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Aluminum-copper (Al-Cu) alloy B206 is a high strength and ductile alloy showing promise for use in automotive suspension components. Incorporation of lightweight B206 alloy in automotive suspension components may significantly reduce overall vehicle weight and increase the vehicle’s fuel efficiency. However, one of the major factors inhibiting the use of B206 is its high susceptibility to hot tearing during casting. Hot tearing is a complex phenomenon attributed to alloy solidification, microstructure and stress/strain development within a casting. Numerous methods (e.g. preheating of mold, grain refinement, elimination of sharp corners in a component) help to reduce the occurrence of hot tears in castings, but the underlying mechanisms responsible for hot tearing remain ambiguous. This research aims to advance the understanding of the mechanisms responsible for hot tearing in B206 Al alloy. In this research, the conditions associated with the formation of hot tears in B206 were investigated via ex situ and in situ methods. Titanium was added in three levels (i.e. unrefined, 0.02 and 0.05 wt%) to investigate the effect of grain refinement on hot tearing. Ex situ neutron diffraction strain mapping was carried out on the three B206 castings to determine casting strain and stress. Further, in situ techniques were used to establish the onset temperature and solid fraction of hot tearing in B206 and to improve the understanding of microstructure development in B206. The results indicate that titanium additions had a significant impact on the hot tearing susceptibility of B206, by effectively reducing grain size and transforming grain morphology from coarse dendrites to fine globular grains. Further, thermal analysis suggested that grain refinement delayed the onset of dendrite coherency in B206 and therefore enhanced the duration of bulk liquid metal feeding for the refined casting conditions. As a result, the interactive effects of such factors resulted in a more uniform distribution of strain, and subsequent higher resistance to hot tearing for the grain refined castings. Finally, in situ analysis determined the onset solid fraction of hot tearing in B206 and provided an understanding of the role of microstructure on hot tearing in B206.

Transmitted/founder (TF) simian-human immunodeficiency viruses (SHIVs) express HIV-1 envelopes modified at position 375 to efficiently infect rhesus macaques while preserving authentic HIV-1 Env biology. TF SHIV.C.CH505 is an extensively characterized virus shown to recapitulate key features of HIV-1 immunobiology, including CCR5-tropism, a tier 2 neutralization profile, reproducible early viral kinetics, and authentic immune responses. SHIV.C.CH505 is used frequently in nonhuman primate studies of HIV, but viral loads after months of infection are variable and typically lower than those in people living with HIV. We hypothesized that additional mutations besides Δ375 might further enhance virus fitness without compromising essential components of CH505 Env biology. From sequence analysis of SHIV.C.CH505-infected macaques across multiple experiments, we identified a signature of envelope mutations associated with higher viremia. We then used short-termin vivomutational selection and competition to identify a minimally adapted SHIV.C.CH505 with just five amino acid changes that substantially improve virus replication fitness in macaques. Next, we validated the performance of the adapted SHIVin vitroandin vivoand identified the mechanistic contributions of selected mutations.In vitro, the adapted SHIV shows improved virus entry, enhanced replication on primary rhesus cells, and preserved neutralization profiles.In vivo, the minimally adapted virus rapidly outcompetes the parental SHIV with an estimated growth advantage of 0.14 days-1and persists through suppressive antiretroviral therapy to rebound at treatment interruption. Here, we report the successful generation of a well-characterized, minimally adapted virus, termed SHIV.C.CH505.v2, with enhanced replication fitness and preserved native Env properties that can serve as a new reagent for NHP studies of HIV-1 transmission, pathogenesis, and cure.Author SummaryThe power of the nonhuman primate model of HIV to predict outcomes in people living with HIV (PLWH) depends on authentic virus-host interactions. In pursuit of viruses that generate infection that mirrors the effects of HIV-1 in PLWH, we developed a minimally adapted version of a commonly used virus, SHIV.C.CH505, which has better fitness than the parental virus while retaining important biological properties. First, we studied virus sequences from SHIV.C.CH505-infected rhesus macaques to identify a signature of mutations common to animals with higher viral loads. We then tested viruses containing the various mutations in the lab and in animals to determine the most fit version and to identify the contribution of each mutation. Ultimately, we identified a minimally adapted version of SHIV.C.CH505 with just 5 amino acid substitutions that enhances virus replication and preserves CH505 envelope properties, including sensitivity to clinically relevant broadly neutralizing antibodies. This new virus, called SHIV.C.CH505.v2 replicates well in macaques over time and persists through antiretroviral therapy. SHIV.C.CH505.v2 could be an important component of nonhuman primate studies of HIV prevention, therapy, and cure.

