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Biomedical subjects

C G Taylor

Publications and source records attributed to C G Taylor.

At least 55 records · Page 3Linked to original sources
PubMed1993

Using claims data for epidemiologic research. The concordance of claims-based criteria with the medical record and patient survey for identifying a hypertensive population.

In this study, a method was developed to identify health plan members with hypertension from insurance claims, using medical records and a patient survey for validation. A sample of 2,079 patients from two study sites with medical service or pharmacy claims indicating a diagnosis of essential hypertension were surveyed, and the medical records of 182 of the 1,275 survey respondents were reviewed. Where the criteria to identify hypertensive patients used both the medical and pharmacy claims, there was 96% agreement with either the medical record or the patient survey. Where the criteria relied on medical claims alone, the agreement rate decreased to 74% with the medical record and 64% with the patient survey. Where the criteria relied on the pharmacy claims alone, the agreement rate was 67% with the medical record and 75% with the patient survey. Combined evidence from medical service and pharmacy claims yielded a high level of agreement with alternative, more costly sources of data in identifying patients with essential hypertension. As it is more thoroughly investigated, claims data should become a more widely accepted resource for epidemiologic research.

Adolescent↗
PubMed1992

Mesangial cell killing by leukocytes: role of leukocyte oxidants and proteolytic enzymes.

Mesangial cells from human and rat kidney were examined for sensitivity to killing by neutrophils. Cells from both species were sensitive to killing by phorbol myristate acetate-stimulated neutrophils. Catalase was highly protective while superoxide dismutase was less protective and a number of protease inhibitors were not protective. Strong protection was also observed with the iron chelators, deferoxamine and phenanthroline, and with the hydroxyl radical scavengers, dimethylthiourea and 5,5-dimethyl-1-pyrroline N-oxide. Pretreatment of the mesangial cells with deferoxamine followed by washing also provided protection. Mesangial cells were also killed by reagent hydrogen peroxide (H2O2) but were much less sensitive to injury by direct application of proteolytic enzymes. The ability of H2O2 to injure mesangial cells was prevented by pre-incubation of the H2O2 with human leukocyte myeloperoxidase. These data suggest that killing is due primarily to the generation of H2O2 by the stimulated neutrophils and its further reduction in an iron-catalyzed reaction. The hydroxyl radical may be the reduction product that actually mediates lethal injury but lack of scavenger specificity prevents definitively concluding this. Mesangial cell killing by activated neutrophils could be significantly inhibited by monoclonal antibodies to CD11/CD18 molecules, suggesting that close contact between the target and effector cells is required for cytotoxicity. Although qualitatively similar to endothelial cells, the mesangial cells appeared to be quantitatively more oxidant sensitive than previously examined human and rat endothelial cells. Taken together, these data show that mesangial cells from rat and human are sensitive to leukocyte-induced injury and that injury results via an oxidant pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Elevation of lung glutathione by oral supplementation of L-2-oxothiazolidine-4-carboxylate protects against oxygen toxicity in protein-energy malnourished rats.

The objectives of this study were to investigate whether oral supplementation of L-2-oxothiazolidine-4-carboxylate (OTC) is effective for increasing tissue glutathione (GSH) concentrations in rats fed a diet very low (0.5%) in protein-a model of wasting malnutrition-and to determine the efficacy of OTC for protection against pulmonary oxygen toxicity. Weanling rats, fed a 0.5 or 15% protein diet for 2 wk, were given an oral supplement of OTC, and tissue GSH concentrations were measured over a 24 h period. OTC supplementation to rats fed 0.5% protein significantly increased GSH concentrations in liver and lung, but not in kidney and blood, when compared with the 0.5% protein unsupplemented group. The liver GSH concentration in the 0.5% protein OTC-supplemented group was higher than the 15% control group. Daily supplementation of OTC protected rats from pulmonary oxygen toxicity during 4 days of 85% oxygen exposure as determined by lung-to-body weight ratios and in vivo proton magnetic resonance imaging. Although hyperoxia exposure increased lung GSH concentrations in all groups, OTC supplementation was effective for increasing lung GSH concentration in rats fed the 0.5% protein diet. This study demonstrated that oral administration of OTC to wasting malnourished rats is an effective procedure to increase GSH concentration rapidly in target organs such as lung, and that daily supplementation of a low dose of OTC has a sustained effect to protect against pulmonary oxygen toxicity during 4 days of hyperoxia exposure.

