Angular Momentum Partitioning and Hexacontatetrapole Moments in Impulsively Excited Argon Ions

We have studied polarized electron collisions with Ar in which the target is simultaneously ionized and excited to form Ar+(3p4(1D)4p) states. We measured the integrated Stokes parameters of the subsequent fluorescence emitted by the 2F7/2, 2F5/2, 2D5/2, and 2P3/2 states along the direction of electron polarization. The Rubin-Bederson hypothesis is shown to hold for the L and S multipoles of these states. The electric quadrupole and hexadecapole of the 1D core are derived. By recoupling these moments with the electric quadrupole moment of the 4p electron, we calculate higher moments of the total ionic orbital angular momentum, including its hexacontatetrapole (64-pole) moment

Angular momentum partitioning and the subshell multipole moments in impulsively excited argon ions

We have investigated collisions between transversely polarized electrons and Ar, in which the Ar is simultaneously ionized and excited to the Ar+*[3p4(+D)4p] states. The Stokes parameters of the fluorescence emitted in the following transitions was measured: (+D)4s 2D/2−(1D)4p 2F7/2 (461.0 nm), (1D)4s 2D5/2 −(1D)4p 2F5/2 (463.7 nm), (1P)3d 2D5/2−(1D)4p 2D5/2 (448.2 nm), and (1D)4s 2D3/2−(1D)4p 2P3/2 (423.7 nm). We develop the angular momentum algebra necessary to extract from these data, starting from the overall atomic J multipoles, the partitioning of orbital angular momentum into the 1D core electric quadrupole and hexadecapole moments, and the outer 4p electric quadrupole moment. The magnetic dipole of the outer electron is also determined. This procedure requires the assumption of good LS coupling for these states, which is justified. We recouple these individual core- and outer-electron moments to calculate the initial electric quadrupoles, hexadecapoles, and hexacontatetrapoles of the initial excited-state manifold. The detailed time structure of the electron-atom collision is considered, as well as the time evolution of the excited ionic state. The Rubin-Bederson hypothesis is thus shown to hold for the initial ionic L and S terms. The consequences of the breakdown of LS coupling are considered. From the circular polarization data, estimates of the relative importance of direct and exchange excitation cross section are made. We discuss experimental issues related to background contributions, Hanle depolarization of the fluorescence signal, and cascade contributions. Nonlinearity of the equations relating the Stokes parameters to the subshell multipole moments complicates the data analysis. Details of the Monte Carlo terrain-search algorithm used to extract multipole data is discussed, and the implications of correlation between the various subshell multipole moments is analyzed. The physical significance of the higher-order multipole moments is discussed, and graphical representations of the effects of these multipoles on the excited ionic charge clouds is presented

Carbon stock growth in a forest stand: the power of age

BACKGROUND: Understanding the relationship between the age of a forest stand and its biomass is essential for managing the forest component of the global carbon cycle. Since biomass increases with stand age, postponing harvesting to the age of biological maturity may result in the formation of a large carbon sink. This article quantifies the carbon sequestration capacity of forests by suggesting a default rule to link carbon stock and stand age. RESULTS: The age dependence of forest biomass is shown to be a power-law monomial where the power of age is theoretically estimated to be 4/5. This theoretical estimate is close to the known empirical estimate; therefore, it provides a scientific basis for a quick and transparent assessment of the benefits of postponing the harvest, suggesting that the annual magnitude of the sink induced by delayed harvest lies in the range of 1–2% of the baseline carbon stock. CONCLUSION: The results of this study imply that forest age could be used as an easily understood and scientifically sound measure of the progress in complying with national targets on the protection and enhancement of forest carbon sinks

Methotrexate-mediated activation of an AMPK-CREB-dependent pathway: a novel mechanism for vascular protection in chronic systemic inflammation

