Country-of-Origin Effect in International Trade

Due to the globalization tendency, the companies are faced with the situation of responding to identical or increasingly similar needs that evolve in the same direction on different markets. However, at the same time, within the new markets, the companies are confronted with the situation of their products’ rejection due to the fact that the physical or economic access of the consumers to the product, the purchasing behaviour, the consume characteristics and the manner in which consumers can dispose of the product, greatly depend on the culture of each country. This article presents the basic elements of the country-of-origin effect. First, it presents the characteristic of this effect. Secondly, it analyzes the forms in which the country-of-origin effect can have for different specialists or different fields of research. This effect can be called the “prism effect” for the global management, “the made-in principle” for marketing management or “country’s brand” for marketers. Thirdly, the present study analyzes the causes which determine the appearance of this effect. There can be social, economic, environmental, development causes but the most important factor of the country-of-origin effect represents the cultural issues. The fourth part consists of a personal analysis of the causes of the problem, and the fifth presents some ways to overcome a negative effect. In conclusion, we suggest that international companies must pay special attention in analyzing the prism effect of their products on the new market in order to adjust certain perceptions by an adequate marketing.country-of-origin effect, stereotype, international management

Experimental validation of a novel technique for ultrasound imaging of cardiac fiber orientation

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Interaction of Model Lipid Vesicles with Alveolar Macrophages

Macrophages are a type of white blood cells that play key roles in host defense by recognizing and engulfing foreign and apoptotic bodies. To accomplish this task, they rely on complex molecular interactions involving both lipids and proteins. Previous studies have shown that surface exposure of phosphatidylserine by apoptotic cells is required for their successful clearance, suggesting specific lipid-protein interactions at least for the initiation of phagocytosis of apoptotic cells. However, macrophages can engulf foreign and apoptotic bodies that substantially vary in size suggesting that non-specific interactions over a range of length scales may be relevant. The purpose of our study is to investigate the correlation between physical properties of lipid bilayers and their engulfment by macrophages. We modify bilayer properties systematically as a function of phospholipid headgroup composition and by addition of ceramide and cholesterol. We use a combination of scattering and spectroscopic methods to quantify lipid interactions and flow cytometry to measure engulfment rates. This study can help distinguish between the role of lipids and proteins in clearance of apoptotic and foreign particles

Large-scale multielectrode recording and stimulation of neural activity

Large circuits of neurons are employed by the brain to encode and process information. How this encoding and processing is carried out is one of the central questions in neuroscience. Since individual neurons communicate with each other through electrical signals (action potentials), the recording of neural activity with arrays of extracellular electrodes is uniquely suited for the investigation of this question. Such recordings provide the combination of the best spatial (individual neurons) and temporal (individual action-potentials) resolutions compared to other large-scale imaging methods. Electrical stimulation of neural activity in turn has two very important applications: it enhances our understanding of neural circuits by allowing active interactions with them, and it is a basis for a large variety of neural prosthetic devices. Until recently, the state-of-the-art in neural activity recording systems consisted of several dozen electrodes with inter-electrode spacing ranging from tens to hundreds of microns. Using silicon microstrip detector expertise acquired in the field of high-energy physics, we created a unique neural activity readout and stimulation framework that consists of high-density electrode arrays, multi-channel custom-designed integrated circuits, a data acquisition system, and data-processing software. Using this framework we developed a number of neural readout and stimulation systems: (1) a 512-electrode system for recording the simultaneous activity of as many as hundreds of neurons, (2) a 61-electrode system for electrical stimulation and readout of neural activity in retinas and brain-tissue slices, and (3) a system with telemetry capabilities for recording neural activity in the intact brain of awake, naturally behaving animals. We will report on these systems, their various applications to the field of neurobiology, and novel scientific results obtained with some of them. We will also outline future directions

Experimental 3-D Ultrasound Imaging with 2-D Sparse Arrays using Focused and Diverging Waves

International audienceThree dimensional ultrasound (3-D US) imaging methods based on 2-D array probes are increasingly investigated. However, the experimental test of new 3-D US approaches is contrasted by the need of controlling very large numbers of probe elements. Although this problem may be overcome by the use of 2-D sparse arrays, just a few experimental results have so far corroborated the validity of this approach. In this paper, we experimentally compare the performance of a fully wired 1024-element (32 × 32) array, assumed as reference, to that of a 256-element random and of an " optimized " 2-D sparse array, in both focused and compounded diverging wave (DW) transmission modes. The experimental results in 3-D focused mode show that the resolution and contrast produced by the optimized sparse array are close to those of the full array while using 25% of elements. Furthermore, the experimental results in 3-D DW mode and 3-D focused mode are also compared for the first time and they show that both the contrast and the resolution performance are higher when using the 3-D DW at volume rates up to 90/second which represent a 36x speed up factor compared to the focused mode

