Exploring the Role of Central Metals in Bulky Phthalocyanines for Dye-Sensitized Solar Cells.

Two series of metallo-(Zn(II), Mg(II), and Ru(II)) and free-base phthalocyanines (Pcs) with a carboxyl anchoring group and well-established bulky peripheral substituents (either tert-butyl or bulky 2,6-diisopropylphenoxy) were synthesized and tested as sensitizers in dye-sensitized solar cells (DSSCs). The trend of photovoltaic efficiencies (PCEs) for free-base and metallo Pcs followed the order Zn(II)Pc>Mg(II)Pc≫H2Pc ≈ Ru(II)Pc regardless of the peripheral substitution. Higher efficiencies (4.

Crystal structure of inhibitor of κB kinase β.

Inhibitor of κB (IκB) kinase (IKK) phosphorylates IκB proteins, leading to their degradation and the liberation of nuclear factor κB for gene transcription. Here we report the crystal structure of IKKβ in complex with an inhibitor, at a resolution of 3.6 Å.

Sensitivity and gene expression profile of fresh human acute myeloid leukemia cells exposed ex vivo to AS602868.

Purpose: The need for new treatment options for acute myeloid leukemia (AML) is increasing. AS602868 is a novel investigational drug with reported activity on AML cells.

Methods: We studied gene expression profiles in AML blasts exposed to AS602868 in order to better understand its mechanism of action.

An adiponectin-like molecule with antidiabetic properties.

Adiponectin increases glucose transport, reduces inflammation, and controls vascular functions. Hence, we propose that treatment with a recombinant globular domain of adiponectin (rgAd110-244) has significant therapeutic potential to treat insulin resistance. Mice were fed for 3 months on a high-fat diet (HFD) to induce insulin resistance, diabetes, and moderate weight gain.

NF-kappaB inhibition triggers death of imatinib-sensitive and imatinib-resistant chronic myeloid leukemia cells including T315I Bcr-Abl mutants.

The Bcr-Abl inhibitor imatinib is the current first-line therapy for all newly diagnosed chronic myeloid leukemia (CML). Nevertheless, resistance to imatinib emerges as CML progresses to an acute deadly phase implying that physiopathologically relevant cellular targets should be validated to develop alternative therapeutic strategies. The NF-kappaB transcription factor that exerts pro-survival actions is found abnormally active in numerous hematologic malignancies.