RESUMO
Cameron Park, Texas, is a colonia (an isolated, unincorporated rural settlement without municipal improvements) on the Texas-Mexico border in the Lower Rio Grande Valley, in Cameron County near Brownsville, Texas. Cameron Park has a population of 5,961 residents, 99.3% of whom are Hispanic. The annual median income is 16,934 US dollars, about one-half of the state median. Fifty-eight percent of families generally and 68% of those with children younger than 5 years have incomes below poverty level. Cameron Park resides geographically in a region where agriculture has been, and continues to be, a dominant industry, a fact consistent with the intensive use of pesticides and increased potential for air, water, and ground contamination. The practice of good environmental health is extremely difficult under these conditions. In 1999 the Texas A&M University Center for Housing and Urban Development's Colonias Program and the Center for Environmental and Rural Health teamed up to create an environmental health education and outreach program called the Cameron Park Project (CPP). The CPP focused on how to reduce potential environmental exposures associated with human illness by providing residents with scientifically sound information on positive health practices and how to deal with environmental hazards. In this article we discuss the research methodology used in the CPP, a methodology specifically chosen to address four challenges presented by colonias to conducting valid and reliable research.
Assuntos
Relações Comunidade-Instituição , Saúde Ambiental , Serviços de Informação , Humanos , Relações Interinstitucionais , Pesquisa/tendências , População Rural , TexasRESUMO
Previous studies have shown that proton magnetic resonance spectroscopy (MRS) is useful in predicting neurologic prognosis in children with traumatic brain injury (TBI). Reductions in N-acetyl derived metabolites and presence of lactate have been predictive of poor outcomes. We examined another spectroscopy metabolite, myoinositol (mI), to determine whether it is altered after TBI. Found primarily in astrocytes, mI functions as an osmolyte and is involved in hormone response pathways and protein-kinase C activation. Myoinositol is elevated in the newborn brain and is increased in a variety of diseases. We studied 38 children (mean age 11 y; range 1.6-17 y) with TBI using quantitative short echo time occipital gray and parietal white matter proton MRS at a mean of 7 d (range 1-17 d) after injury. We found that occipital gray matter mI levels were increased in children with TBI (4.30 +/- 0.73) compared with controls (3.53 +/- 0.48; p = 0.003). We also found that patients with poor outcomes 6-12 mo after injury had higher mI levels (4.78 +/- 0.68) than patients with good outcomes (4.15 +/- 0.69; p < 0.05). Myoinositol is elevated after pediatric TBI and is associated with a poor neurologic outcome. The reasons for its elevation remain unclear but may be due to astrogliosis or to a disturbance in osmotic function.