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K Moore

Publications and source records attributed to K Moore.

At least 37 records · Page 2Linked to original sources
PubMed1990

Phenotypic changes in a CD4+ lymphocyte subset correlate with a conversion from suppressor to helper inducer function.

The monoclonal antibodies WR16 (CD45RA) and WR19 were used to isolate two reciprocal subsets of CD4 lymphocytes by negative selection. The CD4+/WR16-/WR19+ subset exhibited helper-inducer activity in a pokeweed mitogen (PWM)-driven Ig secretion assay, whereas the CD4+/WR16+/WR19- subset showed suppressor activity. When the CD4+/WR16+/WR19- subset was cultured in phytohaemagglutinin (PHA) or purified protein derivative (PPD) there was increased expression of the antigen binding WR19 but the cells remained WR16 negative. Cultures of CD4+/WR16+/WR19- lymphocytes with PHA or PPD induced a phenotypic change that resulted in a population which was CD4+/WR16-/WR19+. Investigation of the functional activity of the CD4+/WR16+/WR19- subset, before and after activation and phenotypic change to WR16-/WR19+, indicated that the change in phenotype correlated with a functional conversion from suppressor to helper-inducer activity. These results suggest that the CD4+/WR16+/WR19- suppressor subset comprises cells that differentiate to WR16-/WR19+ helper-inducer cells after exposure to antigen or mitogen.

CD4 Antigens↗
PubMed1990

Recent advances in childhood cancer.

Major advances during the past 25 years in the treatment of childhood cancer have resulted in a dramatic improvement in disease-free survival for more than 60% of diagnosed patients. Advances in both laboratory and clinical research have demanded a concomitant expansion of nursing skill and practice to keep pace in this area. This article strives to provide an overview of recent advances in pediatric oncology in both the scientific and clinical arenas and to highlight some of the contributions made by pediatric oncology nurses.

Child↗
PubMed1989

SecA protein, a peripheral protein of the Escherichia coli plasma membrane, is essential for the functional binding and translocation of proOmpA.

We have reconstituted protein translocation across plasma membrane vesicles of Escherichia coli using purified proOmpA and trigger factor, a 63 kd soluble protein. Treatment of membrane vesicles with urea inactivates them for translocation unless a factor present in cytoplasmic extracts is added during the translocation reaction. Sedimentation analysis showed that the stimulatory activity is of distinctly higher mol. wt than trigger factor. Cytoplasmic extracts from a strain that greatly overproduces the SecA protein are highly enriched in the stimulatory activity for untreated membranes and restore translocation to urea-treated membranes, suggesting that this protein is the stimulatory factor. This assay was used to monitor the isolation of SecA protein from the overproducing strain. The purified protein is soluble, yet binds peripherally to membranes with high affinity and supports translocation. Using pure proOmpA, SecA protein, trigger factor and urea-treated membranes, the protein export process was resolved into binding and translocation steps. We find that proOmpA binds to membrane vesicles with or without SecA protein, but that translocation only occurs when SecA was bound prior to proOmpA.

Amino Acid Isomerases↗
PubMed1989

Safety and effectiveness of cranial electrotherapy in the treatment of tension headache.

One hundred patients were enrolled in a multicenter double-blind study to evaluate the safety and effectiveness of the Pain Suppressor Unit, a cranial electrotherapy stimulator for the symptomatic treatment of tension headaches. Treatment consisted of extremely low level, high frequency current applied transcranially. Pain scores before and after 20 minute treatments of individual headaches as well as patient and physician global evaluations were the primary efficacy variables. Following use of the active unit, patients reported an average reduction in pain intensity of approximately 35%. Placebo patients reported a reduction of approximately 18%. The difference was statistically significant (p = 0.01). The active unit was rated as moderately or highly effective in 40% by physicians, and in 36% by patients. Both physicians and patients scored the placebo unit moderately or highly effective for only 16%. The difference in ordered outcomes was statistically significant (p = 0.004). Approximately 10% of patients in each group reported at least one minor adverse experience. Cranial electrotherapy stimulation is distinct from TENS, and is safe and often effective in ameliorating the pain intensity of tension headaches. It should be considered as an alternative to the chronic usage of analgesics.

