Biomedical subjects

J W Cameron

Publications and source records attributed to J W Cameron.

13 recordsLinked to original sources

PubMed1998

Simulation methodology for estimating financial effects of telemedicine in West Virginia.

Understanding the full financial effects of telemedicine systems on payers, providers, and patients has been hampered by the lack of data from full-fidelity systems operating at a steady state. The vast majority of telemedicine systems in the United States have yet to achieve their full potential in serving their target populations and are operating well below capacity. The purposes of this research are two-fold: (1) to develop a methodology that compensates for the limited availability of empirical data on the financial effects of telemedicine; and (2) to test this methodology in a comprehensive telemedicine system in West Virginia. The proposed methodology utilizes simulation modeling techniques for evaluating the financial performance of a mature telemedicine system. It is particularly suitable for analyzing large, complex systems that have not yet achieved steady-state operation. Although complex, the methodology can be described simply as consisting of two major steps. The first is the identification of all of the relevant variables and parameters for modeling. The second consists of simulating "real world" decision situations involving all relevant variables and parameters. The relation among the variables and parameters are described in terms of mathematical equations. The ability of the researcher to estimate the financial effects of a given telemedicine system is a function of the extent to which the resulting model approximates conditions of the real world; i.e., the fit between model and reality.

Algorithms↗

PubMed1998

A framework for analyzing and improving nurse practitioners' access to research literature.

Advanced practice nurses are charged with basing their practice on research by evaluating and engaging in research studies. Review of research, however, is often hampered by the difficulty in accessing research. The breadth and depth of the literature on innovation and information dissemination demonstrate that nurse practitioners' (NPs) access to and use of the research literature are not trivial matters. This paper suggests some guidelines that may make research more accessible to the NP community. Because the issue is viewed as a problem of access, a seminal work on patients' access to healthcare services is employed to frame the discussion and proposed solutions.

Diffusion of Innovation↗

PubMed1995

Malnutrition in hospitalized children with congenital heart disease.

OBJECTIVE: To determine the prevalence of malnutrition among hospitalized children with congenital heart disease by age, disease process, and clinical status. DESIGN: Cross-sectional, retrospective chart review. SETTING: Pediatric cardiology units at a 150-bed tertiary care teaching hospital in Ann Arbor, Mich. PATIENTS: Patients (n = 160) were randomly selected from consecutive admissions to the Pediatric Cardiology and Thoracic Surgery Services during a 1-year period. INTERVENTION: None. MAIN OUTCOME MEASURES: Acute and chronic malnutrition, assessed by comparing the patients' weight and height with established means. RESULTS: Acute and chronic malnutrition occurred in 33% and 64% of the patients, respectively. Age, diagnostic category, and symptoms were associated with malnutrition. Eighty percent of infants presented with acute malnutrition compared with 18% of patients of other ages (P < .001). Malnutrition affected 60% of patients with left-to-right shunts, 53% of patients with complex heart disease, and no patients with primary rhythm disturbances. Acute malnutrition affected 11% and chronic malnutrition affected 50% of patients with left-sided heart obstruction. Acute or chronic malnutrition occurred in 70% or more of patients with cyanosis and/or congestive heart failure but in only 30% of patients with neither (P < .001). CONCLUSION: Malnutrition in hospitalized children with congenital heart disease remains common, highlighting the importance of nutritional screening and intervention.

Acute Disease↗

PubMed1989

Preferential activation of 6-aminochrysene and 2-aminoanthracene to mutagenic moieties by different forms of cytochrome P450 in hepatic 9000 X g supernatants from the rat.

6-Aminochrysene and 2-aminoanthracene were activated to metabolites which were mutagenic to Salmonella typhimurium TA98 by hepatocytes or hepatic 9000 X g supernatants (S9s) from control or xenobiotic-treated rats. Hepatocytes from Aroclor-1254-treated rats were more efficient than hepatocytes from untreated rats at activating these aromatic amines. When plate-incorporation and liquid-incubation bacterial mutagenesis assays were performed in the presence of limiting amounts of rat hepatic S9, 2-aminoanthracene was activated to a greater extent in both cases, as judged by his+ revertant formation, by 3-methylcholanthrene-induced hepatic S9 than by phenobarbital-induced or control S9s. In contrast, 6-aminochrysene was activated more efficiently by phenobarbital-induced S9 than by 3-methylcholanthrene-induced or control S9s. This unexpected finding was confirmed employing polyclonal antibodies directed against specific forms of rat cytochrome P450. Thus, when employing Aroclor-1254-induced S9 as a source of metabolic activation, antibody directed against cytochrome P450IA1 inhibited the activation of 2-aminoanthracene but not of 6-aminochrysene. In contrast, antibody directed against cytochrome P450IIB1 inhibited the activation of 6-aminochrysene but not of 2-aminoanthracene. These results suggest that under conditions in which the amounts of S9 added are rate-limiting, the two aromatic amines are preferentially activated by different induced forms of cytochrome P-450.

