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N-type (Si-doped, ND≈1017cm-3) GaAs epitaxial layers (MOCVD) are irradiated at 77 K with oxygen (0.163 GeV), krypton (5.15 GeV), xenon (5.73 GeV) and at 300 K with krypton (5.15 GeV). Hall effect measurements are performed, in situ, with increasing fluence. A decrease of the electron concentration and a degradation of the Hall mobility, respectively due to trapping and to scattering on irradiation-induced point defects are pointed out. In the heavily doped layers, shallow donor impurities merge with the conduction band in distorted band tail. A simple two band conduction model is used as a simulation tool, which allows the carrier Hall concentration variation to be correctly fitted, as a function of both temperature and ion fluence. The Hall mobility versusfluence variation at 77 K, which is mainly limited by screened ionized impurities and defects, is also simulated. From these simulations, the arsenic vacancy levels E1and E2are most likely to correspond respectively to single acceptor (-/0) and single donor (0/+) transitions. The introduction rates of induced defects (in particular VAs) are estimated: the total experimental introduction rate appears to be about 50% of the theoretical atomic displacement rate associated with nuclear collisions, independently of ion nature and of temperature. Although electronic stopping power Seis about 2000 times larger than nuclear stopping power Sn, it is then suggested that irradiation-induced electronic excitation, in the investigated range Se= 1–12 MeV/μm, has no effect on the degradation of n-type GaAs epitaxial layers.

Background: There are studies showing stimulative effect of arginine on insulin secretion. This mechanism is not fully explained. The effects of the impact of arginine on carbohydrate balance under the conditions of ischemia and reperfusion remain to be determined. The aim of this study is the evaluation of the influence of short-term L-arginine supplementation on the concentration of glucose and insulin in blood and insulin binding in rat skeletal muscle under the conditions of ischemia and reperfusion. Methods: The study was conducted on male Wistar rats with average body mass 250 ± 30 g. Animals were divided into four groups: Group I - control, Group II - placebo, Group III - L-arginine 500 mg/kg/24 h for 5 days, Group IV - L-arginine and L-NAME (75 µmol/rat/24 h) for 5 days. Each group was divided into subgroups depending on duration of ischemia and reperfusion. Acute ischemia of hind limb was induced in each group by putting pneumatic tourniquet on the thigh. Blood samples and skeletal muscles were collected from the rats. Plasma concentrations of glucose and insulin were measured. Insulin binding to insulin receptors was determined in skeletal muscle. Results: A clear reduction of insulin binding to receptor was found in the group of animals without ischemia and the group supplemented with L-arginine and subjected to 4-h ischemia and 30- and 120-min reperfusion. A significant increase in insulin level was found in groups of animals with L-arginine and/or L-NAME subjected to 4-h ischemia at all times of reperfusion. Supplementation with L-arginine and/or L-NAME decreased levels of glucose in blood serum of animals undergoing ischemia-reperfusion syndrome compared to the control and placebo groups. Conclusion: Under conditions of ischemia-reperfusion, short-term administration of L-arginine causes a decrease in insulin binding capacity of insulin receptors in skeletal muscle, an increase in insulin level and a decrease in the concentration of glucose in blood serum.

This paper highlights the analysis of the development of fatigue cracks under loading in the region of rolling contact. A surface defect is taken as an irregularity of a convex circular profile on an otherwise regular contact track, on which a rolling element is moving. 2D numerical models with different lengths of cracks were analysed. The results provided an estimation of the influence of the irregularity height and the length of a crack on the stress intensity factors (SIF) at the crack tip, and, as a consequence, on the crack growth rate and direction. A simplified model of contact was used in which the rolling element was replaced by the distribution of displacements equivalent to its interaction. It was assumed that an element in a contact pair having a large mass and moving with a high velocity would not deviate from its initial path while rolling over the irregularity on the track. This allowed the dynamic contact interaction and corresponding crack tip loading to be estimated, despite the use of a quasi—static model for the analyses.

