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Biomedical subjects

M Rogers

Publications and source records attributed to M Rogers.

At least 181 records · Page 10Linked to original sources
PubMed1991

Treatment of macrophages with oxidized low-density lipoprotein increases their intracellular glutathione content.

Macrophages derived from the human monocyte cell line THP-1 or isolated from the peritoneum of C3H/HEJ mice were incubated with oxidized low-density lipoprotein (LDL) and the total glutathione content (oxidized plus reduced) was measured. An initial depletion of glutathione was followed by an increase, such that after a period of 24 h the glutathione content has approximately doubled. This response required the oxidation of the lipid phase of the LDL molecule, since both native LDL and acetylated LDL had little effect on glutathione levels. The response of the cells to oxidized LDL was dependent on the extent of oxidative modification of the protein. It was also found that 4-hydroxynonenal had a similar effect on THP-1 cells, and we suggest that this or other aldehydes present in oxidized LDL causes the induction of glutathione synthesis in response to an initial oxidative stress and consequent glutathione depletion. In addition, we found that both cell types possess transferases and peroxidases capable of detoxifying aldehydes and peroxides. However, treatment of cells with oxidized LDL or 4-hydroxynonenal for a period of 24 h had no effect on the activities of these enzymes.

Aldehydes↗
PubMed1991

Essential fatty acid deficiency impairs macrophage spreading and adherence. Role of arachidonate in cell adhesion.

Dietary polyunsaturated fatty acid manipulation exerts a strikingly protective effect in models of tissue inflammation and injury. A critical element of this effect appears to revolve around leukocyte trafficking but underlying mechanisms are ill understood. In the current study it was observed that essential fatty acid (EFA) deficiency markedly impaired the capacity of resident macrophages to spread and adhere. This effect was not a simple function of the alteration of membrane fatty acid composition. Elicited EFA-deficient macrophages were equally adherent to elicited control cells, despite the fact that they were equally EFA-deficient relative to resident EFA-deficient cells. With respect to the mechanism underlying defective macrophage adherence in EFA deficiency, no change in the expression of cell surface adherence molecules (Fc receptor, Mac-1, or LFA-1) was noted with the deficiency state. Also, an adherence defect could not be induced in normal cells pharmacologically with cyclooxygenase blockade, lipoxygenase blockade, or a platelet-activating factor receptor antagonist. In contrast, phospholipase inhibition was able to induce a spreading and adherence defect in resident macrophages similar to that seen with EFA deficiency. Using several phospholipase inhibitors, a correlation between phospholipase inhibition and impairment of adherence was observed. Adding back exogenous fatty acids to cells after phospholipase inhibition demonstrated that normal adherence was reconstituted with arachidonate. This alteration in macrophage spreading and adherence with EFA deficiency may be an important component of the anti-inflammatory effect of dietary polyunsaturated fatty acid manipulation. Additionally, these results suggest that arachidonate may be an intracellular mediator of leukocyte adherence.

Animals↗
PubMed1991

Prenatal records: a national survey of content.

The uses of prenatal records extend well beyond management of patient care. They are also vehicles for communication, quality assurance, financial compensation, and legal documentation. To serve each of these functions, records should be systematic and detailed. This nationwide study was conducted to assess the extent to which prenatal records in current use include sufficient detail to serve these functions. A random sample of 2746 physicians who listed obstetrics and gynecology, obstetrics, or maternal-fetal medicine as a primary or secondary specialty in the American Medical Association file were contacted by mail and were requested to submit a blank copy of their prenatal records. The records of 969 respondents were examined for the presence or absence of 53 items that corresponded to the five functions identified above. The items of interest were present in 1% to 98% of the records. More than 90% included items of traditional medical-obstetric significance. The percentages of records with items of more contemporary relevance (e.g., cigarette smoking, risk-assessment checklists, psychological stress) were found in lower percentages of the records. Stratified and logistic regression analyses revealed that the most systematic and detailed records were commercially available, were used by physicians in hospital and government program-based practices, and were used by physicians who had completed medical school less than or equal to 15 years before the survey. The findings suggest that physicians who do not use commercially available forms or those who are in private or health maintenance organization practice or have been practicing for more than 15 years should reconsider their prenatal records in light of the functions they will serve in the 1990s and beyond.

