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Biomedical subjects

A Mooney

Publications and source records attributed to A Mooney.

At least 19 recordsLinked to original sources
PubMed2001

Basis of the superiority of cefoperazone amphotericin teicoplanin for isolating Campylobacter upsaliensis from stools.

The optimum method for isolating Campylobacter upsaliensis from stools has not been clearly defined. In a preliminary study, cefoperazone amphotericin teicoplanin (CAT) selective medium isolated six C. upsaliensis strains which were not detected using modified cefoperazone charcoal deoxycholate (mCCDA). In order to identify the factors that underlie the superiority of CAT over mCCDA for isolating C. upsaliensis, we examined the effect of incubation time and antibiotic content of culture media on the growth of C. upsaliensis isolates using semiquantitative methods. The recovery of a subgroup of C. upsaliensis isolates from seeded stool specimens was also evaluated. Differences in growth of C. upsaliensis on CAT and mCCDA were modest and were not explained by the antibiotic profiles of the two media. Recovery of C. upsaliensis from spiked human feces on CAT was superior to that on mCCDA at lower concentrations of organisms (10(3) CFU/ml). We conclude that although CAT is more suitable than mCCDA for the isolation of C. upsaliensis from stools, the superiority of CAT for detecting this organism is not accounted for by the antibiotic composition of the medium.

Amphotericin B↗
PubMed1999

Type IV collagen and laminin regulate glomerular mesangial cell susceptibility to apoptosis via beta(1) integrin-mediated survival signals.

Postinflammatory scarring is characterized by changes in extracellular matrix (ECM) composition and progressive loss of normal resident cells. In glomerular inflammation there is now evidence that unscheduled apoptosis (programmed cell death) of mesangial and other resident cells may mediate progression to irreversible glomerulosclerosis. In the current study we examined the hypothesis that ECM components may differ in their capacity to support mesangial cell survival by suppression of apoptosis. Using a well-established in vitro model of mesangial cell apoptosis, we found that collagen IV and laminin, components of normal mesangial ECM, protected rat mesangial cells from apoptosis induced by serum starvation and DNA damage, by a beta(1) integrin-mediated, but arg-gly-asp (RGD)-independent mechanism. In contrast, collagen I, fibronectin, and osteonectin/SPARC, which are overexpressed in diseased glomeruli, failed to promote rat mesangial cell survival. However, the survival-promoting effect of collagen IV and laminin was not associated with changes in cellular levels of apoptosis regulatory proteins of the Bcl-2 family. These experiments demonstrate that glomerular mesangial cell survival is dependent on interactions with ECM and provide insights into potential mechanisms by which resident cell loss may occur during acute inflammation and postinflammatory scarring of the kidney and other organs.

Animals↗
PubMed1999

Treating patients with hypertriglyceridaemia saves lives: triglyceride revisited.

The statin trials in secondary and primary prevention have shown that lowering LDL cholesterol produces a reduction in coronary event rates of around 35%. The most common dyslipidaemia in MI survivors is mixed hyperlipidaemia rather than hypercholesterolaemia. New evidence from VA-HIT and BIPS suggests that relatively low levels of triglyceride may be associated with a significant increase in coronary risk. In patients with established coronary disease, treatment with a fibrate that lowers triglyceride and raises HDL cholesterol, but which has little effect on LDL cholesterol, slows the rate of progression of coronary lesions. In hypertriglyceridaemic patients who have survived an MI or who have angina pectoris, fibrate treatment reduced the incidence of fatal and non-fatal MI by 40% (p = 0.03) (BIPS). In patients with coronary artery disease, who have low levels of HDL, fibrate treatment reduced the incidence of fatal and non-fatal MI by 22% (p = 0.006) (VA-HIT). These patients represent around 25% of the post-MI population. Work in progress will shortly define the effect of fibrate treatment on coronary event rate in patients with peripheral vascular disease and Type 2 diabetes.

Arteriosclerosis↗
PubMed1999

The terminal sequence of complement plays an essential role in antibody-mediated renal cell apoptosis.

