Fatigue behavior of foreign object damaged 7075 heat treated aluminum alloy coated with PVD WC/C

AbstractThe effect of a physically vapor deposited (PVD) WC/C coating on the fatigue behavior of as produced and foreign object damaged (FOD) solution heat treated and aged 7075 aluminum alloy was studied. Coated and uncoated samples were tested under rotating bending to determine the fatigue strengths between 104 and 106 cycles in both damaged and smooth condition. FOD was produced with single shots of small hard steel spheres impacting at 100 m/s in the minimum cross section. SEM was used to characterize the features of the fracture surfaces

Evaluation of the residual stresses induced by shot peening on some sintered steels

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Study of new heat treatment parameters for increasing mechanical strength and stress corrosion cracking resistance of 7075 Aluminium alloy

For many years 7075 Aluminum alloys have been widely used especially in those applications for which highmechanical performances are required. It is well known that the alloy in the T6 condition is characterized bythe highest ultimate and yield strengths, but, at the same time, by poor stress corrosion cracking (SCC)resistance. For this reason, in the aeronautic applications, new heat treatments have been introduced toproduce T7X conditions, which are characterized by lower mechanical strength, but very good SCC behavior,when compared with the T6condition. The aim of this work is to study the tensile properties and the SCCbehavior of 7075 thick plates when submitted to a single step ageing by varying the ageing times. The tests werecarried out according to the standards and the data obtained from the SCC tests were analyzed quantitatively byan image analysis software. The results show that, if compared with the T7X conditions, the single step ageingperformed in the laboratory can produce acceptable tensile and SCC properties. The data should be confirmedby experiments carried out on thick plates submitted to heat treatments in industrial furnace

Relationships between tensile and fracture mechanics properties and fatigue properties of large plastic mold steel

presentazione oral

Identification of two novel mutations in CDHR1 in consanguineous Spanish families with autosomal recessive retinal dystrophy.

Inherited retinal dystrophies present extensive phenotypic and genetic heterogeneity, posing a challenge for patients' molecular and clinical diagnoses. In this study, we wanted to clinically characterize and investigate the molecular etiology of an atypical form of autosomal recessive retinal dystrophy in two consanguineous Spanish families. Affected members of the respective families exhibited an array of clinical features including reduced visual acuity, photophobia, defective color vision, reduced or absent ERG responses, macular atrophy and pigmentary deposits in the peripheral retina. Genetic investigation included autozygosity mapping coupled with exome sequencing in the first family, whereas autozygome-guided candidate gene screening was performed by means of Sanger DNA sequencing in the second family. Our approach revealed nucleotide changes in CDHR1; a homozygous missense variant (c.1720C > G, p.P574A) and a homozygous single base transition (c.1485 + 2T > C) affecting the canonical 5' splice site of intron 13, respectively. Both changes co-segregated with the disease and were absent among cohorts of unrelated control individuals. To date, only five mutations in CDHR1 have been identified, all resulting in premature stop codons leading to mRNA nonsense mediated decay. Our work reports two previously unidentified homozygous mutations in CDHR1 further expanding the mutational spectrum of this gene

Mutations in the heat-shock protein A9 (HSPA9) gene cause the EVEN-PLUS syndrome of congenital malformations and skeletal dysplasia.

We and others have reported mutations in LONP1, a gene coding for a mitochondrial chaperone and protease, as the cause of the human CODAS (cerebral, ocular, dental, auricular and skeletal) syndrome (MIM 600373). Here, we delineate a similar but distinct condition that shares the epiphyseal, vertebral and ocular changes of CODAS but also included severe microtia, nasal hypoplasia, and other malformations, and for which we propose the name of EVEN-PLUS syndrome for epiphyseal, vertebral, ear, nose, plus associated findings. In three individuals from two families, no mutation in LONP1 was found; instead, we found biallelic mutations in HSPA9, the gene that codes for mHSP70/mortalin, another highly conserved mitochondrial chaperone protein essential in mitochondrial protein import, folding, and degradation. The functional relationship between LONP1 and HSPA9 in mitochondrial protein chaperoning and the overlapping phenotypes of CODAS and EVEN-PLUS delineate a family of "mitochondrial chaperonopathies" and point to an unexplored role of mitochondrial chaperones in human embryonic morphogenesis