Global volumetric reductions across amygdala nuclei in chronic TBI

BACKGROUND: Traumatic brain injury (TBI) may increase susceptibility to neurodegenerative diseases later in life, that is, the accelerated aging hypothesis. This is supported by recent research demonstrating subcortical gray matter atrophy patterns in chronic TBI (M=9 years post-injury) that are similar to some neurodegenerative diseases. Atrophy appears to be global across hippocampal subfields and selective across thalamic nuclei. There have been no investigations into differential atrophy patterns across amygdalar nuclei in chronic TBI. OBJECTIVE: Given the close proximity between the amygdala and hippocampus, and amygdala atrophy implicated in some neurodegenerative conditions, the aims of the present investigation are to determine 1) whether the pattern of amygdala atrophy in chronic TBI follows a global or selective pattern and 2) whether time since injury predicts specific nuclei atrophy. METHOD: 40 TBI and 33 non-TBI participants completed T1 weighted 3T magnetic resonance imaging scans. Amygdalae were segmented into 10 nuclei using freesurfer, summed bilaterally and adjusted for estimated intracranial volume and sex. Unpaired t-tests (alpha Holm adjusted) and Cohen’s D were used to compare groups. Partial correlations (adjusting for age) were used to test the relationship between nuclei and time since injury. RESULTS: Amygdala volumes were smaller in the TBI group than the non-TBI group and this pattern was consistent across all 10 amygdala nuclei suggesting a global pattern. No correlations between amygdala nuclei and time since injury were significant. CONCLUSION: Global changes across amygdala nuclei is evident in chronic TBI. This is similar to the global pattern of atrophy observed across hippocampal subfields and in contrast to selective thalamic atrophy that is evident in these same individuals. Lack of a relationship between nuclei and time since injury does not support the accelerate

Class I HLA-restricted cytotoxic T lymphocyte responses against malaria-elucidation on the basis of HLA peptide binding motifs

In animal models, CD8+ T cells are a critical effector mechanism in the protective immunity against malaria. Conventional approaches to the development of many vaccines, including those against malaria, have however proved inadequate. In particular, an alternative approach is needed for the development of vaccines designed to induce a cellular immune response mediated by CD8+ T cells. Advances in the field of molecular immunology during the past decade have provided an insight into the presentation of peptides by MHC class I molecules and their recognition by CD8+ T cells. These studies have provided a conceptual basis for the development of efficacious parasitic and viral vaccines. By a combination of immunochemical and cellular immunologic analyses based on specific peptide binding motifs, a subunit malaria vaccine that includes CD8+ T cell epitopes restricted by the most common class I HLA alleles, including HLA-A2, can now be constructed