Health Literacy Education in Baccalaureate Nursing Programs in the United States.

AIM: This study's aim was to determine the prevalence of health literacy education in nursing programs. Health literacy content and teaching strategies were also explored. BACKGROUND: Over 75 million Americans have low health literacy, a problem that can cause negative health outcomes. Knowledge about health literacy is important for nurses; yet, the extent to which the topic is included within nursing curricula is unknown. METHOD: An online survey was distributed to 150 nursing programs to obtain information about health literacy education in the curricula. RESULTS: Fifty-seven programs responded, with the majority reporting that health literacy is taught in their curricula. The impact of low health literacy and the importance of plain language were noted as common topics. CONCLUSION: The majority of participants reported inclusion of health literacy in their curricula using various teaching strategies. However, a low response rate prevents generalized conclusions.

Informing best practice with community practice: the community change chronicle method for program documentation and evaluation.

Health promotion professionals are increasingly encouraged to implement evidence-based programs in health departments, communities, and schools. Yet translating evidence-based research into practice is challenging, especially for complex initiatives that emphasize environmental strategies to create community change. The purpose of this article is to provide health promotion practitioners with a method to evaluate the community change process and document successful applications of environmental strategies. The community change chronicle method uses a five-step process: first, develop a logic model; second, select outcomes of interest; third, review programmatic data for these outcomes; fourth, collect and analyze relevant materials; and, fifth, disseminate stories. From 2001 to 2003, the authors validated the use of a youth empowerment model and developed eight community change chronicles that documented the creation of tobacco-free schools policies (n = 2), voluntary policies to reduce secondhand smoke in youth hangouts (n = 3), and policy and program changes in diverse communities (n = 3).

A case study in teaching tobacco policy advocacy at a Historically Black university.

Policy advocacy is increasingly recognized as a crucial component of the training provided to health educators but relatively few universities offer advocacy training as part of their professional preparation programs for health educators. Historically Black colleges and universities (HBCUs) represent a natural setting for creating strong Black leaders in tobacco policy advocacy. This case study focuses on experiential education at an HBCU to develop advocacy skills around tobacco issues among Black college students. The authors describe the structure and content of two tobacco policy courses, their efforts to evaluate these courses, and the lessons they learned planning and conducting them. They believe their experience can prove useful to others developing curricula for teaching policy advocacy skills to health education students.

Retinoid signaling is involved in governing the waiting period for axons in chick hindlimb.

During embryonic development in chick, axons pause in a plexus region for approximately 1 day prior to invading the limb. We have previously shown that this "waiting period" is governed by maturational changes in the limb. Here we provide a detailed description of the spatiotemporal pattern of Raldh2 expression in lumbosacral motoneurons and in the limb, and show that retinoid signaling in the limb contributes significantly to terminating the waiting period. Raldh2, indicative of retinoid signaling, first appears in hindlimb mesenchyme near the end of the waiting period. Transcripts are more abundant in connective tissue associated with predominantly fast muscles than predominantly slow muscles, but are not expressed in muscle cells themselves. The tips of ingrowing axons are always found in association with domains of Raldh2, but development of Raldh2 expression is not regulated by the axons. Instead, retinoid signaling appears to regulate axon entry into the limb. Supplying exogenous retinoic acid to proximal limb during the waiting period caused both motor and sensory axons to invade the limb prematurely and altered the normal stereotyped pattern of axon ingrowth without obvious effects on limb morphogenesis or motoneuron specification. Conversely, locally decreasing retinoid synthesis reduced axon growth into the limb. Retinoic acid significantly enhanced motor axon growth in vitro, suggesting that retinoic acid may directly promote axon growth into the limb in vivo. In addition, retinoid signaling may indirectly affect the waiting period by regulating the maturation of other gate keeping or guidance molecules in the limb. Together these findings reveal a novel function of retinoid signaling in governing the timing and patterning of axon growth into the limb.

Shh influences cell number and the distribution of neuronal subtypes in dorsal root ganglia.

