The Effect of Sequence of Operations on Fatigue Life of LSP Treated Open-hole Aluminium Specimens

Fastener holes in aeronautical structures are typical sources of fatigue cracks due to their induced local stress concentration. A very efficient solution to this problem is to establish compressive residual stresses around the fastener holes that retard the fatigue crack nucleation and its subsequent local propagation. Previous work done on the subject of the application of LSP treatment on thin, open-hole specimens [1] has proven that the LSP effect on fatigue life of treated specimens can be detrimental, if the process is not properly optimized. In fact, it was shown that the capability of the LSP to introduce compressive residual stresses around fastener holes in thin-walled structures representative of typical aircraft constructions was not superior to the performance of conventional techniques, such as cold-working.

Grid-based histogram arithmetic for the probabilistic analysis of functions

The selection of predefined analytic grids (partitions of the numeric ranges) to represent input and output functions as histograms has been proposed as a mechanism of approximation in order to control the tradeoff between accuracy and computation times in several áreas ranging from simulation to constraint solving. In particular, the application of interval methods for probabilistic function characterization has been shown to have advantages over other methods based on the simulation of random samples. However, standard interval arithmetic has always been used for the computation steps. In this paper, we introduce an alternative approximate arithmetic aimed at controlling the cost of the interval operations. Its distinctive feature is that grids are taken into account by the operators. We apply the technique in the context of probability density functions in order to improve the accuracy of the probability estimates. Results show that this approach has advantages over existing approaches in some particular situations, although computation times tend to increase significantly when analyzing large functions.

Meromorphic continuation of functions and arbitrary distribution of interpolation points

We characterize the region of meromorphic continuation of an analytic function ff in terms of the geometric rate of convergence on a compact set of sequences of multi-point rational interpolants of ff. The rational approximants have a bounded number of poles and the distribution of interpolation points is arbitrary.

A synthetic all d-amino acid peptide corresponding to the N-terminal sequence of HIV-1 gp41 recognizes the wild-type fusion peptide in the membrane and inhibits HIV-1 envelope glycoprotein-mediated cell fusion

Recent studies demonstrated that a synthetic fusion peptide of HIV-1 self-associates in phospholipid membranes and inhibits HIV-1 envelope glycoprotein-mediated cell fusion, presumably by interacting with the N-terminal domain of gp41 and forming inactive heteroaggregates [Kliger, Y., Aharoni, A., Rapaport, D., Jones, P., Blumenthal, R. & Shai, Y. (1997) J. Biol. Chem. 272, 13496–13505]. Here, we show that a synthetic all d-amino acid peptide corresponding to the N-terminal sequence of HIV-1 gp41 (D-WT) of HIV-1 associates with its enantiomeric wild-type fusion (WT) peptide in the membrane and inhibits cell fusion mediated by the HIV-1 envelope glycoprotein. D-WT does not inhibit cell fusion mediated by the HIV-2 envelope glycoprotein. WT and D-WT are equally potent in inducing membrane fusion. D-WT peptide but not WT peptide is resistant to proteolytic digestion. Structural analysis showed that the CD spectra of D-WT in trifluoroethanol/water is a mirror image of that of WT, and attenuated total reflectance–fourier transform infrared spectroscopy revealed similar structures and orientation for the two enantiomers in the membrane. The results reveal that the chirality of the synthetic peptide corresponding to the HIV-1 gp41 N-terminal sequence does not play a role in liposome fusion and that the peptides’ chirality is not necessarily required for peptide–peptide interaction within the membrane environment. Furthermore, studies along these lines may provide criteria to design protease-resistant therapeutic agents against HIV and other viruses.

Draft Genome Sequence of Aneurinibacillus migulanus NCTC 7096

ACKNOWLEDGMENTS This project was funded by the Government of Kuwait (to F.N.A.) and the European Union’s Seventh Framework Programme under grant agreement 245268 (ISEFOR; to L.B. and S.W.). Further support came from the SwissBOL project, financed by the Swiss Federal Office for the Environment (grant holder L.B.) and the Sciex–Scientific Exchange Programme NMS.CH (to L.L. and L.B.).

Draft Genome Sequence of Aneurinibacillus migulanus Strain Nagano

ACKNOWLEDGMENTS This project was funded by the Kuwait Government (to F.N.A.), the European Union’s Seventh Framework Programme under grant agreement no. 245268 (ISEFOR; to L.B. and S.W.). Further support came from the SwissBOL project, financed by the Swiss Federal Office for the Environment (grant holder, L.B.) and the Sciex–Scientific Exchange Programme NMS.CH (to L.B. and L.L.).

Sequence of the FRA3B common fragile region: Implications for the mechanism of FHIT deletion

The hypothesis that chromosomal fragile sites may be “weak links” that result in hot spots for cancer-specific chromosome rearrangements was supported by the discovery that numerous cancer cell homozygous deletions and a familial translocation map within the FHIT gene, which encompasses the common fragile site, FRA3B. Sequence analysis of 276 kb of the FRA3B/FHIT locus and 22 associated cancer cell deletion endpoints shows that this locus is a frequent target of homologous recombination between long interspersed nuclear element sequences resulting in FHIT gene internal deletions, probably as a result of carcinogen-induced damage at FRA3B fragile sites.

Nucleotide sequence of the Kaposi sarcoma-associated herpesvirus (HHV8)

The genome of the Kaposi sarcoma-associated herpesvirus (KSHV or HHV8) was mapped with cosmid and phage genomic libraries from the BC-1 cell line. Its nucleotide sequence was determined except for a 3-kb region at the right end of the genome that was refractory to cloning. The BC-1 KSHV genome consists of a 140.5-kb-long unique coding region flanked by multiple G+C-rich 801-bp terminal repeat sequences. A genomic duplication that apparently arose in the parental tumor is present in this cell culture-derived strain. At least 81 ORFs, including 66 with homology to herpesvirus saimiri ORFs, and 5 internal repeat regions are present in the long unique region. The virus encodes homologs to complement-binding proteins, three cytokines (two macrophage inflammatory proteins and interleukin 6), dihydrofolate reductase, bcl-2, interferon regulatory factors, interleukin 8 receptor, neural cell adhesion molecule-like adhesin, and a D-type cyclin, as well as viral structural and metabolic proteins. Terminal repeat analysis of virus DNA from a KS lesion suggests a monoclonal expansion of KSHV in the KS tumor.