Effectiveness of a practice-based intervention to increase vaccination rates and reduce missed opportunities.

BACKGROUND: Although provider feedback and recall/reminder systems have been shown to increase vaccination rates for children, little is known about the effectiveness of less intensive interventions. OBJECTIVE: To determine whether provider prompting at acute care visits in an urban hospital-based outpatient clinic can increase vaccination rates and decrease missed opportunities. DESIGN AND METHODS: Study participants, 3 years or younger, were identified from a managed care organization as receiving primary care at the clinic. Eligibility criteria included 1 or more visits to the clinic without regard to continuity of enrollment. Patients' vaccination records were generated at nursing triage and attached to the encounter sheet. Vaccination and visit data were abstracted from medical records, and comparisons were made between baseline (n = 521) and postintervention (n = 642) groups for up-to-date vaccination rates, missed opportunity rates, and mean numbers of visits. RESULTS: Up-to-date rates at the age of 24 months for 4 diphtheria and tetanus toxoids and pertussis, 3 polio, 1 measles-mumps-rubella, 3 hepatitis B, and 3 Haemophilus influenzae type b vaccines changed from 70% to 78% (P =.07). Up-to-date rates increased significantly to 87% among the subset of children continuously enrolled in the managed care organization and the practice (P<.01). Overall, mean numbers of visits were similar. Missed opportunity rates among children not up-to-date for 4 diphtheria and tetanus toxoids and pertussis, 3 polio, 1 measles-mumps-rubella, 3 hepatitis B, and 3 Haemophilus influenzae type b vaccines at the age of 24 months declined from 65% to 45% (P =.04). Similar trends were noted at the age of 10 months. CONCLUSIONS: In the absence of increased funding, minor changes in standard operating procedures may improve vaccination delivery. Further improvements may require efforts to ensure continuity of provider and plan assignment.

Fox Chase Network: Fox Chase Cancer Center's community hospital affiliation program.

Fox Chase Cancer Center developed a format for affiliation with community providers in 1986. Fox Chase Network was formed to establish hospital-based community cancer centers to increase access to patients involved in clinical research. Under this program, the Fox Chase Network now contributes 500 patients per year to prevention and clinical research studies. As relationships with community providers form, patient referrals have increased at Fox Chase Cancer Center and for each Fox Chase Network member. A dedicated staff is required to operate the central office on a day-to-day basis as well as at each affiliate. We have found this to be a critical element in each program's success. New challenges in the cancer business-increasing volumes with declining revenue-have caused us to reconfigure the services offered to affiliates, while maintaining true to our mission: to reduce the burden of human cancer.

The involvement of a LINE-1 element in a DNA rearrangement upstream of the mdr1a gene in a taxol multidrug-resistant murine cell line.

Two closely related but functionally distinct P-glycoprotein isoforms are encoded by the murine multidrug-resistance genes mdr1a and mdr1b. In a series of independently selected multidrug-resistant (MDR) J774.2 cell lines, mdr gene amplification and/or overexpression and overproduction of either the mdr1a or mdr1b products, or both gene products, correlates with the MDR phenotype. To investigate the possibility that mutations in the promoter regions of the mdr1a or mdr1b genes could influence their differential expression, mdr promoter-specific probes were used to detect and map potential structural alterations. An unusual structural rearrangement was found in the 5'-region of the amplified mdr1a allele in J7.T1, a cell line selected with taxol. To characterize this rearrangement, the regulatory regions of the mdr1a and mdr1b genes were analyzed. Whereas no gross structural alterations were detected by Southern blot hybridization using the mdr1b promoter probe, a novel amplified EcoRI fragment was detected by the mdr1a promoter probe. To determine the precise nature of this mutation, an mdr1a 5'-genomic clone was isolated from J7.T1 cells. Sequence analysis revealed an unusual DNA rearrangement consisting of the mdr1b gene, from its fourth intron toward its 3'-end, upstream of an intact mdr1a promoter on the amplified allele. We propose that this event occurred by an unequal sister chromatid exchange that was mediated by LINE-1 repetitive elements.

Uptake of [3H]serotonin and [3H]glutamate by primary astrocyte cultures. I. Effects of different sera and time in culture.

Na(+)-dependent, fluoxetine-sensitive high-affinity uptake of serotonin and Na(+)-dependent uptake of glutamate were studied in primary astrocyte cultures from 1-day-old rat neocortex. This uptake was independent of time in culture from 1 to 6 weeks. High-affinity serotonin uptake was decreased when cells were grown in horse serum as compared to fetal bovine serum and was almost absent when cells were grown in chemically defined medium. In contrast, glutamate uptake was unaffected by the composition of the medium in which the cultures were grown. The serum effect on serotonin uptake was not due to the greater level of serotonin in the fetal bovine serum and was only reversed by a change of serum over a time period of days.

Swelling-induced release of glutamate, aspartate, and taurine from astrocyte cultures.

Swelling of primary astrocyte cultures by exposing them to hypotonic media caused release of label after the cells had been allowed to accumulate 3H-L-glutamate, 3H-D-aspartate, or 3H-taurine. Comparable release of endogenous L-glutamate or taurine, as measured by high-pressure liquid chromatography (HPLC), was also found. Release of label was not affected by treating the cells with cytochalasin B, indicating that microfilament polymerization was not significantly involved. Hypotonic-induced release did not appear to principally involve reversal of the Na(+)-dependent uptake system since increasing external K+ to depolarize the cells by replacement of external Na+, thus maintaining isotonic conditions, increased release to a lesser extent. Threo beta-hydroxyaspartate, a potent 3H-L-glutamate uptake blocker, added externally stimulated efflux of 3H-L-glutamate independently of the swelling-induced efflux. Upon restoration of swollen cells to isotonic medium they showed an unimpaired ability to take up 3H-L-glutamate. The swelling-induced release of label was inhibited by a number of anion transport inhibitors, one of which has been shown to significantly improve outcome in an experimental brain trauma/hypoxia model in which astrocyte swelling is an early event.