The endoplasmic reticulum (ER) protein translocation channel subunit Sec61β/Sbh1 is non-essential, but contains multiple phosphorylation sites suggesting a regulatory role in ER protein import. We show here that mutating two N-terminal, proline-flanked, phosphorylation sites in the Sbh1 cytosolic domain phenocopies the temperature-sensitivity of a yeast strain lacking SBH1/SBH2, and results in reduced translocation into the ER of an Sbh1-dependent substrate, Gls1. In a microscopic screen we show that about 12% of GFP-tagged secretory proteins depend on Sbh1 for translocation. Sbh1-dependent proteins have targeting sequences with less pronounced hydrophobicity and often no or an inverse charge bias. A subset of these proteins was dependent on N-terminal phosphorylation of Sbh1 and on the phospho-S/T-specific proline isomerase Ess1 (PIN1 in mammals) for ER import. We conclude that Sbh1 promotes ER translocation of substrates with suboptimal targeting sequences and that its activity is regulated by a conformational change induced by N-terminal phosphorylation.

Magnesium alloys are biocompatible, biodegradable and have the ability to promote bone ingrowth, making them ideal candidate materials for replacing auto- and allografts in future treatments of large bone defects. Powder bed fusion-laser beam (PBF-LB) additive manufacturing of these alloys would further allow for the production of complex structures, optimized for bone grafting. However, the corrosion rates of structures processed by PBF-LB remain too high. An improved understanding of the influence of the microstructure generated during PBF-LB on the corrosion properties is considered key to their future implementation in implants. In this study, the effect of PBF-LB processing and subsequent hot isostatic pressing (HIP) on the microstructure and texture in different sample directions was studied and related to the corrosion behavior of a Mg-Y-Nd-Zr alloy. The results were compared with an extruded Mg-Y-Nd-Zr alloy. A higher amount of secondary phases resulted in a higher rate of localized corrosion for the PBF-LB processed material compared to that for the extruded one. Due to growth of the secondary phases, the corrosion rate was further increased after HIP. Moreover, a strong texture was observed in the PBF-LB material, and it was also enhanced in the HIP material. While this affected the electrochemical activity as measured by potentiodynamic polarization tests, any texture effect appeared to be masked by the contribution of the secondary phases in the longer-term mass change and hydrogen evolution tests. Future work should look further into the influence of individual process parameters on the microstructure and the resulting corrosion behavior of the material, to further clarify its interdependence.

Additional file 9: Supplementary Table S2. Analysis of allelic variant on WGS data retrieved from NCBI SRA database of 41 peach accessions. The presence of di1/di1, di2/di2 and di1/di2 genotypes or of PET alleles in Prupe.6G242400 was assessed. References to phenotype information about double-flower and other ornamental traits are also indicated. Accessions with unclear genotype at either di or Di2 loci were also included.

Additional file 7: Supplementary File S1. DNA sequence of the diΔ, di1 and di2 variants. Prupe.2G237700 is highlighted in green with the boxed pre-miR172 sequence. The deletion is indicated in diΔ with strikethrough text while the insertions in di1 and di2 are highlighted in orange and yellow, respectively. Primers used for genotyping are marked as bold, underlined sequences. Primers used for RT-qPCR analysis are shown on a portion of the pre-miR172d sequence.

Eggplant fruits are normally harvested and marketed when they reach the commercial maturity, that precedes the physiological ripening when dramatic changes in taste, composition and peel color take place. The biochemical changes in fruit peel across the developmental stages, characterized also by a sizeable decrement of anthocyanins, were studied in four eggplant genotypes differing for fruit pigmentation. HPLC-DAD, HPLC-ESI-MS and NMR analyses identified naringenin chalcone and naringenin 7-O-glucoside as the main phenolic compounds in extracts from the physiological ripe stage, along with compounds tentatively identified as glycosylated naringenin chalcone, naringenin and kaempferol. On average, the levels of anthocyanins, responsible for the peel pigmentation, dropped by 75% during development, while, surprisingly, the level of total phenols showed a slight decrease of 16%, with a final concentration of more than 1000 mg/100g dw. RT-qPCR expression profiling of nine genes coding for enzymes putatively acting at different steps of the involved pathways showed modulation mostly consistent with the observed changes in phenolic composition, with a remarkable decrease in the activity of flavonol reductase and an increase in flavonol synthase during berry development. Antioxidant activity monitored by peroxyl scavenging was similar at all developmental stages while Fremy's analysis evidenced a slight decrement at full physiological ripening. These results are valuable to address the improvement of eggplant commercial fruit quality and the valorization of unmarketable physiological ripe fruits, especially for the newly accumulation of the health-promoting compounds chalcones and flavanones.

