Effect of soil strength on root growth under different water conditions

The objective of this study was to determine the effects of soil water and soil strength on root growth in situations where the individual effects of both of these factors were important. Three grain legumes were grown from pre-germinated seeds for five days on 50-mm compacted columns of two major soils of Sri Lanka. Four or five levels of bulk density (1.1 to 1.8 Mg.m^–3) and five or six levels of matric potential (–0.02 to–2.0 MPa) were used.Soil strength and matric potential effects on root growth were independently significant for most crop and soil combinations. Under high (wet) matric potential (>–0.77 MPa) soil conditions, the effect of soil water on root growth was evident only in its effect on soil strength. Bulk density had a significant effect on root growth independent of soil strength and matric potential in three cases.For all crops and soils, root penetration was 80% of the maximum or greater when the average soil strength (soil water not limiting) was 0.75 MPa or less, and when the average matric potential (soil strength not limiting) was –0.77 MPa or greater (wetter). Root penetration was 20% of the maximum or less when the soil strength was greater than 3.30 MPa (soil water not limiting), and when matric potential (soil strength not limiting) was less than –3.57 MPa. The use of pre-germinated seeds, which contained imbibed water, combined with a lack of water loss from the closed chambers containing the plants is the probable cause for the very low (–3.57 MPa) matric potential that allowed root growth at 20% of the maximum.     

Fluid pressure relaxation depends upon osteonal microstructure: modeling an oscillatory bending experiment.

When bone is mechanically loaded, bone fluid flow induces shear stresses on bone cells that have been proposed to be involved in bone's mechanosensory system. To investigate bone fluid flow and strain-generated potentials, several theoretical models have been proposed to mimic oscillatory four-point bending experiments performed on thin bone specimens. While these previous models assume that the bone fluid relaxes across the specimen thickness, we hypothesize that the bone fluid relaxes primarily through the vascular porosity (osteonal canals) instead and develop a new poroelastic model that integrates the microstructural details of the lacunar-canalicular porosity, osteonal canals, and the osteonal cement lines. Local fluid pressure profiles are obtained from the model, and we find two different fluid relaxation behaviors in the bone specimen, depending on its microstructure: one associated with the connected osteonal canal system, through which bone fluid relaxes to the nearby osteonal canals; and one associated with the thickness of a homogeneous porous bone specimen (approximately 1 mm in our model), through which bone fluid relaxes between the external surfaces of the bone specimen at relatively lower loading frequencies. Our results suggest that in osteonal bone specimens the fluid pressure response to cyclic loading is not sensitive to the permeability of the osteonal cement lines, while it is sensitive to the applied loading frequency. Our results also reveal that the fluid pressure gradients near the osteonal canals (and thus the fluid shear stresses acting on the nearby osteocytes) are significantly amplified at higher loading frequencies.     

Positioning of nucleosomes in satellite I-containing chromatin of rat liver

The location of nucleosomes on rat satellite I DNA has been investigated using a new approach. Nucleosome cores were prepared from rat liver nuclei with micrococcal nuclease, exonuclease III and nucleases S1. From the total population of core DNA fragments the satellite-containing fragments were isolated by molecular cloning and the complete sequence of 50 clones was determined. The location of nucleosomes along the satellite sequence was found to be non-random. Our results show that nucleosomes occupy a number of positions on satellite I DNA. About 35 to 50% of all nucleosomes are positioned in two corresponding major sites, the remainder in about 16 less preferred sites. The major nucleosome positions are apparently strictly defined with the precision of a single base-pair. These results were confirmed by other approaches, including restriction nuclease digestion experiments. There are good indications of a defined long-range organization of the satellite chromatin fiber in two or more oligonucleosomal arrays with distinct nucleosome configurations.     

The Insulin-like Growth Factor-1 Binding Protein Acid-labile Subunit Alters Mesenchymal Stromal Cell Fate

Age-related osteoporosis is accompanied by an increase in marrow adiposity and a reduction in serum insulin-like growth factor-1 (IGF-1) and the binding proteins that stabilize IGF-1. To determine the relationship between these proteins and bone marrow adiposity, we evaluated the adipogenic potential of marrow-derived mesenchymal stromal cells (MSCs) from mice with decreased serum IGF-1 due to knockdown of IGF-1 production by the liver or knock-out of the binding proteins. We employed 10–16-week-old, liver-specific IGF-1-deficient, IGFBP-3 knock-out (BP3KO) and acid-labile subunit knock-out (ALSKO) mice. We found that expression of the late adipocyte differentiation marker peroxisome proliferator-activated receptor γ was increased in marrow isolated from ALSKO mice. When induced with adipogenic media, MSC cultures from ALSKO mice revealed a significantly greater number of differentiated adipocytes compared with controls. MSCs from ALSKO mice also exhibited decreased alkaline-phosphatase positive colony size in cultures that were stimulated with osteoblast differentiation media. These osteoblast-like cells from ALSKO mice failed to induce osteoclastogenesis of control cells in co-culture assays, indicating that impairment of IGF-1 complex formation with ALS in bone marrow alters cell fate, leading to increased adipogenesis.     

