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Biomedical subjects

N Scolding

Publications and source records attributed to N Scolding.

26 records · Page 2Linked to original sources
PubMed1994

Preliminary evidence from magnetic resonance imaging for reduction in disease activity after lymphocyte depletion in multiple sclerosis.

The central nervous system lesions of multiple sclerosis (MS) can be detected by magnetic resonance imaging (MRI) and the initial perivascular inflammatory component is distinguished by the presence of gadolinium enhancement. To assess the effect of systemic lymphocyte depletion on disease activity, seven patients with MS received a 10-day intravenous course of the humanised monoclonal antibody CAMPATH-1H (anti-CDw52). With some variations in the protocol, enhanced cerebral MR images were obtained monthly for 3-4 months before and at least 6 months after treatment. 28 enhancing areas were detected on the first series of 7 scans; 51 additional active lesions were identified on 18 scans before treatment; 15 were detected on 20 scans done over the next 3 months, but only 2 active lesions were seen on 23 scans during follow-up beyond 3 months. The difference in lesion incidence rate before and after treatment varied and the rate ratio was significantly reduced in only three patients. Collectively, in a "meta-analysis", the rate ratios were 0.15 [corrected] (95% CI 0.09-0.24) for all seven patients and 0.24 (0.14-0.42; p < 0.001) with exclusion of the patient whose scanning schedule differed. The effect of CAMPATH-1H on disease activity provides direct, but preliminary, evidence that disease activity in MS depends on the availability of circulating lymphocytes and can be prevented by lymphocyte depletion. It is too early to say anything about the clinical results of treatment with this agent.

Antigens, CD↗
PubMed1991

The pathogenesis of demyelinating disease: insights from cell biology.

Cellular and humoral immune mechanisms have been implicated in the pathogenesis of human and experimental demyelinating diseases of the CNS. How these interact in the complex sequence of events that culminates in phagocytosis of myelin by macrophages has yet to be resolved. The relationship between leakage of the blood-brain barrier and demyelination, the reason why recurrent inflammatory demyelination occurs--seemingly in the absence of an antigen-specific immune response--and the lack of effective remyelination all require explanation if a coherent account of immunologically mediated demyelination is to be achieved. One approach to these problems is to study in vitro the developmental and cellular biology of oligodendrocytes--the glial cells responsible for the synthesis and maintenance of CNS myelin. This provides experimental opportunities not offered by more direct investigation of the intact nervous system, but carries the clear disadvantage that observations made in vitro cannot necessarily be extrapolated to humans.

Animals↗
PubMed1989

Quantitative magnetic resonance imaging in multiple sclerosis: the effect of high dose intravenous methylprednisolone.

Magnetic resonance imaging was performed on 50 patients with clinically definite or probable multiple sclerosis before and 15 days after starting treatment with intravenous methylprednisolone (0.5 g daily for 5 days). Scans were abnormal in 49 patients. New lesions had appeared on the second scan in nine individuals and in seven a single pre-existing lesion appeared to have become smaller but in no case were lesions seen to disappear. Two patients showed both reduction in the size of an abnormal area and development of a single new lesion indicating that corticosteroids do not appear rapidly to alter the process underlying plaque formation. Measurements of relaxation times were performed in 12 randomly selected patients. All showed elevated values in normal appearing white matter but not cortex before treatment compared with 18 healthy controls. After treatment a significant decrease of T1 and T2 was observed in cortex, and of T1 alone in normal appearing white matter. No significant change could be detected within lesions, a finding attributed to the wide range of relaxation values observed at these sites before treatment. Since brain water content is increased in normal appearing white matter of multiple sclerosis patients, and is significantly reduced by high-dose methylprednisolone, resolution of oedema may contribute to the rapid spontaneous or corticosteroid induced symptomatic recovery that characterises the disease in its early stages.

Adult↗
PubMed1989

Immune mechanisms in the pathogenesis of demyelinating diseases.

The loss of myelin which characterises many human and experimental demyelinating diseases, among them multiple sclerosis, is thought to be immune mediated, but the precise mechanisms responsible remain unknown despite intense research. Normally, myelin in the central nervous system (CNS) is protected from systemic immune responses by the blood brain barrier, which separates nervous tissue from the peripheral circulation. Here we review evidence suggesting that an understanding of the demyelinating disorders may be helped by considering their immune pathogenesis in two stages. The first is damage to the blood brain barrier; this appears to be cell mediated, and allows infiltration into the CNS of other immune effectors. These include complement and also macrophages, which together may mediate the second stage, injury to the myelin/oligodendrocyte complex.

Animals↗
PubMed1986

Guidelines to control heparin treatment.

With new guidelines for the control of heparin infusion rates the proportion of kaolin cephalin clotting time ratios was significantly improved compared with ratios achieved without their use. Further improvement might result from careful preparation and delivery of the infusion.

Heparin↗
PubMed1986

Charcoal and isoniazid pharmacokinetics.

Activated charcoal (10 g) administered 1 h after a 600 mg oral dose of isoniazid to six healthy subjects did not reduce the area under the plasma concentration-time curve for isoniazid significantly. Charcoal administration is unlikely to be of value in isoniazid poisoning if delayed by an hour or more after the overdose.

Acetylation↗