Posthumous Tribute to Professor Marek Dietrich

Although there has been considerable analysis on the effects of trade measures on forest product markets, these have tended to focus on tariffs. There is growing concern about the impact of non-tariff trade measures on the global forest product sector. The objective of this study is to fill a gap and estimate trade and economic impacts of non-tariff barriers and compare them to the impacts of tariffs. Ad-valorem equivalent estimates for a set of well-defined non-tariff trade restrictions are incorporated into a global forest products trade model. Nontariff barriers are found to be less common than tariffs but have similar or bigger aggregate impacts on trade, production, producer revenues, consumer expenditures and value added as tariffs. There is uncertainty in the estimation of ad-valorem equivalence of non-tariff barriers that serves as a caveat on the results. Impacts of reducing tariff and non-tariff barriers are often different across regions and products. While not free from uncertainty, the results underscore the importance of analysing both types of trade policy and the need for continuing comprehensive trade liberalization.

IL-17 is a cytokine produced by a newly identified T-cell subpopulation (TH17/THIL-17). It is a central mediator in inflammatory processes that connects T-cell stimulation with neutrophil mobilization. The role of IL-17 in the immune dysfunction after polytrauma is still not clarified. In a retrospective study, the systemic concentration of IL-17 and IL-6 of 71 polytraumatized patients were analyzed daily by enzyme-linked immunosorbent assay. The patients' collective consist of 55 men and 16 women (43 ± 16 years; injury severity score, 33 ± 13). In only 6% of the patients, an increase in systemic IL-17 was detected. In most patients (94%), no systemic IL-17 was detectable or the IL-17 concentrations in plasma were in the range of the healthy donor group. To identify a possible role of systemic IL-17 in the posttraumatic phase, the patients were divided into two groups. Group A (47 men, 15 women) consists of patients with IL-17 concentrations in the range of normal healthy donors. Group B (8 men, 1 woman) consists of patients with elevated (>45 pg mL−1on at least 3 consecutive days) systemic IL-17 concentrations. Three patients in group B showed highly increased systemic IL-17 concentrations (median, >200 pg mL−1). These patients were male and showed all blunt chest and abdominal trauma with lung contusion and pneumohemothorax. However, there was no conformity in other injury patterns, injury severity score, age, outcome, intensive care period, or clinical complications. After a period of 4 years, we were able to obtain a new blood sample from one patient with high IL-17 level. The systemic IL-17 value of this former patient was now less than the detection limit. However, stimulation of peripheral blood mononuclear cells from this patient revealed elevated numbers of cells with the capacity to produce IL-17-producing cells as determined by enzyme-linked immuno spot assay and flow cytometry compared with peripheral blood mononuclear cells obtained from current polytrauma patients and healthy donors. In conclusion, IL-17 is not suitable as a pathophysiological or predictive marker after polytrauma. Whether highly increased systemic IL-17 concentrations detected in single patients are due to individually increased numbers of TH17 cells as we have demonstrated with one rerecruited patient has to be further analyzed.

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The grid research that has been intensely undertaken in the recent years has resulted in a long list of excellent solutions for the access to and utilization of powerful remote computing resources. Some of these solutions have emerged into standards or good practices widely accepted by the grid community. However, a lot of other important standards are yet to be found and the range of available middleware, protocols and services causes not only a serious problem when deciding on the technology to be used for a particular grid environment, but also poses a major challenge when trying to solve some ongoing issues. The lack of standards and heterogeneity of the grid middleware used is, for example, a big challenge when designing science gateways that are set to provide the scientific community with means of accessing the vast amount of the powerful grid resources delivered by multiple independent grid infrastructures administered by different types of grid management systems. In this paper, we present a method by which we addressed this problem within the PROGRESS project and how it resulted in the design of the grid resource broker plug‐in mechanism, which allows the enabling of resources belonging to heterogeneous grid infrastructures within a computing portal. Copyright © 2007 John Wiley & Sons, Ltd.

Web portals are one of the possible ways to access the remote computing resources offered by Grid environments. Since the emergence of the first middleware for the Grid, works have been conducted on delivering the functionality of Grid services on the Web. Many interesting Grid portal solutions have been designed help organize remote access to Grid resources and applications from within Web browsers. They are technically advanced and more and more widely used around the world, resulting in feedback from the community. Some of these user comments concern the flexibility and user‐friendliness of the developed solutions. In this paper we present how we addressed the need for a flexible and user‐friendly Grid portal environment within the PROGRESS project and how our approach facilitates the use of the Grid within Web portals. Copyright © 2006 John Wiley & Sons, Ltd.

