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Biomedical subjects

S Stevens

Publications and source records attributed to S Stevens.

At least 91 records · Page 5Linked to original sources
PubMed1982

The histochemical features of the Michaelis-Gutmann body and a consideration of the pathophysiological mechanisms of its formation.

The reactions to a number of histochemical stains by Michaelis-Gutmann (MG) bodies in 13 cases of malakoplakia are described. All MG bodies contained calcium and phosphate. Iron was present in six cases. Special stains failed to reveal the presence of micro-organisms. In six cases the MG bodies contained either lecithin or sphingomyelin and in three both phospholipids were present. There was no evidence of phospholipid of bacterial cell membrane derivation. Carbohydrate staining reactions suggested the presence of a neutral polysaccharide and an acidic non-sulphated polysaccharide (such as a sialoglycan). No histochemical evidence could be adduced to implicate bacterial cell membranes in the structure of the organic matrix of the MG body. The implications of these findings in the light of the association between clinical bacterial infection and malakoplakia are discussed.

Adult↗
PubMed1981

Keratoconus.

Explore the source record for details and available documents.

Contact Lenses↗
PubMed1981

Legionnaires' disease at autopsy.

Sporadic deaths from Legionnaires' disease may escape detection at autopsy. Known epidemiological and clinical features of the disease should arouse suspicion and prompt appropriate bacteriological studies. The pathological findings in Legionnaires' disease are almost entirely confined to the lungs and are not distinct from any other severe bacterial bronchopneumonia. The causative organism, Legionella pneumophila, is difficult to identify on a Gram stain but will stain nonspecifically with the Giemsa, Warthin-Starry, and Dieterle techniques. The direct fluorescent antibody method allows specific identification of Legionella in paraffin-embedded tissue sections.

Autopsy↗
PubMed1981

Validity of routine clinical test weighing as a measure of the intake of breast-fed infants.

Routine clinical test weighing was carried out on 100 bottle-fed infants to assess the accuracy of the procedure; the feed intake was measured by weighing the feeding bottles before and after feeding. Test weight was found to be an unreliable indication of feed weight, underestimating the amount of feed actually taken at test weight values below 60 g, and overestimating the amount of feed taken at test weights over 60 g. The errors were largest in infants having test weights at the extremes of the range. Test weighing with clinical baby scales is an unreliable and inaccurate indication of feed intake in breast-fed infants.

Body Weight↗
PubMed1981

Affinity labelling of the human uterine progesterone receptor with 21-, 16 alpha- and 11 alpha-bromoacetoxyprogesterones.

This report describes the use of 21-, 16 alpha- and 11 alpha -[2'-3H]bromoacetoxyprogesterone as affinity labels to characterize the human uterine progesterone receptor (HPR). These three derivatives can bind to and displace progesterone bound to the HPR. This affinity labelling was inhibited by an excess of radioinert progesterone and could not be demonstrated if bovine serum albumin was used in place of the HPR. Bromoacetic acid alone did not affinity label the HPR. Polyacrylamide gel electrophoresis under denaturing conditions showed that all three derivatives bound to a 45,000 molecular weight protein.

Affinity Labels↗
PubMed1980

Binding of 2-hydroxyestradiol to rat anterior pituitary cell membranes.

We have studied the specific binding of 1,3,5(10)-estratrien-2,3,17 beta-triol (2-hydroxyestradiol) to an enriched membrane fraction isolated from the rat anterior pituitary gland. Specific [6,7-(3)H]2-hydroxyestradiol-17 beta ([3H]2-hydroxyestradiol) binding is saturable and displays a high and low affinity binding component. The apparent dissociation constants, KD, are 4 +/- 2 x 10(-10) and 2 x 10(-6) M with 13 fmol and 2.6 pmol bound/mg of protein, respectively. The specific high affinity binding increases linearly with increasing amounts of tissue protein. The binding is both temperature- and pH-dependent, with maximal binding at 37 degrees C and pH 7.4. The 2-hydroxyestradiol binding is shown to be stereospecific. Dopamine and spiroperidol (a dopamine antagonist) competitively inhibit the specific binding of [3H]2-hydroxyestradiol to the high affinity binding site with inhibition constants, KI, of 1 x 10(-6) M and 2 x 10(-5) M, respectively. Related catecholestrogens (2-hydroxyestrone and 2-hydroxyestriol) are also competitive inhibitors of [3H]2-hydroxyestradiol binding with KI values of 1.5 x 10(-5) M and 1.9 x 10(-5) M, respectively. None of the estrogens (estrone, estradiol, estriol) or 2-methoxyestrogen derivatives (2-methoxyestrone, 2-methoxyestradiol, 2-methoxyestriol) inhibits [3H]2-hydroxyestradiol binding at concentrations up to 10(-4) M. Norepinephrine, epinephrine, and serotonin are also ineffective as inhibitors at concentrations of 10(-5) M and inhibited less than 20% at 10(-4) M. Centrifugation through a stepwise discontinuous sucrose density gradient is used to separate subcellular components of the anterior pituitary cells. Approximately 90 per cent of the specific [3H]2-hydroxyestradiol binding is associated with the material at the 47.4 to 52.9% sucrose interface, the layer most highly enriched for 5'-nucleotidase (an enzyme marker for plasma membranes). Studies of tissue specificity indicate that specific 2-hydroxyestradiol binding sites are heterogeneously distributed in nervous tissue with the highest concentration of binding sites in the anterior pituitary, cerebral cortex, and hypothalamus and lower levels found in the thalamus and striatum. Low levels 2-hydroxyestradiol binding sites are also identified in liver and uterus. The present demonstration of specific 2-hydroxyestradiol binding to the anterior pituitary membrane provides information on the mechanism of catecholestrogen action.

