The current studies used a priming methodology to assess the abstractness of children's early syntactic constructions. In the main study, 3-, 4- and 6-year-old children were asked to describe a prime picture by repeating either an active or a passive sentence, and then they were left to their own devices to describe a target picture. For half the children at each age, the prime sentences they repeated had high lexical overlap with the sentence they were likely to produce for the target, whereas for the other half there was very low lexical overlap between prime and target. The main result was that 6-year-old children showed both lexical and structural priming for both the active transitive and passive constructions, whereas 3- and 4-year-old children showed lexical priming only. This pattern of results would seem to indicate that 6-year-old children have relatively abstract representations of these constructions, whereas 3- and 4-year-old children have as an integral part of their representations certain specific lexical items, especially pronouns and some grammatical morphemes. In a second study it was found that children did not need to repeat the prime out loud in order to be primed - suggesting that the priming effect observed concerns not just peripheral production mechanisms but underlying linguistic representations common to comprehension and production. These results support the view that young children develop abstract linguistic representations gradually during the preschool years.
Four normal human subjects were investigated for evidence of auditory-visual interaction in the generation of horizontal saccades. In a first experiment it was shown that the mean amplitudes of initial saccades from primary position to auditory targets were significantly affected by the simultaneous occurrence of a distracting visual stimulus. If both auditory and visual stimuli were in the same hemifield, the mean amplitude of initial saccades to a fixed buzzer position was consistently increased or decreased depending on the position of the visual stimulus. The phenomenon is felt to be analogous to the "centre-of-gravity" effect previously described for two simultaneous visual stimuli. It did not occur if visual and auditory stimuli were in opposite hemifields when a simultaneous visual stimulus caused a slight reduction of mean initial saccadic amplitude compared to the mean amplitude to buzzer alone. In this case the reduction was independent of visual stimulus position. Similar effects were seen for mean final eye positions. In a second experiment, a similar procedure was carried out, but the eyes started by looking at a point at 15 degrees eccentricity. The same pattern of auditory-visual interaction was obtained in both experiments, consistent with the concept of eye-movement related movement of modality-specific sensory "maps" which has recently been shown to occur in the superior colliculus of primates.
The specific mechanisms that underlie childhood stuttering are not fully understood. The current study investigated these mechanisms by comparing the effect on fluency of priming different components of a short sentence. The main findings were that: (1) both children who stutter (CWS) (n = 12, M age = 6;3) and children who do not stutter (CWNS) (n = 12, M age = 6;6) were more fluent after function word (FW) priming than content word (CW) priming, (2) this effect was significantly greater for CWS than for CWNS, and (3) after FW priming, CWS produced CWs with significantly longer duration than did CWNS. These findings are discussed in relation to two competing theories of stuttering: the covert repair hypothesis (CRH) [Kolk, H., & Postma, A. (1997). Stuttering as a covert repair phenomenon. In R. F. Curlee & G. M. Siegel (Eds.), Nature and treatments of stuttering: New directions (pp. 182–203). Needham Heights, MA: Allyn & Bacon] and the developmentally focused model of Howell and Au-Yeung [Howell, P., & Au-Yeung, J. (2002). The EXPLAN theory of fluency control and the diagnosis of stuttering. In E. Fava (Ed.), Current issues in linguistic theory series: Pathology and therapy of speech disorders (pp. 75–94). Amsterdam: John Benjamins].Learning outcomes: After reading this article, the reader will be able to: (1) understand which linguistic levels can be primed in children who stutter; (2) see why EXPLAN predicts asymmetrical effects on fluency when function or content words are primed; (3) appreciate the distinguishing characteristics of CRH and EXPLAN theories.
Over the past decade, immunotherapy delivered novel treatments for many cancer types. However, lung cancer still leads cancer mortality, and non-small-cell lung carcinoma patients with mutant EGFR cannot benefit from checkpoint inhibitors due to toxicity, relying only on palliative chemotherapy and the third-generation tyrosine kinase inhibitor (TKI) osimertinib. This new drug extends lifespan by 9-months vs. second-generation TKIs, but unfortunately, cancers relapse due to resistance mechanisms and the lack of antitumor immune responses. Here we explored the combination of osimertinib with anti-HER3 monoclonal antibodies and observed that the immune system contributed to eliminate tumor cells in mice and co-culture experiments using bone marrow-derived macrophages and human PBMCs. Osimertinib led to apoptosis of tumors but simultaneously, it triggered inositol-requiring-enzyme (IRE1α)-dependent HER3 upregulation, increased macrophage infiltration, and activated cGAS in cancer cells to produce cGAMP (detected by a lentivirally transduced STING activity biosensor), transactivating STING in macrophages. We sought to target osimertinib-induced HER3 upregulation with monoclonal antibodies, which engaged Fc receptor-dependent tumor elimination by macrophages, and STING agonists enhanced macrophage-mediated tumor elimination further. Thus, by engaging a tumor non-autonomous mechanism involving cGAS-STING and innate immunity, the combination of osimertinib and anti-HER3 antibodies could improve the limited therapeutic and stratification options for advanced stage lung cancer patients with mutant EGFR.
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