The molecular mechanisms responsible for specifying the dorsal-ventral pattern of neuronal identities in dorsal root ganglia (DRG) are unclear. Here we demonstrate that Sonic hedgehog (Shh) contributes to patterning early DRG cells. In vitro, Shh increases both proliferation and programmed cell death (PCD). Increasing Shh in vivo enhances PCD in dorsal DRG, while inducing greater proliferation ventrally. In such animals, markers characteristic of ventral sensory neurons are expanded to more dorsal positions. Conversely, reducing Shh function results in decreased proliferation of progenitors in the ventral region and decreased expression of the ventral marker trkC. Later arising trkA(+) afferents make significant pathfinding errors in animals with reduced Shh function, suggesting that accurate navigation of later arising growth cones requires either Shh itself or early arising, Shh-dependent afferents. These results indicate that Shh can regulate both cell number and the distribution of cell types in DRG, thereby playing an important role in the specification, patterning and pathfinding of sensory neurons.

Hoxc10 and Hoxd10 regulate mouse columnar, divisional and motor pool identity of lumbar motoneurons.

A central question in neural development is how the broad diversity of neurons is generated in the vertebrate CNS. We have investigated the function of Hoxc10 and Hoxd10 in mouse lumbar motoneuron development. We show that Hoxc10 and Hoxd10 are initially expressed in most newly generated lumbar motoneurons, but subsequently become restricted to the lateral division of the lateral motor column (lLMC). Disruption of Hoxc10 and Hoxd10 caused severe hindlimb locomotor defects. Motoneurons in rostral lumbar segments were found to adopt the phenotype of thoracic motoneurons. More caudally the lLMC and dorsal-projecting axons were missing, yet most hindlimb muscles were innervated. The loss of the lLMC was not due to decreased production of motoneuron precursors or increased apoptosis. Instead, presumptive lLMC neurons failed to migrate to their normal position, and did not differentiate into other motoneurons or interneurons. Together, these results show that Hoxc10 and Hoxd10 play key roles in establishing lumbar motoneuron columnar, divisional and motor pool identity.

Onset of ETS expression is not accelerated by premature exposure to signals from limb mesenchyme.

The ETS transcription factors ER81 and PEA3 are expressed in discrete populations of sensory and motor neurons and regulate late events in neuronal development and limb innervation. Although initiation of ETS expression requires limb-derived signals, we show here that precocious axon growth into transplanted older donor limbs, which prematurely exposes neurons to limb-derived signals, does not accelerate the onset of expression of Er81 or Pea3. Similarly, neither MN-cadherin, which is reportedly regulated by ER81, nor T-cadherin is expressed precociously in neurons innervating older donor limbs. Thus, neurons must attain a particular level of differentiation to respond to inducing signals from limb. We also show that signals emanating from limb mesenchyme are sufficient to initiate Er81 and Pea3 expression in sensory and motor neurons in the absence of myogenic cells in Sp(d) mutant mice and that induction of ETS expression is unlikely to directly involve retinoid signaling from limb mesenchyme.

Ephrin-A5 inhibits growth of embryonic sensory neurons.

EphA-ephrin signaling has recently been implicated in the establishment of motor innervation patterns, in particular in determining whether motor axons project into dorsal versus ventral nerve trunks in the limb. We investigated whether sensory axons, which grow out together with and can be guided by motor axons, are also influenced by Eph-ephrin signaling. We show that multiple EphA receptors are expressed in DRGs when limb innervation is being established, and EphA receptors are present on growth cones of both NGF-dependent (predominantly cutaneous) and NT3-dependent (predominantly proprioceptive) afferents. Both soluble and membrane-attached ephrin-A5 inhibited growth of approximately half of each population of sensory axons in vitro. On average, growth cones that collapsed in response to soluble ephrin-A5 extended more slowly than those that did not, and ephrin-A5 significantly slowed the extension of NGF-dependent growth cones that did not collapse. Finally, we show that ectopic expression of ephrin-A5 in ovo reduced arborization of cutaneous axons in skin on the limb. Together these results suggest that sensory neurons respond directly to A-class ephrins in the limb. Thus, ephrins appear to pattern sensory axon growth in two ways-both directly, and indirectly via their inhibitory effects on neighboring motor axons.

