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The new theory of democratic phase coherent data-scatter (DPCD-S) is introduced. Basics of UV-visible spectrometry theory and error propagation have been presented. The qualitative spectral analysis provided is point-by-point over the complete data set and not just limited to Lambda-maxima. Equal weightings of the ‘voting’ data scattering algorithm are employed in the analysis of both the calibration and food colour data and this is consequently the democratic algorithm. The paper shows how the technique can be used with UV-visible standards to analyse the wavelength and photometric calibration of a spectrophotometer. The main results relate to the analysis of a series of spectra taken on complex mixtures of three important food dyes and their quantitative analysis using the phase coherent data-scatter technique. This method is shown to offer new possibilities for identifying and archiving UV-visible spectra from a single point in a transform space. Complex spectra can therefore be represented by a single point in this transform space, which is weighted by the ‘votes’ of all the data points in the complex data set. The software allows the user to interrogate the scatter results and locate the scatter point to the specific spectral positions. A new mathematical operator has been introduced to resolve any possible coincidence of two spectral projection points. Analysis of two close spectra from very-different admixtures of food colours shows powerfully the utility of this operator. Error propagation severely limits the accuracy of the usual UV-method of simultaneous equation secondary mixtures analysis.

Resume Treatment of (5H)-2-furanones with LDA gives the corresponding (3H)-2-furanones which react easily in water with dienophiles to give cycloadducts in good yields and high stereoselectivity.

AMLs constitute an heterogeneous group of hematopoietic stem cell disorders of rather poor prognosis. Abnormal activation of signaling pathways including STAT, MAPK and NF-KB have been described in AMLs and could constitute new targets for therapy. In this study, we focused on the PI3K/AKT and mTOR/P70S6K activity in primary blast cells purified from the bone marrow of patients with primary (n = 54) or secondary (n =10) AMLs. Patients with de novo AMLs were issued from the AML2001 French Multicenter Trial directed by the GOELAMS. The FAB classification was the following: M0 (n = 8), M1 (n = 10) M2 (n = 21), M4 (n = 10), M4eo (n = 2), M5 (n = 11), unknown AML (n = 2). In 58% of these patients, a constitutive activation of PI3K/AKT was detected in blast cells by western blot analysis showing AKT and FOXO3a phosphorylation, and confirmed by immunofluorescence confocal microscopy and flow cytometry analysis in CD34+ blast cells. Constitutive GAB1/2 phosphorylation was detected in all PI3K+ patients. However, we did not find any correlation between PI3K activation and FLT3 gene mutations. PTEN and SHIP-1 expression was normal in all tested PI3K+ patients. Proliferation (3H thymidine incorporation) was significantly increased in PI3K+ samples compared to PI3K- samples (p=0.001). The mTOR/P70S6K pathway was activated and the mTOR inhibitor rapamycin selectively reduced proliferation of PI3K+ samples. We determined the expression of the alpha, beta and delta isoforms of the catalytic sub-unit of PI3K (p110) in leukemic cells and found that p110 delta was the only consistently expressed isoform. In 8 PI3K+ samples tested, IC87114 (ICOS Corporation), a specific p110delta inhibitor compound used at 10μM totally suppressed AKT and FOXO3a phosphorylation. IC87114 inhibited proliferation of PI3K+ leukemic cells whereas it did not induce apoptosis. IC87114 did not significantly impaired the proliferation of PI3K- blast cells. Interestingly, IC87114 did not inhibit the proliferation or clonogenicity of CD34+ cord blood cells cultured in SCF, FLT3L and TPO used as controls. Overall, our results report, a/ a constitutive activation of PI3K in 58% of AML, b/ no correlation between FLT3 gene mutations and PI3K positivity, c/ no implication of PTEN or SHIP-1 phosphatases in PI3K activation, d/ a major role of the p110 delta isoform of PI3K in leukemic cell proliferation, e/ a potential therapeutic value of inhibiting mTOR and P110 delta activity.