Administration, Oral↗
PubMed1992

Human umbilical vein endothelial cell killing by activated neutrophils. Loss of sensitivity to injury is accompanied by decreased iron content during in vitro culture and is restored with exogenous iron.

First passage human umbilical vein endothelial cells (HUVECs) were sensitive to killing by activated neutrophils and reagent hydrogen peroxide (H2O2). Catalase and deferoxamine prevented killing whereas soybean trypsin inhibitor and superoxide dismutase did not. In these regards, HUVECs are similar to previously characterized endothelial cells from bovine and rat. Although first passage HUVECs were killed by activated neutrophils, sensitivity fell off rapidly as the cells were maintained in culture. At passage 2 (four population doublings), and beyond, HUVECs were highly resistant. The cells also became resistant to killing by reagent H2O2. The acquisition of resistance to killing was not accompanied by a failure to up-regulate neutrophil adhesion molecules or to support neutrophil adhesion. Levels of intracellular anti-oxidants (total thiols, though not glutathione, glutathione peroxidase or catalase activity) increased as a function of passage in culture. However, levels of glutathione and total thiols in late passage (resistant) HUVECs were similar to levels in late passage rat pulmonary artery endothelial cells, that were sensitive to killing by activated neutrophils. Cell-associated iron in HUVECs fell as a function of time in culture. By passage 2, the amount of total iron measurable with the Ferrozine reagent was only about 30% of the amount recovered from first passage HUVECs. The loss of iron from the cells may underlie much of the concomitant resistance to killing because when the cells were pretreated with iron under conditions in which it could be taken up, sensitivity to killing by activated neutrophils and by H2O2 was restored.

Cells, Cultured↗
PubMed1991

Lymphokine-activated killer cell suppressor factor in malignant effusions.

We examined the possibility that tumor-released products inhibit lymphokine-activated killer cell activation. Lymphokine-activated killer cells from human peripheral blood lymphocytes were activated with recombinant interleukin 2 for 4 days in the presence of malignant effusions or conditioned media from cultured cell lines (10% vol/vol). Eight of 10 malignant effusions/media suppressed the induction of lymphokine-activated killer cell cytotoxicity, as measured in a 4-hour sodium chromate release assay. Seven of 10 effusions/media inhibited lymphokine-activated killer cell proliferation. Suppression was both dose and time dependent. A representative suppressive effusion was fractionated by agarose gel chromatography, treated with detergents disruptive of ionic bonds and lipids, and refractionated using polyacrylamide gel chromatography. Seven suppressive fractions ranging in molecular weight from 1 x 10(5) to 3 x 10(5) d were isolated. It is speculated that this suppressor factor may represent a large multimeric structure with ionic-bonded individual suppressive components.

Cell Division↗
PubMed1991

Diagnosed intellectual and emotional impairment among parents who seriously mistreat their children: prevalence, type, and outcome in a court sample.

A substantial body of research evidence over the past three decades has indicated that intellectual and emotional impairment among parents is a factor contributing to child abuse and neglect. This study examined the court records of 206 seriously abused or neglected children and their families in a large urban area and found that in over half the records a parent had been diagnosed as having an emotional disorder and/or low IQ, with a majority of these diagnoses indicating significant impairment. Although type of impairment (emotional, low IQ, and a subsample of substance abusers) did not predict type of mistreatment, higher predicted risk for continued mistreatment, or greater likelihood of permanent removal of the child by the court, low IQ parents revealed significantly less prior court involvement and greater acceptance of court-ordered services. Parents diagnosed with serious emotional disorders were significantly more likely than less disturbed parents to have their children permanently removed despite findings of no significant differences in risk or compliance factors.

Affective Symptoms↗
PubMed1991

Effect of hyperoxia on oxygen free radical defense enzymes in the lung of zinc-deficient rats.

