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A method is presented for the determination of a triaxial ellipsoid (such as a strain ellipsoid)from three nonparallel plane sections of the ellipsoid. The sections need be neither orthogonal nor central sections of the ellipsoid. Measurement errors are used to adjust the observed plane ellipses so that they are exact sections of the nearest true ellipsoid, whose dimensions and orientation are then found by solution of a system of six linear equations. A solution of the inverse problem is also presented: given a triaxial ellipsoid with known orientation, to determine the shape and orientation of the ellipse on a plane section. The problem is solved by expanding the equation of an ellipsoid with rotated coordinates, then setting one dimension to zero. Also, a method is presented for the projection of a triaxial ellipsoid onto a plane surface. This is solved by taking the derivative of the ellipsoid equation in the direction of the normal to the plane surface.

In a 4-year controlled, prospective trial, histomorphometric analysis was used to compare the tissue-level skeletal effects of fluoride therapy in 43 postmenopausal women (75 mg NaF/day) with those of 35 matching placebo subjects; all subjects received 1500 mg/day elemental calcium supplement. In addition to an initial, baseline biopsy, a second biopsy was obtained after 6, 18, 30 or 48 months. Measurements were made on a third biopsy obtained from 8 subjects following at least 72 months of fluoride therapy. The change in cancellous bone volume or trabecular thickness in fluoride-treated subjects was not different from a change in placebo-treated subjects. However, paired analysis in the fluoride-treated subjects indicated that bone volume was increased between the first and second biopsies (p<0.005). Both osteoid length and width were significantly increased in fluoride compared with placebo subjects; however, only the osteoid surface increased linearly (r=0.63,p<0.001). The mineral apposition rate and relative tetracycline-covered bone surface were not different between fluoride and placebo treatment, although they were decreased in both groups in the second biopsy. The tetracycline-covered bone surface returned to normal in the third biopsy. Definitive evidence for osteomalacia is a prolonged mineralization lag time, which following fluoride treatment was found to be increased 9-fold in the second biopsy and 4-fold in the third biopsy. Further evidence for osteomalacia was increased osteoid thickness by 6 months, evidence of focal areas of interstitial mineralization defects, and broad tetracycline labels of low fluorescence intensity. In the third biopsies, osteoclastic resorption was observed beneath osteoid seams. Fluoride therapy increased the cortical width compared with placebo treatment (p<0.02), and increased the osteoid surface in Haversian canals, but did not change the osteoid width, resorption surface or cortical porosity. After an initial rise, serum fluoride levels remained constant, and the urine values fell slightly. The bone fluoride concentration rose throughout the treatment period, and was correlated with the change in osteoid-covered bone surface (r=0.56,p<0.001). Although we found definitive evidence for osteomalacia, the cause of the osteomalacia was not determined in this study. On the other hand, the presence of bone resorption beneath unmineralized osteoid and of osteocyte halos is suggestive of hyperparathyroidism. Thus, it is possible that the strong stimulus for bone formation brought about by fluoride therapy resulted in relative calcium deficiency.

A reverse phase ion pair HPLC method has been developed in this work for separation not only between sulfonate surfactant (Chevron CHASER XP 1000) and ethoxylated alcohol cosurfactants (Amoco 120 and 122) but also between two Amocos. Amoco 120 and 122, a homolog mixture of C5 and C6 alcohol ethoxylates respectively, were separated according to their alkyl group without influence of the ethylene oxide group.

A strike swing in steeply dipping Silurian strata encloses the southeastern corner of the small Barrack Creek Adamellite stock near Queanbeyan, New South Wales, and at first sight, it appears as though the intrusion of the stock caused deformation. However, minor folds in these strata indicate that the warping was produced by late-stage tectonic folding rather than granite-push. The stock has no primary structures that indicate viscous flow and probably was emplaced by passive stoping up the core of a steeply plunging conical fold. A similar stock nearby (the Googong Granite) has an angular outline and was probably intruded by block-settling or some similar stoping process.

Lower Palaeozoic sedimentary and volcanic rocks east of Queanbeyan, N.S.W., have undergone multiple deformation resulting in four systems of folds. The first of these consists of large isoclinal, recumbent folds (F1). The second generation folds (F2) are the most pronounced; they consist of flattened flexural-slip folds with well developed axial-plane slaty cleavage. Minor variants of this system are associated with meridionally-trending faults. Third and fourth generation folds are minor kink systems.The existence of first generation folds was established on the basis of F2 fold-facing determinations, and their likely form was deduced from the geometrical variations of F2 folds. It is thought that all fold phases developed during the Late Silurian Bowning Orogeny.

The changes in the tibial diaphysis as a result of feeding a high calcium diet to rats previously fed a calcium free diet were determined. The calcium free diet resulted in an increase in the medullary area, and the subsequent feeding of a high calcium diet caused a reduction in medullary area. However, the amount of endosteal bone lost during ten days of feeding a calcium free diet was not completely restored after 78 days of feeding a high calcium diet. The decrease in medullary area was brought about by decreased endosteal bone resorption and particularly by increased endosteal bone formation. Bone formation at the periosteum and at the epiphyses were unchanged, indicating that the high calcium diet did not cause a generalized increase in bone formation. The increase in endosteal bone formation was limited to those sites along endosteum where greatest loss of bone had occurred during the calcium depletion period. This indicates that a local factor is at least partially responsible for the stimulation of endosteal bone formation during calcium repletion. Mechanical stress, which stimulates bone formation, was increased in calcium deficient animals and returned to normal during calcium repletion. In addition, mechanical stress was probably greatest in those sites where the greatest amount of bone repletion occurred and may have been the factor which contributed to the increase in endosteal bone formation during calcium repletion.

AbstractPurpura fulminans is a thrombotic disease that can occur during infections, disseminated intravascular coagulation or in the context of an acquired or congenital protein C or S deficiency. Here we report the case of a 4-year-old child who developed, 5 days after a chickenpox infection, large painful ecchymotic, necrotizing and retiform plaques on the lower extremities. Laboratory analyses revealed very low protein S levels as well as anticardiolipin antibodies. Aggressive treatment by low-molecular-weight heparin, steroids, intravenous immunoglobulins and fresh frozen plasma was able to prevent the extension of the lesions and to correct the coagulation abnormalities. No lesions required skin grafting. As in our patient, an acquired protein S deficiency is probably responsible for most cases of purpura fulminans occurring after varicella, but the concomitant presence of antiphospholipid antibodies may also play a role. Copyright © 2004 S. Karger AG, Basel