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Biomedical subjects

M Fairhurst

Publications and source records attributed to M Fairhurst.

12 recordsLinked to original sources
PubMed2002

Treatment of "Gamekeeper's Thumb" by reconstruction of the ulnar collateral ligament.

This study examines the treatment of 22 thumbs with symptomatic laxity of the ulnar collateral ligament of the metacarpophalangeal joint by ligament reconstruction 1 week to 10 years after injury. The existing ligament remnants were repaired in 13 thumbs and were re-attached to bone, using a bone anchor, in seven cases. Two ligaments were reconstructed using the extensor pollicis brevis tendon. Patients were reviewed at a mean of 16 months. Functional stability was regained in all patients, but two thumbs had ongoing pain in the metacarpophalangeal joint. All but one patient returned to their original work and recreational pastimes. This study suggests that ligament reconstruction for chronic laxity of the ulnar collateral ligament is likely to achieve painless stability of the metacarpophalangeal joint even when reconstruction is delayed. This makes joint fusion unnecessary in most instances.

Adolescent↗
PubMed2001

Improving ARTMAP learning through variable vigilance.

This paper presents a mechanism to vary the vigilance parameter in the RePART fuzzy neural network. This mechanism helps to smooth out the problem of category proliferation which affects ARTMAP-based networks. Empirical experiments show that the use of variable vigilance improves the performance of the RePART model while, at the same time, requiring a less complex structure.

Algorithms↗
PubMed2000

Computer recording of standard tests of visual neglect in stroke patients.

OBJECTIVE: To determine whether a computer-based method for recording standardized assessment of neglect identifies abnormalities in the 'process' as well as in the 'outcome' of such tasks. DESIGN: Prospective sequential assessment of patients admitted to a stroke rehabilitation unit. SUBJECTS: All consecutive patients with right-sided cerebrovascular accident confirmed on computerized tomography (CT) scan including 30 patients with neglect, 57 patients without neglect. An age-matched control group of 13 subjects. INTERVENTION: All patients were tested using the standard Rivermead Behavioural Inattention Test (BIT) and by computer recording of two standard tests for assessing neglect (line bisection and Albert's test). Age-matched controls were tested using computer recording of the two standard tests. MAIN OUTCOME MEASURES: Neglect was defined using the BIT with a cut-off score of 129. Computer recording measured the 'outcome' of tasks, i.e. the deviation from midline and omissions in cancellation, as well as the 'process' of tasks, i.e. time between cancellations, components of cancellation time including premovement, movement and drawing time, and the starting point for cancellation. RESULTS: The computer recording identified significant differences in 'outcome' and 'process' which distinguished neglect from non-neglect patients. There were significant differences between non-neglect patients and age-matched controls with regard to 'process' measures but not with regard to 'outcome' measures. CONCLUSIONS: Computer recording of standard tests for assessing neglect identifies novel impairments with regard to the process of carrying out tasks. These impairments may be used to investigate changes in neglect with time, the response of neglect to treatment and to explore further the neuropsychological changes associated with neglect in stroke patients.

Aged↗
PubMed1999

Developing algorithms to enhance the sensitivity of cancellation tests of visuospatial neglect.

We describe a set of algorithms that enhance the sensitivity of cancellation tests used in assessing visuospatial neglect. The algorithms can be readily implemented on a computer and can provide temporal and nontemporal data on strategies used during cancellation. We also present preliminary results from a group of 68 right-hemisphere brain-damaged patients and 12 age-matched control participants, which demonstrate the clinical significance of the measures we have defined.

Adult↗
PubMed1997

Fibrillin-1 in human cartilage: developmental expression and formation of special banded fibers.

The molecular basis for Marfan's syndrome (MS), a heritable disorder of connective tissue, is now known to reside in mutations in FBN1, the gene for fibrillin-1. Classic phenotypic manifestations of MS include several skeletal abnormalities associated primarily with overgrowth of long bones. As a first step towards understanding how mutations in FBN1 result in skeletal abnormalities, the developmental expression of fibrillin-1 (Fib-1) in human skeletal tissues is documented using immunohistochemistry and monoclonal antibodies demonstrated here to be specific for Fib-1. At around 10-11 weeks of fetal gestation, Fib-1 is limited in tissue distribution to the loose connective tissue surrounding skeletal muscle and tendon in developing limbs. By 16 weeks, Fib-1 is widely expressed in developing limbs and digits, especially in the perichondrium, but it is apparently absent within cartilage matrix. Fib-1 appears as a loose meshwork of fibers within cartilage matrix by 20 weeks of fetal gestation. Until early adolescence, Fib-1 forms loose bundles of microfibrils within cartilage. However, by late adolescence, broad banded fibers composed of Fib-1 are found accumulated pericellularly within cartilage. Because these fibers can be extracted from cartilage using dissociative conditions, we postulate that they are laterally packed and crosslinked microfibrils. On the basis of these findings, we suggest that the growth-regulating function of Fib-1 may reside persistently within the perichondrium. In addition, the accumulation of special laterally crosslinked Fib-1 microfibrils around chondrocytes during late adolescence suggests that growth-regulating activities may also be performed by Fib-1 at these sites.