Animals↗
PubMed1980

A rapid procedure for measurement of DNA repair in human fibroblasts and for complementation analysis of xeroderma pigmentosum cells.

A rapid procedure for measuring unscheduled DNA synthesis has been studied in detail. Human fibroblasts were brought into the non-dividing state by either growing to confluence or starvation for arginine. Residual semi-conservative synthesis was abolished by hydroxyurea. Hydroxyurea-resistant DNA synthesis which was induced by irradiation and chemical mutagens was presumed to represent repair synthesis and provided a very rapid semi-quantitative procedure for its measurement. Problems were encountered, however, when comparing the quantitative response of different cell strains. The variability between experiments was quite large, and we found that the level of repair synthesis depended not only on the mutagen and the genotype of the cell, but also on physiological factors. This led to some anomalous results. The system was able to detect with ease the large defects in UV-induced repair synthesis in fibroblasts from patients with xeroderma pigmentosum (XP) but it would probably not easily detect less than a 50% reduction in the level of repair synthesis. By extension of this procedure, in combination with cell fusion induced by polyethylene glycol, we have developed a method for carrying out genetic complementation of XP fibroblasts, which does not entail the use of either Sendai virus or of autoradiography. Results of complementation analysis of 4 XP cell strains are presented.

Arginine↗
PubMed1980

Studies on a new case of xeroderma pigmentosum (XP3BR) from complementation group G with cellular sensitivity to ionizing radiation.

XP3BR is a fibroblast strain derived from a xeroderma pigmentosum patient exhibiting severe mental retardation in addition to the typical changes in the skin. No tumours have been observed by 6 years of age. Cells from this patient had no detectable excision repair of u.v. damage. The defect in daughter strand repair was also characteristic of excision-defective XP's. The material was assigned to complementation group G and is the second (unrelated) example from this group. XP3BR cells were more sensitive than normal cells to the lethal action not only of u.v. but also of gamma irradiation, in contrast to all other XP cells tested to date including XP2BI, the other representative of complementation group G. The u.v. sensitivity was similar to that of strains from complementation groups A and D, confirming the correlation between extreme u.v. sensitivity and the presence of neurological defects. Following treatment with u.v., XP3BR, and other XPs gave more 6-thioguanine resistant mutants than normal cells whether the comparison was made per unit of dose or per lethal event. After low doses of gamma irradiation XP3BR cells were more mutable than normal or XP2BI cells.

Cell Line↗
PubMed1979

The response of ataxia telangiectasia cells to bleomycin.

The autosomal recessive disorder, ataxia telangiectasia (AT) is characterised by cellular sensitivity to ionizing radiation. The molecular basis of this radiosensitivity is the subject of controversy. We report here that cultured fibroblasts from AT patients are also sensitive to the lethal effects of bleomycin. As with ionizing radiation, no defect has been observed in the overall rejoining of single or double-strand breaks produced by bleomycin. Since, however, only apyrimidinic (and to a lesser extent apurinic) sites and strand breaks are known to be produced by bleomycin, we tentatively suggest that AT cells are unable to rejoin a very small fraction of the total strand breaks. We attribute our inability to detect such unrejoined strand breaks to the relative insensitivity of the sucrose gradient procedures normally used to detect strand breaks.

Ataxia Telangiectasia↗
PubMed1977

The production and repair of double strand breaks in cells from normal humans and from patients with ataxia telangiectasia.

The production and repair of double strand breaks induced by gamma-rays in the DNA of human fibroblasts have been measured by sedimentation in sucrose radients under non-denaturing conditions. Unirradiated DNA formed a rapidly sedimenting gel. Low doses of radiation released freely sedimenting DNA molecules from this gel. Higher doses reduced the rate of sedimentation of the free DNA due to the introduction of double strand breaks. The breakage efficiency was 1 break/1.3 X 10(10) daltons of DNA/krad. Postirradiation incubation after a high dose of radiation resulted in an increase in molecular weight of the free DNA molecules, and after a low dose the rapidly-sedimenting gel was reformed. The data suggest that double strand breaks are repaired in human fibroblasts. No significant differences were found between fibroblasts from two normal donors and four patients with the radiosensitive disorder, ataxia telangiectasia, in either the production or repair of double strand breaks.

Ataxia Telangiectasia↗
PubMed1975

Postreplication repair of DNA in chick cells: studies using photoreactivation.

During replication of DNA after ultraviolet irradiation, gaps are left in the newly-synthesized DNA strands in both bacterial and animal cells and these gaps are subsequently sealed by a process known as postreplication repair. In order to test whether it is the ultraviolet-induced pyrimidine dimers which are responsible for the production of these daughter-strand gaps in animal cells, we have used chick embryo fibroblasts. In these cells the pyrimidine dimers are photoreactivable, i.e. they can be split by an enzymatic process dependent on visible or near ultraviolet light. Our results indicate that chick cells possess a postreplication repair system similar to that in mammalian cells; gaps are produced in the newly-synthesized strands and then filled in. If the ultraviolet-irradiated cells are first photoreactivated to remove most of the dimers, the number of daughter-strand gaps produced is much less than without photoreactivation. This suggests that the dimers are indeed responsible for the formation of many of the gaps in the newly-synthesized DNA. Ultraviolet light also inhibits the overall rate of DNA synthesis. This inhibition is, however, only partly overcome by photoreactivation.

Animals↗