Adult↗
PubMed1989

Immunohistological features of synovitis in ankylosing spondylitis: a comparison with rheumatoid arthritis.

The immunohistological features of the synovial membrane in ankylosing spondylitis, HLA-B27 associated oligoarthritis, and rheumatoid arthritis wer examined with particular reference to T lymphocyte subsets. T helper (CD4+) cells clearly outnumbered T suppressor/cytotoxic (CD8+) cells in rheumatoid arthritis, whereas both cell types were present in equal numbers in ankylosing spondylitis. A reduction of CD4+/CD45R+ suppressor/inducer cells relative to CD4+/UCHL1+ helper/inducer cells was apparent in all diagnostic groups. The observations were suggestive of disease specific inflammatory responses within synovial membrane.

Adult↗
PubMed1989

B-cell markers in the human kidney.

This report describes the reactivity of a panel of 89 monoclonal antibodies with the normal human kidney. The antibodies were all submitted to the B-cell panel of the Third Leukocyte Differentiation Workshop. Several different patterns of staining of renal structures were identified. Most antibodies clustered in defined CD groups showed the same pattern of reactivity in the kidney, but some, notably CD19 antibodies, showed heterogeneity of binding to the kidney. These findings are important for the use of monoclonal antibodies to define phenotype in cell culture and immunohistology experiments.

Antibodies, Monoclonal↗
PubMed1988

Ultrasonic plaque ablation. A new method for recanalization of partially or totally occluded arteries.

The potential application of ultrasonic energy for ablation of atherosclerotic plaques was studied in human atherosclerotic arteries with continuous and pulsed delivery of energy. With a prototype ultrasonic wire probe (n = 79 segments), there was gross reduction in vascular lesions as well as microscopic disruption of fibrous and calcified plaques. Normal portions of vessels appeared unaffected by the application of ultrasound. The prototype ultrasonic wire catheter ablated calcific deposits in less than 10 seconds. With this probe, all 26 complete atherosclerotic occlusions 0.5-5 cm in length were recanalized irrespective of the presence of calcium. Twenty-four of the segments were reopened in less than 20 seconds. By light microscopy, the site of plaque ablation was smooth, concave, and conformed to the shape of the probe tip. In 17 samples, there was evidence of thermal injury, and in six of the 79 samples studied with the prototype probe, there was vascular perforation. No vascular perforation occurred without thermal damage, when pulsed (rather than continuous) ultrasonic energy was used (n = 40) or when the duration of application was less than 30 seconds, with power output less than 25 W and with the probe oriented parallel to the wall (n = 26). Thus, by modifying the duration, mode, and magnitude of the ultrasonic power output, thermal injury and vascular perforation may be avoided. In vivo intra-arterial ultrasonic angioplasty of a canine chronic femoral fibrocellular occlusion was also performed. A preliminary in vivo study demonstrated feasibility of the percutaneous application of intra-arterial ultrasonic recanalization. Thus, ultrasonic energy appears to have potential as a method for ablation of occlusive atherosclerotic plaque.

Angiography↗
PubMed1988

Structure and function of Fc receptors on macrophages and lymphocytes.

