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There is very little change in the quantity of antibodies people produce, of any isotype, with age. However, there is a change in the quality of the antibody response. Older people produce fewer antibodies that are specific for the activating pathogen or vaccine. At the same time, the number of nonspecific antibodies increases. Quite often these antibodies have selfreactivity (e.g., anti-dsDNA). The appearance of these antibodies is not associated with pathogenic autoimmune disease, although it is true that the incidence of some autoimmune diseases increases with age. The authors postulate that the process of antibody affinity maturation is compromised in old age. No evidence was found that the process of hypermutation is compromised with age. However, using graph theory to study the dynamics of a germinal center selection process, a decrease in the extent of selection occurring in the germinal centers of mucosal tissue was observed with age. This is a tissue-specific phenomenon because the decrease was not seen in the germinal centers of spleen. Because selection of highly specific cells in the germinal center depends on a number of factors (number and quality of founder cells, help from T cells, and follicular dendritic cells) these need to be investigated further to determine what is needed to improve the affinity mutation process.

BackgroundThe best method for measuring the degree of platelet inhibition with glycoprotein (GP) IIb-IIIa antagonists during percutaneous coronary intervention (PCI) and the optimal degree of periprocedural inhibition is uncertain. Low molecular weight heparins have been reported to cause less platelet activation than unfractionated heparin. Therefore, compared with unfractionated heparin (UHF), a low molecular weight heparin could enhance measured platelet inhibition. In this study, we compared 3 methods of measuring platelet inhibition and investigated the effects of half doses of abciximab in combination with either UFH or the low molecular weight heparin dalteparin in patients undergoing PCI with planned abciximab administration. MethodsAbciximab-induced platelet inhibition was measured serially by means of 3 assays: 1) GP IIb-IIIa receptor occupancy, 2) binding of the activated GP IIb—IIIa-specific monoclonal antibody PAC1, and 3) agglutination of platelets with fibrinogen-coated beads (RPFA). Forty patients were randomly allocated to receive either UFH (70 U/kg) or dalteparin (60 IU/kg), followed by a half dose of abciximab (0.125 mg/kg) administered twice at 10-minute intervals. Assays were obtained 10 minutes after each half dose of abciximab and 8 to 10 and 24 hours after abciximab administration. ResultsNo differences between UFH and dalteparin were observed. At each time-point measured, the mean percent platelet inhibition as determined by means of the receptor occupancy assay and PAC1 binding assay was less than the degree of inhibition determined by means of the RPFA. ConclusionsThe results of targeted levels of platelet inhibition cannot be extrapolated between different clinical trials of GP IIb-IIIa antagonists unless the same assay is used. Dalteparin, compared with UFH, does not enhance platelet inhibition or receptor occupancy by abciximab, as demonstrated by means of 3 separate assays. (Am Heart J 2003;145:e6.)

Vaccination of mice with the 42-kDa region of Plasmodium yoelii merozoite surface protein 1 (MSP1(42)) or its 19-kDa C-terminal processing product (MSP1(19)) can elicit protective antibody responses in mice. To investigate if the 33-kDa N-terminal fragment (MSP1(33)) of MSP1(42) also induces protection, the gene segment encoding MSP1(33) was expressed as a glutathione S-transferase (GST) fusion protein. C57BL/6 and BALB/c mice were immunized with GST-MSP1(33) and subsequently challenged with the lethal P. yoelii YM blood stage parasite. GST-MSP1(33) failed to induce protection, and all mice developed patent parasitemia at a level similar to that in naive or control (GST-immunized) mice; mice immunized with GST-MSP1(19) were protected, as has been shown previously. Specific prechallenge immunoglobulin G (IgG) antibody responses to MSP1 were analyzed by enzyme-linked immunosorbent assay and immunofluorescence. Despite being unprotected, several mice immunized with MSP1(33) had antibody titers (of all IgG subclasses) that were comparable to or higher than those in mice that were protected following immunization with MSP1(19). The finding that P. yoelii MSP1(33) elicits strong but nonprotective antibody responses may have implications for the design of vaccines for humans based on Plasmodium falciparum or Plasmodium vivax MSP1(42).

ABSTRACTVaccination of mice with the 42-kDa region of Plasmodium yoeliimerozoite surface protein 1 (MSP142) or its 19-kDa C-terminal processing product (MSP119) can elicit protective antibody responses in mice. To investigate if the 33-kDa N-terminal fragment (MSP133) of MSP142also induces protection, the gene segment encoding MSP133was expressed as a glutathione S-transferase (GST) fusion protein. C57BL/6 and BALB/c mice were immunized with GST-MSP133and subsequently challenged with the lethal P. yoeliiYM blood stage parasite. GST-MSP133failed to induce protection, and all mice developed patent parasitemia at a level similar to that in naive or control (GST-immunized) mice; mice immunized with GST-MSP119were protected, as has been shown previously. Specific prechallenge immunoglobulin G (IgG) antibody responses to MSP1 were analyzed by enzyme-linked immunosorbent assay and immunofluorescence. Despite being unprotected, several mice immunized with MSP133had antibody titers (of all IgG subclasses) that were comparable to or higher than those in mice that were protected following immunization with MSP119. The finding that P. yoeliiMSP133elicits strong but nonprotective antibody responses may have implications for the design of vaccines for humans based on Plasmodium falciparumor Plasmodium vivaxMSP142.

This critical review explores the relative lack of changes in behaviour following interventions such as health education, across the age ranges, to reduce the prevalence of fractures due to osteoporosis. Existing research into osteoporosis is briefly critically appraised. Current evaluations of the effects of health education are small-scale and relatively inconclusive. Health belief models explain but appear not to benefit the realities of lack of change of lifestyle required to have an effect on osteoporosis incidence. Screening with education seems to offer a way forward, but requires more research to confirm its efficacy.

Presents information on gout disease. Historical epidemiology; Symptoms and medical management; Comparison between primary and secondary gout; Stages of the disease.

LETTERS THE RACE IS ON! Right, then! Who's going to be first over the starting line, Amstrad or Atari -- or will an unknown come surging through the field to […]

Provides an overview of the physiological aspects of bone transplantation and explores bone banking, a key step in the complex and critical process of bone transplantation. Identification of potential donors; Criteria for donation; Storage and processing of bone.

A letter to the editor is presented in response to the article "The Age of Ooops," by Derrick Jensen in the March/April 2011 issue.