The relation between pitch and gestures in a story-telling task

Anecdotal evidence suggests that both pitch range and gestures contribute to the perception of speakers\u2019 liveliness in speech. However, the relation between speakers\u2019 pitch range and gestures has received little attention. It is possible that variations in pitch range might be accompanied by variations in gestures, and vice versa. In second language speech, the relation between pitch range and gestures might also be affected by speakers\u2019 difficulty in speaking the L2. In this pilot study we compare global pitch range and gesture rate in the speech of 3 native Italian speakers, telling the same story once in Italian and twice in English as part of an in-class oral presentation task. The hypothesis tested is that contextual factors, such as speakers\u2019 nervousness with the task, cause speakers to use narrow pitch range and limited gestures; a greater ease with the task, due to its repetition, cause speakers to use a wider pitch range and more gestures. This experimental hypothesis is partially confirmed by the results of this study

A convivência com diabetes mellitus tipo 2

Estudo qualitativo que teve como objetivo investigar a convivência dos sujeitos da pesquisa com a diabetes mellitus bem como o cuidado dispensado pela família ao diabético. Participaram deste estudo 20 pessoas com diabetes mellitus tipo 2,  usuários do Programa de Atenção Básica, do Município de Concórdia – SC. Os dados foram obtidos por meio de entrevista, e  organizados em quatro categorias: 1 – Reviravolta na vida, caracterizada por ter que seguir dieta, tomar os remédios, fazer atividade física e também como fator de isolamento social; 2 – Desgosto por não aceitar a doença; 3 – Cuidado familiar enumerado como apoio, dar os remédios, ajuda com a dieta, controle do resultado da glicemia, acompanhamento e participação nas consultas; 4 – Auto cuidado. Conclui-se que a diabetes mellitus requerem novas atitudes e a família é um importante fator que influencia na tomada de decisões frente ao novo estilo de vida que esta condição crônica impõe

Physicochemical and biological characterization of chitosan-microRNA nanocomplexes for gene delivery to MCF-7 breast cancer cells

Cancer gene therapy requires the design of non-viral vectors that carry genetic material and selectively deliver it with minimal toxicity. Non-viral vectors based on cationic natural polymers can form electrostatic complexes with negatively-charged polynucleotides such as microRNAs (miRNAs). Here we investigated the physicochemical/biophysical properties of chitosan–hsa-miRNA-145 (CS–miRNA) nanocomplexes and the biological responses of MCF-7 breast cancer cells cultured in vitro. Self-assembled CS–miRNA nanocomplexes were produced with a range of (+/−) charge ratios (from 0.6 to 8) using chitosans with various degrees of acetylation and molecular weight. The Z-average particle diameter of the complexes was <200 nm. The surface charge increased with increasing amount of chitosan. We observed that chitosan induces the base-stacking of miRNA in a concentration dependent manner. Surface plasmon resonance spectroscopy shows that complexes formed by low degree of acetylation chitosans are highly stable, regardless of the molecular weight. We found no evidence that these complexes were cytotoxic towards MCF-7 cells. Furthermore, CS–miRNA nanocomplexes with degree of acetylation 12% and 29% were biologically active, showing successful downregulation of target mRNA expression in MCF-7 cells. Our data, therefore, shows that CS–miRNA complexes offer a promising non-viral platform for breast cancer gene therapy

Identification Of Target Genes Using Gene Expression Profile Of Granulocytes From Patients With Chronic Myeloid Leukemia Treated With Tyrosine Kinase Inhibitors