Mesangial cell (MC) injury is a characteristic feature in the early phase of Thy.1 nephritis. The present study investigates the contribution of complement to MC apoptosis in this experimental model of kidney disease in rats. Thy.1 nephritis was induced by injection of mouse anti-Thy.1 monoclonal antibody (ER4G). To assess the contribution of the terminal sequence of complement on apoptosis, the studies were performed in complement-sufficient PVG/c (PVG/c+) rats and in rats deficient in complement C6 (PVG/c-). Apoptosis was monitored by assessment of the number of condensed nuclei in kidney sections stained with periodic acid-Schiff (PAS) and by the terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) method and expressed as number of apoptotic cells per 50 glomerular cross sections. In the PAS method, 1 h after intravenous injection of ER4G, PVG/c+ rats exhibited 160.9 +/- 49.5 apoptotic cells, whereas PVG/c- rats had only 3.2 +/- 1.4 apoptotic cells. Control rats exhibited 0.9 +/- 0.6 apoptotic cells. These findings were confirmed with the TUNEL method. In PVG/c- rats, a maximum number of 8.8 +/- 3.1 TUNEL-positive (TUNEL+) cells was found at 6 h followed by a decline thereafter. In PVG/c+ rats, apoptosis was associated with deposition of C6 and C5b-9. Restoration of the complement system of PVG/c- rats with purified human C6 resulted in an increase of apoptosis at 1 h after injection of ER4G from minimal numbers to 239.9 +/- 52.4 TUNEL+ cells. These studies appear to indicate for the first time that the terminal sequence of complement is involved in induction of apoptosis.

Analysis of Variance↗
PubMed1998

Immunological detection and mutational analysis of the RNA2-encoded nematode transmission proteins of pea early browning virus.

Pea early browning virus (PEBV) is transmitted between plants by root-feeding trichodorid nematodes. Mutagenesis studies have implicated two non-structural viral proteins in the transmission process. These two proteins [the 29 kDa ('29K') protein and the 23K protein] were expressed in bacteria and used to raise antibodies. In Western blotting experiments, the antibodies detected both of these virus proteins in leaves and roots of infected Nicotiana bethamiana and N. clevelandii plants. Periodate treatment of proteins transferred to nitrocellulose membranes suggested that the PEBV 23K protein may be glycosylated. A PEBV mutant was constructed lacking the complete 23K coding sequence. The mutant was able systemically to infect Nicotiana spp. but caused striking chlorotic ringspot leaf symptoms and stunting of both leaves and roots. These symptoms were absent in plants doubly-infected with the mutant and wild-type PEBV. The 23K gene deletion mutant was transmitted by nematodes at a much reduced frequency compared to wild-type virus, indicating that the 23K protein is involved in but not essential for vector transmission. Western immuno-blot and ELISA experiments revealed that the reduction in the nematode-transmissibility of PEBV carrying mutations in the 23K gene did not result from interference in the expression of the 29K transmission protein or from gross changes in the titre of virus in the roots of infected plants.

Animals↗
PubMed1997

Cytokines promote glomerular mesangial cell survival in vitro by stimulus-dependent inhibition of apoptosis.

