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OSM-Classicis a program designed in Matlab® to provide a method of accurately determining strain in a test sample using an optical imaging technique. Measuring strain for the mechanical characterization of materials is most commonly performed with extensometers, LVDT (linear variable differential transistors), and strain gauges; however, these strain measurement methods suffer from their fragile nature and it is not particularly easy to attach these devices to the material for testing. To alleviate these potential problems, an optical approach that does not require contact with the specimen can be implemented to measure the strain. OSM-Classicis a software that interrogates a series of images to determine elongation in a test sample and hence, strain of the specimen. It was designed to provide a graphical user interface that includes image processing with a dynamic region of interest. Additionally, the stain is calculated directly while providing active feedback during the processing.

A naturally occurring immunodeficiency syndrome has been seen in a captive colony of macaque monkeys. This syndrome is seen primarily in the species Macaca cyclopis. Affected animals died with lymphomas (a rare disease in macaques) or such opportunistic infections as Pneumocystis carinii and noma (necrotizing gingivitis). These M. cyclopis exhibited anemia, neutropenia, and a circulating bizarre immature monocyte. In addition, liver function tests suggested hepatitis. Pokeweed mitogen-, concanavalin A-, and xenogeneic cell-stimulated proliferative responses by lymphocytes of animals with the syndrome were dramatically diminished. The T4 (helper, inducer)/T8 (suppressor, cytotoxic) ratio in the peripheral blood mononuclear T-cell populations of M. cyclopis in this colony are decreased when compared with those from either Macaca mulatta in the same colony or normal humans. Epidemiologic evidence implicates a common source agent in this syndrome. The similarity of this syndrome in macaques to human acquired immunodeficiency syndrome suggests that it may provide an important model for studying the human syndrome.

The naturally occurring immunodeficiency syndrome of macaque monkeys is an important animal model for the acquired immunodeficiency syndrome in humans. A new type D retrovirus, distinct from Mason-Pfizer monkey virus, has been isolated from affected animals at the New England Regional Primate Research Center. We now report the results of experimental infection of macaques with retrovirus D/New England after 13 months of study. Inoculated macaques developed lymphadenopathy without follicular hyperplasia, profound neutropenia, and a transient decrease in peripheral blood lymphocyte blastogenic responsiveness. Despite our varying the strain of virus, the manner in which the virus was grown, the size of the inoculum, and the age of the inoculated animals, infected macaques have not developed opportunistic infections or profound, prolonged loss of T cell function, key features of the macaque immunodeficiency syndrome. Therefore, experimental infection of naive macaques with D/New England has not reproduced the naturally occurring macaque immunodeficiency syndrome.

Restriction on cytolytic T lymphocyte (CTL)-target cell-interactions are studied in the primate S. oedipus, a naturally occurring A + B----A bone marrow-chimeric species. We show that the T cell, B cell, and myelomonocytic progenitor cell populations are chimeric in this species. We selected animals for study that are populated by fully major histocompatibility complex (MHC)-disparate hematopoietic cell populations, using a functional assay system. We then developed an in vitro system for analyzing at the clonal level the genetic restrictions on the trinitrophenyl-specific CTL-target cell interactions of this species. In this system, we have shown that tolerance to foreign MHC determinants was not, of itself, sufficient to facilitate the generation of CTL specific for target cells expressing those foreign MHC determinants. Rather, a marked preference for the expansion of CTL clones with a restriction for target cells bearing the host animals' MHC determinants was seen. Hematopoietically derived cells did not affect the repertoire of these T lymphocytes. These studies represent the first demonstration of the phenomenon of an environment dictating interactional restrictions on CTL in a naturally occurring bone marrow-chimeric animal. This is also the first demonstration of the profound influence of the environment on the repertoire of the T lymphocyte in a primate species.

The nonobese diabetic (NOD) mouse model of type 1 diabetes (T1D) was discovered by coincidence in the 1980s and has since been widely used in the investigation of T1D and diabetic complications. The current in vivo study was originally designed to prospectively assess whether hyperglycemia onset is associated with physical destruction or functional impairment of beta cells under inflammatory insult during T1D progression in diabetes-prone female NOD mice. Prediabetic 16- to 20-wk-old NOD mice were transplanted with green fluorescent protein (GFP)-expressing reporter islets in the anterior chamber of the eye (ACE) that were monitored longitudinally, in addition to glycemia, with and without immune modulation using anti-CD3 monoclonal antibody therapy. However, there was an early and vigorous immune reaction against the GFP-expressing beta cells that lead to their premature destruction independent of autoimmune T1D development in progressor mice that eventually became hyperglycemic. This immune reaction also occurred in nonprogressor NOD recipients. These findings showed a previously unknown reaction of NOD mice to GFP that prevented achieving the original goals of this study but highlighted a new feature of the NOD mice that should be considered when designing experiments using this model in T1D research.