Adolescent↗
PubMed1997

Evaluation of the immunotoxicity of benzoporphyrin derivative (BPD-MA) in mice.

Photodynamic therapy has been shown to selectively eliminate activated lymphocytes in a number of experimental situations. These findings have important implications in therapies involving selective immunomodulation. In this study we report the effects of intravenous dosing with the photosensitizer benzoporphyrin derivative-monoacid A(BPD) on normal immunological function. Therapeutic doses of BPD and light had no effect on natural killer cell activity, the mixed lymphocyte reaction, cell-mediated lympholysis, the primary immune response to sheep red blood cells, or the secondary memory response to T cell-dependent antigens. In non-light treated controls, BPD at concentrations up to 10-fold higher had a limited effect on cell-mediated lympholysis. We conclude that the primary effect of BPD in several therapeutic modalities in not due to a generalized suppression of the immune system.

Animals↗
PubMed1991

Expression of an EL4 tumour-associated determinant on subpopulations of murine T cells in normal and lympho-proliferative autoimmune mice.

It has been demonstrated that the single autosomal recessive lpr and gld genes are responsible for the accumulation of unusual T-cell subsets. Although these subsets have been assigned to the T-cell lineage, they share certain antigenic cell surface markers with mature B lymphocytes. Consequently the maturational pathway(s) of these cells has been difficult to fit in the currently accepted models of T-cell differentiation. Previous work has determined that the YE1/19.1 monoclonal antibody (mAb), developed against the EL4 tumour line, reacts with the accumulating T cells in lpr-expressing mice. In this study we report that YE1/19.1 could also be used as a marker for the accumulating T cells in gld-expressing mice and that the hyporesponsiveness seen in gld mice correlated with these accumulating cells. We then demonstrated that the YE1/19.1 antibody also reacts with a subpopulation of neonatal thymocytes as well as a mitogen non-responsive subpopulation of 'double negative' T cells from the spleens and thymuses of non-autoimmune mice. Our findings indicate that the YE1/19.1 mAb will be a useful probe for helping in the eludication of the intra-thymic maturational pathways of T lymphocytes.

Animals↗
PubMed1988

Detection of malignant melanoma with monoclonal antibodies.

Eleven murine monoclonal antibodies (MoAbs) were isolated that defined unique membrane antigens expressed on human melanoma cells but not detectable on human lymphoid cells by radioimmunometric assays. Five of these MoAbs each identified a separate melanoma cell surface antigen as shown by distinctly different in vitro MoAb binding patterns to a diverse panel of tumor cell lines. One of these 5 monoclonals, MoAb 34.1, reacted specifically with 9/11 melanoma lines and 0/28 other human tumor or lymphoid cell lines. The other 4 MoAbs reacted strongly with melanomas, but also bound to 1 or more non-melanoma lines. The remaining 6 MoAbs defined three distinct regions of a single melanoma cell membrane protein with a molecular weight of 125 kiloDaltons (kD) as shown by antibody crossblocking and gel electrophoresis. A sensitive radioimmunoassay developed with MoAbs to 2 epitopes of this 125 kD protein detected up to 500-fold higher levels of this antigen in extracts of melanoma cells compared to autologous lymphoid cells. The 125 kD antigen also was detected by indirect immunoperoxidase assays with the MoAbs on biopsied tumors in histologic tissue sections of 5/11 metastatic melanomas and 1/11 carcinomas but was found on some normal endothelium and smooth muscle. Another monoclonal, MoAb 705, reacted more broadly with tumor cells in 10/14 biopsied melanomas and 10/11 carcinomas, but also was reactive with basal epidermis and normal fibroblasts. By contrast, MoAb 34.1 bound specifically to tumor cells of 7/11 biopsied metastatic melanomas, but bound 0/10 carcinomas and few normal tissues except for some macrophages. Thus, MoAb 34.1 was the most specific diagnostic reagent for immunohistologic detection of melanoma. The 250 kD antigen defined by MoAb 34.1 is similar to a high molecular weight proteoglycan reported to be an excellent tumor marker for human melanomas. The results of these studies show that murine monoclonal antibodies can be used as sensitive reagents for radioimmunoassays and immunohistology of malignant melanoma.