Eggplant berries are rich in anthocyanins like delphinidin-3-rutinoside (D3R) and nasunin (NAS), which are accumulated at high amounts in the peel. NAS is derived by D3R through acylation and glycosylation steps. The presence of D3R or NAS is usually associated with black-purple or lilac fruit coloration of the most cultivated varieties, respectively. Building on QTL mapping position, a candidate gene approach was used to investigate the involvement of a BAHD anthocyanin acyltransferase (SmelAAT) in determining anthocyanin type. The cDNA sequence comparison revealed the presence of a single-base deletion in D3R-type line ‘305E40’ (305E40_aat) with respect to the NAS-type reference line ‘67/3’. This is predicted to cause a frame shift mutation, leading to a loss of SmelAAT function and, thus, D3R retention. RT-qPCR analyses confirmed SmelAAT and 305E40_aat expression during berry maturation. In D3R-type lines, ‘305E40’ and ‘DR2’, overexpressing the functional SmelAAT allele from ‘67/3’, the transcript levels of the transgene correlated with the accumulation of NAS in fruit peel. Furthermore, it was also found a higher expression of the transcript for glucosyltransferase Smel5GT1, putatively involved with SmelAAT in the last steps of anthocyanin decoration. Finally, an indel marker matching with anthocyanin type in the ‘305E40’ × ’67/3’ segregating population was developed and validated in a wide number of accessions, proving its usefulness for breeding purposes.

Purpose of Review Along with population aging, the incidence of both heart failure (HF) and cancer is increasing. However, little is known about new-onset cancer in HF patients. This review aims at showing recent discoveries concerning this subset of patients. Recent Findings Not only cancer and HF share similar risk factors but also HF itself can stimulate cancer development. Some cytokines produced by the failing heart induce mild inflammation promoting carcinogenesis, as it has been recently suggested by an experimental model of HF in mice. Summary The incidence of new-onset cancer is higher in HF patients compared to the general population, and it significantly worsens their prognosis. Moreover, the management of HF patients developing new-onset cancer is challenging, especially due to the limited therapeutic options for patients affected by both cancer and HF and the higher risk of cardiotoxicity from anticancer drugs.

The present research uses in-situ neutron diffraction to examine the effect of grain refinement on grain growth during solidification of Al-5 wt.% Cu and Mg-5 wt.% Zn alloys. The alloys were grain refined through additions of Al-5Ti-1B and Zr, respectively. The in-situ neutron diffraction experiments were carried out by heating the alloys to temperatures above the liquidus and subsequently cooling in 5 or 10 degrees C temperature steps to temperatures below solidus, while being irradiated by thermal neutrons. With the addition of grain refiners, grain size reductions of 92% were observed for both the Al-5 wt.% Cu and Mg-5 wt.% Zn alloys. The refined and unrefined Al-5 wt.% Cu alloys contained alpha-Al with Al2Cu along the grain boundary regions. Differences in Al2Cu morphology were observed in the grain refined alloys. The Mg-5 wt.% Zn alloy contained MgZn intermetallic phases with primary Mg. The refined Mg-5 wt.% Zn-0.7 wt.% Zr alloy contained Mg, MgZn and Zn2Zr phases. In-situ neutron diffraction enabled quantification of individual plane solid fraction growth for the alpha-Al and Al2Cu phases in the Al-Cu alloys, and for alpha-Mg in the Mg alloys. For the unrefined Al-5 wt.% Cu, the coarse microstructure resulted in a rapid solid fraction rise at temperatures just below liquidus followed by a gradual increase in solid fraction until the sample was fully solid. The grain-refined Al-5 wt.% Cu alloys showed a columnar to equiaxed microstructure transition and a more gradual growth in fraction solid throughout solidification. For the Mg-5 wt.% Zn alloy, the more packed (0002) and (10 (1) over bar1) alpha-Mg plane intensities grew at a slower rate than the (10 (1) over bar0) plane intensity, resulting in an irregular grain structure. With the addition of the Zr grain refiner, the Mg-5 wt.% Zn-0.7 wt.% Zr alloy had (10 (1) over bar0), (0002) and (10 (1) over bar1) planes intensities all increasing at similar rates, especially at the early stages of solidification. FactSage (TM) (version 6.4, Montreal, QC, Canada) equilibrium solidification models followed the fraction solid curves developed by tracking the fastest growing planes of the Mg alloys.

