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Meta-analysis was used to examine curriculum-based measurement in the content areas of social studies and science. Nineteen studies between the years of 1998 and 2020 were reviewed to determine overall mean correlation for criterion validity and examine alternate-form reliability and slope coefficients. An overall mean correlation of 0.59 was found for criterion validity; however, there was significant heterogeneity across studies, suggesting curriculum-based measure (CBM) format or content area may affect findings. Low to high alternative form reliability correlation coefficients were reported across CBM formats between 0.21 and 0.89. Studies investigating slopes included mostly vocabulary-matching formats and reported a range from 0.12 to 0.65 correct items per week with a mean of 0.34. Our findings suggest that additional research in the development of these measures in validity, reliability, and slope is warranted.

The E4 variant of APOE strongly predisposes individuals to late-onset Alzheimer's disease. We demonstrate that in response to lipogenesis, apolipoprotein E (APOE) in astrocytes can avoid translocation into the endoplasmic reticulum (ER) lumen and traffic to lipid droplets (LDs) via membrane bridges at ER-LD contacts. APOE knockdown promotes fewer, larger LDs after a fatty acid pulse, which contain more unsaturated triglyceride after fatty acid pulse-chase. This LD size phenotype was rescued by chimeric APOE that targets only LDs. Like APOE depletion, APOE4-expressing astrocytes form a small number of large LDs enriched in unsaturated triglyceride. Additionally, the LDs in APOE4 cells exhibit impaired turnover and increased sensitivity to lipid peroxidation. Our data indicate that APOE plays a previously unrecognized role as an LD surface protein that regulates LD size and composition. APOE4 causes aberrant LD composition and morphology. Our study contributes to accumulating evidence that APOE4 astrocytes with large, unsaturated LDs are sensitized to lipid peroxidation, which could contribute to Alzheimer's disease risk. [ABSTRACT FROM AUTHOR]

We previously reported a +ACA polymorphism in the minimal BRCA1 promoter region located -600bp from the exon 1a start site (ACATAACAC to ACATAA̱C1A̱ACAC). To determine the frequency of the +ACA in the general population, we genotyped 350 randomly selected women of child-bearing age with no history of breast cancer. Among this cohort, 191/350 (55%) individuals carried at least one polymorphic allele, the allelic frequency was determined to be 32% (226/700), and BRCA1 promoter genotypes (159/350, 45% wt/wt; 156/350, 45% wt/+ACA; and 35/350, 10% +ACA/+ACA) conformed to the Hardy-Weinberg equlibrium. Among breast cancer patients, 33/62 (53%) carried at least one polymorphic allele, and the allelic frequency was determined to be 45/124 (36%), similar to the frequency observed in the general population. However, the genotype distribution (29/62, 47% wt/wt; 21/62, 34% wt/+ACA; and 12/62, 19% +ACA/+ACA) did not conform to the Hardy-Weinberg equilibrium and was significantly different from that of the general population (P = 0.0043). These results suggest that the +ACA BRCA1 promoter polymorphism occurs frequently in the general population and may confer increased susceptibility to breast carcinogenesis. [ABSTRACT FROM AUTHOR]