Suchergebnisse

La lengua como significador social -- Sustantivos, pronombres, preposiciones -- Verbos -- El español en contacto con otras lenguas

Abstract
This study explores variable Spanish subject pronoun expression (e.g., yo veo ~ veo) in Spanish-English speaking children in different regions of the United States (U.S.): Los Angeles (LA), California, and the Tri-Cities area of the state of Washington. We also compare the U.S. children to monolingual Spanish-speaking children in Mexico. Binary logistic regression analyses of 2,064 verb tokens produced by nine U.S. children and nine children in Mexico, ages 5;11 to 7 years old, show that the children are sensitive to linguistic factors that typically influence children's Spanish subject pronoun expression in their respective communities. In addition, we find that the LA children's subject pronoun expression is predicted by lexical frequency. A subsequent analysis of the LA children's frequent verbs uncovers two phrases with high degrees of prefabrication, yo creo and yo no sé, which, we argue, obscure the LA children's sensitivity to Reference, all while acting as central exemplars of a [1sg+cognitive verb] construction.

Explosive blast-induced traumatic brain injury (blast-TBI) in military personnel is a leading cause of injury and persistent neurological abnormalities, including chronic pain. We previously demonstrated that chronic pain after spinal cord injury results from central sensitization in the posterior thalamus (PO). The presence of persistent headaches and back pain in veterans with blast-TBI suggests a similar involvement of thalamic sensitization. Here, we tested the hypothesis that pain after blast-TBI is associated with abnormal increases in activity of neurons in PO thalamus. We developed a novel model with two unique features: (1) blast-TBI was performed in awake, un-anesthetized rats, to simulate the human experience and to eliminate confounds of anesthesia and surgery inherent in other models; (2) only the cranium, rather than the entire body, was exposed to a collimated blast wave, with the blast wave striking the posterior cranium in the region of the occipital crest and foramen magnum. Three weeks after blast-TBI, rats developed persistent, ongoing spontaneous pain. Contrary to our hypothesis, we found no significant differences in the activity of PO neurons, or of neurons in the spinal trigeminal nucleus. There were also no significant changes in gliosis in either of these structures. This novel model will allow future studies on the pathophysiology of chronic pain after blast-TBI.

Explosive blast-induced traumatic brain injury (blast-TBI) in military personnel is a leading cause of injury and persistent neurological abnormalities, including chronic pain. We previously demonstrated that chronic pain after spinal cord injury results from central sensitization in the posterior thalamus (PO). The presence of persistent headaches and back pain in veterans with blast-TBI suggests a similar involvement of thalamic sensitization. Here, we tested the hypothesis that pain after blast-TBI is associated with abnormal increases in activity of neurons in PO thalamus. We developed a novel model with two unique features: (1) blast-TBI was performed in awake, un-anesthetized rats, to simulate the human experience and to eliminate confounds of anesthesia and surgery inherent in other models; (2) only the cranium, rather than the entire body, was exposed to a collimated blast wave, with the blast wave striking the posterior cranium in the region of the occipital crest and foramen magnum. Three weeks after blast-TBI, rats developed persistent, ongoing spontaneous pain. Contrary to our hypothesis, we found no significant differences in the activity of PO neurons, or of neurons in the spinal trigeminal nucleus. There were also no significant changes in gliosis in either of these structures. This novel model will allow future studies on the pathophysiology of chronic pain after blast-TBI. © 2019 The Authors ; U.S. Department of Veterans Affairs 5I01BX001629,I01BX002889. National Institutes of Health 5R01NS099245,R01NS102589 ; https://dx.doi.org/10.1016/j.ynpai.2019.100030