Zeus

Treball desenvolupat dins el marc del programa 'European Project Semester'.Nowadays, being a smart city is becoming more important. It is because of increasing energy use and the costs that come with it, that people all over the world are looking for better methods to decrease the environmental effects and costs. Therefore, the purpose of this research is to find out if there is a better way to use the streetlights in Vilanova i la Geltrú in order to go forward in the direction of being a smart city. Vilanova i la Geltrú currently has 10.800 Streetlights, and the energy consumption for these street lights cost a huge amount of money each year. This number can be decreased by finding new ways. This will be done, by further developing a street light called the ‘Urban Node’. This further development will be based on a previous research done. This Urban Node will be a replacement of the current street light. It includes components like led lights, solar panel and a wind turbine. It generates energy by using wind turbines and a solar panel instead of the current regular street light. In this research a certain methodology has been used, which includes expert interviews, an observation and desk research. As a result of using these methods, there has been made a simulation of a renewed streetlight system mostly revolving around the new product adding to the current system, which is the Urban Node. Concluding the results it has been found that implementing the Urban Node is more cost and energy efficient than the current street light system that has been used within Vilanova i la Geltrù. Furthermore, in this report there will be explained what the Urban Node exactly is, how it is structured, where it should be implemented, how it should be implemented and how it is more cost and energy efficient than the current system

The U.S. Coast Guard public affairs officer: roles, perceptions, and culture – a communication excellence study

U.S. Coast Guard missions have grown considerably since it transferred to the Department of Homeland Security (DHS). Using "best practices" from the excellence theory of public relations and high reliability organizational theory, this study examines whether the current structure of the U.S. Coast Guard public affairs program is sufficient to effectively provide a full spectrum of public affairs services over the range of activities that the service has been engaged in since transferring to DHS. Differences between two types of public affairs officers (PAO), primary duty PAOs and collateral duty PAOs are examined to provide insight into whether the U.S. Coast Guard has the right people in the right place to conduct excellent public affairs at the right time. Based on the survey research results with these two key groups, the researcher recommends creating the External Affairs Limited Duty Officer specialty and provides additional options to increase public affairs effectiveness

Neovascularization and vascular markers in a foreign body reaction to subcutaneously implanted degradable biomaterial in mice

To study the spatiotemporal processes of angiogenesis during a foreign body reaction (FBR), biodegradable bovine collagen type-1 (COL-I) discs were implanted in mice for a period up to 28 days. The cellular infiltration (consisting mainly of macrophages, giant cells and fibroblasts), and the extent of neovascularization into the discs were determined. Also the expression levels and/or distribution of the endothelial cell markers von Willebrand factor (vWF), platelet endothelial cell adhesion molecule-1 (PECAM-1)/CD31, MECA-32 antigens and endomucin, and of the basal lamina marker collagen type IV (Coll IV) were analysed. In time, a strong neovascularization of the discs was observed, with frequently occurring vascular sprouting, and intussusceptive growth of vessels. In this model, vWF, MECA-32 and endomucin antibodies often failed to stain neovessels in the COL-I discs. In contrast, staining for collagen IV basal lamina component in combination with CD31 covered the complete range of neo-vessels. We conclude that the model described in this study is a useful model to study FBR induced angiogenesis because of the active neovascularization taking place during prolonged periods of time.</p

Comparison of effects of anti-thrombin aptamers HD1 and HD22 on aggregation of human platelets, thrombin generation, fibrin formation, and thrombus formation under flow conditions

HD1 and HD22 are two of the most-studied aptamers binding to thrombin exosite I and exosite, respectively. To complete of their pharmacological profiles, the effects of HD1 and HD22 on thrombin-, ristocetin-, and collagen-induced human platelet aggregation, on thrombin generation and fibrin formation in human plasma, as well as on thrombus formation in human whole blood under flow conditions were assessed. The dissociation constants for HD1 and HD22 complexes with thrombin in simulated plasma ionic buffer were also evaluated. HD1 was more potent than HD22 in terms of inhibiting thrombin-induced platelet aggregation in platelet-rich plasma (PRP; 0.05-3 mu M) and in washed platelets (WPs; 0.005-3 mu M): approximately 8.31% (+/- 6.99% SD) and 89.53% (+/- 11.38% SD) for HD1 (0.5 mu M) and HD22 (0.5 mu M), respectively. Neither HD1 nor HD22 (3 mu M) did influence platelets aggregation induced by collagen. Both of them inhibited ristocetin-induced aggregation in PRP. Surprisingly, HD1 and HD22 aptamers (3 mu M) potentiated ristocetin-induced platelet aggregation in WP. HD1 reduced thrombin generation in a concentration-dependent manner [ETP at 3 mu M: 1677.53 +/- 55.77 (nM +/- min) vs. control 2271.71 +/- 423.66 (nM +/- min)], inhibited fibrin formation (lag time at 3 mu M: 33.70 min +/- 8.01 min vs. control 7.91 min +/- 0.91 min) and reduced thrombus formation under flow conditions [AUC(30) at 3 mu M: 758.30 +/- 344.23 (kPa +/- min) vs. control 1553.84 +/- 118.03 (kPa +/- min)]. HD22 (3 mu M) also delayed thrombin generation but increased the thrombin peak. HD22 (3 mu M) shortened the lag time of fibrin generation (5.40 min +/- 0.26 min vs. control 7.58 min +/- 1.14 min) but did not modify thrombus formation (3, 15 mu M). K-d values for the HD1 complex with thrombin was higher (257.8 +/- 15.0 nM) than the K-d for HD22 (97.6 +/- 2.2 nM). In conclusion, HD1 but not HD22 represents a potent anti-thrombotic agent, confirming the major role of exosite I in the action of thrombin. HD22 aptamer blocking exosite II displays weaker anti-platelet and anti-coagulant activity, with surprising activating effects on thrombin and fibrin generation most likely induced by HD22-induced allosteric changes in thrombin dynamic structure.</p

