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Biomedical subjects

J Slack

Publications and source records attributed to J Slack.

At least 73 records · Page 4Linked to original sources
PubMed1985

Screening for Down's syndrome in the North East Thames region.

The suggested strategies for a screening programme for Down's syndrome by maternal serum alpha fetoprotein concentration were examined and tested on the experience of the North East Thames Regional. Screening by maternal serum alpha fetoprotein concentration may be used to identify pregnancies at increased risk, but this is useful only in women aged over 32 whose collective risk is greater than one in 200. The absolute probability of carrying babies with Down's syndrome for individuals in this high risk group can then be calculated and used to decide whether further diagnosis by amniocentesis is desired.

Adult↗
PubMed1983

Vascular mortality in patients with gout and in their families.

A mortality study was performed to determine death rates from coronary and cerebrovascular pathology in 180 patients with gout and their families. Lipid profiles were also analysed. Neither male nor female gout patients after presentation to hospital nor their male or female first-degree relatives were found to have an increased risk of dying from coronary artery or cerebrovascular disease. Families of hyperlipidaemic gout patients had a slightly increased incidence among males of death from coronary artery disease, a finding which may reflect the hypercholesterolaemia found among these relatives. It could have influenced the vascular mortality rate in families of hyperlipidaemic gout patients without any relationship to the diagnosis of gout itself.

Adult↗
PubMed1982

Family study of lipid and purine levels in gout patients.

A family study was performed to determine whether the hypertriglyceridaemia associated with gout is present in families of gout patients or due to the life style of the patient himself. The study revealed the expected hypertriglyceridaemia in gout patients; this was reflected by elevated serum levels of prebetalipoproteins and with reduction in the proportion of beta-lipoprotein. None of these abnormalities were seen in the first-degree relatives. Furthermore, the proportion of high-density lipoproteins was not significantly raised in gout patients.

Female↗
PubMed1981

Effects of delipidated serum and lipoprotein-deficient serum on sterol biosynthesis and efflux in cultured skin fibroblasts - a comparison of the behaviour of cells from a control with those from a heterozygote and homozygote for familial hypercholesterolaemia.

The biosynthesis and efflux of sterols from cells into the medium were investigated in skin fibroblasts from a control, a patient with obligate heterozygous familial hypercholesterolaemia and a patient with the homozygous condition. The behaviour of the cells was studied in two lipid free media (lipoprotein deficient and delipidated serum), with and without the addition of low density lipoproteins (LDL) in order to find experimental conditions which showed maximum differences between the three cell lines. Incorporation of [14C]acetate into sterols in the presence (repression) and absence (induction) of LDL was similar in the normal and heterozygous cells, whereas the homozygous cells showed reduced repression and increased induction. In all three cell lines induction of sterol synthesis was greater with delipidated than lipoprotein deficient serum. The efflux of sterols in both the presence and absence of LDL did not differ between the three cell lines, but it was greater when LDL was added to the medium and when delipidated serum was used. Sterol biosynthesis and efflux from the cells of the heterozygote did not differ significantly from those of the control.

Adult↗
PubMed1980

Subclass restriction of murine antibodies. III. Antigens that stimulate IgG3 in mice stimulate IgG2c in rats.

The IgG subclass distribution of rat antibodies to 13 different antigens was measured. Antibodies to protein and hapten-protein conjugates were predominantly IgG2a. Antigens labeled thymus-independent type 1, based upon responses in mice, stimulated both IgG2b and IgG2c antibodies, but little IgG2a. Polysaccharide and hapten-polysaccharide antigens (thymus-independent type 2) as well as phosphocholine-keyhole limpet hemocyanin, stimulated predominantly IgG2c antibodies. A division of antigens into essentially the same categories has been made on the basis of subclass restriction in mice. Antigens that stimulate IgG2c in rats stimulate IgG3 in mice. Thus, by comparing subclass preference with a variety of antigens, functional analogues among subclasses in different species can be identified.

Animals↗
PubMed1980

Subclass restriction of murine antibodies. II. The IgG plaque-forming cell response to thymus-independent type 1 and type 2 antigens in normal mice and mice expressing an X-linked immunodeficiency.

Antigens have been classified previously into three categories, thymus-dependent (TD), thymus-independent type (TI) 1, and TI-2, based upon thymic dependence and ability to stimulate an immunodeficient strain of mouse, CBA/N. Here we demonstrate that the different antigen classes elicit IgG antibodies of different subclasses. TD antigens stimulate predominantly IgG1 antibodies, with smaller amounts of IgG2 and IgG3 being expressed. TI-1 antigens stimulate almost no IgG1 antibodies and equal amounts of IgG2 and IgG3. TI-2 antigens elicit predominantly IgG3 antibodies. Mice expressing the CBA/N phenotype are known to be nonresponsive to TI-2 antigens. This was confirmed in this study. In addition, we demonstrate that the IgG3 component of the response to TI-1 antigens is virtually absent in mice expressing the CBA/N phenotype, which supports our previous finding that the CBA/N defect may be restricted to a B-lymphocyte subpopulation containing most of the precursors of IgG3-secreting cells.

Animals↗
PubMed1980

Family study of lipid and purine levels in gout patients and analysis of mortality.

A family study was performed to determine whether the hypertriglyceridaemia associated with gout is present in families of gout patients or simply due to their life-style. The study revealed hypertriglyceridaemia in gout patients, reflected by hyperprebetalipoproteinaemia and with reciprocal reduction in the proportion of beta-lipoprotein. These abnormalities were not seen in first-degree relatives. No definite increase in mortality was found from coronary or cerebrovascular disease in male gout patients after presentation to hospital or in their relatives. Families of hyperlipidaemic gout patients did reveal a slight increase in male coronary deaths although the significance of this finding was doubtful since some hypercholesterolaemia was found in these hyperlipidaemic families.

Cholesterol↗