Resolution of glomerular inflammation requires the removal of proliferating resident glomerular mesangial cells, but excessive loss of glomerular cells is a feature of postinflammatory scarring. Because apoptosis regulates mesangial cell number in glomerular inflammation, we have studied the exogenous control of apoptosis triggered in cultured mesangial cells by stimuli likely to be important in vivo. Apoptosis could be induced by serum deprivation to model decreased availability of survival factors, by etoposide as an example of DNA-damaging agents, by ligation of mesangial cell Fas, and by protein synthesis inhibition by cycloheximide. Insulin-like growth factor I (IGF-I), IGF-II, and basic fibroblast growth factor were each able to suppress apoptosis induced by serum deprivation, whereas TGF-beta 1, epidermal growth factor, and platelet-derived growth factor had no effect. IGF-I and IGF-II (but not basic fibroblast growth factor) were also able to protect cells from apoptosis induced by etoposide or cycloheximide. However, Fas-mediated apoptosis was resistant to suppression by all three cytokines. None of the cytokines tested caused a change in the levels of expression of Bcl-2, Bax, Bcl-x, or Bak proteins. The survival-promoting properties of serum-free medium conditioned by mesangial cells was abrogated by neutralizing IGF-I Ab. These experiments are the first to define cytokines that inhibit apoptosis and thereby promote survival of mesangial cells, and the data indicate a paracrine survival signaling role for IGF-I. Finally, the data show that Fas ligation can override cytokine survival signaling, emphasizing a candidate role for this molecule in the undesirable apoptotic loss of mesangial cells during the progression of glomerular scarring.

Animals↗
PubMed1997

Neutrophil fate in experimental glomerular capillary injury in the rat. Emigration exceeds in situ clearance by apoptosis.

Neutrophils (PMNs) and their toxic contents can injure glomeruli, but to date their fate in glomerulonephritis has been unknown. We studied glomerulonephritis induced in rats by formation of concanavalin A (Con A)/anti-Con A immune complexes on glomerular endothelial cells. PMN infiltration, which was almost exclusively confined to the lumen of glomerular capillaries, was transient, peaking at 4 hours, with only 9.0 +/- 4.1% (mean +/- SEM) of the maximum remaining at 24 hours. There was clear evidence of PMN apoptosis leading to phagocytosis in situ by intraluminal macrophages. However, the kinetics of leukocyte infiltration and PMN apoptosis, the preferential location at 24 hours of apoptotic PMNs within occluded capillary loops, and tracking of radiolabeled PMNs all indicated that in situ phagocytic clearance after apoptosis was the fate of a minority of PMNs, amounting to no more than one-fifth of the peak infiltrating load. Instead, the majority of infiltrating PMNs (72.9 +/- 3.1%) had emigrated from inflamed glomeruli by 24 hours, apparently returning to the circulation. We conclude that PMN emigration from inflamed glomeruli is a hitherto unrecognized mechanism for regulation of PMN-mediated glomerular injury.

Animals↗
PubMed1997

Treatment of experimental mesangioproliferative glomerulonephritis with non-anticoagulant heparin: therapeutic efficacy and safety.

Treatment with conventional heparin is effective in experimental mesangioproliferative glomerulonephritis. However, the long-term effects and safety of this therapy, in particular in the presence of mesangiolysis, have not been assessed. In addition, this therapy has been hampered by bleeding complications. In the present study, therefore, we investigated the long-term effects of a short course of non-anticoagulant (NA) heparin treatment in the anti-Thy 1.1 mesangioproliferative glomerulonephritis, in which early immune-mediated mesangiolysis subsequently leads to mesangial hyperproliferation. Rats received continuous ip NA-heparin or vehicle during the active mesangioproliferative phase (Days 2 to 9; early treatment) or during the early resolution phase (Days 10 to 17; late treatment). Whereas NA-heparin in the early treatment group did not affect the glomerular macrophage, lymphocyte, or platelet influx, it did lead to significantly decreased glomerular cellularity, mesangial cell proliferation, alpha-smooth muscle actin, desmin expression (ie, markers of activated mesangial cells), and matrix accumulation as well as to persistent mesangiolytic lesions including microaneurysms. Despite this latter finding, at Day 120, NA-heparin-treated rats of the early treatment group showed significantly better renal function and less proteinuria and glomerulosclerosis than vehicle-infused rats. In contrast, late therapy with NA-heparin neither accelerated resolution of the nephritis or otherwise affected the course of the disease. We conclude that transient NA-heparin therapy is effective in mesangioproliferative glomerulonephritis, both acutely and long term, when it is initiated during the active phase of the disease. Also, NA-heparin therapy is safe even in glomerular diseases accompanied by mesangiolysis.