In situ neutron diffraction was utilized to examine the solidification behavior of aluminum and magnesium alloys for further understanding of solidification, hot tearing, and grain refinement. The experiments consisted of melting samples and allowing them to cool while being irradiated by neutrons. During solidification, solid phases enabled diffraction of neutrons. The diffraction profiles were collected at each temperature step and were used to interpret the growth of individual planes and phases. In situ neutron diffraction enabled determination of fraction solid curves for individual planes and phases, which was not possible with traditional thermal analysis and computational techniques. This paper outlines the method of generation of fraction solid curves from neutron diffraction intensity data, including a technique to account for the effects of the Debye–Waller factor. This method was successful in revealing detailed insights into crystalline solidification. It showed promise in quantifying many other phenomena beyond those discussed.

BACKGROUND: Depression is highly prevalent in Heart Failure (HF). Treatment with sacubitril/valsartan improved quality of life and survival in HF patients. Aim of the study was to investigate prospectively the effect of sacubitril/valsartan on depression in advanced HF patients in waiting list for heart transplant (HT). METHODS: 37 consecutive patients with advanced HF in waiting list for HT were treated with sacubitril/valsartan. We analyzed data derived from the assessment performed the year before the beginning of sacubitril/valsartan, at study entry, and at one year of follow-up. Depression was assessed with Beck Depression Inventory II (BDI) scale. Cognitive function were assessed with Mini-Mental State Examination (MMSE). Functioning was evaluated measuring meters at 6 Minute Walking Test (6MWT) and maximum rate of oxygen consumption (VO2 max). RESULTS: At baseline, 64.9% of HF patients were in NYHA III and 35.1% NYHA IIIB, BDI was 15.2 ± 5.2 with 59.5% of patients with a score > 13. MMSE was 27.8 ± 2.6. After one year of follow-up NYHA class improved significantly, with 56.8% in NYHA II, 40.5% in NYHA III and 2.7% NYHA in IIIB (p 13. MMSE remain stable (28.2 ± 2.1) (p = 0.104). No statistical differences are observed between data collected in the evaluation 1-year before and soon before treatment with sacubitril/valsartan. Multivariate regression analysis demonstrate a relationship between reduction in BDI-II score and improvement in six-minute walking test independently by the effect of sex, age, selective serotonin reuptake inhibitors, VO2 max, NT-proBNP, PAPs, NYHA class differences evaluated at follow-up versus baseline. CONCLUSIONS: Our study showed a reduction in depressive symptomatology in heart transplant waiting list patients treated with sacubitril/valsartan. The improvement in depressive symptomatology was paralleled by 6MWT increase in the follow-up.

Rationale: Dyspnea and exercise limitation are common symptoms in Systemic Sclerosis (SSc) patients. Multiorgan involvement and disease activity could lead patients to different clinical complications and affect prognosis. Aim of this study was to explore the role of cardiopulmonary exercise test (CPET) in the evaluation of exercise limitation and in the characterization of specific phenotypes of organ involvement in SSc patients. Methods: 24 consecutive patients (23 women, 51.3 ± 2.0 mean age) diagnosed with clinically stable SSc (EULAR 2013) underwent resting echocardiography and maximal symptom-limited incremental CPET. Patients were categorized into three groups: A (interstitial lung disease on CT scan), B (pulmonary vascular diesase), C (left ventricular dysfunction). Results were compared with those of 23 healthy controls and among SSc groups. Results: Compared to controls, SSc patients exhibited a significant reduction in functional capacity, ventilatory limitation and a higher estimated pulmonary pressure at echocardiography. Group A (3 patients) exhibited reduced ventilation, lower VO2max, higher PetCO2, and a worse oxygen uptake efficiency slope. Group B (6 patients) was charaterized by higher VE/VCO2 slope, reduced exercise capacity and a peculiar breathing pattern with the presence of exercise oscillatory ventilation. Group C (15 patients) showed lower ventilation, VO2max and VO2/work slope. Conclusion: CPET can unmask early exercise limitation and can be useful in the identification of different clinical phenotypes in SSc patients.

