Constraining predictions of the carbon cycle using data.

We use a carbon-cycle data assimilation system to estimate the terrestrial biospheric CO(2) flux until 2090. The terrestrial sink increases rapidly and the increase is stronger in the presence of climate change. Using a linearized model, we calculate the uncertainty in the flux owing to uncertainty in model parameters. The uncertainty is large and is dominated by the impact of soil moisture on heterotrophic respiration. We show that this uncertainty can be greatly reduced by constraining the model parameters with two decades of atmospheric measurements.

Recent patterns and mechanisms of carbon exchange by terrestrial ecosystems.

Knowledge of carbon exchange between the atmosphere, land and the oceans is important, given that the terrestrial and marine environments are currently absorbing about half of the carbon dioxide that is emitted by fossil-fuel combustion. This carbon uptake is therefore limiting the extent of atmospheric and climatic change, but its long-term nature remains uncertain. Here we provide an overview of the current state of knowledge of global and regional patterns of carbon exchange by terrestrial ecosystems. Atmospheric carbon dioxide and oxygen data confirm that the terrestrial biosphere was largely neutral with respect to net carbon exchange during the 1980s, but became a net carbon sink in the 1990s. This recent sink can be largely attributed to northern extratropical areas, and is roughly split between North America and Eurasia. Tropical land areas, however, were approximately in balance with respect to carbon exchange, implying a carbon sink that offset emissions due to tropical deforestation. The evolution of the terrestrial carbon sink is largely the result of changes in land use over time, such as regrowth on abandoned agricultural land and fire prevention, in addition to responses to environmental changes, such as longer growing seasons, and fertilization by carbon dioxide and nitrogen. Nevertheless, there remain considerable uncertainties as to the magnitude of the sink in different regions and the contribution of different processes.

Travelling wave ultrasonic motor using the B08 flexural mode of a circular membrane.

This paper describes the design, construction, and performance of a piezoelectric motor that uses the travelling B08 mode of an 80-mm diameter circular membrane to drive a rotor by frictional contact. The motor is of a thin planar design, giving high torque of up to 0.33 Nm at low speed and has been developed as a design that can be made with lithographic techniques for miniaturization. Investigations of the free stator with a vibration pattern imager and impedance analyzer gave the resonance frequency, mode, and electromechanical coupling of the stator. Motor speed as a function of frequency for a constant voltage and performance charts of speed, output power, and efficiency against torque are presented for a particular input voltage and rotor pre-load. The effects of two different lead zirconate titanate (PZT) ring dimensions have been investigated. Excitation of the B09 mode has been observed, incommensurate with the piezoelectric excitation of the stator. This is discussed with relation to edge-clamping of the stator. Single standing wave motoring was observed, believed to arise from asymmetry of the stator and its perturbation of the B08 resonance mode. Sources of power loss, including frame vibration and friction interface slip, are considered and discussed.

Identification of A2B5-positive putative oligodendrocyte progenitor cells and A2B5-positive astrocytes in adult human white matter.

Spontaneous remyelination of previously demyelinated axons is found in a substantial minority of acute and chronic lesions in multiple sclerosis. In the rodent, central remyelination restores saltatory conduction and helps restore limb function, and it seems likely that endogenous myelin repair contributes to neurological recovery in multiple sclerosis. However, the identity of the remyelinating cell remains enigmatic. Fully differentiated oligodendrocytes have very limited capacity for recapitulating their developmental activities and re-engaging myelination pathways. Proliferative oligodendrocyte progenitors--often known as O-2A cells because of their ability to differentiate in vitro into either oligodendrocytes or ("type 2") astrocytes--are, in contrast, extremely efficient at myelin repair either spontaneously, or after transplantation into the de- or dysmyelinated CNS. Oligodendrocyte progenitors are present in both developing and adult rodent CNS. We have previously demonstrated that proliferative oligodendrocyte progenitors are present in cultures prepared from the adult human CNS. Here, using fresh tissue print preparations, we report that cells with processes and the A2B5-positive immunophenotype of proliferative oligodendrocyte progenitors are present in situ in adult human white matter. This technique also reveals the occurrence of A2B5-positive astrocytes, a cell also not previously identified in the normal adult human CNS. In the light of the rodent data showing the importance of oligodendrocyte progenitors in myelin repair, our findings suggesting the presence of progenitors in the adult human brain may have significant implications for spontaneous remyelination in multiple sclerosis and other demyelinating conditions.

A proliferative adult human oligodendrocyte progenitor.

The failure of oligodendrocytes to sustain repair of demyelinated axons contributes to the cumulative neurological disability which characterizes multiple sclerosis. In the rodent, transplanted neonatal glial progenitors efficiently remyelinate gliotoxic lesions. Proliferative bipotential progenitors are also present in the adult rat, but have not hitherto been identified in adult human tissue. Here we demonstrate cells in cultures of adult human temporal lobe which are morphologically and immunocytochemically identical to rate progenitors, are bipotential, and exhibit an astrocyte-driven proliferative response. The identification of an adult human oligodendrocyte progenitor is the first step towards developing interventional strategies for promoting repair of demyelinated lesions in patients with multiple sclerosis.