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Biomedical subjects

F J Conway

Publications and source records attributed to F J Conway.

13 recordsLinked to original sources

Integer-driven relational database for clinical outcomes research.

A working database program specifically designed to organize and analyze data for the purpose of generating clinical outcomes reports is presented. Following the author's hypothesis, the database accepts only integer input but can generate reports in textual format. The pilot model database presented here uses only five clinic data items, three outcomes items, and can generate 90 different outcomes reports in the form of charts, graphs, or grids. The program consists of a graphical user interface front end that drives a relational database.

Database Management Systems↗

Diagnosis of a computer-simulated podiatric patient.

The authors discuss the use of computers in medicine. A patient presenting with a condition requiring surgery is represented by a data file in a computer program. The user obtains data from the file by selecting items from a menu. Data are presented on the screen in pop-up windows. By examining the data and making judgments, the user may determine the pathology and make first a provisional and then a definitive diagnosis.

Computer Simulation↗

A proposed model of cancer as the inappropriate expression of non-body introns.

An a posteriori proposal is made that cancer represents an alien non-body phenotype erupting from "silent" gene groups within actively coding regions of a normal cell's genome. Relevant empirical data is garnered from the literature and twelve premises are derived from the data. On the basis of these premises it is hypothesized that the malignant neoplastic phenotype results from interference with non-histone chromosomal proteins causing retention and expression in a body cell of non-body introns. These are asserted to be the same introns which, as exons in a trophoblast cell, direct the normal development of the fetal placenta. Development of a malignant tumor is presented as a pathological recapitulation of the development of a normal placenta. Unrestrained tumor growth is attributed to the inability of endogenous body chalones to suppress the non-body gene groups coding for neoplastic mitosis, while invasion and metastasis result from failure of the non-body genes which code for implantation and mitosis to switch off at the proper time. The hypothesis asserts that all carcinogenic agents alter phosphorylation of non-histone chromosomal proteins, that cancer and normal trophoblast cells are genetically programmed to travel through the body's vascular system to effect immunosuppression in lymphoid tissues, that malignant neoplastic tissue will regress when exposed to trophoblast-based chalones, and that mammals immunized against trophoblast-based antigen will be resistant to the development of malignant tumors.

Animals↗

Human pharmacokinetic and pharmacodynamic studies on the atenolo (ICI 66,082), a new cardioselective beta-adrenoceptor blocking drug.

The beta-adrenoceptor blocking effects of orally administered atenolol on tachycardia induced by intravenous isoprenaline or by exercise have been studied in normal volunteers, and compared with the effects of similar doses of propranolol. The blood levels of atenolol at various times after oral administration were determined by g.l.c. and correlated with the degree of inhibition of tachycardia. Atenolol was shown to be a beta-adrenoceptor blocker in man, as in animals, in that it antagonized the chronotropic effects of isoprenaline and of exercise. The inhibitory effect of atenolol on exercise-induced tachycardia was evident at a concentration in blood of 0.2 mug/ml and virtually complete at 0.5 mug/ml. Higher concentrations than this did not produce significantly greater blockade. The effects of atenolol on exercise-induced tachycardia were similar to those of propranolol but it was less effective in blocking the rise in heart rate and fall in diastolic blood-pressure induced by intravenous infusion of isoprenaline. This separation of effects is considered characteristic of drugs causing preferential blockade of cardiac beta-adrenoreceptors. The half-life of atenolol in blood was calculated to ablut 9 hours.

Adult↗