Evolutive levels of NGF in neurodegenerative disorders.
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Adult↗
Biomedical subjects
M A Robinson
Publications and source records attributed to M A Robinson.
Mitogens, superantigens, and nominal antigens elicit distinctive patterns of TCRB CDR3 diversity.
The third complementarity-determining region (CDR3) is the only nongermline-encoded hypervariable region of the T cell receptor beta (TCRB) chain, and it is the region that has been predicted to confer fine specificity of the TCR for peptide-MHC complexes. For this reason analysis of TCRB CDR3 heterogeneity may provide insight into immune mechanisms operative in infectious and autoimmune diseases. PBMC stimulated with either mitogen (PHA), superantigen (TSST-1), or nominal antigen (tetanus toxoid) have been compared with unstimulated PBMC using a two-dimensional approach. Analysis of the expressed TCRBV gene repertoire CDR3 length profile coupled with SSCP methodology enabled the discrimination of sequences with the same CDR3 length. For both freshly isolated and PHA stimulated PBMC, a normally distributed spectrum of CDR3 lengths (five or more products) was observed. These products differed by 3 bp (1 amino acid) due to the strict requirement for in-frame rearrangements in the CDR3 region of TCR. By contrast, tetanus toxoid stimulated PBMC had restricted profiles for most TCRBV families after as few as 7 days of incubation. The oligoclonal nature of samples showing CDR3 length restriction was revealed by SSCP analysis and confirmed by sequence determination. Superantigen stimulation resulted in unique patterns of diversity, which included polyclonal expansion of specific TCRBV families as well as oligoclonal expansion of most other TCRBV families. These data reveal complex yet distinct patterns of TCR diversity in response to different T cell activation stimuli.
Adult↗
Diversity in the human T cell receptor beta chain.
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Amino Acid Sequence↗
Under lock and key.
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Attitude of Health Personnel↗
[A study of the oxidative stress indicators in elderly monkeys].
INTRODUCTION: Under physiological conditions aerobic cells produce reactive species of oxygen. Cell survival depends on the equilibrium between the oxidation processes and the antioxidant defences. This interaction determines whether the cell suffers oxidation stress or not. Recent studies suggest that a reduced capacity for oxidation metabolism and proinflammatory states contribute to neurodegenerative changes related to age in humans. OBJECTIVE: To obtain information regarding the relation of TNF-mu to oxidation phenomena in nonhuman primates. MATERIAL AND METHODS: In this study we compare serum levels of the activity of superoxide dismutase (SOD) catalase (CAT), the levels of malonyldialdehyde (MDA) and tumor necrosis factor alpha TNF-alpha using spectrophotometric techniques in young and old nonhuman primates. RESULTS AND CONCLUSION: Our results suggest a relationship between the alterations in oxidation metabolism with the neurodegenerative changes which occur in monkeys.
Aging↗
[Changes in nerve growth factor levels related to age and neurotrophic treatment in non-human primate].
INTRODUCTION: To examine the amounts and role of growth factors in different tissues and corporal fluid, new sensitive techniques have to be developed. A major problem is that the normal concentration of trophic substances, such as nerve growth factor (NGF), in central and peripheral nervous system and in fluids is very low (ng pg/ml). A valuable method of research is the sensitive two site enzyme immunoassay using the monoclonal antibody 27/21 to mouse NGF. Materials and methods. The present work applied this enzyme immunoassay to examine the NGF levels in normal non human primate sera (n= 94) and applied this assay to study of NGF levels in two non human primate receiving NGF infusion: one young and one aged. Two groups of non human primate sera were studied one young adult (n= 69) and one aged (n= 25). The serum samples NGF treated non human primate were taken before the infusion and at the 1st week and 1st, 3rd, 6th and 12th month after infusion. RESULTS: To further test the specificity of conjugate binding, dilutions of the non human primate sera were preincubated with an excess of monoclonal NGF antibody 27/21 in solution. With this strategy it was possible to completely block the signal obtained using the enzyme immunoassay. We found very low levels of NGF in aged monkeys (0.054 ng/ml) when compared with young adult group (0.152 ng/ml) (p> 0.01). The NGF levels in aged non human primate treatment with NGF was very low before (0.50 ng/ml) and during NGF treatment evolution time, whereas at the the 12th month showed an increase in NGF levels (0.180 ng/ml). We found normal values of NGF in the young monkey before and during the first year after NGF infusion. CONCLUSIONS: Using the enzyme immunoassay described it is possible to know the serum concentration of NGF immunoreactive in non human primate and this assay is able to detect peripheral changes in NGF levels after intracerebral infusion of NGF.
Age Factors↗
Linkage between T cell receptor genes and susceptibility to multiple sclerosis: a complex issue.
Susceptibility to Multiple Sclerosis (MS) and to other autoimmune diseases has been linked to genes encoded within the HLA complex. More recent evidence indicates linkage between MS and genes encoded within or closely linked to the T cell receptor (TCR) beta chain gene complex. However, not all available data are concordant. Discrepancies are most likely rooted in the complex nature of TCR and MHC genes and interactions of their products in initiating and sustaining autoimmune responses. An evaluation of linkage of TCR and MHC genes to autoimmune disease processes must take into account the nature of polymorphism in the gene complexes, the complexity of autoimmune diseases along with the multigenic nature of genetic predisposition. These factors create a situation in which simple genetic linkage may be the exception rather than the rule. The present report reviews data concerning TCR and MS linkage and enumerates the complexities that arise in evaluating results from such studies.
Genetic Linkage↗
Development of a vibratory white finger prevention program for shipyard workers: an exploratory study.
BACKGROUND: Vibratory White Finger (VWF) disease afflicts many shipyard workers who use vibrating tools over a period of years and can lead to a lifelong disability. Vascular symptoms include cold-induced spasms of the fingers and hands, blanching of the fingers, and atrophic skin changes in the fingertips. Sensorineural symptoms include numbness and tingling in the fingers and hands and reduced sensory perception and manipulative dexterity. The purpose of this study was to develop a screening program for shipyard workers, so that VWF disease could be identified and workers with the disease could be counseled on possible job changes involving reduced exposure to vibration. METHOD: This study was conducted during 1993. The subjects consisted of 39 users of vibrating tools and 10 nonusers. In the shipyard, each subject received a questionnaire dealing with VWF symptoms, followed by tests for multifrequency vibration thresholds, cutaneous sensitivity, and hand and finger strength. Each subject was subsequently examined outside the shipyard by a board-certified occupational health physician. RESULTS: Using discriminant analysis, statistical models for both the vascular and sensorineural stages of the disease were constructed. In general, there was a high level of agreement between the staging obtained from the statistical models and the outside physician's diagnoses, suggesting that the combination of questionnaire and test data was adequate for initial screening for this disease. CONCLUSION: It is not considered practical to perform a complete physician evaluation on every shipyard worker who is at risk for VWF. By using a structured questionnaire together with a limited number of VWF-related tests, and incorporating the data into a statistical model, it is possible to identify the priority candidates for physician follow-up and possibly alter the worksite to prevent serious disability.
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