This Registry demonstrated that PAD program is essential to increase the survivors, in particular in regions with densely populated area and with insufficient road network. In these areas it is essential to increase the number of AED installation and the Cardiopulmonary Resuscitation (CPR) training among the general population. Strong positive predictive factors of outcome were a short delay to defibrillation, bystander CPR and place of collapse.

Craniosynostosis syndromes are rare and prognosis would benefit from early diagnosis and treatment. We tried to establish a fast molecular diagnosis method to detect craniosynostosis syndromes.One patient aged 6 months was observed and diagnosed at first, and then another 10 patients were included in this study. All of them suffered from congenital hydrocephalus with normal head circumference. Karyotype analysis, chromosome genome microarray analysis and whole exome sequencing were used.The first patient was diagnosed as Apert Syndrome based on his clinical features and whole exome sequencing. The other 10 patients were also detected by the same protocol and one of them was found to be with Crouzon Syndrome. Both of the patients with craniosynostosis syndrome were treated in time and benefited from this new diagnosis protocol.Craniosynostosis syndromes cause hearing loss and deformity. It is worthy to detect mutations on FGFR1, FGFR2 and FGFR3 for children who suffer from congenital hydrocephalus with normal head circumference.

Background Cancer-associated cachexia and muscle wasting are considered key determinants of cancer-related death and reduction in the quality of life of cancer patients. A crucial link has been established between activin signaling and skeletal muscle atrophy-hypertrophy. We previously showed that activin-βC, a novel activin-A antagonist, is a tumor modulator that abolishes the cancer-associated cachexia in a mouse genetic model of gonadal tumorigenesis, in which the normal balance of inhibin/activin signalling is disrupted by a targeted mutation in the Inha gene (inhibin α-KO mouse). This study aimed to identify the molecular mechanism by which activin-βC increases survival and abolishes cancer-associated cachexia in α-KO mice. We hypothesized that overexpression of activin-βC modulates the cachexia phenotype by antagonizing the activin signaling pathway and repressing muscle wasting via the ubiquitin-proteasome and the autophagic-lysosomal degradation pathways. Methods Male and female ActC++, α-KO, and α-KO/ActC++ mice and WT littermate controls were studied. Western blot analysis for the specific E3 ubiquitin ligases, atrogin-1 and MuRF1, markers of the autophagic-lysosomal pathway, Beclin-1, p62, and LC3A/B, effectors Smad-2, Smad-3 and myostatin was performed in the gastrocnemius of age-matched mice. Histopathology of the gastrocnemius and survival analysis were also conducted in animals from the same breeding cohort. Serum levels of activin-A, inflammatory cytokines, hormonal profile, and bone density were also assessed. Results Increased levels of atrogin-1, MuRF-1, Beclin-1, p62, LC3A/B-I, Smad-2 and serum levels of activin-A were noted in the α-KO mice. These mice developed gonadal cancers followed by severe weight loss, and reduced survival. Overexpression of activin- βC antagonized the activin signaling cascade, attenuating the ubiquitin-proteasome and the autophagic-lysosomal degradation pathways, and reduced serum levels of activin-A. α-KO/ActC++ mice displayed a less aggressive cachectic phenotype, reduced tumor weight, and prolonged survival. Conclusion Our findings show for the first time a specific effect of activin-βC on muscle wasting and transcription factors involved in muscle protein degradation. The study indicates that activin-βC may be a novel therapy to abrogate cancer-associated weight loss and prolong survival.

Sec61p is the channel-forming subunit of the heterotrimeric Sec61 complex that mediates co-translational protein import into the endoplasmic reticulum (ER). In yeast, proteins can also be post-translationally translocated by the hetero-heptameric Sec complex, composed of the Sec61 and the Sec63 complexes. The Sec61 channel is also a candidate for the dislocation channel for misfolded proteins from the ER to the cytosol during ER-associated degradation (ERAD). The structure of the Sec61 complex is highly conserved, but the roles of its N-terminal acetylation and its amphipathic N-terminal helix are unknown so far. To gain insight into the function of the Sec61p N-terminus, we mutated its N-acetylation site, deleted its amphipathic helix, or both the helix and the N-acetylation site. Mutation of the N-acetylation site on its own had no effect on protein import into the ER in intact cells, but resulted in an ERAD defect. Yeast expressing sec61 without the N-terminal amphipathic helix displayed severe growth defects and had profound defects in post-translational protein import into the ER. Nevertheless the formation of the hetero-heptameric Sec complex was not affected. Instead, the lack of the N-terminal amphipathic helix compromised the integrity of the heterotrimeric Sec61 complex. We conclude that the N-terminal helix of Sec61p is required for post-translational protein import into the ER and Sec61 complex stability, whereas N-terminal acetylation of Sec61p plays a role in ERAD.

