12, exon 13 and exon 18) while no mutation of PDGFRB was detected in the tested CBFLs. CONCLUSION: These data showed that no pathogenic mutations in PDGFRA and PDGFRB were detected in the context of CBFL without KIT and FLT3 mutations. Thus, PDGFR genes do not seem to be involved in CBFL and future studies are needed to establish the genetic causes of the disease in these particular patients

Nature and decay of a JπJ\pi=36+36^{+} resonance in the 24^{24}Mg + 24^{24}Mg reaction

It has been proposed to associate the narrow (\Gamma=170 keV) and high spin ($J\pi$=36^+) resonance in the 24Mg + 24Mg reaction at E_c.m= 45.7 MeV with a hyperdeformed molecular state in 48Cr. Such a description has important consequences for the resonance decay into the favoured inelastic channels. Through fragment- coincidence measurements performed ON and OFF resonance using the PRISMA-CLARA array, we have established that the 24Mg states selectively populated are the 2^+ and 4^+ members of the ground state band