The effects of hyperoxia and the response of oxygen free radical defense enzymes in the lung and extracellular environment of the lung were measured in Zn-deficient rats. Although lung was the target organ as indicated by the increased lung:body weight ratio in all hyperoxia-exposed rats regardless of dietary regimen, 85% oxygen exposure seemed to impose a stress on the whole animal as indicated by decreased feed intake and body weight in ad libitum-fed rats. Hyperoxia exposure superimposed on Zn deficiency did not further reduce the feed intake or body weight of Zn-deficient rats. After 7 d of hyperoxia exposure, the Zn-repleted and ad libitum-fed groups consistently had increased activity of lung CuZn-superoxide dismutase (CuZnSOD), glutathione peroxidase and catalase; but changes in CuZnSOD activity were not related to lung Cu or Zn concentrations. Although Zn-deficient and pair-fed rats were unable to increase CuZnSOD activity, they had an increased lung Zn concentration compared with their air-exposed counterparts. Hyperoxia exposure also caused an increase in ceruloplasmin activity of pair-fed and ad libitum-fed control rats. We concluded that dietary Zn repletion started at the beginning of 85% oxygen exposure was effective for increasing the activity of the lung oxygen free radical defense enzymes, thus preventing hyperoxia-induced lung damage in Zn-deficient rats.

Animals↗
PubMed1991

Increased lung copper-zinc-superoxide dismutase activity and absence of magnetic resonance imaging-detectable lung damage in copper-deficient rats exposed to hyperoxia.

The effects of hyperoxia on physiological responses, pathological lung lesions detected noninvasively by proton magnetic resonance imaging (MRI), and the oxygen free radical defense enzymes were measured in Cu-deficient rats. Exposure to 85% oxygen seemed to impose a stress on the whole animal as indicated by two physiological responses, decreased food intake and decreased body weight of ad libitum-fed rats. However, all rats exposed to 85% oxygen, including the Cu-deficient group, were able to survive 1 wk of hyperoxia exposure. The target organ specificity for hyperoxia exposure was in the lung as indicated by the increased lung:body weight ratio in all hyperoxia-exposed rats regardless of dietary treatment. All dietary treatment groups exposed to hyperoxia had a similar increase in lung:body weight ratio, but none of the hyperoxia-exposed rats had MRI-detectable lung damage. After 7 d of hyperoxia exposure, all dietary treatment groups, including the Cu-deficient rats, had increased activity of lung CuZn-superoxide dismutase (CuZnSOD), but changes in CuZnSOD activity were not related to lung Cu or Zn concentrations. We propose that the ability to increase CuZnSOD activity is the most important factor of the enzymatic oxygen free radical defense system for protection against hyperoxia-induced lung damage detected by MRI. Even though lung Cu concentration was decreased in Cu deficiency, it seems that Cu-deficient rats are still able to increase lung CuZnSOD activity in response to 85% oxygen exposure.

Animals↗
PubMed1991

Characterization of cis-acting sequences regulating root-specific gene expression in tobacco.

The expression of the tobacco root-specific gene TobRB7 was characterized. Gel blot hybridizations to RNA isolated from various tobacco tissues demonstrated that steady-state TobRB7 mRNA is not detected in expanded leaf, stem, or shoot apex tissue. To determine the spatial pattern of expression, in situ hybridization to root sections revealed that TobRB7 expression is localized to root meristem and immature central cylinder regions. The 5' flanking region of the gene was studied with respect to its ability to direct root-specific expression. Deletions of 5' flanking sequence were fused to the beta-glucuronidase (GUS) reporter gene and transformed into tobacco. Our data demonstrated that sequences 636 base pairs from the site of transcription initiation are sufficient to direct the root-specific GUS expression in transgenic tobacco, whereas sequences 299 base pairs from the site of transcription initiation fail to direct root-specific expression. A negative regulatory element was apparent between 813 base pairs and 636 base pairs 5' of the transcription initiation site. Histochemical localization of GUS activity in transgenic plants was consistent with in situ hybridization results: GUS activity was localized to the root meristem and central cylinder regions. GUS activity appeared 2 days post-germination in the primary root meristem. In lateral roots, GUS activity was detected from the time of initiation.

Amino Acid Sequence↗
PubMed1990

Regeneration of immunosorbent surfaces used in clinical, industrial and environmental biosensors. Role of covalent and non-covalent interactions.

