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Apparatus for bone sectioning.

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J S ARNOLD, D H TAYSUM, W S JEE. 1954. Apparatus for bone sectioning.. https://doi.org/10.3109/10520295409115440

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In view of the fact that fractures are the clinically relevant events, risk factors for fractures are discussed first. Bone mineral density (BMD) appears to be a much less important risk factor for the most severe hip fractures than the risk of falling. No results of experimental studies on hormones and fractures at advanced age are available. An overview of the effects of progestins on bone is given. Effects of progestins on bone have been studied by in vitro experiments using cell lines and by more relevant clinical observations. Prospective studies have been conducted following the use of progestins contained in oral contraceptives, alone or in combination with oestrogens; long-term contraception by injection of depot preparations; so-called "add-back" hormonal therapy attempting to reverse the adverse effects of gonadotropin releasing hormone agonists on bone and after different regimens of hormone replacement therapy (HRT) in postmenopausal women. From the data there are no indications that the various progestins, used in clinical practice, have either a bone-protective or an oestrogen antagonistic activity. Progestins do not add or subtract much of the protective action of oestrogens on the bones.

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Metatropic dysplasia lethal variants.

BACKGROUND: The metatropic dysplasia group includes fibrochondrogenesis, Schneckenbecken dysplasia and metatropic dysplasia (various forms). The overlapping features of this group with other dysplasias may cause diagnostic confusion, particularly in perinatal lethal cases. OBJECTIVE: To attempt to classify the radiological findings of the presented eight sporadic cases based on a broad review of the perinatally lethal metatropic group of conditions and to discuss some overlapping features in the light of current knowledge. RESULTS: The first four cases are of recognised conditions, namely lethal metatropic dysplasia (Type 2) or hyperchondrogenesis, lethal hyperplastic metatropic dysplasia (Type 1) and fibrochondrogenesis. The remaining four cases cannot be categorised accurately and are different from each other but with some features of the metatropic group of dysplasias. CONCLUSIONS: The dysplasias within the metatropic dysplasia group are phenotypically distinct from many forms of chondrodysplasia but the pathogenesis still remains poorly understood from the morphological and molecular perspectives. Chondro-osseous morphology might be helpful in all lethal cases especially in our last four cases.

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