Impact of alginate-producing Pseudomonas aeruginosa on alveolar macrophage apoptotic cell clearance

Pseudomonas aeruginosa infection is a hallmark of lung disease in cystic fibrosis. Acute infection with P. aeruginosa profoundly inhibits alveolar macrophage clearance of apoptotic cells (efferocytosis) via direct effect of virulence factors. During chronic infection, P. aeruginosa evades host defense by decreased virulence, which includes the production or, in the case of mucoidy, overproduction of alginate. The impact of alginate on innate immunity, in particular on macrophage clearance of apoptotic cells is not known. We hypothesized that P. aeruginosa strains that exhibit reduced virulence impair macrophage clearance of apoptotic cells and we investigated if the polysaccharide alginate produced by mucoid P. aeruginosa is sufficient to inhibit alveolar macrophage efferocytosis. Rat alveolar or human peripheral blood monocyte (THP-1)-derived macrophage cell lines were exposed in vitro to exogenous alginate or to wild type or alginate-overproducing mucoid P. aeruginosa prior to challenge with apoptotic human Jurkat T-lymphocytes. The importance of LPS contamination and that of structural integrity of alginate polymers was tested using alginate of different purities and alginate lyase, respectively. Alginate inhibited alveolar macrophage efferocytosis in a dose- and time-dependent manner. This effect was augmented but not exclusively attributed to lipopolysaccharide (LPS) present in alginates. Alginate-producing P. aeruginosa inhibited macrophage efferocytosis by more than 50%. A mannuronic-specific alginate lyase did not restore efferocytosis inhibited by exogenous guluronic-rich marine alginate, but had a marked beneficial effect on efferocytosis of alveolar macrophages exposed to mucoid P. aeruginosa. Despite decreased virulence, mucoid P. aeruginosa may contribute to chronic airway inflammation through significant inhibition of alveolar clearance of apoptotic cells and debris. The mechanism by which mucoid bacteria inhibit efferocytosis may involve alginate production and synergy with LPS, suggesting that alginate lyase may be an attractive therapeutic approach to airway inflammation in cystic fibrosis and other chronic obstructive pulmonary diseases characterized by P. aeruginosa colonization

Smoking exposure induces human lung endothelial cell adaptation to apoptotic stress

Prolonged exposure to cigarette smoking is the main risk factor for emphysema, a component of chronic obstructive pulmonary diseases (COPDs) characterized by destruction of alveolar walls. Moreover, smoking is associated with pulmonary artery remodeling and pulmonary hypertension, even in the absence of COPD, through as yet unexplained mechanisms. In murine models, elevations of intra- and paracellular ceramides in response to smoking have been implicated in the induction of lung endothelial cell apoptosis, but the role of ceramides in human cell counterparts is yet unknown. We modeled paracrine increases (outside-in) of palmitoyl ceramide (Cer16) in primary human lung microvascular cells. In naive cells, isolated from nonsmokers, Cer16 significantly reduced cellular proliferation and induced caspase-independent apoptosis via mitochondrial membrane depolarization, apoptosis-inducing factor translocation, and poly(ADP-ribose) polymerase cleavage. In these cells, caspase-3 was inhibited by ceramide-induced Akt phosphorylation, and by the induction of autophagic microtubule-associated protein-1 light-chain 3 lipidation. In contrast, cells isolated from smokers exhibited increased baseline proliferative features associated with lack of p16(INK4a) expression and Akt hyperphosphorylation. These cells were resistant to Cer16-induced apoptosis, despite presence of both endoplasmic reticulum stress response and mitochondrial membrane depolarization. In cells from smokers, the prominent up-regulation of Akt pathways inhibited ceramide-triggered apoptosis, and was associated with elevated sphingosine and high-mobility group box 1, skewing the cell's response toward autophagy and survival. In conclusion, the cell responses to ceramide are modulated by an intricate cross-talk between Akt signaling and sphingolipid metabolites, and profoundly modified by previous cigarette smoke exposure, which selects for an apoptosis-resistant phenotype