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Biomedical subjects

P D Baker

Publications and source records attributed to P D Baker.

10 recordsLinked to original sources
PubMed1997

Theoretical analysis of non-invasive oscillometric maximum amplitude algorithm for estimating mean blood pressure.

A theoretical analysis is performed to evaluate the effect of arterial mechanical and blood pressure pulse properties on the accuracy of non-invasive oscillometric maximum amplitude algorithm (MAA) estimates of the mean blood pressure obtained using air-filled occlusive cuffs. Invasively recorded blood pressure pulses, selected for their varied shapes, are scaled to simulate a wide range of blood pulse pressures (diastolic blood pressure minus systolic blood pressure). Each scaled blood pressure pulse is transformed through an exponential model of an artery to create a series of blood volume pulses from which a simulated oscillometric waveform is created and the corresponding MAA estimate of the mean blood pressure and error (mean blood pressure minus MAA estimate) are determined. The MAA estimates are found to depend on the arterial blood pressure. The errors are found to depend on the arterial mechanical properties, blood pressure pulse shape and blood pulse pressure. These results suggest that there is no direct relationship between the mean blood pressure and MAA estimate, and that multiple variables may affect the accuracy of MAA estimates of the mean blood pressure obtained using air-filled occlusive cuffs.

Algorithms↗
PubMed1997

Antibiotic therapy for diabetic foot infections: comparison of two parenteral-to-oral regimens.

This prospective, randomized, multicenter trial compared the efficacy of two antibiotic regimens for treatment of foot infections in diabetic adults. Patients with infections requiring hospitalization were randomized to receive either intravenous ofloxacin followed by oral ofloxacin or intravenous ampicillin/sulbactam followed by oral amoxicillin/clavulanate (the aminopenicillin regimen) for 14-28 days. Patients with osteomyelitis were eligible for the study if the infected bone was to be removed. Of 108 patients enrolled in the study, 88 who were evaluable had various skin and soft-tissue infections, and 24% had osteomyelitis. For the ofloxacin and aminopenicillin regimens, the mean duration of intravenous therapy was 7.8 and 7.1 days, respectively, the mean duration of oral therapy was 13.2 and 12.0 days, respectively, the rate of eradication of pathogens was 78% and 88%, respectively, and the overall rate of clinical cure or improvement was 85% and 83%, respectively. Thus, about 3 weeks of therapy with either regimen was well tolerated and effective in treating these diabetic foot infections.

Administration, Oral↗
PubMed1996

Upper limb disorders.

Disorders of the upper limb cause significant morbidity and incur substantial costs. These conditions are amongst the most common reasons for attendance to occupational physicians, and they are also commonly encountered in the practice of a wide array of medical specialities (rheumatology, orthopaedic surgery, rehabilitation and neurology). Despite this collective experience, standardized methods for labelling these conditions and algorithms for their clinical evaluation and treatment are only beginning to be developed. The purpose of this review is to outline a classification system for upper limb disorders, to address the features of the clinical history and examination which are of most benefit in reaching a diagnosis, and to briefly outline approaches to investigation and treatment.

Arm↗
PubMed1992

Decreased P-glycoprotein expression in multidrug-sensitive and -resistant human myeloma cells induced by the cytokine leukoregulin.

