Search Results
You are looking at 1 - 4 of 4 items for
- Author: ANNE J. EVANS x
- Refine by access: All content x
Search for other papers by ANNE J. EVANS in
Google Scholar
PubMed
SUMMARY
The release in vitro of β-glucuronidase from rat testicular homogenates under the influence of ovine and bovine prolactin has been investigated further.
A micro modification of the original assay method has been developed, with improved specificity, sensitivity and precision.
Assay results were reproducible over 2½ yr. and were in good agreement with bioassays for prolactin and luteotrophic activity.
Search for other papers by ANNE J. EVANS in
Google Scholar
PubMed
SUMMARY
The effect of prolactin on the activity of β-glucuronidase in the testis of the rat and mouse has been studied in vitro.
Prolactin increased this activity, and a linear log dose-response relationship was found to exist with doses of between 0·3 and 1·2 mg. of a preparation of prolactin containing between 20 and 25 i.u./mg.
The optimal conditions for this effect have been investigated.
Twenty other substances have been tested; none increased the enzymic activity, but six decreased it.
Possible mechanisms for this effect are discussed.
Search for other papers by ANNE J. EVANS in
Google Scholar
PubMed
Search for other papers by K. A. FERGUSON in
Google Scholar
PubMed
Search for other papers by NADA KOVAČIĆ in
Google Scholar
PubMed
SUMMARY
Three preparations of prolactin have been assayed against a reference preparation by different techniques.
These are the prolongation of dioestrus in the mouse, the in vitro method depending on the increase of β-glucuronidase in the rat testis, and the pigeon crop sac method.
The results have been compared and discussed.
Search for other papers by Thomas M Braxton in
Google Scholar
PubMed
Search for other papers by Dionne E A Sarpong in
Google Scholar
PubMed
Search for other papers by Janine L Dovey in
Google Scholar
PubMed
Search for other papers by Anne Guillou in
Google Scholar
PubMed
Search for other papers by Bronwen A J Evans in
Google Scholar
PubMed
Search for other papers by Juan M Castellano in
Google Scholar
PubMed
Search for other papers by Bethany E Keenan in
Google Scholar
PubMed
Search for other papers by Saja Baraghithy in
Google Scholar
PubMed
Search for other papers by Sam L Evans in
Google Scholar
PubMed
CIBER Fisiopatologia de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
Search for other papers by Manuel Tena-Sempere in
Google Scholar
PubMed
Search for other papers by Patrice Mollard in
Google Scholar
PubMed
Search for other papers by Joseph Tam in
Google Scholar
PubMed
Search for other papers by Timothy Wells in
Google Scholar
PubMed
Human Prader–Willi syndrome (PWS) is characterised by impairments of multiple systems including the growth hormone (GH) axis and skeletal growth. To address our lack of knowledge of the influence of PWS on skeletal integrity in mice, we have characterised the endocrine and skeletal phenotype of the PWS-IC del mouse model for ‘full’ PWS and determined the impact of thermoneutrality. Tibial length, epiphyseal plate width and marrow adiposity were reduced by 6, 18 and 79% in male PWS-IC del mice, with osteoclast density being unaffected. Similar reductions in femoral length accompanied a 32% reduction in mid-diaphyseal cortical diameter. Distal femoral Tb.N was reduced by 62%, with individual trabeculae being less plate-like and the lattice being more fragmented (Tb.Pf increased by 63%). Cortical strength (ultimate moment) was reduced by 26% as a result of reductions in calcified tissue strength and the geometric contribution. GH and prolactin contents in PWS-IC del pituitaries were reduced in proportion to their smaller pituitary size, with circulating IGF-1 concentration reduced by 37–47%. Conversely, while pituitary luteinising hormone content was halved, circulating gonadotropin concentrations were unaffected. Although longitudinal growth, marrow adiposity and femoral geometry were unaffected by thermoneutrality, strengthened calcified tissue reversed the weakened cortex of PWS-IC del femora. While underactivity of the GH axis may be due to loss of Snord116 expression and impaired limb bone geometry and strength due to loss of Magel2 expression, comprehensive analysis of skeletal integrity in the single gene deletion models is required. Our data imply that thermoneutrality may ameliorate the elevated fracture risk associated with PWS.