Spatiotemporal distribution of cortical processing of first and second languages in bilinguals. I. Effects of proficiency and linguistic setting

The study determined how spatiotemporal distribution of cortical activity to words in first and second language is affected by language, proficiency, and linguistic setting. Ten early bilinguals and 14 late adult bilinguals listened to pairs of words presented in Arabic (L1), Hebrew (L2), or in mixed pairs and indicated whether both words had the same meaning or not. Source current densities of event‐related potentials were estimated. Activity to first words in the pair lateralized to right hemisphere, higher to L1 than L2 during early processing (<300 ms) among both groups but only among late bilinguals during late processing (>300 ms). During early and late processing, activities were larger in mixed than monolinguistic settings among early bilinguals but lower in mixed than in monolinguistic settings among late bilinguals. Late processing in auditory regions was of larger magnitude in left than right hemispheres among both groups. Activity to second words in the pair was larger in mixed than in monolinguistic settings during both early and late processing among both groups. Early processing of second words in auditory regions lateralized to the right among early bilinguals and to the left among late bilinguals, whereas late processing did not differ between groups. Wernicke's area activity during late processing of L2 was larger on the right, while on the left no significant differences between languages were found. The results show that cortical language processing in bilinguals differs between early and late processing and these differences are modulated by linguistic proficiency and setting. Hum Brain Mapp 34:2863–2881, 2013. © 2012 Wiley Periodicals, Inc.     

White-spot Lesions and Gingivitis Microbiotas in Orthodontic Patients

White-spot lesions (WSL) associated with orthodontic appliances are a cosmetic problem and increase risk for cavities. We characterized the microbiota of WSL, accounting for confounding due to gingivitis. Participants were 60 children with fixed appliances, aged between 10 and 19 yrs, half with WSL. Plaque samples were assayed by a 16S rRNA-based microarray (HOMIM) and by PCR. Mean gingival index was positively associated with WSL (p = 0.018). Taxa associated with WSL by microarray included Granulicatella elegans (p = 0.01), Veillonellaceae sp. HOT 155 (p < 0.01), and Bifidobacterium Cluster 1 (p = 0.11), and by qPCR, Streptococcus mutans (p = 0.008) and Scardovia wiggsiae (p = 0.04) Taxa associated with gingivitis by microarray included: Gemella sanguinis (p = 0.002), Actinomyces sp. HOT 448 (p = 0.003), Prevotella cluster IV (p = 0.021), and Streptococcus sp. HOT 071/070 (p = 0.023); and levels of S. mutans (p = 0.02) and Bifidobacteriaceae (p = 0.012) by qPCR. Species' associations with WSL were minimally changed with adjustment for gingivitis level. Partial least-squares discriminant analysis yielded good discrimination between children with and those without WSL. Granulicatella, Veillonellaceae and Bifidobacteriaceae, in addition to S. mutans and S. wiggsiae, were associated with the presence of WSL in adolescents undergoing orthodontic treatment. Many taxa showed a stronger association with gingivitis than with WSL.     

Dental caries in a cohort of very young American Indian children

Objectives: This paper reports the prevalence and severity of caries in a group of 16‐month‐old American Indian children. Methods: The study is an ongoing longitudinal study of risk factors for caries in children from a Northern Plains Tribal community. Children were examined for caries and risk factor data collected at approximately 1, 4, 8, 12, and 16 months of age. Surface‐specific caries data were collected and the presence of precavitated “white spot” lesions was recorded at the subject level. Results: The mean age was 15.4 months for the sample of 232 children. Caries prevalence was 31.9 percent, while an additional 29.3 percent had white spot lesions only. Mean dmfs was 1.57, and ranged from 0 to 44 surfaces. Nearly 3 percent of all erupted tooth surfaces were affected and maxillary central incisors had the highest prevalence of caries (22 percent). Conclusions: Among the very youngest children, dental caries prevalence was very high among these American Indian children.     

Genetic enhancement of cognition in a kindred with cone-rod dystrophy due to RIMS1 mutation

Background

The genetic basis of variation in human cognitive abilities is poorly understood. RIMS1 encodes a synapse active‐zone protein with important roles in the maintenance of normal synaptic function: mice lacking this protein have greatly reduced learning ability and memory function.

Objective

An established paradigm examining the structural and functional effects of mutations in genes expressed in the eye and the brain was used to study a kindred with an inherited retinal dystrophy due to RIMS1 mutation.

Materials and methods

Neuropsychological tests and high‐resolution MRI brain scanning were undertaken in the kindred. In a population cohort, neuropsychological scores were associated with common variation in RIMS1. Additionally, RIMS1 was sequenced in top‐scoring individuals. Evolution of RIMS1 was assessed, and its expression in developing human brain was studied.

Results

Affected individuals showed significantly enhanced cognitive abilities across a range of domains. Analysis suggests that factors other than RIMS1 mutation were unlikely to explain enhanced cognition. No association with common variation and verbal IQ was found in the population cohort, and no other mutations in RIMS1 were detected in the highest scoring individuals from this cohort. RIMS1 protein is expressed in developing human brain, but RIMS1 does not seem to have been subjected to accelerated evolution in man.

