Concept to Ensure the Company against Exchange Rate Risk

Ve své bakalářské práci se zabývám návrhem optimálního zajištění podniku proti kusovým rizikům. Metod jak se může podnik zajistit je více např. přirozený hedging, forward, futures, swap a opce.The subject of my bachelor’s thesis is a proposal of ensuring a company against exchange rate risk. There are several methods such as natural hedging, forward, futures, swap and put.

Trichoderma longibrachiatum and Aspergillus fischeri Infection as a Cause of Skin Graft Failure in a Patient with Critical Burns after Liver Transplantation

Infectious complications are responsible for the majority of mortalities and morbidities of patients with critical burns. Although bacteria are the predominant etiological agents in such patients, yeasts and fungi have become relatively common causes of infections over the last decade. Here, we report a case of a young man with critical burns on 88% TBSA (total body surface area) arising as a part of polytrauma. The patient's history of orthotopic liver transplantation associated with the patient's need to use combined immunosuppressant therapy was an additional complication. Due to deep burns in the forearm region, we have (after a suitable wound bed preparation) applied a new bi-layered dermal substitute. The patient, however, developed a combined fungal infection in the region of this dermal substitute caused by Trichoderma longibrachiatum and Aspergillus fischeri (the first case ever reported). The infection caused the loss of the split-thickness skin grafts (STSGs); we had to perform repeated hydrosurgical and mechanical debridement and a systemic antifungal treatment prior to re-application of the STSGs. The subsequent skin transplant was successful

Exploring the planetary boundary for chemical pollution

Rockström et al. (2009a, 2009b) have warned that humanity must reduce anthropogenic impacts defined by nine planetary boundaries if “unacceptable global change” is to be avoided. Chemical pollution was identified as one of those boundaries for which continued impacts could erode the resilience of ecosystems and humanity. The central concept of the planetary boundary (or boundaries) for chemical pollution (PBCP or PBCPs) is that the Earth has a finite assimilative capacity for chemical pollution, which includes persistent, as well as readily degradable chemicals released at local to regional scales, which in aggregate threaten ecosystem and human viability. The PBCP allows humanity to explicitly address the increasingly global aspects of chemical pollution throughout a chemical's life cycle and the need for a global response of internationally coordinated control measures. We submit that sufficient evidence shows stresses on ecosystem and human health at local to global scales, suggesting that conditions are transgressing the safe operating space delimited by a PBCP. As such, current local to global pollution control measures are insufficient. However, while the PBCP is an important conceptual step forward, at this point single or multiple PBCPs are challenging to operationalize due to the extremely large number of commercial chemicals or mixtures of chemicals that cause myriad adverse effects to innumerable species and ecosystems, and the complex linkages between emissions, environmental concentrations, exposures and adverse effects. As well, the normative nature of a PBCP presents challenges of negotiating pollution limits amongst societal groups with differing viewpoints. Thus, a combination of approaches is recommended as follows: develop indicators of chemical pollution, for both control and response variables, that will aid in quantifying a PBCP(s) and gauging progress towards reducing chemical pollution; develop new technologies and technical and social approaches to mitigate global chemical pollution that emphasize a preventative approach; coordinate pollution control and sustainability efforts; and facilitate implementation of multiple (and potentially decentralized) control efforts involving scientists, civil society, government, non-governmental organizations and international bodies

On the Relationship Between the Optical Emission-Line and X-ray Luminosities in Seyfert 1 Galaxies

We have explored the relationship between the [O III] $\lambda$5007 and the 2--10 keV luminosities for a sample of Broad- and Narrow-Line Seyfert 1 galaxies (BLSy1 and NLSy1, respectively). We find that both types of Seyferts span the same range in luminosity and possess similar [O III]/X-ray ratios. The NLSy1s are more luminous than BLSy1s, when normalized to their central black hole masses, which is attributed to higher mass accretion rates. However, we find no evidence for elevated [O III]/X-ray ratios in NLSy1s, which would have been expected if they had excess EUV continuum emission compared to BLSy1s. Also, other studies suggest that the gas in narrow-line regions (NLR) of NLSy1s and NLSy1s span a similar range in ionization, contrary to what is expected if those of the former are exposed to a stronger flux of EUV radiation. The simplest interpretation is that, like BLSy1s, a large EUV bump is not present in NLSy1s. However, we show that the [OIII]/X-ray ratio can be lowered as a result of absorption of the ionizing continuum by gas close to the central source, although there is no evidence that intrinsic line-of-sight absorption is more common among NLSy1s, as would be expected if there were a larger amount of circumnuclear gas. Other possible explanations include: 1) anisotropic emission of the ionizing radiation, 2) higher gas densities in the NLR of NLSy1s, resulting in lower average ionization, or 3) the presence of strong winds in the the nuclei of NLSy1s which may drive off much of the gas in the narrow-line region, resulting in lower cover fraction and weaker [O III] emission.Comment: 18 pages, including 3 figures, 2 tables. Accepted for publication in The Astrophysical Journa

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Linka pro odbavování kamenné sutě

Import 20/04/2006Prezenční výpůjčkaVŠB - Technická univerzita Ostrava. Fakulta strojní. Katedra (340) výrobních strojů a konstruován

Initiative for an International Panel on Chemical Pollution (IPCP)

ISSN:0944-1344ISSN:1614-749