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Biomedical subjects

T Gilmer

Publications and source records attributed to T Gilmer.

10 recordsLinked to original sources

Prevalence, expenditures, utilization, and payment for persons with MS in insured populations.

OBJECTIVE: To determine the prevalence, expenditures, and utilization of enrollees with MS relative to all enrollees in privately insured, Medicare, and Medicaid populations. METHODS: The authors used insurer administrative billing data to identify persons with MS, their insured medical expenditures and utilization, and benchmark general insured population expenditures and utilization. Three samples of insurer billing data were analyzed: nationally representative samples for the privately insured (1994 through 1995) and Medicare (1996 though 1997) populations, and Medicaid data for disabled (1991 through 1996) populations from six states. RESULTS: Using 2 years of diagnoses on claims, the prevalence of MS in the privately insured population was 24 per 10,000, 36 per 10,000 in the Medicare population, and 71 per 10,000 in the Medicaid disabled population. Annual insured expenditures were $7,677 per privately insured enrollee with MS vs $2,394 for all privately insured enrollees, $13,048 per Medicare beneficiary with MS compared with $6,006 for all Medicare beneficiaries, and $7,352 per Medicaid disabled recipient with MS vs $4,088 per disabled recipient without MS. Home health expenditures were very high for Medicare beneficiaries with MS and nursing facility expenditures were very high for Medicaid disabled recipients with MS. A small proportion of enrollees with MS accounted for most expenditures. CONCLUSIONS: Insured enrollees with MS are two to three times more expensive than average insured enrollees. If the premiums that employers or governments pay health insurers and the capitation amounts that insurers pay health care providers do not account for these higher costs, a disincentive is created for the enrollment and care of persons with MS.

Adolescent↗

The Medicaid Rx model: pharmacy-based risk adjustment for public programs.

BACKGROUND: Risk adjustment models typically use diagnoses from claims or encounter records to assess illness severity. However, concerns about the availability and reliability of diagnostic data raise the potential for alternative methods of risk adjustment. Here, we explore the use of pharmacy data as an alternative or complement to diagnostic data in risk adjustment. OBJECTIVES: To develop and test a pharmacy-based risk adjustment model for SSI and TANF Medicaid populations. RESEARCH DESIGN: Pharmacological review combined with empirical evaluation. We developed the Medicaid Rx model, a system that classifies a subset of the National Drug Codes into categories that can be used for risk-assessment and risk-adjusted payment. SUBJECTS: Subjects consisted of 362,370 persons with disability and 1.5 million AFDC and TANF beneficiaries in California, Colorado, Georgia, and Tennessee during 1990-1999. MEASURES: We compare pharmacy and diagnostic classification for three chronic diseases. We also compare R2 statistics and use simulated health plans to evaluate the performance of alternative models. RESULTS: Pharmacy and diagnostic classification vary in their ability to identify specific chronic disease. Using simulated plans, diagnostic models are better at predicting expenditures than are pharmacy-based models for disabled Medicaid beneficiaries, although the models perform similarly for TANF Medicaid beneficiaries. Models that combine diagnostic and pharmacy data have superior overall performance. CONCLUSIONS: The performance of risk adjustment models using a combination of pharmacy and diagnostic data are superior to that of models using either data source alone, particularly among TANF beneficiaries. Concerns regarding variations in prescribing patterns and the incentives that may follow from linking payment to pharmacy use warrant further research.

Adult↗

The Ras/p120 GTPase-activating protein (GAP) interaction is regulated by the p120 GAP pleckstrin homology domain.

Pleckstrin homology domains are structurally conserved functional domains that can undergo both protein/protein and protein/lipid interactions. Pleckstrin homology domains can mediate inter- and intra-molecular binding events to regulate enzyme activity. They occur in numerous proteins including many that interact with Ras superfamily members, such as p120 GAP. The pleckstrin homology domain of p120 GAP is located in the NH(2)-terminal, noncatalytic region of p120 GAP. Overexpression of the noncatalytic domains of p120 GAP may modulate Ras signal transduction pathways. Here, we demonstrate that expression of the isolated pleckstrin homology domain of p120 GAP specifically inhibits Ras-mediated signaling and transformation but not normal cellular growth. Furthermore, we show that the pleckstrin homology domain binds the catalytic domain of p120 GAP and interferes with the Ras/GAP interaction. Thus, we suggest that the pleckstrin homology domain of p120 GAP may specifically regulate the interaction of Ras with p120 GAP via competitive intra-molecular binding.

3T3 Cells↗

Impact of ethics consultations in the intensive care setting: a randomized, controlled trial.

OBJECTIVE: To determine the following: a) whether ethics consultations in the intensive care setting reduce nonbeneficial treatments, defined as days in the intensive care unit (ICU) and treatments delivered to those patients who ultimately fail to survive to hospital discharge; and b) whether physicians, nurses, social workers, and patients/families agree that ethics consultations in the ICU are beneficial in addressing treatment conflicts. DESIGN: Prospective, randomized, controlled trial of ethics consultations. SETTING: Medical and pediatric ICUs in a university medical center. PATIENTS: Seventy-four patients in whom value-based treatment conflicts arose during the course of treatment. INTERVENTIONS: The patients were randomly assigned to an intervention (ethics consultation offered) or nonintervention (ethics consultation not offered) arm of the trial. MEASUREMENTS: Medical data and ICU hospital days were compared between the intervention and control groups before and after the randomization. Likert scale and commentary responses were recorded to structured and open-ended interviews with the responsible physicians, nurses, social workers, and families of patients assigned to the intervention arm within 1 month after the patient's death or hospital discharge. Interviewees were asked whether ethics consultations helped with the following: a) to identify ethical issues; b) to analyze ethical issues; c) to resolve ethical issues; d) to educate about ethical issues; and e) to present personal views. MAIN RESULTS: There were no differences in overall mortality between the control patients and patients receiving ethics consultations. However, ethics consultations were associated with reductions in ICU hospital days and life-sustaining treatments in those patients who ultimately failed to survive to discharge. Also, ethics consultations were regarded favorably by most participants. CONCLUSIONS: Ethics consultations seem to be useful in resolving conflicts that may be inappropriately prolonging futile or unwanted treatments and are perceived to be beneficial.

