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1.
Front Physiol ; 9: 1152, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-30233386

RESUMEN

Coarticulation is the tendency for speech vocalization and articulation even at the phonemic level to change with context, and compensation for coarticulation (CfC) reflects the striking human ability to perceive phonemic stability despite this variability. A current controversy centers on whether CfC depends on contrast between formants of a speech-signal spectrogram-specifically, contrast between offset formants concluding context stimuli and onset formants opening the target sound-or on speech-sound variability specific to the coordinative movement of speech articulators (e.g., vocal folds, postural muscles, lips, tongues). This manuscript aims to encode that coordinative-movement context in terms of speech-signal multifractal structure and to determine whether speech's multifractal structure might explain the crucial gestural support for any proposed spectral contrast. We asked human participants to categorize individual target stimuli drawn from an 11-step [ga]-to-[da] continuum as either phonemes "GA" or "DA." Three groups each heard a specific-type context stimulus preceding target stimuli: either real-speech [al] or [a], sine-wave tones at the third-formant offset frequency of either [al] or [aɹ], and either simulated-speech contexts [al] or [aɹ]. Here, simulating speech contexts involved randomizing the sequence of relatively homogeneous pitch periods within vowel-sound [a] of each [al] and [aɹ]. Crucially, simulated-speech contexts had the same offset and extremely similar vowel formants as and, to additional naïve participants, sounded identical to real-speech contexts. However, randomization distorted original speech-context multifractality, and effects of spectral contrast following speech only appeared after regression modeling of trial-by-trial "GA" judgments controlled for context-stimulus multifractality. Furthermore, simulated-speech contexts elicited faster responses (like tone contexts do) and weakened known biases in CfC, suggesting that spectral contrast depends on the nonlinear interactions across multiple scales that articulatory gestures express through the speech signal. Traditional mouse-tracking behaviors measured as participants moved their computer-mouse cursor to register their "GA"-or-"DA" decisions with mouse-clicks suggest that listening to speech leads the movement system to resonate with the multifractality of context stimuli. We interpret these results as shedding light on a new multifractal terrain upon which to found a better understanding in which movement systems play an important role in shaping how speech perception makes use of acoustic information.

2.
J Phys Chem A ; 114(34): 9289-99, 2010 Sep 02.
Artículo en Inglés | MEDLINE | ID: mdl-20681535

RESUMEN

The FT-microwave spectrum of germylcyclohexane, c-C(6)H(11)GeH(3), has been recorded, and more than 40 transitions for the (70)Ge, (72)Ge, and (74)Ge isotopomers (isotopologues) have been assigned for the chair-equatorial conformer. The heavy atom adjusted r(0) structural parameters have been determined [distances, C(gamma)-C(delta) = 1.533(3) A, C(gamma)-C(beta) = 1.532(3) A, C(alpha)-C(beta) = 1.540(3) A, C(alpha)-Ge = 1.957(3) A; angles, angleC(gamma)C(delta)C(beta) = 111.2(5) degrees , angleGeC(alpha)C(beta) = 111.1(5) degrees , with the dihedral angle angleC(gamma)C(delta)C(beta)C(alpha) = 55.6(10) degrees ]. Raman and/or infrared spectra of gas, liquid, and solid germylcyclohexane have been recorded. The temperature dependency of the Raman spectrum of the conformer pair 712 (equatorial)/683 (axial) cm(-1) gives an enthalpy difference of 453 +/- 38 cm(-1) (1.30 +/- 0.11 kcal/mol) with the chair-equatorial conformer the more stable form. At ambient temperature, the abundance of the axial conformer is 11 +/- 1%. Substituent effects on the enthalpy difference and structure of monosubstituted cyclohexanes are discussed for a number of molecules.

3.
Toxicol Appl Pharmacol ; 247(2): 146-57, 2010 Sep 01.
Artículo en Inglés | MEDLINE | ID: mdl-20600219

RESUMEN

Microbial stimuli and atmospheric particulate matter (PM) interact to amplify the release of inflammatory and immune-modulating cytokines. The basis of this interaction, however, is not known. Cultured human lung fibroblasts (HLF) were used to determine whether various protein kinase pathways were involved in the release of IL-6 following combined exposure to the PM-derived metal, Ni, and M. fermentans-derived macrophage-activating lipopeptide 2 (MALP-2), a toll-like receptor 2 agonist. Synergistic release of IL-6 by MALP-2 and NiSO4 was obvious after 8h of co-stimulation and correlated with a late phase accumulation of IL-6 mRNA. Ni and MALP-2, alone or together, all led to rapid and transient phosphorylations of ERK(1/2) and JNK/SAPK of similar magnitude. p38 phosphorylation, however, was observed only after prolonged treatment of cells with both stimuli together. A constitutive level of PI3K-dependent Akt phosphorylation remained unchanged by Ni and/or MALP-2 exposure. IL-6 induced by Ni/MALP-2 co-exposure was partially dependent on activity of HIF-1alpha and COX-2 as shown by targeted knockdown using siRNA. IL-6 release in response to Ni/MALP-2 was partially sensitive to pharmacological inhibition of ERK(1/2), p38, and PI3K signaling. The protein kinase inhibitors had minimal or no effects on Ni/MALP-2-induced accumulation of HIF-1alpha protein, however, COX-2 expression and, more markedly PGE(2) production, were suppressed by LY294002, SB203580, and U0126. Thus, Ni/MALP-2 interactions involve multiple protein kinase pathways (ERK(1/2), p38, and PI3K) that modulate events downstream from the early accumulation of HIF-1alpha to promote IL-6 gene expression directly or secondarily, through COX-2-derived autocrine products like PGE(2).


Asunto(s)
Interleucina-6/metabolismo , Lipopéptidos/toxicidad , Níquel/toxicidad , Proteínas Quinasas/metabolismo , Transducción de Señal/efectos de los fármacos , Receptor Toll-Like 2/agonistas , Células Cultivadas , Ciclooxigenasa 2/metabolismo , Sinergismo Farmacológico , Fibroblastos , Humanos , Subunidad alfa del Factor 1 Inducible por Hipoxia/metabolismo , Pulmón , Proteínas Quinasas Activadas por Mitógenos/antagonistas & inhibidores , Proteínas Quinasas Activadas por Mitógenos/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo
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