| 911. |
|
|
| 912. |
- Rudäng, Robert, et al.
(författare)
-
Hip fracture prevalence in grandfathers is associated with reduced cortical cross-sectional bone area in their young adult grandsons
- 2010
-
Ingår i: The Journal of Clinical Endocrinology and Metabolism. - 1945-7197. ; 95:3, s. 1105-1114
-
Tidskriftsartikel (refereegranskat)abstract
- Context: Parent hip fracture prevalence is a known risk factor for osteoporosis. The role of hip fracture prevalence in grandparents on areal bone mineral density (aBMD) and bone size in their grandsons remains unknown. Objective: The objective of the study was to examine whether hip fracture prevalence in grandparents was associated with lower aBMD and reduced cortical bone size in their grandsons. Design and Setting: This was a population-based cohort study in Sweden. Study Subjects: Subjects included 1015 grandsons (18.9 ± 0.6) (mean ± sd) and 3688 grandparents. Main Outcome Measures: aBMD, cortical bone size, volumetric bone mineral density and polar strength strain index of the cortex in the grandsons in relation to hip fracture prevalence in their grandparents were measured. Results: Grandsons of grandparents with hip fracture (n = 269) had lower aBMD at the total body, radius, and lumbar spine, but not at the hip, as well as reduced cortical cross-sectional area at the radius (P < 0.05) than grandsons of grandparents without hip fracture. Subgroup analysis demonstrated that grandsons of grandfathers with hip fracture (n = 99) had substantially lower aBMD at the lumbar spine (4.9%, P < 0.001) and total femur (4.1%, P = 0.003) and lower cortical cross-sectional area of the radius (4.1%, P < 0.001) and tibia (3.3%, P < 0.011). Adjusting bone variables for grandson age, weight, height, smoking, calcium intake, and physical activity and taking grandparent age at register entry, years in register, and grandparent sex into account strengthened or did not affect these associations. Conclusions: Family history of a grandfather with hip fracture was associated with reduced aBMD and cortical bone size in 19-yr-old men, indicating that patient history of hip fracture in a grandfather could be of value when evaluating the risk of low bone mass in men.
|
|
| 913. |
|
|
| 914. |
- Saenger, P, et al.
(författare)
-
Recommendations for the diagnosis and management of Turner syndrome.
- 2001
-
Ingår i: The Journal of clinical endocrinology and metabolism. - : The Endocrine Society. - 0021-972X. ; 86:7, s. 3061-9
-
Tidskriftsartikel (refereegranskat)abstract
- Comprehensive recommendations on the diagnosis of Turner syndrome (TS) and the care of affected individuals were published in 1994. In the light of recent advances in diagnosis and treatment of TS, an international multidisciplinary workshop was convened in March 2000, in Naples, Italy, in conjunction with the Fifth International Symposium on Turner Syndrome to update these recommendations. The present paper details the outcome from this workshop. The genetics and diagnosis of the syndrome are described, and practical treatment guidelines are presented.
|
|
| 915. |
|
|
| 916. |
- Sandberg, Tove, et al.
(författare)
-
Paracrine stimulation of capillary endothelial cell migration by endometrial tissue involves epidermal growth factor and is mediated via up-regulation of the urokinase plasminogen activator receptor
- 2001
-
Ingår i: Journal of Clinical Endocrinology and Metabolism. - 1945-7197. ; 86:4, s. 1724-1730
-
Tidskriftsartikel (refereegranskat)abstract
- Endometrial angiogenesis is not well studied, but has potential as a model for studies of physiological angiogenesis. Migration as well as proliferation of vascular endothelial cells are modulated by other endometrial cells. This study analyzes the chemotactic signal released from endometrial tissue in a wound assay using human microvascular endothelial cells. Endometrial tissue explants stimulate migration, and this effect is significantly weaker with explants taken at midcycle than those obtained earlier or later in the cycle. Migration is inhibited more than 50% by either blocking antibodies to the urokinase plasminogen activator receptor (uPAR) or enzymatic removal of uPAR from the cell surface. Also, migration is inhibited more than 50% by antibodies to epidermal growth factor (EGF), but not by antibodies to vascular endothelial growth factor or basic fibroblast growth factor. The combination, of anti-EGF and anti-uPAR antibodies does not further reduce the response, suggesting that these antibodies target a common pathway. Conditioned medium from endometrial explants contains EGF, and EGF stimulates the migration of endothelial cells in a dose-dependent way. This effect is completely blocked by antibodies to uPAR. These data suggest up-regulation of the uPA system by EGF. Conditioned medium from EGF-treated cells contains less uPA than medium from control cells. In contrast, binding of radiolabeled uPA reveals an increased number of uPA-binding sites in EGF-treated cells. Increased expression of uPAR potentially increases the activation and assembly of focal adhesion sites, a prerequisite for cell migration. We conclude that the endometrial migratory signal has two components. The major part of the signal is blocked by antibodies to EGF, and the response is mediated via upregulation of uPAR in the endothelial cells. The other part of the signal is unknown, and the response does not involve uPAR. Decreased endometrial chemotactic signal at midcycle is probably related to decreased release of EGF, which is secondary to increased binding to endometrial cell membranes.
|
|
| 917. |
|
|
| 918. |
|
|
| 919. |
|
|
| 920. |
|
|
