Local wood demand, land cover change and the state of Albany Thicket on an urban commonage in the Eastern Cape, South Africa.

Understanding the rates and causes of land-use change is crucial in identifying solutions, especially in sensitive landscapes and ecosystems, as well as in places undergoing rapid political, socioeconomic or ecological change. Despite considerable concern at the rate of transformation and degradation of the biodiversity-rich Albany Thicket biome in South Africa, most knowledge is gleaned from private commercial lands and state conservation areas. In comparison, there is limited work in communal areas where land uses include biomass extraction, especially for firewood and construction timber. We used aerial photographs to analyze land use and cover change in the high- and low-use zones of an urban commonage and an adjacent protected area over almost six decades, which included a major political transition. Field sampling was undertaken to characterize the current state of the vegetation and soils of the commonage and protected area and to determine the supply and demand for firewood and construction timber. Between the 1950s and 1980s, there was a clear increase in woody vegetation cover, which was reversed after the political transition in the mid-1990s. However, current woody plant standing stocks and sustainable annual production rates are well above current firewood demand, suggesting other probable causes for the decline in woody plant cover. The fragmentation of woody plant cover is paralleled by increases in grassy areas and bare ground, an increase in soil compaction, and decreases in soil moisture, carbon, and nutrients.

The human G1m1 allotype associates with CD4+ T-cell responsiveness to a highly conserved IgG1 constant region peptide and confers an asparaginyl endopeptidase cleavage site.

The human G1m1 allotype comprises two amino acids, D12 and L14, in the CH3 domain of IGHG1. Although the G1m1 allotype is prevalent in human populations, ~40% of Caucasiods are homozygous for the nG1m1 allotype corresponding to E12 and M14. Peptides derived from the G1m1 region were tested for their ability to induce CD4+ T-cell proliferative responses in vitro. A peptide immediately downstream from the G1m1 sequence was recognized by CD4+ T cells in a large percentage of donors (peptide CH315-29). CD4+ T-cell proliferative responses to CH315-29 were found at an increased frequency in nG1m1 homozygous donors. Homozygous nG1m1 donors possessing the HLA-DRB1*07 allele displayed the highest magnitudes of proliferation. CD4+ T cells from donors homozygous for nG1m1 proliferated to G1m1-carrying Fc-fragment proteins, whereas CD4+ T cells from G1m1 homozygous donors did not. The G1m1 sequence creates an enzymatic cleavage site for asparaginyl endopeptidase in vitro. Proteolytic activity at D12 may allow the presentation of the CH315-29 peptide, which in turn may result in the establishment of tolerance to this peptide in G1m1-positive donors. Homozygous nG1m1 patients may be more likely to develop CD4+ T-cell-mediated immune responses to therapeutic antibodies carrying the G1m1 allotype.

The HLA-DR2 haplotype is associated with an increased proliferative response to the immunodominant CD4(+) T-cell epitope in human interferon-beta.

Human CD4(+) T-cell epitopes were identified in interferon-beta (IFN-beta)-1b. A prominent peptide epitope region was found that induced a proliferative response in 16% of all donors tested. Responses corresponded to the presence of the HLA-DR2 haplotype. Responsive donors expressing the HLA-DQ6 allele showed an increased level of proliferation to the epitope as compared to peptide-responsive HLA-DQ6 negative donors. A similar result was found for HLA-DR15-expressing donors. PBMC from donors expressing HLA-DR15 were more likely to proliferate in response to IFN-beta in a whole-protein in vitro assay than donors who did not carry this haplotype. It is striking that the common DQ6 allele HLA-DQB1(*)0602 is found in linkage disequilibrium with HLA-DRB1(*)1501, and this combination defines the HLA genotype associated with the development of multiple sclerosis. The HLA association between a response to IFN-beta and MS might explain the prevalence of neutralizing antibody development, and may underlie the etiology of the disease.

Peritoneal B-cell development depends on strain, radiation, and time.

