WinEcon Fiscal Pathways: A Computer Based Learning Module for the Subject Macroeconomic Theory and Policy

trade reforms, manufacturing performance, Australia

Evaluation of Shugor, Dubasi and Watish subtypes of Sudan Desert sheep at the El-Huda National Sheep Research Station, Gezira Province, Sudan

Presents results obtained from a trial conducted at El-Huda National Sheep Research Station, Sudan, Shugor, Dubasi and Watish subtypes of Sudan Desert sheep to compare productivity, reproductivity and animal performance, with particular reference to lambing, lambing intervals, body weight, growth rates and mortality rates, incl. recommendations for further investigations

Gallium oxide and gadolinium gallium oxide insulators on Si δ-doped GaAs/AlGaAs heterostructures

Test devices have been fabricated on two specially grown GaAs/AlGaAs wafers with 10 nm thick gate dielectrics composed of either Ga<sub>2</sub>O<sub>3</sub> or a stack of Ga<sub>2</sub>O<sub>3</sub> and Gd<sub>0.25</sub>Ga<sub>0.15</sub>O<sub>0.6</sub>. The wafers have two GaAs transport channels either side of an AlGaAs barrier containing a Si delta-doping layer. Temperature dependent capacitance-voltage (C-V) and current-voltage (I-V) studies have been performed at temperatures between 10 and 300 K. Bias cooling experiments reveal the presence of DX centers in both wafers. Both wafers show a forward bias gate leakage that is by a single activated channel at higher temperatures and by tunneling at lower temperatures. When Gd<sub>0.25</sub>Ga<sub>0.15</sub>O<sub>0.6</sub> is included in a stack with 1 nm of Ga<sub>2</sub>O<sub>3</sub> at the interface, the gate leakage is greatly reduced due to the larger band gap of the Gd<sub>0.25</sub>Ga<sub>0.15</sub>O<sub>0.6</sub> layer. The different band gaps of the two oxides result in a difference in the gate voltage at the onset of leakage of ~3 V. However, the inclusion of Gd<sub>0.25</sub>Ga<sub>0.15</sub>O<sub>0.6</sub> in the gate insulator introduces many oxide states (≤4.70Ã�Â�10<sup>12</sup> cm<sup>âÂ�Â�2</sup>). Transmission electron microscope images of the interface region show that the growth of a Gd<sub>0.25</sub>Ga<sub>0.15</sub>O<sub>0.6</sub> layer on Ga<sub>2</sub>O<sub>3</sub> disturbs the well ordered Ga<sub>2</sub>O<sub>3</sub>/GaAs interface. We therefore conclude that while including Gd<sub>0.25</sub>Ga<sub>0.15</sub>O<sub>0.6</sub> in a dielectric stack with Ga<sub>2</sub>O<sub>3</sub> is necessary for use in device applications, the inclusion of Gd decreases the quality of the Ga<sub>2</sub>O<sub>3</sub>/GaAs interface and near interface region by introducing roughness and a large number of defect states

Monte Carlo simulations of high-performance implant free In_0.3Ga_0.7 nano-MOSFETs for low-power CMOS applications

No abstract available

A shift in balance between profibrinolytic and antifibrinolytic factors causes enhanced fibrinolysis in cirrhosis

The aim of this study was to assess the cause of enhanced fibrinolysis in cirrhosis by studying the balance between profibrinolytic and antifibrinolytic proteins in 24 patients with mild or severe cirrhosis. Antigen levels of both tissue-type plasminogen activator and plasminogen-activator inhibitor 1 were increased in mild and severe cirrhosis. Activity levels showed a very wide variability, but median activity levels of both proteins were normal. In most patients, the increase in tissue-type plasminogen activator was counterbalanced by the increased levels of plasminogen-activator inhibitor 1, but in a subgroup of patients the change in balance resulted in extremely high tissue-type plasminogen-activator levels. The specific activity of both proteins (activity/ antigen quotient) was reduced in either mild or severe cirrhosis. This finding indicates either that more enzyme-inhibitor complexes circulate in the blood of patients with cirrhosis than in normal individuals or that dysfunctional molecules circulate. Plasminogen and α2-antiplasmin antigen and activity levels were decreased in both mild and severe cirrhosis. The binding of α2-antiplasmin to fibrin was decreased in severe cirrhosis, making fibrin clots more susceptible to lysis. Clot lysis experiments were performed to see if equal decreases in plasminogen and α2-antiplasmin levels, as found in cirrhosis, result in a change in the rate of fibrinolysis. It was found that the proportionate decreases led to enhancement of fibrinolysis, indicating that the inhibitor depletion is more important than the proenzyme depletion. The authors conclude that enhanced fibrinolysis frequently found in cirrhosis may be attributed to an increased tissuetype plasminogen-activator activity relative to plasminogen-activator-inhibitor activity and decreased levels of α2-antiplasmin, resulting in a reduced binding of α2-antiplasmin to fibrin.</p