Attitude of Health Personnel↗

Improving health-based payment for Medicaid beneficiaries: CDPS.

This article describes the Chronic Illness and Disability Payment System (CDPS), a diagnostic classification system that Medicaid programs can use to make health-based capitated payments for TANF and disabled Medicaid beneficiaries. The authors describe the diversity of diagnoses and different burdens of illness among disabled and AFDC Medicaid beneficiaries. Claims from seven States are analyzed, and payment weights are provided that States can use when adjusting HMO payments. The authors also compare the taxonomy and statistical performance of CDPS to other leading diagnostic classification systems and find that the new model performs better in a number of respects.

Adult↗

A new ligand for the peroxisome proliferator-activated receptor-gamma (PPAR-gamma), GW7845, inhibits rat mammary carcinogenesis.

We have tested a new ligand for peroxisome proliferator-activated receptor-gamma, GW7845, as an inhibitor of experimental mammary carcinogenesis, using the classic rat model with nitrosomethylurea as carcinogen. Rats were first treated with a single dose of nitrosomethylurea (50 mg/kg body weight, i.p.). Starting 1 week later, they were fed GW7845, at either 60 or 30 mg/kg of diet, for 2 months. This agent significantly reduced tumor incidence, tumor number, and tumor weight at both doses. This is the first report of the use of a ligand for peroxisome proliferator-activated receptor-gamma to prevent experimental breast cancer.

Animals↗

Peptide inhibitors of src SH3-SH2-phosphoprotein interactions.

Activated pp60c-src has been implicated in a number of human malignancies including colon carcinoma and breast adenocarcinoma. Association of the src SH2 domain with tyrosine-phosphorylated proteins plays a role in src-mediated signal transduction. Inhibitors of src SH2 domain-phosphoprotein interactions are, thus, of great interest in defining the role(s) of src in signal transduction pathways. To facilitate such studies, an enzyme-linked immunosorbent assay (ELISA) was developed to detect inhibitors of src SH2-phosphoprotein interactions. This assay measures inhibition of binding of a fusion construct (glutathione S-transferase src SH3-SH2) with autophosphorylated epidermal growth factor receptor tyrosine kinase domain. Activities of phosphopeptide segments derived from potential src SH2 cognate phosphoprotein partners were determined, with the focal adhesion kinase-derived segment VSETDDY*AEIIDE yielding the highest inhibitory activity. Structure activity studies starting from acetyl (Ac)-Y*EEIE have identified Ac-Y*Y*Y*IE as the most active compound screened in the ELISA. This compound is at least 20-fold more active than the parent peptide Ac-Y*EEIE. A high resolution (2 A) crystal structure of human src SH2 complexed with Ac-Y*EEIE was obtained and provided a useful framework for understanding the structure-activity relationships. Additionally, Ac-Y*EEIE was able to block interactions between src and its cellular phosphoprotein partners in vanadate-treated cell lysates from MDA-MB-468 breast carcinoma cells. However, it is unable to abrogate proliferation of MDA-MB-468 cells in culture, presumably because of poor cell penetration and/or lability of the phosphate group on tyrosine.

Amino Acid Sequence↗

Mouse retroviral sequences acquired by cell lines after passaging through nude mice detected by hybridization of the fms probe pSM3.

The expression of a large RNA transcript, 8.5 to 9.5 kilobases, possibly related to the fms oncogene in mouse, rat, and human tumor cells, has been described in the literature. However, the pSM3 fms probe used to detect this gene transcript contains a significant amount of the pol gene of the Susan McDonough strain of feline sarcoma virus from which it was derived. Using a fms probe which does not contain any viral pol sequences, no such "fms-related" transcripts were detected in cell lines previously reported to express the large transcripts. These cell lines did express a large 9.5-kilobase transcript which hybridized to a probe for murine leukemia virus. Partial sequence analysis of the 9.5-kilobase transcript detected with the pSM3 probe in transformed rat cells indicated sequence homology with AKV murine leukemia virus. Thus, the presence of large RNA transcripts, interpreted by us and others as being related to the oncogene fms, appears to be due to the expression of mouse retroviral sequences which hybridize to the viral pol region contained in the pSM3 fms probe. In the case of rat and human cells, such sequences appear to be acquired after the cells have been passaged in nude mice. These results should serve as a reminder of the important biohazard and data interpretation implications for investigations in which cells transfected with retroviral vector constructs are injected into nude mice, because rescue of the recombinant sequences in these cells could occur following infection by endogenous murine retroviral particles.

Animals↗

Explaining the decline in health insurance coverage, 1979-1995.

The decline in health insurance coverage among workers from 1979 to 1995 can be accounted for almost entirely by the fact that per capita health care spending rose much more rapidly than personal income during this time period. We simulate health insurance coverage levels for 1996-2005 under alternative assumptions concerning the rate of growth of spending. We conclude that reduction in spending growth creates measurable increases in health insurance coverage for low-income workers and that the rapid increase in health care spending over the past fifteen years has created a large pool of low-income workers for whom health insurance is unaffordable.

Adult↗