Cell surface receptors for the Fc portion of immunoglobulin confer on most cells of the immune system the ability to communicate with the humoral antibody response. These Fc receptors are known to be particularly important for the function of various effector cells, such as macrophages, since they are involved in mediating a variety of activities including endocytosis, antibody-dependent cellular cytotoxicity, and triggering the release of potent inflammatory agents. Over the past few years, a considerable amount has been learned about the structure and functions of the Fc receptors expressed by murine and human cells, due to the availability of specific anti-receptor antibodies and the isolation of Fc receptor cDNA clones. In general, these receptors are transmembrane proteins whose extracellular domains contain two immunoglobulin-like regions and are thus members of the immunoglobulin gene family. Their domain structure consists of a glycosylated extracellular domain, a single membrane-spanning segment, and a relatively long cytoplasmic domain. The cytoplasmic tails exhibit a surprising degree of variation in length and amino acid sequence. This review summarizes some recent information concerning the structure and expression of the Fc receptors found on murine and human macrophages and lymphocytes. Particular attention is paid to the functional activities of these receptors, and the possible relationship between receptor function and receptor structure.

Animals↗
PubMed1988

An immunohistological study of CD4+ lymphocyte subsets within inflammatory lesions with special reference to rheumatoid arthritis and inflammatory bowel disease.

The monoclonal antibodies (mAbs) WR16, UCHL1 and WR19 identify subsets of CD4+ lymphocytes that have been functionally characterized as suppressor inducer cells or helper inducer cells. These were applied as components of a panel of lymphocyte-specific mAbs for the phenotypic analysis of lymphocyte populations within biopsies taken from rheumatoid synovial membrane and normal and inflamed gut. The phenotype of peripheral blood lymphocytes from patients with rheumatoid arthritis were also compared to normal controls. The rheumatoid synovium was characterized immunohistologically by a lymphocytic infiltrate composed predominantly of CD4+ lymphocytes and a CD4:CD8 ratio of 2.4. The CD4+ population was composed of UCHL1+ cells to the exclusion of WR16+ cells. This finding was confirmed by double immunofluorescence staining using directly conjugated Leu-3a and WR16. The UCHL1+/WR16-/CD4+ phenotype was maintained in the synovial biopsies regardless of whether the patient had commenced treatment with disease modifying drugs. The absence of WR16+ cells within the rheumatoid synovium was shown to be a localized phenomenon as there was a slight elevation of circulating WR16+ lymphocytes in the peripheral blood of rheumatoids whilst the levels of UCHL1+ and WR19+ lymphocytes remained unchanged. As no appropriate normal control tissue is available for comparison to the rheumatoid synovium we also examined the lymphocytes present within Crohn's disease-involved bowel biopsies and compared them to normal gut tissue lymphocytes using WR16 and UCHL1 mAbs. The CD3+ lymphocytes present within normal tissue comprised a mixture of WR16+ and UCHL1+ cells. In contrast the CD3+ lymphocytes within Crohn's involved tissue were exclusively UCHL1+ as previously observed in the rheumatoid synovium. These data indicate that the CD4+ lymphocyte infiltrate present within inflammatory lesions of presumed distinct aetiology exhibit a localized selective loss of cells with the CD45R+/CD4+ suppressor inducer phenotype. This may be a consequence of the selective extravasation of CD4+ helper induced cells or more likely, in view of the previously documented loss of the p220 molecule identified by CD45R mAbs upon T-cell activation, the result of CD4+ T-cell activation at sites of inflammation.

Arthritis, Rheumatoid↗
PubMed1988

Nurse executive effectiveness.

Community hospital chief nurse executives (CNEs) and chief executive officers (CEOs) ranked, in a nationwide survey, seven characteristics of nurse executive effectiveness. Human management skill was ranked first by both groups. CNEs cited CEO support as the second most important factor in their effectiveness, while CEOs ranked total organizational view second. Both groups cited the need for fiscal management skills for CNEs. Results differ from an earlier study of university hospital based CNEs and CEOs. Such discrepancies, including differences in education, tenure, and salary, hold strong implications for the pursuit of careers in nursing administration.

Administrative Personnel↗
PubMed1987

A comparison of spleen and lymph node cells as fusion partners for the raising of monoclonal antibodies after different routes of immunisation.