The durability and regeneration of antibodies immobilized to commercial immunosorbents were investigated by monitoring Ag-Ab dissociation. Solutions consisting of 0.01 M hydrochloric acid (HCl), 10% propionic acid, 50% ethylene glycol and 10% SDS in 6 M urea were used in the evaluation of antigen dissociation from antibody covalently immobilized to glass and polystyrene beads, microtiter plates and Immobilon filters. RAH-IgG, used as a model antibody, bound strongly to all covalent surfaces. However, on adsorption to Nunc-1 microtiter plates, 25-60% of RAH-IgG was removed by all dissociating solutions. Covalent binding to Sanger beads was weakest relative to other covalent surfaces, exhibiting 30% and 65% detachment with ethylene glycol and SDS in urea, respectively. Although all four solutions dissociated antigen from surface-bound antibody, HCl and propionic acid were more effective on most surfaces. The antibody remained functional following antigen dissociation and reassociated to nearly 100% on all surfaces except Sanger beads and Nunc-1 microtiter plates. This study was initiated to evaluate regeneration and reuse of microelisa plates and emerging biosensors as a means of reducing routine laboratory analysis costs. Data are presented to demonstrate the reusability of microtiter plates in ELISAs following antigen dissociation from covalently bound antibody.

Antigen-Antibody Complex↗
PubMed1990

A feasibility study of the MTT assay for chemosensitivity testing in ovarian malignancy.

We assess the feasibility of using the MTT assay as a measure of cell viability in chemosensitivity testing in ovarian malignancy. The assay utilises the conversion of the tetrazolium salt MTT to formazan by dehydrogenase enzymes in living cells. We show that the optical density of the formazan produced from MTT is directly proportional to the number of live cells tested. Optimum MTT conversion occurred after 4 h incubation and dimethyl sulphoxide was found to be the most suitable solvent for the formazan. Seventy-five samples of ascitic fluid and/or solid tumour were collected from 56 patients with FIGO stage III-IV ovarian adenocarcinoma. Malignant cell suspensions with a viability greater than 75% were prepared from 95% of ascitic fluid and 75% of biopsy samples by simple techniques. The effect of cytotoxic drugs was assessed in 91% of patients included in the study. Variation in drug effect between patients was evident following a 48 h incubation period and was reproducible. Overall platinum and anthraquinone analogues produced the greater effect but resistance did occur. Our results mirrored reported clinical response rates. Only one sample tested against chlorambucil showed any drug effect. As this assay produces results in a high percentage of tests and is rapid and simple it appears suitable for prospective clinical trials to correlate the in vitro results with in vivo response.

Adenocarcinoma↗
PubMed1990

Alterations of cellular characteristics of a human ovarian teratocarcinoma cell line after in vitro treatment with retinoids.

Differentiation of the human teratocarcinoma derived cell line. PA-1, with retinoids was examined at concentrations (10(-6)-10(-8) M) that did not exhibit an antiproliferative effect during log-phase growth. Treatment with naturally occurring retinoic acid or certain synthetic retinoids (13-cis retinoic acid, Ro10-9359, and Ro13-7410), while not significantly altering the log-phase growth rate, decreased the saturation cell density and mitotic indices after confluence. Retinoid treatment also induced changes in cell morphology, which appear to be related to reorganization of microtubules and microfilaments. Following retinoid treatment, the expression of cell glycoproteins (of 162 kDa, 152 kDa, 143 kDa. and 51 kDa) was altered. Treated cells also exhibited decreased expression of alkaline phosphatase, as well as an increased capacity for intercellular communication as evidenced by gap-junctional transfer of the phosphorylated toxic intermediate of 6-thioguanine to HPRT- cells. Treatment with retinoic acid dramatically reduced the quantity of shed plasma membrane material and altered its composition.

Alkaline Phosphatase↗
PubMed1990

Preliminary clinical study of transferrin-adriamycin conjugate for drug delivery to acute leukemia patients.

Seven patients with acute leukemia were treated intravenously with low doses of transferrin-Adriamycin conjugate. The total amount of drug given each patient was far below known toxicity levels for free Adriamycin. The number of tumor cells in peripheral blood diminished in treated patients, and bone marrow aspirates showed no evidence of disease progression. Two patients gave a febrile response and no hypersensitivity reactions were observed. Results of parallel basic research have shown that transferrin receptors on acute leukemia cells bind transferrin-Adriamycin conjugates, and kill by mechanisms at either the plasma membrane or nuclear levels, or both. Such conjugates may provide an alternative to monoclonal antibody drug targeting.

