Analysis of outpatient referral failures.

BACKGROUND: The purpose of this study was to measure the rate at which outpatient referrals failed to be completed, and to analyze predisposing factors for referral failure in the family practice of a medical center. METHODS: Structured questionnaires were completed by referring physicians whenever a referral was initiated during a 4-month period. On the 60th day after referral, an investigator contacted the referred patients by telephone and also reviewed their charts. RESULTS: During the 4-month period, 604 referrals (2.28%) were made from 26,476 encounters at the study clinic. Sixty-four patients (10.6%) failed to complete the referral processes within a 60-day period. The most frequent reasons for referral failure were administrative factors, ie, too long a wait (59.4%), and the patient's belief that the referral was not necessary (23.4%). The physician's or patients's opinion of referral necessity, the level of experience of the referring physician, and the method of contact with the consultant all had significant influence on the referral failure rate. CONCLUSIONS: Improving administrative efficiency, enhancing communication between physicians and between physicians and patients, assessing the willingness of patients to follow through on a referral, and the method used to initiate the referral by the physician may reduce the referral failure rate.

2,4-Diamino-5-benzylpyrimidines and analogues as antibacterial agents. 9. Lipophilic trimethoprim analogues as antigonococcal agents.

Lipophilic analogues of trimethoprim (1) bearing 3,5-dialkyl-4-hydroxy substituents in the benzene ring are much more active in vitro against Neisseria gonorrhoeae than is 1. The 3,5-diisopropyl-4-hydroxy derivative (2) was selected as a candidate for clinical evaluation as an antigonococcal agent, and as part of the preliminary evaluation it was submitted to extended pharmacokinetic and metabolism studies in dogs. Although the compound was not extensively conjugated by metabolic enzymes, one of the methyl groups was metabolized to produce a 3-isopropyl-4-hydroxy-5-(alpha-carboxyethyl)benzyl derivative (43), which was rapidly excreted. Related analogues were likewise extensively metabolized.

Indoleacetic acid complementation and its relation to host range specifying genes on the Ti plasmid of Agrobacterium tumefaciens.

Host range variations were noted when 23 wild-type strains of Agrobacterium tumefaciens were tested on 27 different plant species. Because we have shown previously that host range specificity is conferred by the pTi plasmid, these variations in host specificity implicated genetic differences among pTi plasmids within the A. tumefaciens population that was tested. Host specificity was independent of the type of opine utilized and biotype of the strain used. These data suggested that separate genetic determinants operate for host specificity. This hypothesis was confirmed by Tn5 mutagenesis of the pTi plasmid, which generated mutants affected in host specificity. The regions of host specifying genes were located by displacement analysis of mutant pTi-plasmid-DNA restriction fragments. There are at least two sites on the pTiC58 plasmid: one within the T-region and the other about 75-77 kb to the right of this region. Mutations within the T-region were chemically complemented by indoleacetic acid, which restored the host range of the mutants. Such complementations were not observed with mutants outside the T-region.

The metabolism of isamoxole in the rat and guinea-pig.

1. The absorption, metabolism and excretion of isamoxole, (2-methyl-N-butyl-N-(4-methyloxazol-2-yl)propanamide), a compound with anti-allergy properties, has been studied in the rat and guinea-pig. 2. The compound was well-absorbed by both species after oral doses of 50 to 150 mg/kg. It underwent extensive first-pass metabolism in the liver, and was excreted as a mixture of metabolites, predominantly in the urine, within 48 h. 3. Three major routes of metabolism were involved, namely deacylation, oxidative ring scission and alkyl oxidation. 4. A major plasma and urine metabolite was 1-butyl-3-(1-carboxyethyl)urea, and this was accompanied by low levels of its cyclized product 3-butyl-5-methylhydantoin.