Chronic High Fructose Intake Reduces Serum 1,25 (OH)2D3 Levels in Calcium-Sufficient Rodents

Excessive fructose consumption inhibits adaptive increases in intestinal Ca²⁺ transport in lactating and weanling rats with increased Ca²⁺ requirements by preventing the increase in serum levels of 1,25(OH)₂D₃. Here we tested the hypothesis that chronic fructose intake decreases 1,25(OH)₂D₃ levels independent of increases in Ca²⁺ requirements. Adult mice fed for five wk a high glucose-low Ca²⁺ diet displayed expected compensatory increases in intestinal and renal Ca²⁺ transporter expression and activity, in renal CYP27B1 (coding for 1α-hydroxylase) expression as well as in serum 1,25(OH)₂D₃ levels, compared with mice fed isocaloric glucose- or fructose-normal Ca²⁺ diets. Replacing glucose with fructose prevented these increases in Ca²⁺ transporter, CYP27B1, and 1,25(OH)₂D₃ levels induced by a low Ca²⁺ diet. In adult mice fed for three mo a normal Ca²⁺ diet, renal expression of CYP27B1 and of CYP24A1 (24-hydroxylase) decreased and increased, respectively, when the carbohydrate source was fructose instead of glucose or starch. Intestinal and renal Ca²⁺ transporter activity and expression did not vary with dietary carbohydrate. To determine the time course of fructose effects, a high fructose or glucose diet with normal Ca²⁺ levels was fed to adult rats for three mo. Serum levels of 1,25(OH)₂D₃ decreased and of FGF23 increased significantly over time. Renal expression of CYP27B1 and serum levels of 1,25(OH)₂D₃ still decreased in fructose- compared to those in glucose-fed rats after three mo. Serum parathyroid hormone, Ca²⁺ and phosphate levels were normal and independent of dietary sugar as well as time of feeding. Thus, chronically high fructose intakes can decrease serum levels of 1,25(OH)₂D₃ in adult rodents experiencing no Ca²⁺ stress and fed sufficient levels of dietary Ca²⁺. This finding is highly significant because fructose constitutes a substantial portion of the average diet of Americans already deficient in vitamin D.     

Dynamic permeability of the lacunar–canalicular system in human cortical bone

A new method for the experimental determination of the permeability of a small sample of a fluid-saturated hierarchically structured porous material is described and applied to the determination of the lacunar–canalicular permeability \((K_\mathrm{LC})\) in bone. The interest in the permeability of the lacunar–canalicular pore system (LCS) is due to the fact that the LCS is considered to be the site of bone mechanotransduction due to the loading-driven fluid flow over cellular structures. The permeability of this space has been estimated to be anywhere from \(10^{-17}\;\) to \(10^{-25}\; \hbox {m}^{2}\) . However, the vascular pore system and LCS are intertwined, rendering the permeability of the much smaller-dimensioned LCS challenging to measure. In this study, we report a combined experimental and analytical approach that allowed the accurate determination of the \(K_\mathrm{LC}\) to be on the order of \(10^{-22}\; \hbox {m}^{2}\) for human osteonal bone. It was found that the \(K_\mathrm{LC}\) has a linear dependence on loading frequency, decreasing at a rate of \(2 \times 10^{-24}\; \hbox {m}^{2}\) /Hz from 1 to 100 Hz, and using the proposed model, the porosity alone was able to explain 86 % of the \(K_\mathrm{LC}\) variability.     

On bone adaptation due to venous stasis

This paper addresses the question of whether or not interstitial fluid flow due to the blood circulation accounts for the observed periosteal bone formation associated with comprised venous return (venous stasis). Increased interstitial fluid flow induced by increased intramedullary pressure has been proposed to account for the periosteal response in venous stasis. To investigate the shear stresses acting on bone cell processes due to the blood circulation-driven interstitial fluid flow, a poroelastic model is extended to the situation in which the interstitial fluid flow in an osteon is driven by the pulsatile extravascular pressure in the osteonal canal as well as by the applied cyclic mechanical loading. Our results show that under normal conditions, the pulsatile extravascular pressure in the osteonal canal due to cardiac contraction (10mm Hg at 2Hz) and skeletal muscle contraction (30mm Hg at 1Hz) induce peak shear stresses on the osteocyte cell processes that are two orders of magnitude lower than those induced by physiological mechanical loading (100 microstrain at 1Hz). In venous stasis the induced peak shear stress is reduced further compared to the normal conditions because, although the mean intramedullary pressure is increased, the amplitude of its pulsatile component is decreased. These results suggest that the interstitial fluid flow is unlikely to cause the periosteal bone formation in venous stasis. However, the mean interstitial fluid pressure is found to increase in venous stasis, which may pressurize the periosteum and thus play a role in periosteal bone formation.     

Analysis of avian bone response to mechanical loading, Part Two: Development of a computational connected cellular network to study bone intercellular communication

Mechanical loading-induced signals are hypothesized to be transmitted and integrated by connected bone cells before reaching the bone surfaces where adaptation occurs. A computational connected cellular network (CCCN) model is developed to explore how bone cells perceive and transmit the signals through intercellular communication. This is part two of a two-part study in which a CCCN is developed to study the intercellular communication within a grid of bone cells. The excitation signal was computed as the loading-induced bone fluid shear stress in part one. Experimentally determined bone adaptation responses (Gross et al. in J Bone Miner Res 12:982-988, 1997 and Judex et al. in J Bone Miner Res 12:1737-1745, 1997) are correlated with the fluid shear stress by the CCCN, which adjusts cell sensitivities (loading and signal thresholds) and connection weights. Intercellular communication patterns extracted by the CCCN indicate the cell population responsible for perceiving the loading-induced signal, and loading threshold is shown to play an important role in regulating the bone response.