Administration of antigen (human insulin) via the rear footpads of BALB/c mice with subsequent fusion of popliteal and inguinal lymph node lymphocytes induced a higher frequency of hybridomas (100%) secreting specific antibody than either intradermal immunisation and lymph node cell fusion (53%) or conventional subcutaneous immunisation and intraperitoneal boost followed by splenic lymphocyte fusion (8%). The rank order of serum antibody titres was found to correlate with the order of fusion efficiencies. Lymph node cell fusions also produced a greater spectrum of antibody specificities. Such differences in fusion efficiencies were also observed using bovine intestinal alkaline phosphatase.

Alkaline Phosphatase↗
PubMed1987

Histone-H1 inhibits translation by reticulocyte lysates with relative mRNA selectivity.

Histone-H1 purified from rat skeletal muscle is a relatively potent inhibitor of peptide chain initiation in a cell free system, the rabbit reticulocyte lysate (50% inhibition at approximately 0.4 microM). H1 does not inhibit formation of the ternary complex nor its attachment to 40S ribosomes; the data are compatible with H1 binding to mRNA. The inhibition shows mRNA selectivity: translation of beta-globin mRNA is more affected than that of alpha-globin mRNA and hepatic albumin mRNA more than total hepatic mRNA. Whether or not histone-H1 plays a role in translational regulation in intact cells is conjectural, it may serve as a useful model for protein-mRNA interactions.

Animals↗
PubMed1987

Glycerol metabolism in higher plants: glycerol kinase.

Glycerol kinase activity was identified in extracts of higher plant seeds and seedlings, and was partially purified and characterized from cucumber radicle tissue. The enzyme was localized in the post-mitochondrial supernatant of the cell, and catalyzed the formation of glycerol-3-phosphate. The pH optiumum was 9.0. ATP, CTP, GTP or UTP could be used as the phosphoryl group donor. The Km for glycerol was 55 microM and Km values for the nucleoside triphosphates were 145-620 microM. The Vmax for the reaction was 40-78 pmol product per min. Kinetic data indicate that the enzyme has a sequential mechanism.

Glycerol↗
PubMed1987

Reconstitution of rabbit thrombomodulin into phospholipid vesicles.

The influence of phospholipid on thrombin-thrombomodulin-catalyzed activation of protein C has been studied by incorporating thrombomodulin into vesicles by dialysis from octyl glucoside-phospholipid mixtures. Thrombomodulin was incorporated into vesicles ranging from neutral (100% phosphatidylcholine) to highly charged (30% phosphatidylserine and 70% phosphatidylcholine). Thrombomodulin is randomly oriented in vesicles of different phospholipid composition. Incorporation of thrombomodulin into phosphatidylcholine, with or without phosphatidylserine, alters the Ca2+ concentration dependence of protein C activation. Soluble thrombomodulin showed a half-maximal rate of activation at 580 microM Ca2+, whereas half-maximal rates of activation of liposome-reconstituted thrombomodulin were obtained between 500 microM Ca2+ and 2 mM Ca2+, depending on the composition (protein:phospholipid) of the liposomes. The Ca2+ dependence of protein C activation fits a simple hyperbola for the soluble activator, while the Ca2+ dependence of the membrane-associated complex is distinctly sigmoidal with a Hill coefficient greater than 2.4. In contrast, the Ca2+ dependence of gamma-carboxyglutamic acid (Gla) domainless protein C activation is unchanged by membrane reconstitution (1/2 max = 53 +/- 10 microM) and fits a simple rectangular hyperbola. Incorporation of thrombomodulin into pure phosphatidylcholine vesicles reduces the Km for protein C from 7.6 +/- 2 to 0.7 +/- 0.2 microM. Increasing phosphatidylserine to 20% decreased the Km for protein C further to 0.1 +/- 0.02 microM. Membrane incorporation has no influence on the activation of protein C from which the Gla residues are removed proteolytically (Km = 6.4 +/- 0.5 microM). The Km for protein C observed on endothelial cells is more similar to the Km observed when thrombomodulin (TM) is incorporated into pure phosphatidylcholine vesicles than into negatively charged vesicles, suggesting that the protein C-binding site on endothelial cells does not involve negatively charged phospholipids. In support of this concept, we observed that prothrombin and fragment 1, which bind to negatively charged phospholipids, do not inhibit protein C activation on endothelial cells or TM incorporated into phosphatidylcholine vesicles, but do inhibit when TM is incorporated into phosphatidylcholine:phosphatidylserine vesicles. These studies suggest that neutral phospholipids lead to exposure of a site, probably on thrombomodulin, capable of recognizing the Gla domain of protein C.