OBJECTIVE: B-1a, B-1b, and B-2 cells represent the three B-cell subsets in mice. Previous studies have demonstrated that peritoneal B-1a cell development is absent, or nearly so, from adult bone marrow transfers into irradiated adult hosts. The majority of these studies have been performed under a limited set of conditions with irradiated host mice. Here we examined that under a variety of conditions, peritoneal B-1a cells can develop in significant numbers from adult bone marrow transfers into severe combined immunodeficient (SCID) and recombination activation gene 2(-) (RAG-2(-)) mice. MATERIALS AND METHODS: Adult bone marrow was transferred into various strains of irradiated and nonirradiated adult immunodeficient RAG-2(-) and SCID mice. Peritoneal B-cell engraftment was examined by fluorescein-activated cell sorting analysis and unpaired t-tests were used to determine significant differences of B-cell engraftment among the various conditions of cell transfer. RESULTS: The level of B-1a cell engraftment was variously affected by the type of host immunodeficiency, the combination of donor and host strains, and the time allowed for engraftment. Irradiation of SCID, but not RAG-2(-), host mice inhibited B-1a-cell engraftment. Additionally, decreasing the number of bone marrow progenitor cells transferred was not found to preferentially affect B-1a cell development in irradiated RAG-2(-) hosts. CONCLUSION: In the context of these strains, we conclude that adult murine bone marrow contains progenitors that have the capacity to reconstitute peritoneal B-1a cell populations to donor levels.

CD4+ T-cell epitope determination using unexposed human donor peripheral blood mononuclear cells.

The engineering of protein therapeutics to improve their stability, their efficacy, or to create "humanized" versions introduces changes to the amino acid sequence that are potential T-cell epitopes. Until now, there has been no available assay to detect primary T-cell responses to novel epitopes in humans. Currently available in vitro protocols for epitope determination rely on peripheral blood lymphocytes from environmentally exposed or disease-bearing donors. This severely limits the opportunity to confirm T-cell epitopes in novel proteins, because exposed donors are not available to novel or engineered proteins. Other methods for determining T-cell epitopes are either computer-modeled predictions based on potential binding to HLA molecules or the identification of peptides presented by HLA molecules removed from the surface of tumor cells or protein-pulsed antigen-presenting cells. Because HLA binding is necessary, but not sufficient, for T-cell responses, these methods must be validated by in vitro presentation assays. The authors describe a dendritic cell-based assay that identifies CD4+ T-cell epitopes in novel proteins using unexposed donors. Predicted T-cell epitopes in the protein of interest were confirmed using cells from two verified exposed donors. The major CD4+ T-cell epitope of the novel protein examined in this study associated with the expression of HLA DRb1*15. This assay reflects de novo priming in vitro, and it accurately identifies primary T-cell epitopes. This assay is a powerful tool for determining relevant immunostimulatory T-cell epitopes for all types of immunoregulatory applications.

Reengineering the front office: cashing in on the cash cow.

If a company can reengineer its business processes into modules that can be linked, unlinked, and relinked inexpensively, seamlessly, and instantly, it will be able to provide unique value to each and every customer. A modular approach presents a unique opportunity to create significant value and offer customers a proposition that is impossible or at least extremely difficult for your competition to duplicate. This article explains how to reengineer individual processes in light of the overall business strategy chosen by a company.

Strategy: the key to financial payback from reengineering.

This article will present the differences between restructuring, reengineering, and reinventing. It will identify a process for developing a leadership position that is difficult or impossible to duplicate and show how to develop a business strategy that leads to correctly identifying the core value-added processes of your business--the right ones to reengineer.

p24 antibody production in p24 antibody-negative HIV-infected subjects.

To determine if HIV-infected patients with no detectable serum antibodies to p24 are producing antibodies to p24 (anti-p24), blood was obtained from 49 HIV-infected patients at various stages of infection. Serum p24 antigen levels were measured and peripheral blood mononuclear cells were cultured for 1 week without mitogenic stimulation. The presence of anti-p24 in culture supernatants and sera was determined by radioimmunoprecipitation assays. Cells from 89% of the patients who had anti-p24 in their sera spontaneously synthesized anti-p24 in vitro. Similarly, cells from 83% of the HIV-infected patients who had no detectable anti-p24 in their sera spontaneously produced anti-p24 in vitro. Thus the absence of anti-p24 in serum did not reflect suppression in the ability of patients' cells to synthesize and secrete antibodies to p24. However, cells from patients whose sera contained anti-p24 spontaneously synthesized more anti-p24 than did cells from patients whose sera lacked anti-p24, suggesting that these two groups of patients may represent individuals with inherently high or low responses to p24 epitopes, respectively.