OBJECTIVE: To examine the possible impact of changes in the organization and management of the Medicaid program on hospitalization patterns for children with chronic and nonchronic conditions between January 1, 1991, and December 31, 1998. DESIGN: Longitudinal retrospective study of hospitalization patterns of children in 4 strata: Medicaid, non-Medicaid, chronic conditions, and nonchronic conditions. SETTING: Washington State. PATIENTS: Hospital discharge abstract records for all children aged 0 to 17 years profiled into those with and without a chronic condition, Medicaid, and non-Medicaid using a diagnosis-based classification system. MAIN OUTCOME MEASURES: Hospitalization and multiple hospitalization rates and length of hospital stay. RESULTS: In 1991, hospitalization and multiple hospitalization rates were higher for all Medicaid vs non-Medicaid children. From 1991 to 1998, there was a decrease in the hospitalization and multiple hospitalization rates for Medicaid children only. By 1998, rates for Medicaid children approximated those for non-Medicaid children. This decrease was greater for nonchronically ill children than for chronically ill children. Total hospitalizations in Medicaid children decreased by 4.5%. The mean length of stay in 1991 for all Medicaid hospitalized children was higher than that for non-Medicaid children (6.1 vs 5.1 days). By 1998, the length of stay decreased for both groups (5.7 vs 4.9 days). CONCLUSION: The declines in hospitalization and multiple hospitalization rates observed in Washington State Medicaid children from 1991 to 1998 may be the result of many statewide efforts to increase access and improve management for this population.

Adolescent↗

PubMedDate not supplied

Transgenic mice expressing a truncated form of CREB-binding protein (CBP) exhibit deficits in hippocampal synaptic plasticity and memory storage.

Deletions, translocations, or point mutations in the CREB-binding protein (CBP) gene have been associated with Rubinstein-Taybi Syndrome; a human developmental disorder characterized by retarded growth and reduced mental function. To examine the role of CBP in memory, transgenic mice were generated in which the CaMKII alpha promoter drives expression of an inhibitory truncated CBP protein in forebrain neurons. Examination of hippocampal long-term potentiation (LTP), a form of synaptic plasticity thought to underlie memory storage, revealed significantly reduced late-phase LTP induced by dopamine-regulated potentiation in hippocampal slices from CBP transgenic mice. However, four-train induced late-phase LTP is normal. Behaviorally, CBP transgenic mice exhibited memory deficits in spatial learning in the Morris water maze and deficits in long-term memory for contextual fear conditioning, two hippocampus-dependent tasks. Together, these results demonstrate that CBP is involved in specific forms of hippocampal synaptic plasticity and hippocampus-dependent long-term memory formation.

Animals↗