Conclusions

A possible role for RIMS1 in the enhancement of cognitive function at least in this kindred is suggested. Although further work is clearly required to explore these findings before a role for RIMS1 in human cognition can be formally accepted, the findings suggest that genetic mutation may enhance human cognition in some cases.A genetic contribution to variation in human intelligence is well established, but the identities of the genes responsible remain elusive. Many mutations are associated with impaired cognition:¹ no definite genetic causes of enhanced cognition are established,² and there are no known cognition‐enhancing “gain‐of‐function” mutations in genes otherwise associated with cognitive impairment. Therapeutic possibilities deriving from the discovery of any such genes or variants are potentially important: cognitive decline reduces the quality of life,³ and low intelligence test scores are associated with increased morbidity and shorter life‐span.⁴ Accelerated evolution of genes subserving neurodevelopment figures in molecular explanations of the advance of the human nervous system: many of the identified genes regulate brain size and behaviour, some encoding critical synaptic proteins.⁵To identify genes influencing human brain development and function, including cognitive function, we use a paradigm evaluating cerebral structure and function in individuals with known mutations in genes co‐expressed in the lineage‐sharing eye and brain, ascertained by their obvious ocular phenotype, but in whom a neurological phenotype was not fully appreciated. Using this paradigm, we demonstrated roles for the genes PAX6, PITX2, SOX2 and OTX2 in human brain development, cognitive function and memory.^{6,7,8,9,10,11}We now report on the functional and structural effects of mutation in the eye‐ and brain‐expressed gene RIMS1, through the study of individuals from a family already reported to have retinal dystrophy caused by RIMS1 mutation.^12,13 To our knowledge, this is the only family so far reported with such a mutation: the eye phenotype is homogeneous in the family, and has been documented in detail.¹³ The orthologous murine Rim1α encodes a synaptic active‐zone protein necessary for preserving the normal probability of synaptic neurotransmitter release and for long‐term presynaptic potentiation.^14,15Rim1α is also expressed in retinal ribbon synapses.¹⁶ Mice lacking Rim1α protein show severely impaired learning and memory.¹⁷ In our kindred, RIMS1 mutation (Arg844His) causes a late‐onset dominantly inherited cone–rod dystrophy (CORD7; OMIM 603649), leading to varying degrees of visual loss starting from the third decade onwards.¹³ Because RIMS1/Rim1α is also expressed in the brain, we hypothesised that this RIMS1 mutation would produce a structural and functional neurological phenotype.     

Insurance reimbursement in a university-based pediatric weight management clinic

OBJECTIVES: To compare third-party payor reimbursement for patients evaluated in a university-based pediatric weight management clinic in central Kentucky. STUDY DESIGN: Demographic and reimbursement data were reviewed for 120 patients evaluated January to December 2004. Statistical analysis included Kruskal-Wallis test and Friedman's test. RESULTS: Overall, median reimbursement was 60%. For new appointments, contracted (56%) and capitated (60%) reimbursements were higher than Medicaid (55%). For established appointments, Medicaid reimbursement (100%) was higher than contracted (37%) and capitated (58%). CONCLUSION: Our data suggest that reimbursement is influenced by regional factors and is improving in central Kentucky.     

In vitro effect of antibodies to dna on the template activity of DNA

Blood samples containing antibodies to DNA were obtained from patients with systemic lupus erythematosus (SLE) and rabbits immunized with denatured DNA complexed to methylated bovine serum albumin. The immunoglobulin fractions from these sources did not decrease the over-all template activity of singlestranded DNA with DNA polymerase or DNA-dependent RNA polymerase. In competition studies, both DNA polymerase and DNA-dependent RNA polymerase inhibited the binding of DNA antibodies to single-stranded DNA, as evidenced by inhibition of micro-complement fixation. These findings suggest that antibodies to DNA fail to decrease denatured DNA template activity because the enzymes which use a single-stranded DNA template can displace or block the antibodies from the denatured DNA as a result of greater binding affinity to the denatured DNA. The anti-DNA antibodies associated with SLE, therefore, may not be involved in the pathogenesis of the intracellular abnormalities associated with the disease.     

Obesity is Associated with Worse Outcomes Among Abdominal Trauma Patients Undergoing Laparotomy: A Propensity-Matched Nationwide Cohort Study

Introduction

Obesity is associated with increased morbidity and mortality in abdominal trauma patients. The characteristics of abdominal trauma patients with poor outcomes related to obesity require evaluation. We hypothesize that obesity is related to increased mortality and length of stay (LOS) among abdominal trauma patients undergoing laparotomies.

Methods

Abdominal trauma patients were identified from the National Trauma Data Bank between 2013 and 2015. Patients who received laparotomies were analyzed using propensity score matching (PSM) to evaluate the mortality rate and LOS between obese and non-obese patients. Patients without laparotomies were analyzed as a control group using PSM cohort analysis.

Results

A total of 33,798 abdominal trauma patients were evaluated, 10,987 of them received laparotomies. Of these patients, the proportion of obesity in deceased patients was significantly higher when compared to the survivors (33.1% vs. 26.2%, p < 0.001). Elevation of one kg/m² of body mass index independently resulted in 2.5% increased odds of mortality. After a well-balanced PSM, obese patients undergoing laparotomies had significantly higher mortality rates [3.7% vs. 2.4%, standardized difference (SD) = 0.241], longer hospital LOS (11.1 vs. 9.6 days, SD = 0.135), and longer intensive care unit LOS (3.5 vs. 2.3 days, SD = 0.171) than non-obese patients undergoing laparotomies.

Conclusions

Obesity is associated with increased mortality in abdominal trauma patients who received laparotomies versus those who did not. Obesity requires a careful evaluation of alternatives to laparotomy in injured patients.