A shift in balance between profibrinolytic and antifibrinolytic factors causes enhanced fibrinolysis in cirrhosis

The aim of this study was to assess the cause of enhanced fibrinolysis in cirrhosis by studying the balance between profibrinolytic and antifibrinolytic proteins in 24 patients with mild or severe cirrhosis. Antigen levels of both tissue-type plasminogen activator and plasminogen-activator inhibitor 1 were increased in mild and severe cirrhosis. Activity levels showed a very wide variability, but median activity levels of both proteins were normal. In most patients, the increase in tissue-type plasminogen activator was counterbalanced by the increased levels of plasminogen-activator inhibitor 1, but in a subgroup of patients the change in balance resulted in extremely high tissue-type plasminogen-activator levels. The specific activity of both proteins (activity/ antigen quotient) was reduced in either mild or severe cirrhosis. This finding indicates either that more enzyme-inhibitor complexes circulate in the blood of patients with cirrhosis than in normal individuals or that dysfunctional molecules circulate. Plasminogen and α2-antiplasmin antigen and activity levels were decreased in both mild and severe cirrhosis. The binding of α2-antiplasmin to fibrin was decreased in severe cirrhosis, making fibrin clots more susceptible to lysis. Clot lysis experiments were performed to see if equal decreases in plasminogen and α2-antiplasmin levels, as found in cirrhosis, result in a change in the rate of fibrinolysis. It was found that the proportionate decreases led to enhancement of fibrinolysis, indicating that the inhibitor depletion is more important than the proenzyme depletion. The authors conclude that enhanced fibrinolysis frequently found in cirrhosis may be attributed to an increased tissuetype plasminogen-activator activity relative to plasminogen-activator-inhibitor activity and decreased levels of α2-antiplasmin, resulting in a reduced binding of α2-antiplasmin to fibrin.</p

Periaqueductal grey EP3 receptors facilitate spinal nociception in arthritic secondary hypersensitivity

Descending controls on spinal nociceptive processing play a pivotal role in shaping the pain experience following tissue injury. Secondary hypersensitivity develops within undamaged tissue adjacent, and distant to, damaged sites. Spinal neuronal pools innervating regions of secondary hypersensitivity are dominated by descending facilitation that amplifies spinal inputs from un-sensitized peripheral nociceptors. Cyclooxygenase–prostaglandin E2 signaling within the ventrolateral periaqueductal grey (vlPAG) is pro-nociceptive in naïve and acutely inflamed animals but its contributions in more prolonged inflammation and, importantly, secondary hypersensitivity remain unknown. In naïve rats, prostaglandin EP3 receptor (EP3R) antagonism in vlPAG modulated noxious withdrawal reflex (EMG) thresholds to preferential C-, but not A-, nociceptor activation, and raised thermal withdrawal thresholds in awake animals. In rats with inflammatory arthritis, secondary mechanical and thermal hypersensitivity of the hind-paw developed, and this was associated with spinal sensitization to Anociceptor inputs alone. In arthritic rats, blockade of vlPAG EP3R raised EMG thresholds to C-nociceptor activation in the area of secondary hypersensitivity to a degree equivalent to that evoked by the same manipulation in naïve rats

Stationary power applications for polymer electrolyte fuel cells

The benefits provided by Polymer Electrolyte Fuel Cells (PEFC) for power generation (e.g. low operating temperatures, and non-corrosive and stable electrolyte), as well as advances in recent years in lowering their cost and improving anode poisoning tolerance, are stimulating interest in the system for stationary power applications. A significant market potentially exists for PEFCs in certain stationary applications where PEFC technology is a more attractive alternative to other fuel cell technologies. A difficulty with the PEFC is its operation on reformed fuels containing CO, which poisons the anode catalyst. This difficulty can be alleviated in several ways. One possible approach is described whereby the product reformate is purified using a relatively low cost, high-throughput hydrogen permselective separator. Preliminary experiments demonstrate the utility of the concept