Differential gene expression analysis by suppression subtractive hybridization with correlation to the metabolic pathways involved in chronic myeloid leukemia (CML) may provide a new insight into the pathogenesis of CML. Among the overexpressed genes found in CML at diagnosis are SEPT5, RUNX1, MIER1, KPNA6 and FLT3, while PAN3, TOB1 and ITCH were decreased when compared to healthy volunteers. Some genes were identified and involved in CML for the first time, including TOB1, which showed a low expression in patients with CML during tyrosine kinase inhibitor treatment with no complete cytogenetic response. In agreement, reduced expression of TOB1 was also observed in resistant patients with CML compared to responsive patients. This might be related to the deregulation of apoptosis and the signaling pathway leading to resistance. Most of the identified genes were related to the regulation of nuclear factor κB (NF-κB), AKT, interferon and interleukin-4 (IL-4) in healthy cells. The results of this study combined with literature data show specific gene pathways that might be explored as markers to assess the evolution and prognosis of CML as well as identify new therapeutic targets. © 2014 Informa UK, Ltd.55818611869Luatti, S., Additional chromosomal abnormalities in Philadelphia-positive clone: Adverse prognostic influence on frontline imatinib therapy: A GIMEMA Working Party on CML analysis (2012) Blood, 120, pp. 761-767Deininger, M.W., Goldman, J.M., Melo, J.V., The molecular biology of chronic myeloid leukemia (2000) Blood, 96, pp. 3343-3356Baran, Y., Saydam, G., Cumulative clinical experience from a decade of use: Imatinib as first-line treatment of chronic myeloid leukemia (2012) J Blood Med, 3, pp. 139-150Melo, J.V., Hughes, T.P., Apperley, J.F., Chronic myeloid leukemia (2003) Hematology Am Soc Hematol Educ Program, pp. 132-152Mascarenhas, C.C., New mutations detected by denaturing high performance liquid chromatography during screening of exon 6 bcr-abl mutations in patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors (2009) Leuk Lymphoma, 50, pp. 1148-1154Wong, S., Sole BCR-ABL inhibition is insufficient to eliminate all myeloproliferative disorder cell populations (2004) Proc Natl Acad Sci USA, 101, pp. 17456-17461Inokuchi, K., Chronic myelogenous leukemia: From molecular biology to clinical aspects and novel targeted therapies (2006) J Nippon Med Sch, 73, pp. 178-192Park, S., Application of array comparative genomic hybridization in chronic myeloid leukemia (2013) Methods Mol Biol, 973, pp. 55-68Remsing Rix, L.L., Global target profile of the kinase inhibitor bosutinib in primary chronic myeloid leukemia cells (2009) Leukemia, 23, pp. 477-485Canalli, A.A., Granulocytic adhesive interactions and their role in sickle cell vaso-occlusion (2005) Hematology, 10, pp. 419-425Diatchenko, L., Suppression subtractive hybridization: A method for generating diff erentially regulated or tissue-specific cDNA probes and libraries (1996) Proc Natl Acad Sci USA, 93, pp. 6025-6030Diatchenko, L., Suppression subtractive hybridization: A versatile method for identifying diff erentially expressed genes (1999) Methods Enzymol, 303, pp. 349-380Hillmann, A., Dunne, E., Kenny, D., CDNA amplification by SMARTPCR and suppression subtractive hybridization (SSH)-PCR (2009) Methods Mol Biol, 496, pp. 223-243Ewing, B., Base-calling of automated sequencer traces using phred I. Accuracy assessment (1998) Genome Res, 8, pp. 175-185Ghosh, S., Global gene expression and Ingenuity biological functions analysis on PCBs 153 and 138 induced human PBMC in vitro reveals diff erential mode(s) of action in developing toxicities (2011) Environ Int, 37, pp. 838-857Gilmore, T.D., The Rel/NF-kappaB signal transduction pathway: Introduction (1999) Oncogene, 18, pp. 6842-6844Samy, R.P., Identification of a novel Calotropis procera protein that can suppress tumor growth in breast cancer through the suppression of NF-kappaB pathway (2012) PLoS One, 7, pp. e48514Albensi, B.C., Mattson, M.P., Evidence for the involvement of TNF and NF-kappaB in hippocampal synaptic plasticity (2000) Synapse, 35, pp. 151-159Li, F., Sethi, G., Targeting transcription factor NF-kappaB to overcome chemoresistance and radioresistance in cancer therapy (2010) Biochim Biophys Acta, 1805, pp. 167-180Pezzolesi, M.G., Comparative genomic and functional analyses reveal a novel cis-acting PTEN regulatory element as a highly conserved functional E-box motif deleted in Cowden syndrome (2007) Hum Mol Genet, 16, pp. 1058-1071Bidere, N., Casein kinase 1alpha governs antigen-receptorinduced NF-kappaB activation and human lymphoma cell survival (2009) Nature, 458, pp. 92-96Cerveira, N., Bizarro, S., Teixeira, M.R., MLL-SEPTIN gene fusions in hematological malignancies (2011) Biol Chem, 392, pp. 713-724Zhao, L.J., Functional features of RUNX1 mutants in acute transformation of chronic myeloid leukemia and their contribution to inducing murine full-blown leukemia (2012) Blood, 119, pp. 2873-2882Ichikawa, M., AML-1 is required for megakaryocytic maturation and lymphocytic diff erentiation, but not for maintenance of hematopoietic stem cells in adult hematopoiesis (2004) Nat Med, 10, pp. 299-304Blackmore, T.M., The transcriptional cofactor MIER1-beta negatively regulates histone acetyltransferase activity of the CREBbinding protein (2008) BMC Res Notes, 1, p. 68Kohler, M., Evidence for distinct substrate specificities of importin alpha family members in nuclear protein import (1999) Mol Cell Biol, 19, pp. 7782-7791Murati, A., Myeloid malignancies: Mutations, models and management (2012) BMC Cancer, 12, p. 304Daver, N., FLT3 mutations in myelodysplastic syndrome and chronic myelomonocytic leukemia (2013) Am J Hematol, 88, pp. 56-59Bai, Y., Itch E3 ligase-mediated regulation of TGF-beta signaling by modulating smad2 phosphorylation (2004) Mol Cell, 15, pp. 825-831Tzachanis, D., Tob is a negative regulator of activation that is expressed in anergic and quiescent T cells (2001) Nat Immunol, 2, pp. 1174-1182Naka, K., TGF-beta-FOXO signalling maintains leukaemiainitiating cells in chronic myeloid leukaemia (2010) Nature, 463, pp. 676-680Ezzeddine, N., Human TOB, an antiproliferative transcription factor, is a poly(A)-binding protein-dependent positive regulator of cytoplasmic mRNA deadenylation (2007) Mol Cell Biol, 27, pp. 7791-7801Kundu, J., Tob1 induces apoptosis and inhibits proliferation, migration and invasion of gastric cancer cells by activating Smad4 and inhibiting betacatenin signaling (2012) Int J Oncol, 41, pp. 839-84