Retraction and Generalized Extension of Computing with Words

Fuzzy automata, whose input alphabet is a set of numbers or symbols, are a formal model of computing with values. Motivated by Zadeh's paradigm of computing with words rather than numbers, Ying proposed a kind of fuzzy automata, whose input alphabet consists of all fuzzy subsets of a set of symbols, as a formal model of computing with all words. In this paper, we introduce a somewhat general formal model of computing with (some special) words. The new features of the model are that the input alphabet only comprises some (not necessarily all) fuzzy subsets of a set of symbols and the fuzzy transition function can be specified arbitrarily. By employing the methodology of fuzzy control, we establish a retraction principle from computing with words to computing with values for handling crisp inputs and a generalized extension principle from computing with words to computing with all words for handling fuzzy inputs. These principles show that computing with values and computing with all words can be respectively implemented by computing with words. Some algebraic properties of retractions and generalized extensions are addressed as well.Comment: 13 double column pages; 3 figures; to be published in the IEEE Transactions on Fuzzy System

Probing the C-H Activation of Linear and Cyclic Ethers at (PNP)Ir

Interaction of the amido/bis(phosphine)-supported (PNP)Ir fragment with a series of linear and cyclic ethers is shown to afford, depending on substrate, products of α,α-dehydrogenation (carbenes), α,β-dehydrogenation (vinyl ethers), or decarbonylation. While carbenes are exclusively obtained from tert-amyl methyl ether, sec-butyl methyl ether (SBME), n-butyl methyl ether (NBME), and tetrahydrofuran (THF), vinyl ethers or their adducts are observed upon reaction with diethyl ether and 1,4-dioxane. Decarbonylation occurs upon interaction of (PNP)Ir with benzyl methyl ether, and a mechanism is proposed for this unusual transformation, which occurs via a series of C−H, C−O, and C−C bond cleavage events. The intermediates characterized for several of these reactions as well as the α,α-dehydrogenation of tert-butyl methyl ether (MTBE) are used to outline a reaction pathway for the generation of PNP-supported iridium(I) carbene complexes, and it is shown that the long-lived, observable intermediates are substrate-dependent and differ for the related cases of MTBE and THF. Taken together, these findings highlight the variety of pathways utilized by the electron-rich, unsaturated (PNP)Ir fragment to stabilize itself by transferring electron density to ethereal substrates through oxidative addition and/or the formation of π-acidic ligands

Deferoxamine retinopathy: spectral domain-optical coherence tomography findings

Al-Djamiʿ li Ibn al-BaïtharNumérisation effectuée à partir d'un document de substitution

Deferoxamine retinopathy: spectral domain-optical coherence tomography findings

BACKGROUND: To describe the spectral domain optical coherence tomography (SD-OCT) findings of a patient who developed pigmentary retinopathy following high-dose deferoxamine administration. CASE PRESENTATION: A 34-year-old man with thalassemia major complained of nyctalopia and decreased vision following high-dose intravenous deferoxamine to treat systemic iron overload. Fundus examination revealed multiple discrete hypo-pigmented lesions at the posterior pole and mid-peripheral retina. Recovery was partial following cessation of desferrioxamine six weeks later. A follow-up SD-OCT showed multiple accumulated hyper-reflective deposits primarily in the choroid, retina pigment epithelium (RPE), and inner segment and outer segment (IS/OS) junction. CONCLUSION: Deferoxamine retinopathy primarily targets the RPE–Bruch membrane–photoreceptor complex, extending from the peri-fovea to the peripheral retina with foveola sparing. An SD-OCT examination can serve as a simple, noninvasive tool for early detection and long-term follow-up

Macrophage activation increases the invasive properties of hepatoma cells by destabilization of the adherens junction