Animals↗
PubMed1987

Antigen-specific T-cell hyporesponsiveness in MRL congenic mice can be explained by two independent cellular defects.

MRL-+, MRL-lpr and B6-lpr have been shown to be useful models in studying systemic lupus erythematosus. MRL-lpr and B6-lpr differ from their congenic counterparts by the presence and expression of the homozygous recessive lymphoproliferation (lpr) gene. One manifestation of this gene is a massive T-cell proliferation that results in a generalized lymphadenopathy in older animals. A paradox that has developed out of the work utilizing the congenic mice is that the gene responsible for lymphoproliferation also appears to be responsible for the inability of T cells to respond to proliferative signals in vitro. In this paper we investigate the basis for this hyporesponsiveness in antigen-induced activation of proliferation and antibody synthesis. We have demonstrated that spleen cells from both MRL-+ and MRL-lpr mice gave minimal stimulation in a one-way mixed lymphocyte reaction against allogeneic T cells. These findings were extended to include antigen-specific proliferation involving antigen that must be processed and presented to responder lymphocytes in a H-2 restricted manner. Thus, MRL-+ and MRL-lpr spleen cells pulsed with ferredoxin also failed to stimulate ferredoxin-primed T cells from B10.Br animals in vitro. We then investigated whether any T-cell defect(s) was also contributing to this proliferative hyporesponsiveness. T lymphocytes from the spleen of MRL-+, 2-month-old MRL-lpr, and 6-month-old MRL-lpr were tested in a one-way mixed lymphocyte reaction. It was found that only the MRL-+ T cells gave responses approaching normal, suggesting lpr gene involvement in T-cell non-responsiveness. This was confirmed by the demonstration of an age-onset T-cell proliferative hyporesponsiveness in B6-lpr mice. This lpr gene-linked non-responsiveness was also shown to extend to T-cell helper function in a positive allogeneic effect assay. We can conclude from these studies that antigenic nonresponsiveness in MRL congenic mice can be explained by two defects: the failure of antigen-presenting cells in MRL-+ and MRL-lpr mice to provide the necessary signal(s) to immunocompetent T cells, this defect not being associated with the lpr gene, and the lpr gene controlled outgrowth of a unique T-cell population that cannot respond in our assay systems.

Animals↗
PubMed1986

Correction of defective IL 3 responses of T lymphocytes from autoimmune mice.

MRL-+ and MRL-lpr congenic mice differ by the presence and expression of the homozygous recessive lymphoproliferation (lpr) gene. One manifestation of this gene is a massive T cell proliferation that results in a generalized lymphadenopathy in older animals. Interleukin 3 (IL 3), a recently described lymphokine, has been shown to influence lymphocyte differentiation. It was possible that abberrant IL 3 production was the mechanism responsible for the lpr controlled lymphadenopathy. Consequently, in this paper we tested the MRL congenic mice for their ability to produce IL 3. We report that the T lymphocytes from MRL-+ and MRL-lpr could neither respond to pokeweed mitogen in the induction of proliferation nor produce IL 3. Moreover, IL 3 was not produced constitutively nor could be induced at any time period up to 5 days in vitro. This hyporesponsiveness was shown to be controlled at the accessory cell level. Addition of T cell-depleted peritoneal exudate cells from normal major histocompatibility complex (MHC) compatible mice was able to restore the ability to secrete IL 3 in response to pokeweed mitogen in MRL-+ and young MRL-lpr mice. The defect in the accessory cells could be overridden by two means: the incorporation of phorbol myristate acetate in the induction system and preincubation of the cells in tissue culture.

Animals↗
PubMed1976

Synergism between immune complexes and serum from tumor-bearing mice in the suppression of mitogen responses.

Immune complexes either adhering to the cells, or added to cultures, synergized with an inhibitor present in serum to suppress the proliferative response of lymphocytes to specific antigens or to B cell or T cell mitogens. The suppressive effect was dependent on the concentration of both the complex and the serum and was substantially higher when the serum was taken from tumor-bearing, rather than normal mice. Immune complexes alone were not suppressive, but appeared to activate or increase the effectiveness of an inhibitor present in serum. Complexes of syngeneic mouse serum or specifically purified rabbit or sheep antibody, as well as heat aggregated mouse or rabbit Ig, were all effective, whereas heat-aggregated F(ab')2 fragments of rabbit Ig were not, suggesting that any aggregate hearing exposed Fc fragments could mediate synergy. Purified T lymphocytes were equally as sensitive to inhibition as the whole spleen cell population, implying that the suppression acted directly on responding cells rather than via an accessory cell.

Animals↗