The use of discourse markers (DMs) is present in speech to both structure and organize the discourse (Fung & Carter, 2007). However, despite the different studies about the use of DMs, less attention has been paid to specific Spanish DMs such as pues, ‘so, well’ luego, ‘then, therefore’ and entonces ‘so, then’ about their reduction. The focus of this study is on the phonetic variation of these DMs from a corpus of speakers of Mexican Spanish from Salinas, California (Brown & Alba, 2017). This paper analyzed dependent and independent variables to show their influence on the reduction of DMs. Also, chunking phenomena and special reduction were part of the study as they can reflect patterns of change in the language.

Oscillatory perturbations with varying amplitudes and frequencies have been found to significantly affect human standing balance. However, previous studies have only applied perturbation in either the anterior-posterior (AP) or the medio-lateral (ML) directions. Little is currently known about the impacts of 2D oscillatory perturbations on postural stability, which are more commonly seen in daily life (i.e., while traveling on trains, ships, etc.). This study investigated the effects of applying 2D perturbations vs 1D perturbations on standing stability, and how increasing the frequency and amplitude of perturbation impacts postural stability. A dual-axis robotic platform was utilized to simulate various oscillatory perturbations and evaluate standing postural stability. Fifteen young healthy subjects were recruited to perform quiet stance on the platform. Impacts of perturbation direction (i.e., 1D versus 2D), amplitude, and frequency on postural stability were investigated by analyzing different stability measures, specifically AP/ML/2D Center-of-Pressure (COP) path length, AP/ML/2D Time-to-Boundary (TtB), and sway area. Standing postural stability was compromised more by 2D perturbations than 1D perturbations, evidenced by a significant increase in COP path length and sway area and decrease in TtB. Further, the stability decreased as 2D perturbation amplitude and frequency increased. A significant increase in COP path length and decrease in TtB were consistently observed as the 2D perturbation amplitude and frequency increased. However, sway area showed a considerable increase only with increasing perturbation amplitude but not with increasing frequency.

A growing body of research suggests a link between adverse childhood experiences and negative health outcomes. However, less is known about where racial discrimination ranks compared to other adverse childhood experiences, such as maltreatment. To address this issue, I conducted two systematic reviews of meta-analyses to compare the magnitudes of the links between racial discrimination and depressive symptoms and childhood maltreatment and depressive symptoms. My aim was to establish if racial discrimination should be considered an adverse childhood experience. My results demonstrated that the link between racial discrimination and depressive symptoms (r = 0.27) is comparable to the links between 4 different manifestations of maltreatment and depressive symptoms (physical abuse: r = 0.257, emotional abuse: r = 0.301, neglect: r = 0.381, sexual abuse: r = 0.408). I discuss the implications of these findings and propose future research directions.

Down syndrome (DS) is a common genetic developmental disorder characterized by the trisomy of chromosome 21 (Hsa21). All individuals with DS have some kind of intellectual disability, associated with dysfunction in cognition-related structures, including the frontal cortex. Studies have examined developmental changes in the frontal cortex during prenatal stages in DS, however little is known about cortical lamination and neuronal differentiation in postnatal periods in this neurodevelopmental disorder. Therefore, we examined the quantitative and qualitative distribution of neuronal profiles containing the neuronal migration protein doublecortin (DCX), the non-phosphorylated high-molecular-weight neurofilament SMI-32, the calcium-binding proteins calbindin D-28K (Calb), calretinin (Calr), and parvalbumin (Parv), as well as human β-amyloid and APP (6E10), Aβ1-42, and phospho-tau (CP-13) in the supragranular (SG, II/III) and infragranular (IG, V/VI) layers in the DS postnatal frontal cortex compared to neurotypically developing (NTD) controls from ages 28 weeks to 196.4 weeks using immunohistochemistry. Furthermore, cortical lamination was evaluated using thionin, a Nissl stain. We found DCX-immunoreactive (-ir) cells in both the SG and IG layers in younger cases, but not in the oldest cases in both groups. Strong expression of SMI-32 immunoreactivity was observed in pyramidal cells in layers III and V in the oldest cases in both groups, however SMI-32-ir cells appeared much earlier in NTD compared to DS. We found small and fusiform Calb-ir cells in the younger cases (28 to 44 weeks), while in the oldest cases, Calb immunoreactivity was also found in pyramidal cells. Calr-ir cells appeared earlier in DS at 32 weeks compared to NTD at 44 weeks, however both groups showed large bipolar fusiform-shaped Calr-ir cells in the oldest cases. Diffuse APP/Aβ-ir plaque-like accumulations were found in the frontal cortex grey and white matter at all ages, but no Aβ1-42 immunoreactivity was detected in any case. Furthermore, neuropil (but not cellular) granular CP-13 immunostaining was seen in layer I only at 41 weeks NTD and 33 weeks DS. Cell counts show a significantly higher cell number in SG compared to IG for all the neuronal markers in both groups, except in Calb and SMI-32. In NTD, age and brain weight showed the strongest correlations with all cellular counts, except in thionin where DS had a stronger negative correlation with age and brain weight compared to NTD. In addition, height and body weight showed a strong negative correlation in NTD with the migration and neurogenesis marker DCX. These findings suggest that trisomy 21 affects the postnatal frontal cortex lamination, neuronal migration<br/>eurogenesis, and differentiation of projection pyramidal cells and interneurons, which contribute to the disruption of the local and projection inhibitory and excitatory circuitries that may underlie the cognitive disabilities in DS.