Physician perceptions of the types of roles interpreters play in limited English proficient pediatric encounters and how they evaluate the quality of interpretation.

PURPOSE: The purpose of this study is to understand different roles that interpreters play in a pediatric, limited English proficient (LEP) health care encounter and to describe what factors within each role inform physicians' assessment of the overall quality of interpretation. BACKGROUND: Language barriers contribute to lower quality of care in LEP pediatric patients compared to their English-speaking counterparts. Use of professional medical interpreters has been shown to improve communication and decrease medical errors in pediatric LEP patients. In addition, in many pediatric encounters, interpreters take on roles beyond that of a pure language conduit. METHODS: We conducted 11 semi-structured interviews with pediatricians and family medicine physicians in one health system. Transcripts were audio-recorded and transcribed verbatim. We analyzed our data using directed content analysis. Two study team members coded all transcripts, reviewed agreement, and resolved discrepancies. FINDINGS: Physicians described four different interpreter roles: language conduit, flow manager, relationship builder, and cultural insider. Within each role, physicians described components of quality that informed their assessment of the overall quality of interpretation during a pediatric encounter. We found that for many physicians, a high-quality interpreted encounter involves multiple roles beyond language transmission. It is important for health care systems to understand how health care staff conceptualize these relationships so that they can develop appropriate expectations and trainings for medical interpreters in order to improve health outcomes in pediatric LEP patients.

Informing physician strategies to overcome language barriers in encounters with pediatric patients.

OBJECTIVES: To describe physician perceptions of differences in limited English proficient (LEP) pediatric encounters and the behavioral adaptations they make to provide quality care to LEP pediatric patients. METHODS: We conducted 30min, semi-structured interviews with 6 family physicians and 5 pediatricians in one health system. Audiotapes from each interview were transcribed verbatim then coded using content analysis. RESULTS: Multiple aspects of the LEP pediatric encounter were perceived by physicians as different from other encounters: trust and relationship between physician and LEP child/child's family, continuity of care, encounter's structure and flow, patient assessment, and communication barriers. Within each of these themes, physicians identified how they adapt their behavior to improve the quality of care provided to LEP children and families. CONCLUSIONS: Physicians' made both positive and negative adaptations in LEP pediatric encounters that may impact the quality of care provided to these patients. PRACTICE IMPLICATIONS: By identification of specific positive and negative behavioral adaptations, this study emphasizes intervention targets, such as demonstrating interest in an LEP pediatric patient's family story and individuality and using common niceties in conversations with LEP children.

Age-dependent differences in microglial responses to systemic inflammation are evident as early as middle age.

Whereas age increases microglial inflammatory activities and impairs their ability to effectively regulate their immune response, it is unclear at what age these exaggerated responses begin. We tested the hypotheses that augmented microglial responses to inflammatory challenge are present as early as middle age and that repeated stimulation of primed microglia in vivo would reveal microglial senescence. Microglial gene expression was investigated in a mouse model of repeated systemic inflammation induced by intraperitoneal injection of bacterial lipopolysaccharide (LPS). Following LPS, microglia from middle-aged mice (9-10 mo) displayed larger increases in Tnfα, Il-6, and Il-1ß gene expression compared with young adults (2 mo). Similar results were observed in the spleens of middle-aged mice, indicating that exaggeration of both central and peripheral immune responses are already evident at early middle age. Interestingly, despite greater proinflammatory responses to the first LPS challenge in the aged mice, there were no age-dependent differences in either microglia or spleen following a subsequent LPS dose, suggesting that animals at this age retain the ability to effectively control their immune response following repeated challenge. The exacerbated microglial immune response to systemic inflammation at early middle age suggests that the CNS may be vulnerable to age-dependent alterations earlier than previously appreciated.

Microglial numbers attain adult levels after undergoing a rapid decrease in cell number in the third postnatal week.

During postnatal development, microglia, CNS resident innate immune cells, are essential for synaptic pruning, neuronal apoptosis and remodeling. During this period microglia undergo morphological and phenotypic transformations; however, little is known about how microglial number and density is regulated during postnatal CNS development. We found that after an initial increase during the first 14 postnatal days, microglial numbers in mouse brain began declining in the third postnatal week and were reduced by 50% by 6weeks of age; these "adult" levels were maintained until at least 9months of age. Microglial CD11b levels increased, whereas CD45 and ER-MP58 declined between P10 and adulthood, consistent with a maturing microglial phenotype. Our data indicate that both increased microglial apoptosis and a decreased proliferative capacity contribute to the developmental reduction in microglial numbers. We found no correlation between developmental reductions in microglial numbers and brain mRNA levels of Cd200, Cx3Cl1, M-Csf or Il-34. We tested the ability of M-Csf-overexpression, a key growth factor promoting microglial proliferation and survival, to prevent microglial loss in the third postnatal week. Mice overexpressing M-Csf in astrocytes had higher numbers of microglia at all ages tested. However, the developmental decline in microglial numbers still occurred, suggesting that chronically elevated M-CSF is unable to overcome the developmental decrease in microglial numbers. Whereas the identity of the factor(s) regulating microglial number and density during development remains to be determined, it is likely that microglia respond to a "maturation" signal since the reduction in microglial numbers coincides with CNS maturation.

Spinal but not cortical microglia acquire an atypical phenotype with high VEGF, galectin-3 and osteopontin, and blunted inflammatory responses in ALS rats.

Activation of microglia, CNS resident immune cells, is a pathological hallmark of amyotrophic lateral sclerosis (ALS), a neurodegenerative disorder affecting motor neurons. Despite evidence that microglia contribute to disease progression, the exact role of these cells in ALS pathology remains unknown. We immunomagnetically isolated microglia from different CNS regions of SOD1(G93A) rats at three different points in disease progression: presymptomatic, symptom onset and end-stage. We observed no differences in microglial number or phenotype in presymptomatic rats compared to wild-type controls. Although after disease onset there was no macrophage infiltration, there were significant increases in microglial numbers in the spinal cord, but not cortex. At disease end-stage, microglia were characterized by high expression of galectin-3, osteopontin and VEGF, and concomitant downregulated expression of TNFα, IL-6, BDNF and arginase-1. Flow cytometry revealed the presence of at least two phenotypically distinct microglial populations in the spinal cord. Immunohistochemistry showed that galectin-3/osteopontin positive microglia were restricted to the ventral horns of the spinal cord, regions with severe motor neuron degeneration. End-stage SOD1(G93A) microglia from the cortex, a less affected region, displayed similar gene expression profiles to microglia from wild-type rats, and displayed normal responses to systemic inflammation induced by LPS. On the other hand, end-stage SOD1(G93A) spinal microglia had blunted responses to systemic LPS suggesting that in addition to their phenotypic changes, they may also be functionally impaired. Thus, after disease onset, microglia acquired unique characteristics that do not conform to typical M1 (inflammatory) or M2 (anti-inflammatory) phenotypes. This transformation was observed only in the most affected CNS regions, suggesting that overexpression of mutated hSOD1 is not sufficient to trigger these changes in microglia. These novel observations suggest that microglial regional and phenotypic heterogeneity may be an important consideration when designing new therapeutic strategies targeting microglia and neuroinflammation in ALS.