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| 2. |
- Grant, Adrian, et al.
(författare)
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Routine formal fetal movement counting and risk of antepartum late death in normally formed singletons
- 1989
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Ingår i: The Lancet. - 1474-547X. ; 334:8659, s. 345-349
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Tidskriftsartikel (refereegranskat)abstract
- The routine recommendation to women to count fetal movements daily during late pregnancy for the prevention of antepartum late fetal death in normally formed singletons has been evaluated. 68,000 women were randomly allocated within thirty-three pairs of clusters either to a policy of routine counting or to standard care, which might involve selective use of formal counting or informal noting of movements. Antepartum death rates for normally formed singletons were similar in the two groups, regardless of cause of prior risk status. Despite the counting policy, most of these fetuses were dead by the time the mothers received medical attention. The study does not rule out a beneficial effect, but at best, the policy would have to be used by about 1250 women to prevent 1 unexplained antepartum late fetal death, and an adverse effect is just as likely. In addition, formal routine counting would use considerable extra resources.
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| 3. |
- Hammarström, Lennart, et al.
(författare)
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Transfer of IgA deficiency to a bone-marrow-grafted patient with aplastic anaemia
- 1985
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Ingår i: The Lancet. - 1474-547X. ; 325:8432, s. 778-781
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Tidskriftsartikel (refereegranskat)abstract
- IgA deficiency developed in a 2-year-old boy with aplastic anaemia who received a bone-marrow graft from his HLA-identical, 6-year-old, IgA-deficient sister. Southern blot analysis revealed the presence of alpha-genes in both children, thus suggesting a defect of lymphocyte stem-cell differentiation as a cause of IgA deficiency. Tissue typing showed homozygosity of HLA A1, B8, DR3, the haplotype associated with IgA deficiency in healthy people. Despite normal serum levels of IgG subclasses in both donor and recipient, both children showed a relative lack of specific IgG2 anticarbohydrate antibodies. This suggests that their IgA deficiency is part of a more fundamental aberration of immunoglobulin class and subclass distribution.
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| 4. |
- Hjalmarson, Å, et al.
(författare)
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Effect on mortality of metoprolol in acute myocardial infarction
- 1981
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Ingår i: The Lancet. - : The Lancet Publishing Group. - 0140-6736 .- 1474-547X. ; 318:8251, s. 823-827
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Tidskriftsartikel (refereegranskat)abstract
- The effect of metoprolol on mortality was compared with that of placebo in a double-blind randomised trial in patients with definite or suspected acute myocardial infarction. Treatment with metoprolol or placebo started as soon as possible after the patient's arrival in hospital and was continued for 90 days. Metoprolol was given as a 15 mg intravenous dose followed by oral administration of 100 mg twice daily. 1395 patients (697 on placebo and 698 on metoprolol) were included in the trial. Definite acute myocardial infarction developed in 809 and probable infarction in 162. Patients were allocated to various risk groups and within each group patients were randomly assigned to treatment with metoprolol or placebo. There were 62 deaths in the placebo group (8·9%) and 40 deaths in the metoprolol group (5·7%), a reduction of 36% (p<0·03). Mortality rates are given according to the treatment group to which the patients were initially randomly allocated.
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| 5. |
- Islam, M. Shahidul
(författare)
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Drug policy in the Third World
- 1985
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Ingår i: The Lancet. - 0140-6736 .- 1474-547X. ; 2:8445, s. 46-47
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Tidskriftsartikel (refereegranskat)
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| 6. |
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| 7. |
- Palsdottir, A, et al.
(författare)
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Mutation in cystatin C gene causes hereditary brain haemorrhage
- 1988
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Ingår i: The Lancet. - 1474-547X. ; 332:8611, s. 603-604
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Tidskriftsartikel (refereegranskat)abstract
- Hereditary cystatin C amyloid angiopathy (HCCAA) is an autosomal dominant disorder in which a cysteine proteinase inhibitor, cystatin C, is deposited as amyloid fibrils in the cerebral arteries of patients and leads to massive brain haemorrhage and death in young adults. A full length cystatin C cDNA probe revealed a mutation in the codon for leucine at position 68 which abolishes an Alu I restriction site in the cystatin C gene of HCCAA patients. The Alu I marker has been used to show that this mutation is transmitted only in affected members of all eight families investigated, and that the mutated cystatin C gene causes HCCAA.
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| 8. |
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| 9. |
- Saxne, Tore, et al.
(författare)
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Difference in cartilage proteoglycan level in synovial fluid in early rheumatoid arthritis and reactive arthritis.
- 1985
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Ingår i: The Lancet. - 1474-547X. ; 2/8447:8447, s. 127-128
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Tidskriftsartikel (refereegranskat)abstract
- Cartilage proteoglycans were measured, by the use of an enzyme-linked immunosorbent assay, in synovial fluids obtained from 109 unselected patients attending an outpatient rheumatology clinic because of inflammation of the knee. The content of proteoglycans in synovial fluid was inversely related to the degree of joint destruction shown on X-ray. The proteoglycan concentrations in knee-joint exudates were higher in patients with reactive arthritis than in patients with rheumatoid arthritis having synovitis of corresponding duration and lacking radiological evidence of cartilage destruction. The measurement of proteoglycan levels may therefore be useful in differentiating between the two conditions.
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| 10. |
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