The temporal response of bone to unloading

Rats were suspended by their tails with the forelimbs bearing the weight load to simulate the weightlessness of space flight. Growth in bone mass ceased by 1 week in the hindlimbs and lumbar vertebrae in growing rats, while growth in the forelimbs and cervical vertebrae remained unaffected. The effects of selective skeletal unloading on bone formation during 2 weeks of suspension was investigated using radio iostope incorporation (with Ca-45 and H-3 proline) and histomorphometry (with tetracycline labeling). The results of these studies were confirmed by histomorphometric measurements of bone formation using triple tetracycline labeling. This model of simulated weightlessness results in an initial inhibition of bone formation in the unloaded bones. This temporary cessation of bone formation is followed in the accretion of bone mass, which then resumes at a normal rate by 14 days, despite continued skeletal unloading. This cycle of inhibition and resumption of bone formation has profound implication for understanding bone dynamics durng space flight, immobilization, or bed rest and offers an opportunity to study the hormonal and mechanical factors that regulate bone formation

A 14-day ground-based hypokinesia study in nonhuman primates: A compilation of results

A 14 day ground based hypokinesia study with rhesus monkeys was conducted to determine if a spaceflight of similar duration might affect bone remodeling and calcium homeostatis. The monkeys were placed in total body casts and sacrificed either immediately upon decasting or 14 days after decasting. Changes in vertebral strength were noted and further deterioration of bone strength continued during the recovery phase. Resorption in the vertebrae increased dramatically while formation decreased. Cortical bone formation was impaired in the long bones. The immobilized animals showed a progressive decrease in total serum calcium which rebounded upon remobilization. Most mandibular parameters remained unchanged during casting except for retardation of osteon birth or maturation rate and density distribution of matrix and mineral moieties

Magic Numbers for the Photoelectron Anisotropy in Li-Doped Dimethyl Ether Clusters

Photoelectron velocity map imaging of Li(CH$_3$OCH$_3$)$_n$ clusters (1 $\leq$ n $\leq$ 175) is used to search for magic numbers related to the photoelectron anisotropy. Comparison with density functional calculations reveals magic numbers at n=4, 5, and 6, resulting from the symmetric charge distribution with high s-character of the highest occupied molecular orbital. Since each of these three cluster sizes correspond to the completion of a first coordination shell, they can be considered as 'isomeric motifs of the first coordination shell'. Differences in the photoelectron anisotropy, the vertical ionization energies and the enthalpies of vaporization between Li(CH$_3$OCH$_3$)$_n$ and Na(CH$_3$OCH$_3$)$_n$ can be rationalized in terms of differences in their solvation shells, atomic ionization energies, polarizabilities, metal-oxygen bonds, ligand-ligand interactions, and by cooperative effects

Colourings of cubic graphs inducing isomorphic monochromatic subgraphs

A $k$-bisection of a bridgeless cubic graph $G$ is a $2$-colouring of its vertex set such that the colour classes have the same cardinality and all connected components in the two subgraphs induced by the colour classes (monochromatic components in what follows) have order at most $k$. Ban and Linial conjectured that every bridgeless cubic graph admits a $2$-bisection except for the Petersen graph. A similar problem for the edge set of cubic graphs has been studied: Wormald conjectured that every cubic graph $G$ with $|E(G)| \equiv 0 \pmod 2$ has a $2$-edge colouring such that the two monochromatic subgraphs are isomorphic linear forests (i.e. a forest whose components are paths). Finally, Ando conjectured that every cubic graph admits a bisection such that the two induced monochromatic subgraphs are isomorphic. In this paper, we give a detailed insight into the conjectures of Ban-Linial and Wormald and provide evidence of a strong relation of both of them with Ando's conjecture. Furthermore, we also give computational and theoretical evidence in their support. As a result, we pose some open problems stronger than the above mentioned conjectures. Moreover, we prove Ban-Linial's conjecture for cubic cycle permutation graphs. As a by-product of studying $2$-edge colourings of cubic graphs having linear forests as monochromatic components, we also give a negative answer to a problem posed by Jackson and Wormald about certain decompositions of cubic graphs into linear forests.Comment: 33 pages; submitted for publicatio

The role of 1,25-dihydroxyvitamin D in the inhibition of bone formation induced by skeletal unloading

Skeletal unloading results in osteopenia. To examine the involvement of vitamin D in this process, the rear limbs of growing rats were unloaded and alterations in bone calcium and bone histology were related to changes in serum calcium (Ca), inorganic phosphorus (P sub i), 25-hydroxyvitamin D (25-OH-D), 24,25-dihydroxyvitamin D (24,25(OH)2D and 1,25-dihydroxyvitamin D (1,25(OH)2D. Acute skeletal unloading induced a transitory inhibition of Ca accumulation in unloaded bones. This was accompanied by a transitory rise in serum Ca, a 21% decrease in longitudinal bone growth (P 0.01), a 32% decrease in bone surface lined with osteoblasts (P .05), no change in bone surface lined with osteoclasts and a decrease in circulating (1,25(OH)2D. No significant changes in the serum concentrations of P sub i, 25-OH-D or 24,25(OH)2D were observed. After 2 weeks of unloading, bone Ca stabilized at approximately 70% of control and serum Ca and 1,25(OH)2D returned to control values. Maintenance of a constant serum 1,25(OH)2D concentration by chronic infusion of 1,25(OH)2D (Alza osmotic minipump) throughout the study period did not prevent the bone changes induced by acute unloading. These results suggest that acute skeletal unloading in the growing rat produces a transitory inhibition of bone formation which in turn produces a transitory hypercalcemia