Biomedical subjects

A Aase

Publications and source records attributed to A Aase.

41 records · Page 3Linked to original sources

PubMed1989

C1q binding to chimeric monoclonal IgG3 antibodies consisting of mouse variable regions and human constant regions with shortened hinge containing 15 to 47 amino acids.

We have constructed four different deletion mutants of a chimeric mouse-human IgG3 anti-(4-hydroxy-3-nitrophenyl)acetyl/(5-iodo-4 hydroxy-3 nitrophenyl) acetyl (NP/NIP) antibody lacking one or more of the four exons coding for the hinge region. The mutant variants all retained intact hinge region epitopes since they all reacted with IgG3 hinge-specific antibodies. Surprisingly, all the deletion mutants bound C1q equally well or even better than the wild type. Thus the high C1q binding activity of IgG3 compared to IgG1 is apparently not due to the total length of the IgG3 hinge, which is 62 amino acids, nor is it due to the length of the upper hinge which is the stretch from the end of CH1 to the first inter-heavy chain disulfide bond.

Amino Acid Sequence↗

PubMed1989

Regionalizing mortality data: ischaemic heart disease in Norway.

The way regions are delimited has a bearing on the geographical patterns and time trends which emerge from cause specific mortality analysis. Whenever possible, alternative regionalizations should be used to explore the full information potential of the data. For statistical reasons, the size of the regional units (populations-at-risk) should be selected according to the frequency of the cause of death, number of years in the time period, etc. A geographical mortality information system for Norway, based on individual death records and with quick and flexible retrieval options is described. As a demonstration, geographical time trends in ischaemic heart disease from 1970 to 1985 are studied, using different schemes of regionalization. A clear tendency towards regional convergence appears in the rural-urban dimension, but there is no convergence between the five subnational regions of the country. There is no evidence that counties which have received heart disease intervention projects fare any better than those which have not, but here a more thorough analysis is recommended. Within the intervention counties, there are large variations both in mortality levels and trends.

Aged↗

PubMed1989

The diffusion of cardiovascular disease in the Norwegian farming community: a combination of morbidity and mortality data.

This article analyses an observed increase in cardiovascular morbidity among male farmers in Norway during the last decade in the light of the traditionally low mortality in farmers. Three hypotheses to explain the increases in CVD morbidity are tested, of which one, stating that there is a time lag in the spread of risk factors, proves to be most fruitful. Mortality data for agricultural communities show no increase in overall CVD rates, but when age-specific rates are analysed, an increase in the younger age groups emerges, especially for ischaemic heart disease. If this process continues, farmers and farming areas may change from low to high mortality, relatively speaking. It is argued that this change is due to a time lag in two waves, first an increase in risk factors such as smoking, more fatty diets and less physically demanding work, then improved lifestyles due to a better perception of risk factors. Both waves may be affecting rural areas later than the urban centres. Knowledge of such geographical and socio-economic diffusion processes is important in the planning and implementation of prevention programmes.

Aged↗

PubMed1989

The IgG subclass pattern of complement activation depends on epitope density and antibody and complement concentration.

Using a matched series of human-mouse chimaeric IgG anti-5-iodo-4-hydroxy-3-nitrophenacetyl (anti-NIP) antibodies and NIP-bovine serum albumin (NIP-BSA) we examined how different variables influence the activation pattern of complement. When BSA was used with different hapten densities and the input of NIP-BSA was altered, we observed a change in the subclass reaction pattern. IgG3 fixed more Clq than IgG1 and IgG2 in all situations. IgG1 was slightly better than IgG3 and IgG2 at high antigen concentrations at activating C4 and C3 and inducing formation of the terminal complement complex (TCC). When the epitope density and/or the NIP-BSA concentration was reduced, IgG3 became best, followed by IgG1 and IgG2. IgG1 now revealed a marked prozone. Furthermore, IgG4 was found to activate C3 and mediate TCC formation at high epitope and complement concentrations.

Antibodies↗

PubMed1988

Human rheumatoid factor reacting with rabbit IgG but not with human IgG.

A patient, O.A., had in her serum an IgM rheumatoid factor (RF) of high titer which reacted equally well with monomeric and polymeric rabbit IgG, but showed no reaction with homologous or autologous monomeric and polymeric IgG, neither in hemagglutination nor in ELISA tests. In contrast to the usual specificity of RFs crossreacting with rabbit and human IgG, which require the presence of both the CH2 end CH3 domains, the O.A. RF showed reaction only against the CH3 domain. The existence of human RF not reacting with human IgG could challenge the notion that RF production is necessarily induced by autologous IgG and thus playing an important role in potentiating and regulating secondary immune responses. The O.A. RF might represent 1: an extreme case of heteroclitic antibody, 2: the internal image of a hypothetical Fc-receptor reacting with rabbit IgG but not with human IgG, 3: a result of polyclonal B cell activation, 4: an antigenic crossreaction with an unknown antigen with similarities to rabbit IgG but not to human IgG.

Agglutination Tests↗