Search

During the past two years our laboratory has isolated Propionibacterium—an anaerobic Gram-positive rod—on 40 occasions from the drainage fluid of 25 patients on CAPD and eight on IPD. Most patients had no symptoms and the fluid was sent for culture after treatment of peritonitis, during training period, and occasionally because it was cloudy. No association was found with patients' age, length on dialysis, or previous peritonitis episodes. The only statisti cally significant association (=0.033) was with recent (<30 days) catheter insertion. Patients with Propionibacterium as the only organism in their dialysis fluid had normal leucocyte count in the effluent, minimal or no symptoms, and received no treatment. In order to establish the frequency of positive cultures of asymptomatic patients, we cultured 95 dialysate effluents from 33 asymptomatic CAPD patients. Cultures were observed for 4 weeks. We found seven positive fluids (7.4%) in four patients (12%), aerobic sporeformer (2), (2) and (1). The mean time to grow was 18.6 days. In conclusion, effluents from asymptomatic CAPD patients may contain bacteria. The organisms are commensals requiring prolonged incubation to grow. Propionibacterium isolated from peritoneal effluent of patients with minimal or no symptoms does not require treatment. These findings suggest that errors in the technique of CAPD are not rare but when the number of organisms is small and the organism has low virulence, peritonitis does not occur. [ABSTRACT FROM PUBLISHER]

The effect of prior administration of two classes of 7S mouse anti-sheep red blood cell (SRBC) antibodies on the primary immune response to SRBC was studied. Mouse γG1 and γG2 immunoglobulins were isolated from serum by zone electrophoresis and density gradient isolectric focusing. The immunoglobulins were defined by qualitative and quantitative studies, and their effects on the primary response were determined by administering doses ranging from 0.5 to 0.001 mg of immunoglobulin 2 hours before injection of antigen. Gamma G1, antibody suppressed the response to SRBC at all concentrations. High doses of γG2 antibody partially suppressed 19S plaque-forming cells (PFC), but had no significant effect on serum haemagglutinin (HA) levels. Low doses of γG2 antibody specifically augmented both the 19S PFC and serum HA levels. It is concluded that the specific suppressing and augmenting influences of antibodies on the primary response are a function of class. In addition, it is proposed that &gammaG1, and γG2 antibodies can aet as specific regulatory elements during the primary response by exerting these two competing biological effects on antibody synthesis. [ABSTRACT FROM AUTHOR]

The production of complement was investigated using a modification of Jerne's haemolytic plaque technique. Guinea-pig spleen and bone marrow cells were suspended in layers of agarose containing, as indicator cells, sensitized sheep erythrocytes (EA) or intermediate products consisting of EA and some of the components of complement. R reagents or serum, in which certain components of the C′3 complex had been inactivated, were added after incubation. No plaque formation due to release of complement components was observed. Bone marrow and spleen cells produced plaques when incubated with sensitized or non-sensitized erythrocytes and a reagent containing cobra venom. A method was developed for the preparation of thin films of agarose in which tissue cells and erythrocytes were suspended in a single cell layer. Single cells and clumps of cells present in the peritoneal exudate of normal guinea-pigs produced plaques when incubated with EA or EAC′4 and R1. Occasionally, similar clumps of cells also produced plaques with EA or EAC′1 and R4. The plaque-forming cells appeared to be macrophages. Plaques were not detected with R2 or R3. No plaques were produced by spleen cells under similar experimental conditions. Bone marrow cells produced plaques with both sensitized and non-sensitized erythrocytes after prolonged incubation. Optimal plaque formation occurred when R1 or R4 was added before incubation. Plaques were not produced if the tissue cells were pre-incubated in suspension cultures for 2 hours or longer before plating. Treatment of the peritoneal exudate cells with KCN or with dinitrophenol prevented plaque formation. [ABSTRACT FROM AUTHOR]

Background: Excess alcohol consumption has serious adverse effects on health and results in violence-related harm. Objective: This study investigated the impact of change in community alcohol availability on alcohol consumption and alcohol-related harms to health, assessing the effect of population migration and small-area deprivation. Design: A natural experiment of change in alcohol outlet density between 2006 and 2011 measured at census Lower Layer Super Output Area level using observational record-linked data. Setting: Wales, UK; population of 2.5 million aged ≥ 16 years. Outcome measures: Alcohol consumption, alcohol-related hospital admissions, accident and emergency (A&E) department attendances from midnight to 06.00 and violent crime against the person. Data sources: Licensing Act 2003 [Great Britain. Licensing Act 2003. London: The Stationery Office; 2003. URL: www.legislation.gov.uk/ukpga/2003/17/contents (accessed 8 June 2015)] data on alcohol outlets held by the 22 local authorities in Wales, alcohol consumption data from annual Welsh Health Surveys 2008–12, hospital admission data 2006–11 from the Patient Episode Database for Wales (PEDW) and A&E attendance data 2009–11 were anonymously record linked to the Welsh Demographic Service age–sex register within the Secure Anonymised Information Linkage Databank. A final data source was recorded crime 2008–11 from the four police forces in Wales. Methods: Outlet density was estimated (1) as the number of outlets per capita for the 2006 static population and the per quarterly updated population to assess the impact of population migration and (2) using new methods of network analysis of distances between each household and alcohol outlets within 10 minutes of walking and driving. Alcohol availability was measured by three variables: (1) the previous quarterly value; (2) positive and negative change over the preceding five quarters; and (3) volatility, a measure of absolute quarterly changes during the preceding five quarters. Longitudinal statistical analysis used multilevel Poisson models of consumption and Geographically Weighted Regression (GWR) spatial models of binge drinking, Cox regression models of hospital admissions and A&E attendance and GWR models of violent crime against the person, each as a function of alcohol availability adjusting for confounding variables. The impact on health inequalities was investigated by stratifying models within quintiles of the Welsh Index of Multiple Deprivation. Results: The main finding was that change in walking outlet density was associated with alcohol-related harms: consumption, hospital admissions and violent crime against the person each tracked the quarterly changes in outlet density. Alcohol-related A&E attendances were not clinically coded and the association was less conclusive. In general, social deprivation was strongly associated with the outcome measures but did not substantially modify the associations between the outcomes and alcohol availability. We found no evidence for an important effect of population migration. Limitations: Limitations included the absence of any standardised methods of alcohol outlet data collation, processing and validation, and incomplete data on on-sales and off-sales. We were dependent on the quality of clinical coding and administrative records and could not identify alcohol-related attendances in the A&E data set. Conclusion: This complex interdisciplinary study found that important alcohol-related harms were associated with change in alcohol outlet density. Future work recommendations include defining a research standard for recording outlet data and classification of outlet type, the methodological development of residence-based density measures and a health economic analysis of model-predicted harms. Funding: The National Institute for Health Research Public Health Research programme. Additional technical and computing support was provided by the Farr Institute at Swansea University, made possible by the following grant:: Centre for the Improvement of Population Health through E-records Research (CIPHER) and Farr Institute capital enhancement. CIPHER and the Farr Institute are funded by Arthritis Research UK, the British Heart Foundation, Cancer Research UK, the Chief Scientist Office (Scottish Government Health Directorates), the Economic and Social Research Council, the Engineering and Physical Sciences Research Council, the Medical Research Council, the National Institute for Health Research, the National Institute for Social Care and Health Research (Welsh Government) and the Wellcome Trust (grant reference MR/K006525/1).