Subject(s)
Duodenal Neoplasms/genetics , Loss of Function Mutation , Membrane Glycoproteins/genetics , Nerve Tissue Proteins/genetics , Animals , Brunner Glands/metabolism , Duodenal Neoplasms/metabolism , Duodenal Neoplasms/pathology , ErbB Receptors/genetics , ErbB Receptors/metabolism , Gene Expression Regulation, Neoplastic , Gene Knockout Techniques , Membrane Glycoproteins/metabolism , Mice , Nerve Tissue Proteins/metabolism , Receptor, ErbB-3/metabolismABSTRACT
OBJECTIVE: To examine the effects of 15 months of resistance training on bone mineral density (BMD) in female adolescents (aged 14 to 17 years). STUDY DESIGN: Participants were randomly assigned to either a training (n = 46) or control group (n = 21). BMD and body composition were measured by using dual-energy x-ray absorptiometry. Strength was assessed by means of one-repetition maximums for the leg press and bench press. The exercise group trained 30 to 45 minutes a day, 3 days per week, using 15 different resistance exercises. Control participants remained sedentary (<2 hours of exercise per week). RESULTS: Leg strength increased significantly (40%) in the exercise group, but there were no changes in the control group. Femoral neck BMD increased significantly in the training group (1.035 to 1.073 g/cm(2), P <.01) but not in the control group (1.034 to 1.048 g/cm(2)). No significant changes were seen in either group in lumbar spine BMD (1.113 to 1.142 g/cm(2) and 1.158 to 1.190 g/cm(2), respectively) or total body BMD (1.103 to 1.134 g/cm(2) and 1.111 to 1.129 g/cm(2), respectively). CONCLUSION: Resistance training is a potential method for increasing bone density in adolescents, although such a program would be best done as part of the school curriculum.
Subject(s)
Bone Density/physiology , Exercise/physiology , Absorptiometry, Photon , Adolescent , Adolescent Nutritional Physiological Phenomena/physiology , Body Composition/physiology , Female , Femur Neck/diagnostic imaging , Femur Neck/physiology , Humans , Lumbar Vertebrae/diagnostic imaging , Lumbar Vertebrae/physiology , Muscle, Skeletal/diagnostic imaging , Muscle, Skeletal/physiology , Time FactorsABSTRACT
Acute maternal hypervitaminosis A established on Day 9 of gestation in Sprague-Dawley-derived rats caused a dose-related increase in the resorption of implants. The median embryolethal dose was 189,000 i.u./kg. In addition to suppression of the allantois leading to placental agenesis, damaged embryos showed retarded somatic development and hydraemia, all apparent 24 h after treatment. At about Day 11 the hydraemia involved the visceral wall of the yolk sac causing death of the embryo soon after. The fluid in the vitelline vessels continued to collect until Day 13 when it absorbed following necrosis of the wall of the yolk sac. Two mechanisms are suggested for the embryonal hydraemia: either the excess fluid resulted from a permeability disorder induced by the vitamin A; or it was retained metabolic water or water specifically absorbed to inflate the allantois and, being unused for this purpose, it pooled in the blood vessels of the embryo. The yolk sac hydraemia is more likely to have followed injury to the proximal endoderm.
