Can handwashing practices be changed?
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Biomedical subjects
Publications and source records attributed to M Moore.
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The efficacy of various mitogens for growing human lymphocyte colonies in semisolid agar cultures was tested. Protein A as well as phytohemagglutinin (PHA) exhibited a strong stimulatory capacity in contrast to Cowan I strain of Staphylococcus aureus (Cowan I). Pokeweed mitogen (PWM) was effective and generated a sizeable number of colonies. Plating efficiency of lymphocytes from different donors and for the same donors cultured on different days were highly variable. Regardless of mitogen, colonies grew predominantly on the upper and lower surfaces of the agar and these were predominantly composed of T lymphocytes. A much smaller number of colonies grew within the agar and these were found to be monocytes or a mixture of monocytes granulocytes. Under chosen concentrations of agar and mitogens, dose responses of colony number per number of cultured cells were determined. These were found to be characteristic for each of the mitogens but none were linear. The possibility of cell-cell interactions being important for proliferation is therefore raised.
The natural cytotoxic activity of lymphoid cell populations from control and BCG-stimulated rats was examined using four target cell lines, K562, CCRF/CEM, Bri8 and Mc40. In control rats, the cytotoxicity of peritoneal cells was below that of spleen cells but above that of peripheral lymph node cells. Intraperitoneal injection of BCG induced a significant dose and time-dependent augmentation of cytotoxicity by peritoneal cells from W/Not and PVG/c rats, against all four cell lines. The increased activity reached a peak on days 4 and 5 after injection and returned to control levels by day 12. Spleen and lymph node cells from stimulated rats did not show increased cytotoxicity. K562 and CCRF/CEM target cells were considerably more susceptible to killing than Bri8 and Mc40 target cells. Separation of peritoneal cells from BCG-treated rats by density-gradient centrifugation gave an interface population, enriched with mononuclear cells showing high cytotoxic activity and a pellet population enriched with polymorphs showing very low activity. Nylon-fibre column filtration gave non-adherent and adherent cytotoxic populations. Cytotoxic activity was not diminished by removing cells adhering to Sephadex G10 or cells phagocytosing carbonyl iron, suggesting that much of the activity in this system was due to non-phagocytic mononuclear cell populations.
This report was designed to describe and characterize the proportion of of hypercholesterolemic children and adults in the Lipid Research Clinics collaborative prevalence study whose elevated total plasma cholesterol levels were accounted for by elevated high density lipoprotein cholesterol (C-HDL), not by elevated levels of low density lipoprotein cholesterol (C-LDL). In randomly recalled 6-19 year old children having age-, race-, an sex-specific plasma cholesterol levels greater than or equal to 95th percentile levels, 22% of white males, 22% of white females, and 44% of black males had C-HDL, but not C-LDL greater than or equal to age-, sex-, and race-specific 95th percentile levels. In contrast, for adults (ages 20-79 years), 3% of white males, 10% of white females, 17% of black males, and 25% of black females had predominant hyperalphalipoproteinemia which accounted for their hypercholesterolemia. In participants defined as hypercholesterolemic on the basis of two examinations it was observed that the majority of children and adults were in the C-LDL elevated and C-HDL not elevated category. Hypercholesterolemic adults were not as likely as the hypercholesterolemic children to be in the C-HDL elevated and C-LDL not elevated category. For both children and adults, blacks were more likely to have predominant hyperalphalipoproteinemia accounting for their elevated total plasma cholesterol levels than were whites. For hyperalphalipoproteinemic, hypercholesterolemic children and adults, the mean ratio of C-LDL to C-HDL ranged from 1.3 to 1.4 (in children) and 1.4 to 2.1 (in adults), levels well below the overall mean ratio for the entire Lipid Research Clinics random recall group of 2.7 for children and 4.2 for adults. An understanding of the multiple etiologies of hyperalphalipoproteinemic-hypercholesterolemics may be useful in considering programs designed to elevate C-HDL over time, with an aim at reducing CHD risk.
Cyclopenta(cd)pyrene, a constituent of environmental emissions, has been found to mutate and transform mammalian cells in culture. Cyclopenta(cd)pyrene 3,4-oxide, a presumed metabolite, was found to be a direct-acting mutagen and to transform mammalian cells. These results suggest that cyclopenta(cd)pyrene 3,4-oxide may be an ultimate mutagenic form of the parent hydrocarbon.