Animals↗
PubMed1987

Use of the monoclonal antibody WR17, identifying the CD37 gp40-45 Kd antigen complex, in the diagnosis of B-lymphoid malignancy.

The distribution of the gp40-45 Kd antigen bound by the WR17 monoclonal antibody of IgG2 subclass in normal lymphoid tissue was characterized by immunohistochemistry and immunofluorescence staining with flow cytometric analysis. The predominant staining pattern observed was characteristic of an anti-pan-B-lymphocyte reagent. Weak reactions were observed by immunofluorescence staining of viable cell suspensions with all neutrophils and T-lymphocytes in some normal donors. In tissue sections, B-lymphocytes were stained and no cross reactions were observed with T-lymphocytes, although macrophages stained in some sections. A range of T- and B-cell malignancies were stained with WR17 and the reactivity compared to that observed with other monoclonal antibodies in the CD19, CD21 and CD22 clusters. All B-non-Hodgkin's lymphomas, B-chronic lymphocytic, prolymphocytic and hairy cell leukaemia cells examined were stained by WR17 in indirect immunofluorescence assays, whilst the T-cell tumours were negative. The same pattern was observed in cryostat sections of malignant tissue and in addition some tissue macrophages expressed the CD37 antigen cytoplasmically. Intra-tumour heterogeneity of staining was observed with all the monoclonal antibodies tested, although overall WR17 consistently stained B-cell tumours even when expression of the CD19 pan-B-lymphocyte antigen could not be detected with some monoclonals. Monoclonal antibodies, such as WR17, within the CD37 cluster and binding to the gp 40-45 Kd molecule, bind to mature B-lymphocytes and identify the majority of B-cell malignancies.

Antibodies, Monoclonal↗
PubMed1987

Abnormal subcellular distribution of beta-glucuronidase in mice with a genetic alteration in enzyme structure.

Liver beta-glucuronidase is structurally altered in inbred strain PAC so that a peptide subunit with a more basic isoelectric point, GUS-SN, is produced. This allele of beta-glucuronidase was transferred to strain C57BL/6J by 12 backcross matings to form the congenic line B6 X PAC-Gus(n). Liver beta-glucuronidase activity was halved in males of the congenic strain compared to normal males. The lowered activity was specifically accounted for by a decrease in the lysosomal component. There was no alteration in the concentration of microsomal activity. This alteration in the subcellular distribution of beta-glucuronidase in Gus(n)/Gus(n) mice was confirmed by two independent gel electrophoretic systems which separate microsomal and lysosomal components. beta-Glucuronidase activity was likewise approximately halved in mutant spleen, lung, and brain, organs which contain exclusively or predominantly lysosomal beta-glucuronidase. The loss of liver lysosomal beta-glucuronidase activity was shown by immunotitration to be due to a decrease in the number of beta-glucuronidase molecules in lysosomes of the congenic strain. The Gus(n) structural alteration likely causes the lowered lysosomal beta-glucuronidase activity since the two traits remain in congenic animals. Heterozygous Gus(n)/Gus(b) animals had intermediate levels of liver beta-glucuronidase. Also, the effect was specific, in that three other lysosomal enzymes were not reproducibly lower in Gus(n)/Gus(n) mice. Gus(n) is, therefore, an unusual example of a mutation which causes a change in the subcellular distribution of a two-site enzyme.

Animals↗