Acute Disease↗
PubMed1989

Appraisal of the MTT assay as a rapid test of chemosensitivity in acute myeloid leukaemia.

We describe the application of a simple, rapid, semi-automated assay to the sensitivity testing of cytotoxic drugs in 23 patients with acute myeloid leukaemia (AML). The survival of blast cells from the bone marrow was measured by the MTT assay after 48 h continuous exposure to drugs both singly and in combination. There was a linear relationship between the number of leukaemic cells and the optical density of the formazan produced. The assay demonstrated a variation in drug sensitivity between patients. The technique was reproducible and there was no significant difference in response between blast cells obtained from bone marrow or from peripheral blood. Preliminary results show a correlation between in vitro and in vivo data. The test can be repeated throughout the course of the disease to help identify any change in tumour sensitivity. This technique appears to give useful information to assist in the management of acute myeloid leukaemia.

Colorimetry↗
PubMed1988

Characterization of plasma membrane shedding from murine melanoma cells.

Tumor cells release intact portions of their plasma membranes in the process of membrane fragment shedding. This released material has been shown to inhibit various synthetic functions of normal cells, which may play an important role in certain patho-physiological events occurring in advanced-stage cancer patients. Our studies on metastatic variants of the murine B16 melanoma, B16-F1 (low incidence of lung colonization) and B16-F10 (high incidence of lung colonization) indicate that the shed membrane fragment material is composed predominantly of vesicles, ranging in size from 20 to 100 nm in diameter. The release of membrane fragments represents a small percentage (approximately 16%) of the total shedding of plasma membrane components. Membrane fragments were shed at a higher rate from the highly "metastatic" (colonizing) B16-F10 cells than from poorly metastatic B16-F1 cells, resulting in a 2-fold greater accumulation of membrane fragment material by cultures of B16-F10 cells than by B16-F1 cultures during the 48-hr assay period. The study of various intracellu ar metabolic processes (protein and RNA synthesis, glycosylation, and generation of ATP) required for the shedding of membrane fragments indicated that the shedding event is only dependent on energy when inhibitors of the above processes are present for 2 hr. Treatment of cells with these inhibitors for 8 hr results in cessation of the shedding process, indicating both a limited pool of components to be shed and the requirement for further synthesis of the shed material. Glycoprotein components of the shed membrane fragments were analyzed by SDS-polyacrylamide gel electrophoresis. In addition to quantitative differences, 2 additional bands were present in fluorographs from SDS-PAGE gels from the B16-F10 membrane fragment material which were not present in fluorographs from B16-F1 fragments. The glycoprotein components of shed membrane fragments were shown to represent selected domains of the cell's plasma membranes, in that only certain plasma membrane glycoproteins are shed as part of membrane fragments. The glycoproteins released as non-particulate molecules into the extracellular environment failed to exhibit these quantitative and qualitative differences.

Adenosine Triphosphate↗
PubMed1988

Effect of dietary zinc or copper deficiency on the primary free radical defense system in rats.

The effect of dietary Zn or Cu deficiency on the primary free radical defense system was examined in the lungs and livers of 6-wk-old rats. Enzymatic components (superoxide dismutase, catalase and glutathione peroxidase) and nonenzymatic components (alpha-tocopherol, ascorbate, glutathione and metallothionein) of the primary free radical defense system, as well as tissue concentrations of Cu, Zn and Fe, were measured. Liver CuZn-superoxide dismutase and liver catalase activities were significantly lower (P less than 0.05), and lung metallothionein and liver ascorbate concentrations were significantly higher (P less than 0.05) in Cu-deficient rats than in either pair-fed or ad libitum-fed controls. Zn-deficient rats had a significantly lower (P less than 0.05) concentration of liver metallothionein than either control group. Other changes in the enzymatic and nonenzymatic components of the primary free radical defense system could be attributed to the reduction in feed intake by Zn- or Cu-deficient rats and not to a direct effect of the Zn or Cu deficiency per se. The primary free radical defense system in lung and liver of severely Zn- or Cu-deficient rats was not seriously compromised.

Animals↗