A global budget for fine root biomass, surface area, and nutrient contents

Global biogeochemical models have improved dramatically in the last decade in their representation of the biosphere. Although leaf area data are an important input to such models and are readily available globally, global root distributions for modeling water and nutrient uptake and carbon cycling have not been available. This analysis provides global distributions for fine root biomass, length, and surface area with depth in the soil, and global estimates of nutrient pools in fine roots. Calculated root surface area is almost always greater than leaf area, more than an order of magnitude so in grasslands. The average C:N:P ratio in living fine roots is 450:11:1, and global fine root carbon is more than 5% of all carbon contained in the atmosphere. Assuming conservatively that fine roots turn over once per year, they represent 33% of global annual net primary productivity.

Partial molar volume, surface area, and hydration changes for equilibrium unfolding and formation of aggregation transition state: High-pressure and cosolute studies on recombinant human IFN-γ

The equilibrium dissociation of recombinant human IFN-γ was monitored as a function of pressure and sucrose concentration. The partial molar volume change for dissociation was −209 ± 13 ml/mol of dimer. The specific molar surface area change for dissociation was 12.7 ± 1.6 nm2/molecule of dimer. The first-order aggregation rate of recombinant human IFN-γ in 0.45 M guanidine hydrochloride was studied as a function of sucrose concentration and pressure. Aggregation proceeded through a transition-state species, N*. Sucrose reduced aggregation rate by shifting the equilibrium between native state (N) and N* toward the more compact N. Pressure increased aggregation rate through increased solvation of the protein, which exposes more surface area, thus shifting the equilibrium away from N toward N*. The changes in partial molar volume and specific molar surface area between the N* and N were −41 ± 9 ml/mol of dimer and 3.5 ± 0.2 nm2/molecule, respectively. Thus, the structural change required for the formation of the transition state for aggregation is small relative to the difference between N and the dissociated state. Changes in waters of hydration were estimated from both specific molar surface area and partial molar volume data. From partial molar volume data, estimates were 25 and 128 mol H2O/mol dimer for formation of the aggregation transition state and for dissociation, respectively. From surface area data, estimates were 27 and 98 mol H2O/mol dimer. Osmotic stress theory yielded values ≈4-fold larger for both transitions.

Chronic morphine induces visible changes in the morphology of mesolimbic dopamine neurons.

The mesolimbic dopamine system, which arises in the ventral tegmental area (VTA), is an important neural substrate for opiate reinforcement and addiction. Chronic exposure to opiates is known to produce biochemical adaptations in this brain region. We now show that these adaptations are associated with structural changes in VTA dopamine neurons. Individual VTA neurons in paraformaldehyde-fixed brain sections from control or morphine-treated rats were injected with the fluorescent dye Lucifer yellow. The identity of the injected cells as dopaminergic or nondopaminergic was determined by immunohistochemical labeling of the sections for tyrosine hydroxylase. Chronic morphine treatment resulted in a mean approximately 25% reduction in the area and perimeter of VTA dopamine neurons. This reduction in cell size was prevented by concomitant treatment of rats with naltrexone, an opioid receptor antagonist, as well as by intra-VTA infusion of brain-derived neurotrophic factor. In contrast, chronic morphine treatment did not alter the size of nondopaminergic neurons in the VTA, nor did it affect the total number of dopaminergic neurons in this brain region. The results of these studies provide direct evidence for structural alterations in VTA dopamine neurons as a consequence of chronic opiate exposure, which could contribute to changes in mesolimbic dopamine function associated with addiction.