Animals↗

PubMed1986

Analysis of the interlaboratory and intralaboratory reproducibility of the enhancement of simian adenovirus SA7 transformation of Syrian hamster embryo cells by model carcinogenic and noncarcinogenic compounds.

The intralaboratory and interlaboratory reproducibility of a DNA virus (SA7) transformation enhancement assay was investigated using nine carcinogenic and noncarcinogenic compounds representing a variety of chemical classes. By the use of standardized procedures designed to limit assay variables, replicate assay data were collected in two independent laboratories and analyzed for concurrence. The carcinogens, 7,12-dimethylbenz(a)anthracene, benzo(a)pyrene, and N-methyl-N'-nitro-N-nitrosoguanidine yielded reproducible dose-dependent cytotoxicity and positive transformation effects (defined as statistically significant [p less than or equal to 0.05] enhancement of virus transformation at two or more consecutive dose levels) in all experiments in both laboratories. The carcinogens lead chromate, diethylnitrosamine, 4-nitroquinoline-N-oxide, and 2-acetylaminofluorene demonstrated enhancement of SA7 transformation at two or more dose levels in 40-50% of the assays. The noncarcinogenic structural analogs anthracene and pyrene consistently did not produce positive assay responses when tested at dose levels up to the limits of solubility. Good interlaboratory concurrence was demonstrated for these model compounds in the Syrian hamster embryo cell-SA7 assay.

2-Acetylaminofluorene↗

PubMed1986

Chemical enhancement of SA7 virus transformation of hamster embryo cells: evaluation by interlaboratory testing of diverse chemicals.

Twelve chemicals from diverse structural classes were tested under code for their capacity to enhance the transformation of Syrian hamster embryo cells by simian adenovirus SA7 in two independent laboratories. Pretreatment of hamster cells with eight of those chemicals (reserpine, dichlorvos, methapyrilene hydrochloride, benzidine dihydrochloride, diphenylhydantoin, cinnamyl anthranilate, 11-aminoundecanoic acid, and 4,4'-oxydianiline) produced repeatable enhancement of SA7 transformation at two or more consecutive dose levels, which constitutes clear evidence of enhancing activity in this assay. Both toxic and nontoxic doses of each of these chemicals caused enhancement of virus transformation. Two chemicals (2,6-dichloro-p-phenylenediamine and cinnamaldehyde) produced some evidence of enhancing activity (repeatable transformation enhancement at one dose). Dose ranges for cytotoxicity and enhancement of SA7 transformation were similar in both laboratories for all chemicals producing activity. The final two chemicals, chloramphenicol sodium succinate and ethylene thiourea, failed to reproducibly demonstrate either significant cytotoxicity or enhancement of SA7 transformation at concentrations up to 10-20 mM. The test results for these 12 chemicals were combined with the test results for 9 known carcinogens and noncarcinogens in order to evaluate relationships between activity, dose response, and lowest effective enhancing concentration for these compounds, as well as to correlate them with rodent carcinogenesis classifications. The Syrian hamster embryo cell-SA7 system demonstrated reproducible test responses in both intra- and interlaboratory studies and detected 13 out of 15 known rodent carcinogens.

Adenoviridae↗

PubMed1985

Dealkylation of pentoxyresorufin: a rapid and sensitive assay for measuring induction of cytochrome(s) P-450 by phenobarbital and other xenobiotics in the rat.

The O-dealkylation of pentoxyresorufin (7-pentoxyphenoxazone) by rat liver microsomes was examined. The reaction appeared highly specific for certain phenobarbital inducible forms of cytochrome P-450 and was increased 95- to 140-fold by animal pretreatment with phenobarbital (75 mg/kg/day, four ip injections) and approximately 50-fold by Aroclor 1254 (500 mg/kg, one ip injection) while animal pretreatment with 3-methylcholanthrene (50 mg/kg/day, three ip injections) resulted in less than a 2-fold increase over the rate detected in control microsomes. It was observed that this activity, in microsomes for Aroclor-pretreated rats, was dependent on O2 and was inhibited by metyrapone and SKF 525-A, indicative of cytochrome(s) P-450 mediation in the reaction. When antibodies directed against purified cytochrome(s) P-450s were employed to inhibit the pentoxyresorufin O-dealkylation reaction, antibodies to P-450PB-B greatly inhibited the reaction (greater than 90%), while antibodies to P-450PB-C or P-450PB/PCN-E had minimal effects. Assay of hepatic microsomes from rats which were pretreated with varying doses of phenobarbital (0.9-75 mg/kg/day, four ip injections) indicated that while aminopyrine-N-demethylase activity was induced only 2-fold at the maximum dose (75 mg/kg/day), pentoxyresorufin O-dealkylase activity was induced approximately 140-fold at this dose and approximately 4-fold by a dose of phenobarbital as low as 0.9 mg/kg.

Aminopyrine N-Demethylase↗

PubMed1985