To evaluate the role of soluble mediators released after interaction of leukocytes with biomaterials on cells of the implant microenvironment, the surface expression of adhesion molecules (CD11b, CD62L, CD66b, ICAM-1) on freshly isolated whole blood leukocytes (WBL) was analyzed by flow cytometry after incubation in leukocyte/nickel-titanium shape-memory alloy (NiTi-SMA)-conditioned media. NiTi-SMA samples were either coated with calcium phosphate by dipping in oversaturated calcium phosphate solution (CaP-coating) or were non-coated. Peripheral blood mononuclear cells (PBMC) and polymorphonuclear neutrophil leukocytes (PMN) were isolated and seeded on both samples to generate respective conditioned media. In comparison with conditioned media obtained by non-coated NiTi-SMA, the expression of CD11b, CD66b, and ICAM-1 on WBL was upregulated by conditioned media obtained from CaP-coated samples. In contrast, the expression of CD62L on WBL was decreased after incubation in conditioned medium obtained from CaP-coated NiTi-samples compared to non-coated NiTi. These data demonstrate the possible influence of released mediators elicited by leukocyte-biomaterial interactions on cells of the implant microenvironment.

A staple from nickel‐titanium shape memory alloy for foot surgery was prepared by metal injection moulding (powder metallurgy). After a thorough characterisation with a multitude of physical, chemical, mechanical, and biological methods, the prototype appears to be well suited for clinical use where a shape‐memory effect is useful.

Previous studies have shown that laparoscopic interventions are associated with increases in intracranial pressure. However, the consequences on cerebral blood flow (CBF) are unknown. This study investigates the effects of carbon dioxide (CO2) pneumoperitoneum on CBF in pigs. Ten pigs (weight, 20–26 kg) were anesthetized with 1.4 isoflurane and fentanyl (1 g/kg per minute). Mechanical ventilation (fraction of inspired oxygen 0.4) was set to maintain normocapnia (end-tidal CO2tension 35 mm Hg). Arterial and central venous catheters were placed for measurement of mean arterial blood pressure and central venous pressure. Bilateral internal carotid artery blood flow was measured using two transient time flow probes placed around both carotid arteries (with ligated external carotid arteries). Cortical and subcortical cerebral blood flow was measured using laser Doppler flowmetry. Sagittal sinus pressure was measured via a superior sagittal sinus catheter. After baseline measurements, the peritoneal cavity of the animals was insufflated with CO2to achieve an intraabdominal pressure of 12-mm Hg. After 10 minutes of stable CO2, pneumoperitoneum measurements were repeated. Increases in central venous pressure (6.3 ± 2.1 to 11.1 ± 3.0 mm Hg) and sagittal sinus pressure (8.0 ± 2.8 to 11.9 ± 3.0 mm Hg) were noted during CO2pneumoperitoneum (P< .05). Bilateral internal carotid artery blood flow (46.0 ± 7.4 vs 47.7 ± 7.1 mL/100g per minute), cortical CBF (263 ± 115 vs 259 ± 158 tissue perfusion units), and subcortical CBF (131 ± 145 vs 133 ± 149 tissue perfusion units) did not change during CO2pneumoperitoneum. The current data show that CO2pneumoperitoneum increases sagittal sinus pressure without changing CBF. Increases in sagittal sinus pressure are likely related to decreases in cerebral venous drainage caused by increases in intraabdominal pressure.

We have investigated the effects of xenon on regional cerebral blood flow (rCBF) and autoregulation in pigs sedated with propofol 4 mg kg-1 h-1. Balloon-tipped catheters were placed into the descending aorta and inferior vena cava of 15 Göttingen Minipigs for manipulation of arterial pressure and blood sampling. rCBF was measured using the sagittal sinus outflow technique. Xenon was adjusted randomly to end-tidal fractions (FE'Xe) of 0, 0.30, 0.50 and 0.70. After baseline measurements of heart rate (HR), mean arterial pressure (MAP), rCBF, sagittal sinus pressure (SSP) and calculation of regional cerebrovascular resistance (rCVR) at each respective FE'Xe, autoregulation was tested in the MAP range 60-120 mm Hg. Increasing FE'Xe had no effect on HR, MAP, rCBF or SSP. rCVR increased with increases in MAP, regardless of FE'Xe. Autoregulation was not impaired. We conclude that xenon inhalation had no effect on rCBF and autoregulation in our model, which could suggest that xenon is an adequate adjunct for neurosurgical anaesthesia.