Study of the microstructure resulting from brazed aluminium materials used in heat exchangers

Re-solidification of AA4343 cladding after brazing as well as the related precipitation in the modified AA3003 core material have been investigated. Analysis of the re-solidified material showed that partial dissolution of the core alloy occurs in both the brazing joints and away of them. Far from the brazing joints, the dissolution is, however, limited and diffusion of silicon from the liquid into the core material leads to solid-state precipitation in the so-called “band of dense precipitates” (BDP). On the contrary, the dissolution is enhanced in the brazing joint to such an extent that no BDP could be observed. The intermetallic phases present in the resolidified areas as well as in the core material have been analyzed and found to be mainly cubic alpha-Al(Mn,Fe)Si. These results were then compared to predictions made with available phase diagram information

Effect of intensive melt shearing on the formation of Fe-containing intermetallics in LM24 Al-alloy

Fe is one of the inevitable and detrimental impurities in aluminium alloys that degrade the mechanical performance of castings. In the present work, intensive melt shearing has been demonstrated to modify the morphology of Fe-containing intermetallic compounds by promoting the formation of compact α-Al(Fe,Mn)Si at the expense of needle-shaped β-AlFeSi, leading to an improved mechanical properties of LM24 alloy processed by MC-HPDC process. The promotion of the formation of α -Al(Fe, Mn)Si phase is resulted from the enhanced nucleation on the well dispersed MgAl 2O 4 particles in the melt. The Fe tolerance of LM24 alloy can be effectively improved by combining Mn alloying and intensive melt shearing

Multiperiodicity in the large-amplitude rapidly-rotating β\beta Ceph ei star HD 203664

We perform a seismic study of the young massive $\beta$Cephei star HD 203664 with the goal to constrain its interior structure. Our study is based on a time series of 328 new Geneva 7-colour photometric data of the star spread over 496.8 days. The data confirm the frequency of the dominant mode of the star which we refine to $f_1=6.02885$c d$^{-1}$. The mode has a large amplitude of 37 mmag in V and is unambiguously identified as a dipole mode ($\ell=2$) from its amplitude ratios and non-adiabatic computations. Besides $f_1$, we discover two additional new frequencies in the star with amplitudes above $4\sigma$: $f_2=6.82902$c d$^{-1}$ and $f_3=4.81543$c d$^{-1}$ or one of their daily aliases. The amplitudes of these two modes are only between 3 and 4 mmag which explains why they were not detected before. Their amplitude ratios are too uncertain for mode identification. We show that the observed oscillation spectrum of HD 203664 is compatible with standard stellar models but that we have insufficient information for asteroseismic inferences. Among the large-amplitude $\beta$Cephei stars, HD 203664 stands out as the only one rotating at a significant fraction of its critical rotation velocity ($\sim 40$).Comment: 7 pages, 5 figures, accepted for publication in A&A (Astronomy & Astrophysics

Towards ensemble asteroseismology of the young open clusters Chi Persei and NGC 6910

As a result of the variability survey in Chi Persei and NGC6910, the number of Beta Cep stars that are members of these two open clusters is increased to twenty stars, nine in NGC6910 and eleven in Chi Persei. We compare pulsational properties, in particular the frequency spectra, of Beta Cep stars in both clusters and explain the differences in terms of the global parameters of the clusters. We also indicate that the more complicated pattern of the variability among B type stars in Chi Persei is very likely caused by higher rotational velocities of stars in this cluster. We conclude that the sample of pulsating stars in the two open clusters constitutes a very good starting point for the ensemble asteroseismology of Beta Cep-type stars and maybe also for other B-type pulsators.Comment: 4 pages, Astronomische Nachrichten, HELAS IV Conference, Arecife, Lanzarote, Feb 2010, submitte

Cytosolic phospholipase A2α gene silencing in monocytes alters development of Th1 responses and reduces autoimmune arthritis

International audienc

Apolipoprotein E and Coronary Disease: A Puzzling Paradox

Reilly and Rader discuss a new study in PLoS Medicine that shows an association between apoE levels and cardiovascular disease mortality

PCSK9, apolipoprotein E and lipoviral particles in chronic hepatitis C genotype 3: evidence for genotype-specific regulation of lipoprotein metabolism.