Communication↗
PubMed1991

Acoustic reflectometry for airway measurement. Principles, limitations and previous work.

Acoustic pulse reflectometry is a relatively recent technique which allows the non-invasive measurement of human airways. The technique consists of guiding an acoustic impulse through the subject's mouth and into the airway. Suitable analysis of the resulting reflection (the 'echo') allows a reconstruction of the area-distance function. The non-invasive nature of the technique offers significant advantages over the established methods of x-ray cephalometry and CT scanning, and makes it very attractive for the investigation of ENT problems and sleep apnoea, and in the anaesthetic management of patients. This paper describes the theory and limitations of acoustic reflectometry, discusses previous work, and suggests some modifications: it is currently being implemented clinically.

Acoustics↗
PubMed1991

Lack of correlation between maternal antibodies to V3 loop peptides of gp120 and perinatal HIV-1 transmission. The NYC Perinatal HIV Transmission Collaborative Study.

Recent reports have suggested that maternal antibodies to specific epitopes of the variable region 3 (V3 loop) of gp120 of HIV-1 might protect against perinatal transmission. In an attempt to confirm these findings, sera from 34 HIV-1-seropositive mothers, representing 13 episodes of mother-to-infant transmission and 23 episodes of non-transmission (two mothers had two pregnancies each during the study period), were tested for the presence of antibodies to various regions of the gp120 V3 loop. Synthetic peptides were generated from HIV-1MN. Of the four peptides tested by enzyme-linked immunosorbent assay (ELISA), only antibody to the C53 peptide (Env310-322, principal neutralizing determinant) was present in maternal sera. Antibody to the C53 sequence was present in 11 specimens from transmitting mothers and 21 from non-transmitting mothers (84.6 and 91.3%, respectively, P = 0.6). No reactivity was detected against the C51, C57, or C58 peptide sequences, located on the sides of the V3 loop. In an antigen-limited ELISA, only two specimens from transmitting mothers and two specimens from non-transmitting mothers had detectable 'high-affinity' antibodies to C53 at low antigen concentrations (15.4 and 8.7%, respectively; P = 0.6). Our results do not support previous reports that epitope-specific antibodies to the V3 loop peptides protect against perinatal transmission. Further research is required to determine whether any specific maternal humoral response might influence HIV-1 perinatal transmission.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Naproxen induced pseudoporphyria in juvenile chronic arthritis.

We report 6 cases of porphyria-like skin reactions in children taking naproxen for juvenile chronic arthritis. The lesions mimicked either erythropoietic protoporphyria or porphyria cutanea tarda, with both forms occurring in 2 patients. Biochemical studies excluded abnormal porphyrin metabolism.

Adolescent↗
PubMed1991

The use of the Roy Adaptation Model in nursing administration.

In recent years, considerable attention has been paid to the use of a nursing conceptual model for nursing practice. Although many of the theorists and early writers on the subject suggested that a nursing conceptual model could be used to guide nursing administration, there has been little attention given to this in the literature. This article describes the process that one hospital engaged in as they implemented the Roy Adaptation Model for nursing administration. The article discusses the use of the Roy Model in creating a nursing philosophy, mission statements, standards of practice, job descriptions, performance planning and appraisal system and a quality monitoring system. The authors conclude that the use of the Roy Model has contributed to the development of a highly integrated system of nursing administration and practice.

Adaptation, Psychological↗
PubMed1990

Manipulation of the acute inflammatory response by dietary polyunsaturated fatty acid modulation.

