Scoring Federal Legislation for Equity: Definition, Framework, and Potential Application

Federal legislation is fundamental to building a nation in which all can participate, prosper, and reach their full potential. Since our nation's founding, in many ways, federal legislation has created and exacerbated racial inequities, leaving one-third of the population experiencing material poverty and preventing our democracy from realizing the promise of equity. To ensure the federal government serves us all, we must accurately understand and assess whether every policy advances or impedes equity. The Equity Scoring Initiative (ESI) exists to establish the foundation for a new legislative scoring regime. By scoring for equity, we can begin to create an accountable, responsive democracy

Binding of an RNA trafficking response element to heterogeneous nuclear ribonucleoproteins A1 and A2

Heterogeneous nuclear ribonucleoprotein (hnRNP) A2 binds a 21-nucleotide myelin basic protein mRNA response element, the A2RE, and A2RE-like sequences in other localized mRNAs, and is a trans-acting factor in oligodendrocyte cytoplasmic RNA trafficking. Recombinant human hnRNPs A1 and A2 were used in a biosensor to explore interactions with A2RE and the cognate oligodeoxyribonucleotide. Both proteins have a single site that bound oligonucleotides with markedly different sequences but did not bind in the presence of heparin. Both also possess a second, specific site that bound only A2RE and was unaffected by heparin, hnRNP A2 bound A2RE in the latter site with a K-d near 50 nM, whereas the K-d for hnRNP A1 was above 10 muM. UV cross-linking assays led to a similar conclusion. Mutant A2RE sequences, that in earlier qualitative studies appeared not to bind hnRNP A2 or support RNA trafficking in oligodendrocytes, had dissociation constants above 5 muM for this protein. The two concatenated RNA recognition motifs (RRMs), but not the individual RRMs, mimicked the binding behavior of hnRNP A2. These data highlight the specificity of the interaction of A2RE with these hnRNPs and suggest that the sequence-specific A2RE-binding site on hnRNP A2 is formed by both RRMs acting in cis

A comparison of the health status of freshmen at Oregon State University from 1930 to 1960

The data gathered for the study of the health status of freshmen at Oregon State University were derived by an analysis of health history records. These were obtained from the Oregon State University Health Service. The years sampled were 1930, 1940, 1950 and 1960; 300 freshman male and 300 freshman female names were chosen at random for each sample year, giving a total of 2400 students studied. The data for each sex were computed separately. Final statistical evaluation was based on range, mean, and standard deviation of the data gained. This gave an average image of the female and male freshman students for each year studied. Included in the study were certain data pertaining to the health status of the student's parents and relatives. Findings The following findings were found in an analysis of the data gathered in the research. 1. Both female and male freshmen show a gain in height and weight with each succeeding year sampled. The greatest mean height was in 1950 and the greatest mean weight was in 1960. 2. While there was a leveling off or decrease in the incidence of communicable diseases, essentially the severe ones, there appeared an increase in non-communicable diseases. 3. Mothers and fathers of freshman students are getting younger. While there is still some difference in age, the father's mean age is approaching that of the mother's. 4. Data on relatives show a decrease in reported cases of tuberculosis. Heart disease, cancer and diabetes all increased greatly, with diabetes showing the greatest percentage of increase. Conclusions 1. Freshmen at Oregon State University are gaining in stature and future generations will probably be heavier and possibly taller. 2. Freshmen at Oregon State University are healthier in the sense that they have a lower case incidence of the communicable, more common severe diseases. However, their chances of developing non-communicable diseases are increasing. 3. The parents of Oregon State University freshmen are successively younger with each decade. 4. If the trend indicated in the study continues relatives of freshmen at Oregon State University will experience an increase in the incidence of organic diseases. Recommendations Criteria for health status should be established and health record cards should be designed to reflect these criteria. Other studies should be initiated to provide comparisons with this study. In this way up-to-date norms can be established for local, regional and national utilization

cAMP-dependent regulation of IKs single-channel kinetics

International audienceThe delayed potassium rectifier current, IKs, is composed of KCNQ1 and KCNE1 subunits and plays an important role in cardiac action potential repolarization. During β-adrenergic stimulation, 3′-5′-cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) phosphorylates KCNQ1, producing an increase in IKs current and a shortening of the action potential. Here, using cell-attached macropatches and single-channel recordings, we investigate the microscopic mechanisms underlying the cAMP-dependent increase in IKs current. A membrane-permeable cAMP analog, 8-(4-chlorophenylthio)-cAMP (8-CPT-cAMP), causes a marked leftward shift of the conductance–voltage relation in macropatches, with or without an increase in current size. Single channels exhibit fewer silent sweeps, reduced first latency to opening (control, 1.61 ± 0.13 s; cAMP, 1.06 ± 0.11 s), and increased higher-subconductance-level occupancy in the presence of cAMP. The E160R/R237E and S209F KCNQ1 mutants, which show fixed and enhanced voltage sensor activation, respectively, largely abolish the effect of cAMP. The phosphomimetic KCNQ1 mutations, S27D and S27D/S92D, are much less and not at all responsive, respectively, to the effects of PKA phosphorylation (first latency of S27D + KCNE1 channels: control, 1.81 ± 0.1 s; 8-CPT-cAMP, 1.44 ± 0.1 s, P < 0.05; latency of S27D/S92D + KCNE1: control, 1.62 ± 0.1 s; cAMP, 1.43 ± 0.1 s, nonsignificant). Using total internal reflection fluorescence microscopy, we find no overall increase in surface expression of the channel during exposure to 8-CPT-cAMP. Our data suggest that the cAMP-dependent increase in IKs current is caused by an increase in the likelihood of channel opening, combined with faster openings and greater occupancy of higher subconductance levels, and is mediated by enhanced voltage sensor activation