Search results for "PIP"
showing 10 items of 1156 documents
Amine basicity: measurements of ion pair stability in ionic liquid media
2007
Abstract The stability constants relevant to the formation of amine/p-nitrophenol ion pairs have been determined in [bmim][BF4] solution, in the presence of butylamine, piperidine, and triethylamine, by using spectrophotometric measurements. In order to evaluate how the ion pair stability is affected by ionic liquid structure, piperidine has been chosen as model amine for studies in [bmim][PF6], [bmim][NTf2], [bm2im][NTf2] and in several [bmim][BF4]/1,4-dioxane binary mixtures. Data obtained in ionic liquid solutions have been compared with those previously reported in conventional organic solvents.
Investigation of Diketopiperazines Containing a Guanidino-Functionalized Sidechain as Potential Catalysts of Enantioselective Strecker Reactions
2005
Diketopiperazine 1 consisting of L-(γ-guanidino-α-amino)butyric acid and L-phenylalanine was synthesized as the hydroacetate and as the hydronitrate. Its structure was confirmed by X-ray analysis. In contrast to reports in the literature (Lipton et al.), compound 1 does not induce enantioselevtive catalysis of Strecker reactions. (© Wiley-VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2005)
Evidence for a modulatory role of cannabinoids on the excitatory NANC neurotransmission in mouse colon
2007
Abstract It is well accepted that endogenous cannabinoids and CB1 receptors are involved in the regulation of smooth muscle contractility and intestinal motility, through a mechanism mainly related to reduction of acetylcholine release from cholinergic nerve endings. Because, few data exist on a possible modulatory action of the cannabinoid agents on the non-adrenergic non-cholinergic (NANC) excitatory and inhibitory neurotransmission, the aim of the present study was to investigate the effects of cannabinoid drugs on the NANC responses elicited by electrical field stimulation (EFS) in the circular muscle of mouse proximal colon. Colonic contractions were monitored as changes in endoluminal…
Cytomegalovirus‐specific T‐cell immunity and DNAemia in patients with chronic lymphocytic leukaemia undergoing treatment with ibrutinib
2021
Epidemiologia delle Malattie Cardiovascolari
2004
CRiSPy-CUDA: Computing Species Richness in 16S rRNA Pyrosequencing Datasets with CUDA
2011
Pyrosequencing technologies are frequently used for sequencing the 16S rRNA marker gene for metagenomic studies of microbial communities. Computing a pairwise genetic distance matrix from the produced reads is an important but highly time consuming task. In this paper, we present a parallelized tool (called CRiSPy) for scalable pairwise genetic distance matrix computation and clustering that is based on the processing pipeline of the popular ESPRIT software package. To achieve high computational efficiency, we have designed massively parallel CUDA algorithms for pairwise k-mer distance and pairwise genetic distance computation. We have also implemented a memory-efficient sparse matrix clust…
Novel pathway in Bcr-Abl signal transduction involves Akt-independent, PLC-γ1-driven activation of mTOR/p70S6-kinase pathway
2009
In chronic myeloid leukemia, activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway is crucial for survival and proliferation of leukemic cells. Essential downstream molecules involve mammalian target of rapamycin (mTOR) and S6-kinase. Here, we present a comprehensive analysis of the molecular events involved in activation of these key signaling pathways. We provide evidence for a previously unrecognized phospholipase C-gamma1 (PLC-gamma1)-controlled mechanism of mTOR/p70S6-kinase activation, which operates in parallel to the classical Akt-dependent machinery. Short-term imatinib treatment of Bcr-Abl-positive cells caused dephosphorylation of p70S6-K and S6-protein without inactivat…
The new iodoacetamidobenzofuran derivative TR120 decreases STAT5 expression and induces antitumor effects in imatinib-sensitive and imatinib-resistan…
2013
The identification of novel compounds modulating the expression/activity of molecular targets downstream to BCR-ABL could be a new approach in the treatment of chronic myeloid leukemias (CMLs) resistant to imatinib or other BCR-ABL-targeted molecules. Recently, we synthesized a new class of substituted 2-(3,4,5-trimethoxybenzoyl)-2-N,N-dimethylamino-benzo[b]furans, and among these 3-iodoacetylamino-6-methoxybenzofuran-2-yl(3,5-trimethoxyphenyl)methanone (TR120) showed marked cytotoxic activity in BCR-ABL-expressing cells. Interestingly, TR120 was more potent than imatinib in cell growth inhibition and apoptosis induction in both BCR-ABL-expressing K562 and KCL22 cells. Moreover, it showed a…
In BCR-ABL-positive cells, STAT-5 tyrosine-phosphorylation integrates signals induced by imatinib mesylate and Ara-C.
2003
In BCR-ABL-positive cells, the transcription factor STAT-5 is constitutively activated by tyrosine phosphorylation. STAT-5 activation results in upregulation of bcl-X(L) and increased resistance to induction of apoptosis. Here, we investigated the effects of imatinib mesylate and cytosine arabinoside (Ara-C) on STAT-5 tyrosine-phosphorylation, cellular proliferation and induction of apoptosis in cell lines and primary hematopoietic cells. Imatinib mesylate treatment strongly suppressed STAT-5 tyrosine-phosphorylation in K562 and primary CML blasts. In contrast to JAK-2 and PI-3-kinase inhibition, exposure of K562 cells to imatinib mesylate resulted in obvious suppression of proliferation. R…
Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells
2008
Resistance to imatinib mesylate is an emergent problem in the treatment of Bcr-Abl expressing myelogenous leukemias and additional therapeutic strategies are required. We observed that galangin, a non-toxic, naturally occurring flavonoid was effective as anti-proliferative, and apoptotic agent in Bcr-Abl expressing K562 and KCL22 cells and in imatinib mesylate resistant K562-R and KCL22-R cells. Galangin induced an arrest of cells in G0–G1phase of cell cycle and a decrease in pRb, cdk4, cdk1, cycline B levels; moreover, it was able to induce a monocytic differentiation of leukemic Bcr-Abl+ cells. Of note, galangin caused a decrease in Bcl-2 levels and markedly increased the apoptotic activi…