Dietary polyunsaturated fatty acid modulation has been used as an anti-inflammatory strategy in experimental models of disease as well as in clinical trials. To elucidate the mechanisms underlying the anti-inflammatory effects of manipulating dietary polyunsaturated fatty acids, the in vivo effects of essential fatty acid (EFA) deficiency and (n-3) fatty acid supplementation were contrasted using a model of acute inflammation induced by the i.p. injection of zymosan into mice. Both diets led to a substantial decrease in tissue (n-6) fatty acid content. EFA deficiency was also characterized by the accumulation of (n-9) fatty acids, particularly 20:3 (n-9), the fatty acid that uniquely characterizes the deficiency state. Dietary (n-3) fatty acid supplementation led instead to marked increases in (n-3) fatty acids, especially 20:5 (n-3). With respect to the antiinflammatory effects of the two diets, EFA deficiency, but not (n-3) fatty acid supplementation, depleted levels of resident peritoneal macrophages. EFA deficiency was also more effective than (n-3) fatty acid supplementation in inhibiting the influx of polymorphonuclear neutrophils in response to zymosan. The effect of the two diets on the in vivo generation of leukotriene(LT)B also differed markedly. EFA deficiency completely inhibited the synthesis of LTB. Dietary (n-3) fatty acid supplementation, in contrast, reduced the production of LTB4 by only 50%. With (n-3) fatty acid supplementation LTB5 was produced. The more modest effect of (n-3) fatty acid supplementation in decreasing LTB4 generation was not due to blockade of the cyclooxygenase pathway. EFA deficiency, but not (n-3) fatty acid supplementation, was associated with the decreased synthesis of thromboxane. Although dietary fatty acid modulation has been shown to diminish platelet activating factor (PAF) synthesis, studies using the PAF receptor blocker, L659989, established that PAF was not a significant factor in the elicitation of leukocytes in this model of inflammation. In summary, the anti-inflammatory effect of EFA deficiency was more marked that that of dietary (n-3) fatty acid supplementation in acute inflammation. This difference in anti-inflammatory potential appeared to be due to either the greater effect of EFA deficiency in decreasing levels of resident peritoneal macrophages or in suppressing the in vivo generation of LTB4.

Acute Disease↗
PubMed1990

Involvement of dihydropyridine-sensitive calcium channels in nerve growth factor-dependent neurite outgrowth by sympathetic neurons.

We have used a number of pharmacological manipulations of calcium influx to alter the nerve growth factor (NGF)-elicited neurite outgrowth response of SCG neurons. Our results indicate that influx of extracellular calcium is critical to sympathetic SCG neurite outgrowth. Effective blockade of this process was produced by the inorganic calcium channel blockers Cd2+ (with an IC50 of 48 microM), Co2+ (129 microM), and Ni2+ (180 microM). More specifically, there is a significant contribution from dihydropyridine-sensitive L-type calcium channels to NGF-activated neurite outgrowth, as evidenced by the significant inhibition of neurite outgrowth by diltiazem (IC50 of 17 microM) and nifedipine (3 microM). Further, increases in calcium influx can elicit an enhanced neurite outgrowth response, as shown by the calcium channel agonist Bay K 8644 which potentiated neurite outgrowth by up to 40%.

Animals↗
PubMed1990

Retinoid-enhanced gap junctional communication is achieved by increased levels of connexin 43 mRNA and protein.

Natural and synthetic retinoids are potent inhibitors of experimental carcinogenesis in animals and cause reversion of premalignant lesions in humans. In the model C3H 10T1/2 cell system, retinoids enhance postconfluent growth control, reversibly inhibit carcinogen-induced transformation, and enhance gap junctional intercellular communication. These effects are highly correlated. 10T1/2 cells were found to express low levels of connexin 43, a gap junctional protein first found in the heart. After treatment of confluent 10T1/2 cells with the synthetic retinoid tetrahydrotetramethylnapthalenylpropenylbenzoic acid (TTNPB), levels of connexin 43 mRNA and protein increased within 6 h of treatment, while elevation of junctional communication was detected within 12-18 h. The maximally effective concentration of TTNPB (10(-8) M) caused an approximate 10-fold elevation of connexin 43 gene transcripts after 72 h. Indirect immunofluorescence microscopy using a polyclonal antibody to the synthetic C-terminal region of connexin 43 demonstrated that TTNPB induced many fluorescent plaques in regions of cell-cell contact. These results provide a molecular basis for the retinoid-enhanced junctional communication in 10T1/2 cells. It is proposed that one action of retinoids is to modulate the intercellular transfer of signal molecules. These could mediate many of the physiological actions of retinoids on growth control and carcinogenesis.

Animals↗