Aneurysm↗
PubMed1996

What role does apoptosis play in progression of renal disease?

Apoptosis (programmed cell death) is now recognized to play an important role in regulating the number of renal cells in health and disease. Apoptosis may mediate beneficial deletion both of leukocytes and of excess resident cells from the inflamed glomerulus. However, this review focuses on the growing evidence that inappropriate engagement of the cell death 'program' contributes to the progression of renal diseases such as polycystic kidney disease and glomerulonephritis, mediating the loss of 'desirable' cells and eventual development of the hypocellular end-stage kidney.

Animals↗
PubMed1995

Basic fibroblast growth factor augments podocyte injury and induces glomerulosclerosis in rats with experimental membranous nephropathy.

Podocyte injury is believed to contribute to glomerulosclerosis in membranous nephropathy. To identify the factors involved, we investigated the effects of basic fibroblast growth factor (bFGF), a cytokine produced by podocytes, on rats with membranous nephropathy (passive Heymann nephritis [PHN]). All rats received a daily i.v. bolus of 10 microg bFGF or vehicle from days 3-8 after PHN induction. In proteinuric PHN rats on day 8, bFGF injections further increased proteinuria. Podocytes of bFGF-injected PHN rats showed dramatic increases in mitoses, pseudocyst formation, foot process retraction, focal detachment from the glomerular basement membrane, and desmin expression. bFGF injections in PHN rats did not alter antibody or complement deposition or glomerular leukocyte influx. bFGF-injected PHN rats developed increased glomerulosclerosis when compared with control PHN rats. Also, bFGF induced proteinuria and podocyte damage in rats injected with 10% of the regular PHN-serum dose. None of these changes occurred in bFGF-injected normal rats, complement-depleted PHN rats or rats injected with 5% of the regular PHN serum dose. These divergent bFGF effects were explained in part by upregulated glomerular bFGF receptor expression, induced by PHN serum. Thus, bFGF can augment podocyte damage, resulting in increased glomerular protein permeability and accelerated glomerulosclerosis. This bFGF action is confined to previously injured podocytes. Release of bFGF from glomerular sources (including podocytes themselves) during injury may represent an important mechanism by which podocyte damage is enhanced or becomes self sustained.

Animals↗
PubMed1995

Four hugs a day using therapeutic touch.

Imagine a prescription which prescribed four hugs per day to a patient suffering from depression. Hanning described findings that four hugs per day was an antidote for depression, eight hugs per day would achieve mental stability and twelve hugs per day would achieve real psychological growth. If this is the case, touch has a greater significance than most of us would realise. The following assignment was written whilst I was undertaking ENB 176 using reflective practice to explain the benefits or problems in using certain techniques.

Adult↗
PubMed1994

Mesangial cell apoptosis: the major mechanism for resolution of glomerular hypercellularity in experimental mesangial proliferative nephritis.

Increases in mesangial cell number may herald glomerular scarring, but they are not irreversible. This study sought mechanisms by which surplus glomerular mesangial cells can be cleared. A small proportion of cultured mesangial cells exhibited typical morphological features of apoptosis (programmed cell death), which was increased by growth factor deprivation or exposure to cycloheximide, stimuli known to increase apoptosis in other cell types. Apoptosis was confirmed by typical internucleosomal chromatin cleavage. In vivo, clear morphological evidence of mesangial apoptosis leading to phagocytosis by neighboring mesangial cells was obtained in self-limited mesangial proliferation induced in rats by Thy1.1 antibody, apoptosis occurring approximately 10-fold more frequently than in the healthy rat glomerulus. Indeed, changes in glomerular cell number in Thy1.1 nephritis strongly suggested that apoptosis is the major cell clearance mechanism counterbalancing cell division, thereby mediating resolution of glomerular hypercellularity in experimental mesangial proliferation.

Animals↗
PubMed1990

Teaching reading comprehension skills to spina bifida children.