AbstractTumor-associated macrophages play an important role in tumor progression, but whether they exert a tumor-progressive effect remains controversial. Here, we demonstrated that activated macrophage-conditioned medium (AMCM) obtained from RAW macrophages (RAW/AMCM) induced epithelial-mesenchymal transition (EMT) and stimulated the migratory and invasive activities of HepG2 cells, whereas control conditioned media had no effect. Epithelial-cadherin (E-cadherin) and β-catenin staining patterns were altered at the adherens junctions by RAW/AMCM treatment, with an approximately 50% decrease in E-cadherin and β-catenin in the cell membrane. Importantly, levels of β-catenin-associated E-cadherin were also decreased. Following RAW/AMCM treatment, enhanced activation of c-Src was seen prior to increased tyrosine phosphorylation of β-catenin, and this led to the destabilization of adherens junctions. Pretreatment of HepG2 cells with the Src kinase inhibitor, PP2, completely abolished the effects of RAW/AMCM on the EMT, migration, invasion, and expression and association of E-cadherin and β-catenin. AMCMs obtained from human THP-1 monocytes and mouse peritoneal macrophages also caused disassembly of the adherens junctions and migration of HepG2 cells. Furthermore, inhibition of the epidermal growth factor receptor (EGFR) with gefitinib partially prevented the downregulation of E-cadherin and β-catenin at the adherens junctions and migration behavior induced by RAW/AMCM. Our results suggest that activated macrophages have a tumor-progressive effect on HepG2 cells which involves the c-Src- and EGFR-dependent signaling cascades

Survivin counteracts the therapeutic effect of microtubule de-stabilizers by stabilizing tubulin polymers

<p>Abstract</p> <p>Background</p> <p>Survivin is a dual function protein. It inhibits the apoptosis of cells by inhibiting caspases, and also promotes cell growth by stabilizing microtubules during mitosis. Over-expression of survivin has been demonstrated to induce drug-resistance to various chemo-therapeutic agents such as cisplatin (DNA damaging agent) and paclitaxel (microtubule stabilizer) in cancers. However, survivin-induced resistance to microtubule de-stabilizers such as <it>Vinca </it>alkaloids and Combretastatin A-4 (CA-4)-related compounds were seldom demonstrated in the past. Furthermore, the question remains as to whether survivin plays a dominant role in processing cytokinesis or inhibiting caspases activity in cells treated with anti-mitotic compounds. The purpose of this study is to evaluate the effect of survivin on the resistance and susceptibility of human cancer cells to microtubule de-stabilizer-induced cell death.</p> <p>Results</p> <p>BPR0L075 is a CA-4 analog that induces microtubule de-polymerization and subsequent caspase-dependent apoptosis. To study the relationship between the expression of survivin and the resistance to microtubule de-stabilizers, a KB-derived BPR0L075-resistant cancer cell line, KB-<it>L30</it>, was generated for this study. Here, we found that survivin was over-expressed in the KB-<it>L30 </it>cells. Down-regulation of survivin by siRNA induced hyper-sensitivity to BPR0L075 in KB cells and partially re-stored sensitivity to BPR0L075 in KB-<it>L30 </it>cells. Western blot analysis revealed that down-regulation of survivin induced microtubule de-stabilization in both KB and KB-<it>L30 </it>cells. However, the same treatment did not enhance the down-stream caspase-3/-7 activities in BPR0L075-treated KB cells. Translocation of a caspase-independent apoptosis-related molecule, apoptosis-inducing factor (AIF), from cytoplasm to the nucleus was observed in survivin-targeted KB cells under BPR0L075 treatment.</p> <p>Conclusion</p> <p>In this study, survivin plays an important role in the stability of microtubules, but not with caspases inhibition. Over-expression of survivin counteracts the therapeutic effect of microtubule de-stabilizer BPR0L075 probably by stabilizing tubulin polymers, instead of the inhibition of caspase activity in cancer cells. Besides microtubule-related caspase-dependent cell death, caspase-independent mitotic cell death could be initiated in survivin/BPR0L075 combination treatments. We suggest that combining microtubule de-stabilizers with a survivin inhibitor may attribute to a better clinical outcome than the use of anti-mitotic monotherapy in clinical situations.</p