Modulation of the expression of P-glycoprotein, a plasma membrane protein associated with multidrug resistance, was examined in drug-sensitive and drug-resistant tumor cells treated with leukoregulin, a M(r) 50,000 cytokine from human lymphocytes that rapidly permeabilizes the plasma membrane of many tumor cells facilitating the uptake of doxorubicin and other tumor-inhibitory antibiotics. P-glycoprotein expression was measured flow cytometrically by the binding of C219 or MRK16 monoclonal antibody to multidrug-sensitive human K562 erythroleukemia and 8226/S myeloma cells, compared to multidrug-resistant 8226/DOX40 myeloma cells. Cells were treated for up to 2 h with up to 80 units of leukoregulin/ml or one of a variety of unrelated cytokines including interleukin 1 alpha (IL-1 alpha), IL-1 beta, IL-2, IL-3, IL-4, IL-5, IL-6, colony-stimulating factor, macrophage colony-stimulating factor, granulocyte macrophage colony-stimulating factor, tumor necrosis factor alpha, gamma-interferon, alpha-interferon, epidermal growth factor, platelet-derived growth factor AA, platelet-derived growth factor BB, insulin-like growth factor I, insulin-like growth factor II, fibroblast growth factor, or transforming growth factor beta. Leukoregulin caused a concentration-dependent decrease in P-glycoprotein expression; however, P-glycoprotein expression was unaffected by the other cytokines (< 12% decrease in expression). Leukoregulin-induced membrane permeabilization, determined flow cytometrically by intracellular fluorescein efflux, and decreased P-glycoprotein expression occurred simultaneously within 15 min in drug-sensitive and -resistant cells. Enhanced doxorubicin uptake, measured flow cytometrically by doxorubicin influx, was also present within 15 min. Leukoregulin enhancement of doxorubicin uptake and increased membrane permeability varied directly with the decrease in P-glycoprotein expression. Leukoregulin in combination with doxorubicin enhanced the inhibition of cell proliferation in 8226/DOX40 multidrug-resistant cells over expressing P-glycoprotein. In contrast, combined treatment of HL-60/MX2 multidrug-resistant human promyelocytic leukemia cells that do not overexpress P-glycoprotein in association with their multidrug resistance resulted in no greater growth inhibition than observed with HL-60/MX2 cells treated with doxorubicin alone. This is the first demonstration that a naturally occurring macromolecule with anticancer activities can modulate the expression of P-glycoprotein concomitant with enhanced drug uptake and inhibition of cell proliferation.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1988

Tumor-inhibitory antibiotic uptake facilitated by leukoregulin: a new approach to drug delivery.

The uptake of tumor-inhibitory antibiotics by human K562 erythroleukemia cells was examined in the presence of leukoregulin to determine if the lymphokine's ability to increase the plasma membrane permeability of tumor cells facilitates concurrent entry of pharmacologically active molecules. K562 cells were exposed to 0.25-2.0 micrograms of doxorubicin/mL for up to 60 minutes at 37 degrees C. Commencing within 15 minutes, leukoregulin increased the entry of doxorubicin approximately twofold and the uptake of mitomycin, mithramycin, and propidium iodide twofold to tenfold. This finding indicates the potential biotherapeutic value of leukoregulin in promoting the selective entry of pharmacologically active molecules into leukoregulin-sensitive target cells.

Antibiotics, Antineoplastic↗
PubMedDate not supplied

Influence of endogenous Thy1.1 cells upon the efficacy of an anti-Thy1.1 antibody-diphtheria toxin conjugate.

The chemical conjugation of antibodies to protein toxins results in cell-specific cytotoxic agents that can be defined in terms of in vitro potency and efficacy; however, it is the in vivo utilities that are largely being pursued in clinical trials. The nature of in vivo target cell depletion by toxin conjugates is largely unknown. The anti-murine Thy1.1 antibody-diphtheria toxin conjugate possesses high in vitro efficacy, and because mice are remarkably resistant to the native toxin, the conjugate possesses in vivo efficacy. When administered intravenously, the conjugate is shown to deplete peripheral blood Thy1.1+ target cells in a concentration-dependent fashion. When the log kill of Thy1.1+ tumor cells was analyzed by the life span extension method, it was determined, however, that the log kill is inversely proportional to the number of target cells. That is, the presence of an endogenous cell population, which is expressing the same surface antigen targeted by the antibody conjugate as on the pathological cell, may drastically lower the clinical efficacy of the immunotoxin. Thus, the greatest potential for antibody-toxin conjugates will be for low target cell burdens and for pathogenic cell populations expressing unique surface antigens. These are important considerations in the design of bioconjugates to insure high in vivo efficacy in elimination of intended target cells.

Animals↗