RESUMO
In Oklahoma, the infant mortality rate is higher than the national rate. Fetal Infant Mortality Review (FIMR) is an effective perinatal systems intervention. FIMR gathers information from medical, social, and community sources taking a comprehensive look at how well these systems are serving women and infants. It is important to understand that FIMR is a method to develop community-based plans to reduce fetal and infant mortality. It is not a quick-fix solution to a complex problem, a research study, an institutional review, or a system for assigning blame or responsibility for a death. FIMR has been instrumental in identifying what health care providers, community leaders, and citizens can do to improve the health and lives of babies in Oklahoma. Key steps include: (1.) Data abstraction (2.) A home interview (3.) A review of individual case summaries (4.) Development of community-based solutions and interventions designed to improve service systems and resources
Assuntos
Serviços de Saúde da Criança/estatística & dados numéricos , Mortalidade Infantil , Serviços de Saúde Materna/estatística & dados numéricos , Adulto , Feminino , Guias como Assunto , Inquéritos Epidemiológicos , Humanos , Incidência , Lactente , Comunicação Interdisciplinar , Oklahoma/epidemiologia , Avaliação de Resultados em Cuidados de Saúde , Gravidez , Saúde PúblicaRESUMO
The malaria parasite Plasmodium falciparum infects humans and first targets the liver where liver-stage parasites undergo pre-erythrocytic replication. Liver-stage antigen-1 (LSA-1) is currently the only identified P. falciparum protein for which expression is restricted to liver stages. Yet, the importance of LSA-1 for liver-stage parasite development remains unknown. Here we deleted LSA-1 in the NF54 strain of P. falciparum and analysed the lsa-1(-) parasites throughout their life cycle. lsa-1(-) sporozoites had normal gliding motility and invasion into hepatocytes. Six days after infection of a hepatocytic cell line, lsa-1(-) parasites exhibited a moderate phenotype with an ~50% reduction of late liver-stage forms when compared with wild type. Strikingly, lsa-1(-) parasites growing in SCID/Alb-uPA mice with humanized livers showed a severe defect in late liver-stage differentiation and exo-erythrocytic merozoite formation 7 days after infection, a time point when wild-type parasites develop into mature merozoites. The lsa-1(-) parasites also showed aberrant liver-stage expression of key parasite proteins apical membrane antigen-1 and circumsporozoite protein. Our data show that LSA-1 plays a critical role during late liver-stage schizogony and is thus important in the parasite transition from the liver to blood. LSA-1 is the first P. falciparum protein identified to be required for this transitional stage of the parasite life cycle.