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Nuclei from hepatoma tissue culture (HTC) cells were isolated by standard methods and incubated in media commonly used for nuclease digestions (DNAase I and micrococcal nuclease) and for in vitro RNA synthesis. During the incubation, histones can be deacetylated from both control cells and cells treated with 6 mM sodium butyrate to enhance the levels of histone acetylation. Deacetylation of histone is much more apparent in nuclei isolated from sodium butyrate-treated cells. Inclusion of 6 mM sodium butyrate in the incubation medium effectively inhibits the endogenous deacetylase activity acting on histones H3 and H4, whereas sodium acetate at the same concentration has very little inhibitory effect.
Histone acetate is hydrolyzed rapidly in logarithmically dividing hepatoma tissue culture cells (Jackson, V., Shires, A., Chalkley, R. and Granner, D.K. (1975) J. Biol. Chem. 250, 4856--4863). The phenomenon has been analyzed further in hepatoma tissue culture cells at various stages of the cell cycle, in stationary phase, and in the presence of actinomycin D. We also investigated the phenomenon in Tetrahymena pyriformis macronuclei, bovine thymocytes, and human foreskin fibroblasts. The data suggest that this highly metabolically active histone acetylation while altered in mitotic cells, is independent of the overall rate of cell division, and is only slightly sensitive to actinomycin D. Finally, we conclude that the same general phenomenon is found in both cancerous and normal cells and is apparently common to cells from various stages of the evolutionary scale.
Three children developed extensive extrapulmonary disease in the course of fatal adenovirus type 7 pneumonia. Several clinical features, including the unexpected onset of coma, suggested the development of Reye syndrome, but biochemical and histopathologic findings were inconsistent with this diagnosis. Virologic and pathologic studies did not reveal evidence of extrapulmonary adenovirus infection, despite clinical involvement of the liver, skeletal muscle, and central nervous system. The detection in premortem sera from all three patients of adenovirus penton antigen, known to be cytotoxic in vitro, suggests a possible mechanism for the production of extrapulmonary pathology in the absence of extrapulmonary virus infection.
Single-cell suspensions prepared by enzymatic disaggregation of an immunogenic 3-methylcholanthrene-induced sarcoma (Mc40A) contain a significant proportion of infiltrating leucocytes (approximately 42%), comprising T lymphocytes, macrophages and non-phagocytic FcR+ lymphoid-like cells. Tumour-infiltrating lymphocytes (TIL) were isolated and purified by successive passage over Sephadex G-10 columns and their cytotoxic activity in vitro compared with that of lymphoid cells from normal rats and from tumour-bearers at different times after implantation. For this purpose, surviving target cells were quantified by incorporation of the gamma-emitting analogue of methionine, 75Sel-methionine, in a 48-h assay which detected both cytotoxic and cytostatic effects. The reactivity of TIL, which was consistently demonstrable from 11 days after tumour transplantation, was essentially similar to that of normal splenic lymphocytes in magnitude and specificity. Reciprocal cytotoxicity tests using TIL and cultured targets from an antigenically unrelated tumour of similar aetiology (Mc57) showed that the manifestation of TIL cytotoxicity was determined, not by the tumour of origin, but by the susceptibility of the target cells. Evidence that the effector function of TIL was mediated in part by natural killer (NK) cells was derived from concurrent experiments using human myeloid cells (K562) as targets in an 18h 51Cr-release assay. In this system the level of NK activity was critically dependent on the numbers of tumour cells in the TIL population; contamination in excess of 2% gave rise to dose-dependent inhibition of NK function. The results show that within a progressively growing tumour known to possess rejection antigens, NK reactivity was detected in the absence of a demonstrable tumour-specific cytotoxic component.
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An attempt to set up a management information system for individual drug abuse programs throughout a state is described. The principles upon which the system is based are discussed along with the problems encountered in its implementation. A series of guidelines for establishing management information systems in operating human services agencies is included.
The spontaneous cytotoxicity of human peripheral blood lymphocyte preparations from normal donors for K562 target cells was examined. Effector cells were separated into SRBC rosette forming cell (RFC) and non-rosette forming cell (non-RFC) fractions using optimal and suboptimal rosetting procedures. RFC and non-RFC fractions both had high cytotoxic activity irrespective of the rosetting procedure. Owing to the larger size of the RFC fraction, it contained a higher proportion of the total activity in the preparation. Nylon fibre column adherent and non-adherent fractions also both produced cytotoxicity. Nylon fibre non-adherent cells separated by SRBC separation gave a RFC fraction with low activity and a non-RFC fraction with high activity. Separation of nylon fibre adherent cells gave RFC and non-RFC fractions with high cytotoxic activity. Therefore cytotoxic cells did not form a discrete subpopulation and either occur in several lymphocyte subsets or show a variable capacity to form SRBC rosettes and adhere to nylon fibre.