BACKGROUND & AIMS: Hepatitis C virus (HCV) associates with lipoproteins to form "lipoviral particles" (LVPs) that can facilitate viral entry into hepatocytes. Initial attachment occurs via heparan sulphate proteoglycans and low-density lipoprotein receptor (LDLR); CD81 then mediates a post-attachment event. Proprotein convertase subtilisin kexin type 9 (PCSK9) enhances the degradation of the LDLR and modulates liver CD81 levels. We measured LVP and PCSK9 in patients chronically infected with HCV genotype (G)3. PCSK9 concentrations were also measured in HCV-G1 to indirectly examine the role of LDLR in LVP clearance. METHODS: HCV RNA, LVP (d1.07g/ml) fractions, were quantified in patients with HCV-G3 (n=39) by real time RT-PCR and LVP ratios (LVPr; LVP/(LVP+non-LVP)) were calculated. Insulin resistance (IR) was assessed using the homeostasis model assessment of IR (HOMA-IR). Plasma PCSK9 concentrations were measured by ELISA in HCV-G3 and HCV-G1 (n=51). RESULTS: In HCV-G3 LVP load correlated inversely with HDL-C (r=-0.421; p=0.008), and apoE (r=-0.428; p=0.013). The LVPr varied more than 35-fold (median 0.286; range 0.027 to 0.969); PCSK9 was the strongest negative predictor of LVPr (R(2)=16.2%; p=0.012). HOMA-IR was not associated with LVP load or LVPr. PCSK9 concentrations were significantly lower in HCV-G3 compared to HCV-G1 (p<0.001). PCSK9 did not correlate with LDL-C in HCV-G3 or G1. CONCLUSIONS: The inverse correlation of LVP with apoE in HCV-G3, compared to the reverse in HCV-G1 suggests HCV genotype-specific differences in apoE mediated viral entry. Lower PCSK9 and LDL concentrations imply upregulated LDLR activity in HCV-G3

Block of death-receptor apoptosis protects mouse cytomegalovirus from macrophages and is a determinant of virulence in immunodeficient hosts.

The inhibition of death-receptor apoptosis is a conserved viral function. The murine cytomegalovirus (MCMV) gene M36 is a sequence and functional homologue of the human cytomegalovirus gene UL36, and it encodes an inhibitor of apoptosis that binds to caspase-8, blocks downstream signaling and thus contributes to viral fitness in macrophages and in vivo. Here we show a direct link between the inability of mutants lacking the M36 gene (ΔM36) to inhibit apoptosis, poor viral growth in macrophage cell cultures and viral in vivo fitness and virulence. ΔM36 grew poorly in RAG1 knockout mice and in RAG/IL-2-receptor common gamma chain double knockout mice (RAGγC(-/-)), but the depletion of macrophages in either mouse strain rescued the growth of ΔM36 to almost wild-type levels. This was consistent with the observation that activated macrophages were sufficient to impair ΔM36 growth in vitro. Namely, spiking fibroblast cell cultures with activated macrophages had a suppressive effect on ΔM36 growth, which could be reverted by z-VAD-fmk, a chemical apoptosis inhibitor. TNFα from activated macrophages synergized with IFNγ in target cells to inhibit ΔM36 growth. Hence, our data show that poor ΔM36 growth in macrophages does not reflect a defect in tropism, but rather a defect in the suppression of antiviral mediators secreted by macrophages. To the best of our knowledge, this shows for the first time an immune evasion mechanism that protects MCMV selectively from the antiviral activity of macrophages, and thus critically contributes to viral pathogenicity in the immunocompromised host devoid of the adaptive immune system

Measurement of χ c1 and χ c2 production with s√ = 7 TeV pp collisions at ATLAS

The prompt and non-prompt production cross-sections for the χ c1 and χ c2 charmonium states are measured in pp collisions at s√ = 7 TeV with the ATLAS detector at the LHC using 4.5 fb−1 of integrated luminosity. The χ c states are reconstructed through the radiative decay χ c → J/ψγ (with J/ψ → μ + μ −) where photons are reconstructed from γ → e + e − conversions. The production rate of the χ c2 state relative to the χ c1 state is measured for prompt and non-prompt χ c as a function of J/ψ transverse momentum. The prompt χ c cross-sections are combined with existing measurements of prompt J/ψ production to derive the fraction of prompt J/ψ produced in feed-down from χ c decays. The fractions of χ c1 and χ c2 produced in b-hadron decays are also measured