State-coordinated services for traumatic brain injury survivors: toward a model delivery system

Since 1985, the state of Minnesota, through a variety of advocacy, legislative, and interagency efforts, has made incremental gains in public policy and service development for persons with traumatic brain injury (TBI). This article reviews the roles and functions of select state programs and departments in coordinating TBI services. Key initiatives, as well as the current model of public policy and services, are outlined. Current and future service development and initiatives are discussed. Finally, specific implementation recommendations are proposed.     

The formation of intramolecular disulfide bridges is required for induction of the Sindbis virus mutant ts23 phenotype

The Sindbis virus envelope protein spike is a hetero-oligomeric complex composed of a trimer of glycoprotein E1-E2 heterodimers. Spike assembly is a multistep process which occurs in the endoplasmic reticulum (ER) and is required for the export of E1 from the ER. PE2 (precursor to E2), however, can transit through the secretory pathway and be expressed at the cell surface in the absence of E1. Although oligomer formation does not appear to be required for the export of PE2, there is evidence that defects in E1 folding can affect PE2 transit from the ER. Temperature-sensitive mutant ts23 of Sindbis virus contains two amino acid substitutions in E1, while PE2 and capsid protein have the wild-type sequence; however, at the nonpermissive temperature, both E1 and PE2 are retained within the ER and can be isolated in protein aggregates with the molecular chaperone GRP78-BiP. We previously demonstrated that the temperature sensitivity for ts23 was lost as oligomer formation took place at the permissive temperature, suggesting that temperature sensitivity is initiated early in the process of viral spike assembly (M. Carleton and D. T. Brown, J. Virol. 70:952-959, 1996). Experiments described herein investigated the defects in envelope protein maturation that occur in ts23-infected cells and which result in retention of both envelope proteins in the ER. The data demonstrate that in ts23-infected cells incubated at the nonpermissive temperature, E1 folding is disrupted early after synthesis, resulting in the rapid incorporation of both E1 and PE2 into disulfide-stabilized aggregates. Furthermore, the aberrant E1 conformation which is responsible for induction of the ts phenotype requires the formation of intramolecular disulfide bridges formed prior to E1 association with PE2 and the completion of E1 folding.     

Movement of axoplasmic organelles on actin filaments from skeletal muscle

It was recently shown that, in addition to the well-established microtubule-dependent mechanism, fast transport of organelles in squid giant axons also occurs in the presence of actin filaments [Kuznetsov et al., 1992, Nature 356:722-725]. The objectives of this study were to obtain direct evidence of axoplasmic organelle movement on actin filaments and to demonstrate that these organelles are able to move on skeletal muscle actin filaments. Organelles and actin filaments were visualized by video-enhanced contrast differential interference contrast (AVEC-DIC) microscopy and by video intensified fluorescence microscopy. Actin filaments, prepared by polymerization of monomeric actin purified from rabbit skeletal muscle, were stabilized with rhodamine-phalloidin and adsorbed to cover slips. When axoplasm was extruded on these cover slips in the buffer containing cytochalasin B that prevents the formation of endogenous axonal actin filaments, organelles were observed to move at the fast transport rate. Also, axoplasmic organelles were observed to move on bundles of actin filaments that were of sufficient thickness to be detected directly by AVEC-DIC microscopy. The range of average velocities of movement on the muscle actin filaments was not statistically different from that on axonal filaments. The level of motile activity (number of organelles moving/min/field) on the exogenous filaments was less than on endogenous filaments probably due to the entanglement of filaments on the cover slip surface. We also found that calmodulin (CaM) increased the level of motile activity of organelles on actin filaments. In addition, CaM stimulated the movement of elongated membranous organelles that appeared to be tubular elements of smooth endoplasmic reticulum or extensions of prelysosomes. These studies provide the first direct evidence that organelles from higher animal cells such as neurons move on biochemically defined actin filaments.     

School feeding in Jamaica: a review of its evaluation

This paper reviews two studies that evaluated the school feeding program in Jamaica. The first examined 115 children aged 12-13 y who were enrolled in three classes in a poor, rural school. One class was served the standard school meal at 0900 whereas the other two classes served as controls. The outcome variables included school achievement, attendance, and weight gain. After one semester, the class receiving the meal showed improved arithmetic scores and school attendance compared with the control classes; however, they showed no weight gain. The academic improvement remained significant after school attendance was controlled for. It was therefore hypothesized that the gains in arithmetic resulted from the alleviation of hunger in the classroom. The other study, conducted in a metabolic ward, examined the effects of missing breakfast on cognitive function in 90 children aged 9-10 y and of differing nutritional status. Using a crossover design, the investigators tested each child on two mornings 1 wk apart, once after serving them breakfast and second without. Breakfast, consisting of the school program meal, was served at 0800. When severely malnourished, stunted, or wasted children received no breakfast, their performance in various cognitive tests deteriorated. These results indicate that alleviation of hunger was one of the mechanisms by which school feeding improved academic achievement in the previous study. Undernourished children are more likely to benefit from school feeding programs than are adequately nourished children.