The presence of highly compressible soft soil layers can expose infrastructure networks (roads, bridges, pipelines, etc.) to settlements that can compromise their serviceability or even their stability. The analysis/forecast of the induced effects can follow empirical, analytical, numerical approaches at different levels of analysis referring to samples of exposed elements whose number decreases as the level of required details increases. The present work proposes an original procedure for investigating bridge settlement-induced damage via the generation of empirical fragility curves based on the integration of visible damage surveys on statically indeterminate bridges (both masonry and concrete) with widespread remote sensing-derived settlement measurements. The procedure is tested in Amsterdam city (The Netherlands) worldwide famous for its dense network of bridges resting with their foundations on a subsoil of thick layers of organic clay and peat alternating with sands. These bridges currently suffer from settlement-induced damages of different severity that yearly require expensive maintenance and repair works. The obtained results seem promising under the perspective of prioritizing interventions on those bridges for which detailed and demanding coupled/uncoupled geotechnical-structural models need to be set up.

Activins and inhibins, members of the TGF-β superfamily, are growth and differentiation factors involved in the regulation of several biological processes, including reproduction, development, and fertility. Previous studies have shown that the activin-β

The acylphosphatase from Sulfolobus solfataricus (Sso AcP) is a globular protein able to aggregate in vitro from a native-like conformational ensemble without the need for a transition across the major unfolding energy barrier. This process leads to the formation of assemblies in which the protein retains its native-like structure, which subsequently convert into amyloid-like aggregates. Here, we investigate the mechanism by which Sso AcP aggregates in vivo to form bacterial inclusion bodies after expression in E. coli . Shortly after the initiation of expression, Sso AcP is incorporated into inclusion bodies as a native-like protein, still exhibiting small but significant enzymatic activity. Additional experiments revealed that this overall process of aggregation is enhanced by the presence of the unfolded N-terminal region of the sequence and by destabilization of the globular segment of the protein. At later times, the Sso AcP molecules in the inclusion bodies lose their native-like properties and convert into β -sheet-rich amyloid-like structures, as indicated by their ability to bind thioflavin T and Congo red. These results show that the aggregation behavior of this protein is similar in vivo to that observed in vitro, and that, at least for a predominant part of the protein population, the transition from a native to an amyloid-like structure occurs within the aggregate state.

In this study, the hot cracking susceptibility of AZ91E and AE42 magnesium alloys was assessed using the moving torch Varestraint test method. Plates of 3 mm thickness were sliced from AZ91E and AE42 ingots and subsequently tested. Quantitative cracking data in terms of maximum crack length was used for evaluating the cracking susceptibility. Scanning electron microscopy (SEM) was carried out and the results suggest that AE42 showed a higher resistance to hot cracking in comparison to the AZ91E alloy. This was attributed to the difference in microstructure between the two alloys. In the fusion zone and heat affected zone of AE42, the brittle needle-like Al11RE3 phase was seen to decompose to the more ductile particle-like Al2RE phase, thereby increasing the alloy’s resistance to hot cracking. In contrast, SEM fractography revealed that brittle Al6Mn and Mg17Al12 intermetallic particles segregated to grain boundaries and triggered hot cracking in AZ91E. Dans cette etude, on a evalue la susceptibilite a la ...

The most commonly used aluminum alloy for automotive engine blocks is 319, which possesses good strength and castability. In this research, 319 Al alloy engine blocks were analysed in the as-cast, heat-treated and service-tested conditions. Extensive microscopy and hardness measurements were carried out on samples extracted from top to bottom along the interbore region of each cylinder. The results suggest that a variation in cooling rate along the cylinders caused a refinement in microstructure at the bottom of the cylinders. Although the morphology of the secondary phases changed, the increased cooling rate did not lead to the formation of different secondary phases, which is indicated by the fact that no significant difference in hardness of the secondary phases was observed at the top and bottom of the cylinder. Furthermore, the results from nanoindentation indicate that Al 2Cu has a stronger bond with the matrix compared to Si and Al 17Fe 3.2Mn 0.8Si 2. � 2011 Indian Institute of Metals.