An early broad competence of motoneurons to express ER81 is later sculpted by the periphery.

The ETS transcription factor ER81 is expressed in sensory neurons and motoneurons that innervate the adductor and femorotibialis muscles in chick hindlimb and is essential for the development of monosynaptic connections between these two populations of neurons. Neurons need a signal(s) from limb bud mesoderm to initiate ER81 expression. It is not known whether the mature expression pattern arises because adductor and femorotibialis motoneurons are uniquely competent to respond to peripheral signals and express ER81, or whether all motoneurons are competent to express ER81, but normally only adductor and femorotibialis motoneurons are exposed to the requisite activating signal. To investigate these possibilities, we examined ER81 expression in motoneurons that encountered limb tissue surgically mismatched with their target identity at stages after motor pool identities are established. We found that ER81 expression was not invariably linked to motor pool identity or target innervation and was more malleable in later-born femorotibialis motoneurons than in earlier-born adductor motoneurons. We also found that ER81 expression is regulated differently in sensory neurons and motoneurons. Most striking was the observation that motoneurons caudal to the normal adductor and femorotibialis pools could express ER81 when exposed to the appropriate peripheral signals, although this competence did not extend through the entire lumbosacral (LS) region. Thus, it appears that a prepattern of competence to express ER81 is established in early LS motoneurons, most likely in concert with their target identity, and that the expression domains of motoneurons are subsequently refined by peripheral signals at later stages.

Development of "normal" dermatomes and somatotopic maps by "abnormal" populations of cutaneous neurons.

During development, motor and sensory axons grow to peripheral targets with remarkable precision. Whereas much has been learned about the development of motoneuron connectivity, less is known about the regulation of cutaneous innervation. In adults, dorsal root ganglia (DRG) innervate characteristic skin regions, termed dermatomes, and their axons project somatotopically in the dorsal horn. Here, we have investigated whether cutaneous neurons are selectively matched with specific skin regions, and whether peripheral target skin influences the central connections of cutaneous neurons. To address these questions, we shifted limb buds rostrally in chick embryos prior to axon outgrowth, causing DRGs to innervate novel skin regions, and mapped the resulting dermatomes and central projections. Following limb shifts, cutaneous innervation arose from more rostral and from fewer DRGs than normal, but the overall dermatome pattern was preserved. Thus, DRGs parcel out innervation of skin in a consistent manner, with no indication of matching between skin and DRGs. Similarly, cutaneous nerves established a "normal" somatotopic map in the dorsal horn, but in more rostral segments than usual. Thus, the peripheral target skin may influence the pattern of CNS projections, but does not direct cutaneous axons to specific populations of neurons in the dorsal horn.

In vivo analysis of Schwann cell programmed cell death in the embryonic chick: regulation by axons and glial growth factor.

The present study uses the embryonic chick to examine in vivo the mechanisms and regulation of Schwann cell programmed cell death (PCD) in spinal and cranial peripheral nerves. Schwann cells are highly dependent on the presence of axons for survival because the in ovo administration of NMDA, which excitotoxically eliminates motoneurons and their axons by necrosis, results in a significant increase in apoptotic Schwann cell death. Additionally, pharmacological and surgical manipulation of axon numbers also affects the relative amounts of Schwann cell PCD. Schwann cells undergoing both normal and induced PCD display an apoptotic-like cell death, using a caspase-dependent pathway. Furthermore, axon elimination results in upregulation of the p75 and platelet-derived growth factor receptors in mature Schwann cells within the degenerating ventral root. During early development, Schwann cells are also dependent on axon-derived mitogens; the loss of axons results in a decrease in Schwann cell proliferation. Axon removal during late embryonic stages, however, elicits an increase in proliferation, as is expected from these more differentiated Schwann cells. In rodents, Schwann cell survival is regulated by glial growth factor (GGF), a member of the neuregulin family of growth factors. GGF administration to chick embryos selectively rescued Schwann cells during both normal PCD and after the loss of axons, whereas other trophic factors tested had no effect on Schwann cell survival. In conclusion, avian Schwann cells exhibit many similarities to mammalian Schwann cells in terms of their dependence on axon-derived signals during early and later stages of development.