Women, infants, and children cash value voucher (CVV) use in Arizona: a qualitative exploration of barriers and strategies related to fruit and vegetable purchases.

OBJECTIVE: Women, Infants, and Children (WIC) cash value vouchers (CVV) have been inconsistently redeemed in Arizona. The objective of this study was to explore perceived barriers to use of CVV as well as strategies participants use to overcome them. DESIGN: Eight focus groups were conducted to explore attitudes and behaviors related to CVV use. SETTING: Focus groups were conducted at 2 WIC clinics in metro-Phoenix, AZ. PARTICIPANTS: Participants in WIC who were at least 18 years of age and primarily responsible for buying and preparing food for their households. PHENOMENON OF INTEREST: Perceived barriers to CVV use and strategies used to maximize their purchasing value. ANALYSIS: Transcripts were analyzed using a general inductive approach to identify emergent themes. RESULTS: Among 41 participants, multiple perceived barriers emerged, such as negative interactions in stores or confusion over WIC rules. Among experienced shoppers, WIC strategies also emerged to deal with barriers and maximize CVV value, including strategic choice of times and locations at which to shop and use of price-matching, rewards points, and other ways to increase purchasing power. CONCLUSIONS AND IMPLICATIONS: Arizona WIC participants perceived barriers that limit easy redemption of CVV. Useful strategies were also identified that could be important to explore further to improve WIC CVV purchasing experiences.

Participant-centered education: building a new WIC nutrition education model.

OBJECTIVE: To assess the readiness of the Western Region Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) states to implement participant-centered nutrition education (PCE) and to develop a PCE model for WIC service delivery. DESIGN: Formative research including on-line survey, qualitative in-depth interviews, focus groups, and observational assessments. SETTING: WIC clinics within the Western Region WIC states. PARTICIPANTS: State and local staff and WIC clients within 8 states, 2 tribal organizations, and 2 territories. PHENOMENON OF INTEREST: Readiness indicators of states to implement and expand PCE elements to include in PCE model development. ANALYSIS: On-line surveys were collected and analyzed. On-site assessment forms, interviews, and focus group findings were collected, coded, and summarized by themes. RESULTS: Key themes from state and local findings guided the model development for PCE implementation in the Western Region WIC states. The PCE model must be flexible and systems oriented, contain strong training and mentoring components, and integrate cultural sensitivity to best reach program participants. CONCLUSIONS AND IMPLICATIONS: The PCE model has the potential to improve WIC nutrition services and enable participants to make positive health-related behavior changes that will influence long-term health issues. Further outcome studies are needed to determine the success of PCE implementation in the Western Region WIC states.

Animal models for genetic neuromuscular diseases.

The neuromuscular disorders are a heterogeneous group of genetic diseases, caused by mutations in genes coding sarcolemmal, sarcomeric, and citosolic muscle proteins. Deficiencies or loss of function of these proteins leads to variable degree of progressive loss of motor ability. Several animal models, manifesting phenotypes observed in neuromuscular diseases, have been identified in nature or generated in laboratory. These models generally present physiological alterations observed in human patients and can be used as important tools for genetic, clinic, and histopathological studies. The mdx mouse is the most widely used animal model for Duchenne muscular dystrophy (DMD). Although it is a good genetic and biochemical model, presenting total deficiency of the protein dystrophin in the muscle, this mouse is not useful for clinical trials because of its very mild phenotype. The canine golden retriever MD model represents a more clinically similar model of DMD due to its larger size and significant muscle weakness. Autosomal recessive limb-girdle MD forms models include the SJL/J mice, which develop a spontaneous myopathy resulting from a mutation in the Dysferlin gene, being a model for LGMD2B. For the human sarcoglycanopahties (SG), the BIO14.6 hamster is the spontaneous animal model for delta-SG deficiency, whereas some canine models with deficiency of SG proteins have also been identified. More recently, using the homologous recombination technique in embryonic stem cell, several mouse models have been developed with null mutations in each one of the four SG genes. All sarcoglycan-null animals display a progressive muscular dystrophy of variable severity and share the property of a significant secondary reduction in the expression of the other members of the sarcoglycan subcomplex and other components of the Dystrophin-glycoprotein complex. Mouse models for congenital MD include the dy/dy (dystrophia-muscularis) mouse and the allelic mutant dy(2J)/dy(2J) mouse, both presenting significant reduction of alpha2-laminin in the muscle and a severe phenotype. The myodystrophy mouse (Large(myd)) harbors a mutation in the glycosyltransferase Large, which leads to altered glycosylation of alpha-DG, and also a severe phenotype. Other informative models for muscle proteins include the knockout mouse for myostatin, which demonstrated that this protein is a negative regulator of muscle growth. Additionally, the stress syndrome in pigs, caused by mutations in the porcine RYR1 gene, helped to localize the gene causing malignant hypertermia and Central Core myopathy in humans. The study of animal models for genetic diseases, in spite of the existence of differences in some phenotypes, can provide important clues to the understanding of the pathogenesis of these disorders and are also very valuable for testing strategies for therapeutic approaches.