Comparison of Effects of Anti-thrombin Aptamers HD1 and HD22 on Aggregation of Human Platelets, Thrombin Generation, Fibrin Formation, and Thrombus Formation Under Flow Conditions

HD1 and HD22 are two of the most-studied aptamers binding to thrombin exosite I and exosite, respectively. To complete of their pharmacological profiles, the effects of HD1 and HD22 on thrombin-, ristocetin-, and collagen-induced human platelet aggregation, on thrombin generation and fibrin formation in human plasma, as well as on thrombus formation in human whole blood under flow conditions were assessed. The dissociation constants for HD1 and HD22 complexes with thrombin in simulated plasma ionic buffer were also evaluated. HD1 was more potent than HD22 in terms of inhibiting thrombin-induced platelet aggregation in platelet-rich plasma (PRP; 0.05–3 μM) and in washed platelets (WPs; 0.005–3 μM): approximately 8.31% (±6.99% SD) and 89.53% (±11.38% SD) for HD1 (0.5 μM) and HD22 (0.5 μM), respectively. Neither HD1 nor HD22 (3 μM) did influence platelets aggregation induced by collagen. Both of them inhibited ristocetin-induced aggregation in PRP. Surprisingly, HD1 and HD22 aptamers (3 μM) potentiated ristocetin-induced platelet aggregation in WP. HD1 reduced thrombin generation in a concentration-dependent manner [ETP at 3 μM: 1677.53 ± 55.77 (nM⋅min) vs. control 2271.71 ± 423.66 (nM⋅min)], inhibited fibrin formation (lag time at 3 μM: 33.70 min ± 8.01 min vs. control 7.91 min ± 0.91 min) and reduced thrombus formation under flow conditions [AUC30 at 3 μM: 758.30 ± 344.23 (kPa⋅min) vs. control 1553.84 ± 118.03 (kPa⋅min)]. HD22 (3 μM) also delayed thrombin generation but increased the thrombin peak. HD22 (3 μM) shortened the lag time of fibrin generation (5.40 min ± 0.26 min vs. control 7.58 min ± 1.14 min) but did not modify thrombus formation (3, 15 μM). Kd values for the HD1 complex with thrombin was higher (257.8 ± 15.0 nM) than the Kd for HD22 (97.6 ± 2.2 nM). In conclusion, HD1 but not HD22 represents a potent anti-thrombotic agent, confirming the major role of exosite I in the action of thrombin. HD22 aptamer blocking exosite II displays weaker anti-platelet and anti-coagulant activity, with surprising activating effects on thrombin and fibrin generation most likely induced by HD22-induced allosteric changes in thrombin dynamic structure

Tumor Vascular Morphology Undergoes Dramatic Changes during Outgrowth of B16 Melanoma While Proangiogenic Gene Expression Remains Unchanged

In established tumors, angiogenic endothelial cells (ECs) coexist next to “quiescent” EC in matured vessels. We hypothesized that angio-gene expression of B16.F10 melanoma would differ depending on the growth stage. Unraveling the spatiotemporal nature thereof is essential for drug regimen design aimed to affect multiple neovascularization stages. We determined the angiogenic phenotype—represented by 52 angio-genes—and vascular morphology of small, intermediate, and large s.c. growing mouse B16.F10 tumors and demonstrated that expression of these genes did not differ between the different growth stages. Yet vascular morphology changed dramatically from small vessels without lumen in small to larger vessels with increased lumen size in intermediate/large tumors. Separate analysis of these vascular morphologies revealed a significant difference in αSMA expression in relation to vessel morphology, while no relation with VEGF, HIF-1α, nor Dll4 expression levels was observed. We conclude that the tumor vasculature remains actively engaged in angiogenesis during B16.F10 melanoma outgrowth and that the major change in tumor vascular morphology does not follow molecular concepts generated in other angiogenesis models