Detection of immune complexes by inhibition of antibody-dependent cellular cytotoxicity (ADCC) is based on the principle that soluble complexes can compete with target cell-bound antibody for receptors (FcR) on cytotoxic lymphocytes. The objective of this study was to define a cytotoxicity system for the determination of soluble immune complexes in the sera of patients with inflammatory bowel disease (IBD). For this purpose, the conditions under which soluble complexes of rat serum albumin (RSA) and rabbit anti-RSA inhibited human K-cell mediated lysis of sensitized Chang cells were examined, on the assumption that the behaviour in the system of circulating immune complexes putatively present in inflammatory bowel disease, is similar to that of artificial immune complexes. Inhibition of ADCC by a standard amount of artificial complex in different normal human sera was relatively uniform provided that the final concentration of the latter did not exceed 10% of the culture medium. In the absence of extraneous complexes, the effect of both normal and IBD sera on ADCC varied widely. Differential inhibition of ADCC by sera from patients with IBD and normal subjects was thus expressed as a function of ADCC in a standard batch of foetal bovine serum (FBS). Under these conditions differences between pathological (n = 51) and normal (n = 52) sera were highly significant (P less than 0.001), which could not be explained by the presence in the patients' sera of HL-A antibodies reactive with the effector cells, nor by a deficit in nutritional support of ADCC. The absence of a correlation between inhibition of ADCC and total serum IgG or IgM inferred that inhibition was attributable to immune complexes in the IBD sera. The limitations of this assay for assessment of the incidence of immune complexes in pathological sera are discussed.
Takayasu's disease is a nonspecific arteritis of unknown cause with predilection for the aortic arch and its branches; approximately 20% of those affected are children or adolescents, predominantly females. The purpose of this article is to report the case of a young girl in which the mode of presentation was microscopic hematuria and proteinuria. Subsequently, aortic valvular insufficiency developed and there was evidence of aortitis in the thoracic and abdominal aorta, as well as in the arch. All functional and anatomical cardiac derangements were documented by ultrasound and angiocardiography. Renal biopsies showed progressive glomerular involvement characterized by focal and segmental glomerulonephritis. It is postulated that a common immunologic mechanism was responsible for the aortic and glomerular lesions.
Rosette formation between human lymphocytes and mouse red blood cells (MRBC) was examined as a marker for B lymphocytes and as a method of B lymphocyte separation. A small proportion of lymphocytes formed spontaneous rosettes with MRBC (mean value 6%) and the number was considerably increased by pretreating the lymphocytes with neuraminidase (mean value 16%). Double marker tests demonstrated that lymphocytes forming MRBC rosette were immunoglobulin (Ig) bearing cells, with a high proportion of IgM bearing cells, but not all Ig bearing cells formed MRBC rosettes. Lymphocyte populations enriched with T or B lymphocytes, by SRBC rosette sedimentation and nylon column filtration, gave values for MRBC rosettes consistent with a subpopulation of Ig bearing cells. Separation of MRBC rosette-forming cells gave a relatively poor degree of separation and rerosetting with MRBC produced variable results.
The natural (spontaneous) cytotoxicity (NC) of cell populations from different lymphoid organs of the rat were examined using a human myeloid cell line (K562) and a rat fibrosarcoma cell line (Mc40) as target cells. Rat blood and spleen lymphoid cell populations gave high cytotoxicity against K562, while lymph node cells and bone-marrow cells gave low levels of cytotoxicity and thymus cells virtually no activity. Addition of thymus or lymph node cells to spleen effector cells did not suppress the high cytotoxicity of spleen cells. A similar organ distribution of reactivity was observed against Mc40 cells, but the levels of cytotoxicity were much lower than for K562. A strain difference was monitored in the levels of natural cytotoxicity and cell populations from inbred Wistar rats consistently gave higher activity on a cell-to-cell basis than the corresponding population from PVG/c rats. Natural cytotoxicity was not removed when spleen cell populations were depleted of cells adhering to nylon-fibre columns or plastic surfaces, or depleted of cells ingesting carbonyl iron. In agreement with other studies using human and animal lymphoid cells, the natural killer cell in this system was found to be non-adherent and non-phagocytic and its distribution did not correspond to the established organ distribution of T or B lymphocytes.
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