Four years of experience with an interactive health care system.
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Biomedical subjects
Publications and source records attributed to H Peterson.
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From cultures of V79 Chinese hamster cells, 10 independent clones of 8-azaguanine resistant cells were isolated and subcultured. Cells from all ten clones were resistant to 1 mg/ml levels of 8-azaguanine (8-AzG), contained less than 3% of the wild type levels of the enzyme, hypoxanthine guanine phosphoribosyl transferase (HGPRT), and were unable to grow in HAT medium. The ten clones were classified according to the conditions under which they reverted to the wild type phenotype. Clones in classes I and II reverted spontaneously with frequencies of 40-10(-5) and about 3-10(-5) respectively, and the reversion frequency was independent of the density of cells of all but one of the clones in the culture medium used. Class II clones evinced increased reversion frequencies with ethyl methanesulfonate (EMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and to a lesser extent with 5-bromo-2'-deoxyuridine (budR), suggesting that these clones contained point mutations in a locus which controls HGPRT activity. The processes of reversion and toxicity appeared to be associated. Class III clones did not revert spontaneously or with BUdR and MNNG, but did revert with EMS. The reversion frequency of class I clones was not increased after treatment with EMS, MNNG or BUdR.
Twenty-three difficult to control patients with 1 or more seizures per week despite diphenylhydantoin (DPH), phenobarbital and/or primidone in near and toxic doses and blood levels were entered in the study. 3 had grand mal. 8 psychomotor seizures and 12 had both. During a 6 1/2 month study period the patient received active drug and placebo for 3 months each; randomized, double-blind. The dose was to be increased within 4 weeks up to 6 capsules per day equal to 1,200 mg of carbamazepine (C), while the doses or previously taken (basis) anticonvulsants were to remain unchanged. Hematopoetic system and heptic functions were monitored. Complete seizure control attributable to C was not achieved in any, but up to 50% improvement occurred in 12 patients. Questionable improvement was thought to take place in 3 patients, no change occurred in 7, and psychomotor seizures became more frequent in 1 patient. A clear-cut psychotropic effect was not observed. Adverse effects attributable to C were a decline of WBC below 4,000 with relative neutropenia in 3 patients followed by at return to the previous after discontinuation of C. Nystagmus and unsteadiness were seen in about half of the patients, and some headache and drowsiness occurred in one quarter. The highest C blood level was 11.8 mug/ml, the lowest 3.8 mug/ml (average 5.6 mug/ml) during 1,200 mg intake. It seemed, generally, that intoxication occurred with lower blood levels of carbamazepine in those patients whose basis anticonvulsant blood levels were highest.
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We propose a likelihood method for estimating parameters in generalized linear models with missing covariates and a non-ignorable missing data mechanism. In this paper, we focus on one missing covariate. We use a logistic model for the probability that the covariate is missing, and allow this probability to depend on the incomplete covariate. We allow the covariates, including the incomplete covariate, to be either categorical or continuous. We propose an EM algorithm in this case. For a missing categorical covariate, we derive a closed form expression for the E- and M-steps of the EM algorithm for obtaining the maximum likelihood estimates (MLEs). For a missing continuous covariate, we use a Monte Carlo version of the EM algorithm to obtain the MLEs via the Gibbs sampler. The methodology is illustrated using an example from a breast cancer clinical trial in which time to disease progression is the outcome, and the incomplete covariate is a quality of life physical well-being score taken after the start of therapy. This score may be missing because the patients are sicker, so this covariate could be non-ignorably missing.
The financial data of all patients (535) admitted to the Nutritional Support Service (NSS) during 1985, including charges, true care costs, and actual reimbursement including pass-through payments (which are Medicare funds given directly to hospitals for education and capital equipment, and vary significantly from hospital to hospital), were analyzed. The NSS Medicare patients fell into 98 diagnostic related groups (DRGs). All 3,939 Medicare patients admitted in 1985 with the same DRGs as the NSS patients were also identified and their financial data analyzed. The NSS patients lost $999,643 because of the 266 medicare reimbursed NSS patients sustained high losses which overwhelmed the modest profits of the 269 non-Medicare patients. When data from all Medicare patients (which includes both NSS and non-NSS patients) with the same DRGs are analyzed, large profits are realized. These profits are totally due to pass-through payments received. Without pass throughs the loss for all 3,939 Medicare patients in these 98 DRGs would have been $1,641,273. The impact of eliminating pass throughs in the next few years needs to be determined. NSS patients represent a group that generates high financial losses under the federal prospective reimbursement system. However, present Medicare reimbursement of other less seriously ill patients with similar DRGs more than compensate these losses if pass throughs are used in determining reimbursements.