Aims Premature cardiovascular events complicate chronic inflammatory conditions. Low-dose weekly methotrexate (MTX), the most widely used disease-modifying drug for rheumatoid arthritis (RA), reduces disease-associated cardiovascular mortality. MTX increases intracellular accumulation of adenosine monophosphate (AMP) and 5-aminoimidazole-4-carboxamide ribonucleotide which activates AMP-activated protein kinase (AMPK). We hypothesised that MTX specifically protects the vascular endothelium against inflammatory injury via induction of AMPK-regulated protective genes. Methods/results In the (NZW×BXSB)F1 murine model of inflammatory vasculopathy, MTX 1 mg/kg/week significantly reduced intramyocardial vasculopathy and attenuated end-organ damage. Studies of human umbilical vein endothelial cells (HUVEC) and arterial endothelial cells (HAEC) showed that therapeutically relevant concentrations of MTX phosphorylate AMPKαThr172, and induce cytoprotective genes including manganese superoxide dismutase (MnSOD) and haem oxygenase-1 (HO-1). These responses were preserved when HUVECs were pretreated with tumour necrosis factor-α to mimic dysfunctional endothelium. Furthermore, MTX protected against glucose deprivation-induced endothelial apoptosis. Mechanistically, MTX treatment led to cyclic AMP response element-binding protein (CREB)Ser133 phosphorylation, while AMPK depletion attenuated this response and the induction of MnSOD and HO-1. CREB siRNA inhibited upregulation of both cytoprotective genes by MTX, while chromatin immunoprecipitation demonstrated CREB binding to the MnSOD promoter in MTX-treated EC. Likewise, treatment of (NZW×BXSB)F1 mice with MTX enhanced AMPKαThr172 phosphorylation and MnSOD, and reduced aortic intercellular adhesion molecule-1 expression. Conclusions These data suggest that MTX therapeutically conditions vascular endothelium via activation of AMPK-CREB. We propose that this mechanism contributes to the protection against cardiovascular events seen in patients with RA treated with MTX

Internet of Things for Sustainable Forestry

Forests and grasslands play an important role in water and air purification, prevention of the soil erosion, and in provision of habitat to wildlife. Internet of Things has a tremendous potential to play a vital role in the forest ecosystem management and stability. The conservation of species and habitats, timber production, prevention of forest soil degradation, forest fire prediction, mitigation, and control can be attained through forest management using Internet of Things. The use and adoption of IoT in forest ecosystem management is challenging due to many factors. Vast geographical areas and limited resources in terms of budget and equipment are some of the limiting factors. In digital forestry, IoT deployment offers effective operations, control, and forecasts for soil erosion, fires, and undesirable depositions. In this chapter, IoT sensing and communication applications are presented for digital forestry systems. Different IoT systems for digital forest monitoring applications are also discussed

Disturbance and the resilience of coupled carbon and nitrogen cycling in a north temperate forest

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/96419/1/jgrg864.pd

Changes in timber haul emissions in the context of shifting forest management and infrastructure

<p>Abstract</p> <p>Background</p> <p>Although significant amounts of carbon may be stored in harvested wood products, the extraction of that carbon from the forest generally entails combustion of fossil fuels. The transport of timber from the forest to primary milling facilities may in particular create emissions that reduce the net sequestration value of product carbon storage. However, attempts to quantify the effects of transport on the net effects of forest management typically use relatively sparse survey data to determine transportation emission factors. We developed an approach for systematically determining transport emissions using: 1) -remotely sensed maps to estimate the spatial distribution of harvests, and 2) - industry data to determine landscape-level harvest volumes as well as the location and processing totals of individual mills. These data support spatial network analysis that can produce estimates of fossil carbon released in timber transport.</p> <p>Results</p> <p>Transport-related emissions, evaluated as a fraction of transported wood carbon at 4 points in time on a landscape in western Montana (USA), rose from 0.5% in 1988 to 1.7% in 2004 as local mills closed and spatial patterns of harvest shifted due to decreased logging on federal lands.</p> <p>Conclusion</p> <p>The apparent sensitivity of transport emissions to harvest and infrastructure patterns suggests that timber haul is a dynamic component of forest carbon management that bears further study both across regions and over time. The monitoring approach used here, which draws only from widely available monitoring data, could readily be adapted to provide current and historical estimates of transport emissions in a consistent way across large areas.</p

The transcription factor ERG regulates a low shear stress-induced anti-thrombotic pathway in the microvasculature.

Endothelial cells actively maintain an anti-thrombotic environment; loss of this protective function may lead to thrombosis and systemic coagulopathy. The transcription factor ERG is essential to maintain endothelial homeostasis. Here, we show that inducible endothelial ERG deletion (ErgiEC-KO) in mice is associated with spontaneous thrombosis, hemorrhages and systemic coagulopathy. We find that ERG drives transcription of the anticoagulant thrombomodulin (TM), as shown by reporter assays and chromatin immunoprecipitation. TM expression is regulated by shear stress (SS) via Krüppel-like factor 2 (KLF2). In vitro, ERG regulates TM expression under low SS conditions, by facilitating KLF2 binding to the TM promoter. However, ERG is dispensable for TM expression in high SS conditions. In ErgiEC-KO mice, TM expression is decreased in liver and lung microvasculature exposed to low SS but not in blood vessels exposed to high SS. Our study identifies an endogenous, vascular bed-specific anticoagulant pathway in microvasculature exposed to low SS