Thirteen children with spina bifida (mean age 11 yrs 11 mths) and a mean reading comprehension reading deficit of 10.5 mths were enrolled into a remedial programme. The withdrawal single case study methodology was used (baseline--5 weeks, treatment--5 weeks, withdrawal--12 weeks). Each child was seen twice a week for 15 minutes during both the baseline and treatment stages. A teaching programme based on a close technique was utilized only during the treatment stage. The technique involved teaching each child a strategy for systematically examining a text for meaning. A halving of the comprehension deficit was observed by the end of the treatment stage, with a mean regression of almost 3 months at the end of the withdrawal stage. No relationship between IQ and gains in reading comprehension was observed. The results may indicate that, in part, reading comprehension deficits are performance deficits which, in turn, may be mediated by attentional strategies.

Adolescent↗
PubMed1990

Type of childcare at 18 months--I. Differences in interactional experience.

A longitudinal study has followed two-parent families and their first-born child. The families were chosen so that there were three groups of dual-earner families using relatives, childminders and nurseries for day care and one group of single-earner families. At 18 mths of age children in the study were observed in the four types of childcare setting. The data from the detailed observations were used to compare the children's interactional experience. The results indicate marked variation in the quality of children's experiences between different childcare settings. Possible reasons for such variation are discussed.

Attention↗
PubMed1990

Type of childcare at 18 months--II. Relations with cognitive and language development.

In a longitudinal study of women and their first-born children the relationship between type of day care experience and cognitive and language development at 18 mths of age was considered. There was a strong association between socio-economic characteristics and type of day care and analyses allowed for this. The results for cognitive development indicate a relationship with mother's education but not with type of day care. For language development the results indicate that children who experience group care were less likely to show much production of different word combinations, but that this was related to the children's language environments.

Child Care↗
PubMed1983

Unemployment and health in the context of economic change.

Evidence relating unemployment to health is found at every level of social science analysis from national population rates to individual psychophysiological stress response. At the population level of analysis, increase in the unemployment rate indicates recession and/or structural economic decline. At the individual level, unemployment is interpreted as a stressful life event. In both cases, inverse associations are found between measures of unemployment and indicators of health. We identify social science literatures associating health indicators with each of the following: economic growth, socioeconomic status, sociocultural change, economic instability, the status of being unemployed, social stress and work stress. Outstanding research issues include the requirements to identify and measure the effects of conditional factors and control variables in multivariate analysis and to examine a broader range of both severity of unemployment and severity of health outcomes. A research agenda proposes studies at the macro, meso and micro levels of analysis. We urge such research for its potential contribution both to analytic social science and to economic and social policy.

Health↗
PubMed1982

Economic change and sex-specific cardiovascular mortality in Britain 1955-1976.

Analyses directed toward recent declines in cardiovascular disease mortality rates have typically focused on alterations in important physiological and behavioral risk factors resulting from lifestyle changes and medical advances. In this study, a multivariate model of the impact of more fundamental changes in the socioeconomic and bio-physical environments has been developed and applied to cardiovascular disease mortality rates, by sex, in England and Wales and Scotland during 1955-1976. The predictive model includes factors associated with (1) long-term growth in the economy, (2) deleterious behavioral risk factors loosely associated with economic growth--especially cigarette consumption per capita, (3) economic instability--especially recession as indicated by factors related to unemployment, income loss, and recessional declines in average weekly hours worked in manufacturing industries, (4) health care, and (5) physical environmental disturbances--especially very cold temperatures. This model proves to be an excellent instrument for the statistical explanation of trends and fluctuations in CVD mortality rates for both sexes and both regions in Britain in the post-War period. In general, the overall exponential rate of economic growth is found to be the most powerful factor in the long-term decline in CVD mortality rates. Similarly, disturbances to the national and regional economic situations--especially recessions--have regularly been associated with elevated death rates for all populations observed. Cigarette and unusually high spirits consumption, as well as particularly cold winter temperatures, have also had important deleterious effects on CVD mortality. The proportion of government expenditures devoted to health care is associated with a reduction in CVD mortality in England and Wales.

Adult↗