Apparent texture symmetry deviations in aluminum sheet.

An ultrasonic texture measurement system for sheet metal is being developed using rotating electromagnetic acoustic transducers (EMATs). We report on further investigations of deviation from theoretically predicted symmetries in the elastic constants (as measured ultrasonically using the aforementioned system) of cold-rolled aluminum sheet reported in earlier publications. A study of the effects of annealing and deliberate deformation (both elastic and plastic) are used to develop an explanation of the nature and likely origin of this asymmetry. These deviations from symmetry cannot be detected by ultrasonic Lamb wave measurement in three directions alone. Texture asymmetry is relevant to the sheet metal manufacturer as it affects formability and may indicate processing problems. Results indicate that the asymmetry in the measured ultrasonic Lamb wave velocities on either side of the rolling direction is due to a stress effect rather than crystallographic

Mutations in the clathrin-assembly gene Picalm are responsible for the hematopoietic and iron metabolism abnormalities in fit1 mice.

Recessive N-ethyl-N-nitrosourea (ENU)-induced mutations recovered at the fitness-1 (fit1) locus in mouse chromosome 7 cause hematopoietic abnormalities, growth retardation, and shortened life span, with varying severity of the defects in different alleles. Abnormal iron distribution and metabolism and frequent scoliosis have also been associated with an allele of intermediate severity (fit14R). We report that fit14R, as well as the most severe fit15R allele, are nonsense point mutations in the mouse ortholog of the human phosphatidylinositol-binding clathrin assembly protein (PICALM) gene, whose product is involved in clathrin-mediated endocytosis. A variety of leukemias and lymphomas have been associated with translocations that fuse human PICALM with the putative transcription factor gene AF10. The Picalmfit1-5R and Picalmfit1-4R mutations are splice-donor alterations resulting in transcripts that are less abundant than normal and missing exons 4 and 17, respectively. These exon deletions introduce premature termination codons predicted to truncate the proteins near the N and C termini, respectively. No mutations in the genes encoding Picalm, clathrin, or components of the adaptor protein complex 2 (AP2) have been previously described in which the suite of disorders present in the Picalmfit1 mutant mice is apparent. These mutants thus provide unique models for exploring how the endocytic function of mouse Picalm and the transport processes mediated by clathrin and the AP2 complex contribute to normal hematopoiesis, iron metabolism, and growth.