Książki na temat „Linear block codes”

Mathematics is the perfect language needed for describing how the theory of relativity applies to the physical Universe and all of spacetime, and that description includes the strange behaviour that occurs near black holes. ‘Navigating through spacetime’ explains some of the complicated mathematical language using spacetime diagrams. It describes world-lines—the path left behind as an object journeys through spacetime—and light cones. Black holes profoundly affect the orientations of the light cones. As a particle approaches a black hole, its future light cone tilts more and more towards the black hole. When the particle crosses the event horizon, all of its possible future trajectories end inside the black hole.

Color and luminance interact in many ways in the human visual system. For instance, the colors in an afterimage, which are due to adaptation of retinal cones, are especially vivid when test contours, presented after the adapting image, coincide with the blurred edges of the afterimage. A single colored adapting pattern can give rise to two differently colored afterimages, according to the position of black lines in the test field. This shows that colors seen by the low-acuity chromatic pathways will diffuse outward along, but not across, luminance contours. This is also true for real colors. Finally, flicker-augmented contrast shows that the visual system, when given a choice, will select the most salient color/luminance borders in a stimulus.

Policing Intimacy analyzes literary depictions of sexual policing of the color line across multiple spaces with diverse colonial histories: Mississippi through William Faulkner’s work, Louisiana through Ernest Gaines’s novels, Haiti through the work of Marie Chauvet and Edwidge Danticat, and the Dominican Republic through writing by Julia Alvarez, Junot Díaz, and Nelly Rosario. This literature exposes the continuing coloniality that links depictions of U.S. democracy with Caribbean dictatorships in the twentieth century, revealing a set of interrelated features characterizing the transformation of colonial forms of racial and sexual control into neocolonial reconfigurations. Patterns are discernable, as a result of systemic inequality and large-scale historical events, revealing the ways in which private relations can reflect national occurrences and the intimate can be brought under public scrutiny. Acknowledging the widespread effects of racial and sexual policing that persist in current legal, economic, and political infrastructures across the circum-Caribbean can in turn bring to light permutations of resistance to the violent discriminations of the status quo. By drawing on colonial documents, such as early law systems like the 1685 French Code Noir instated in Haiti, the 1724 Code Noir in Louisiana, and the 1865 Black Code in Mississippi, in tandem with examples drawn from twentieth-century literature, Policing Intimacy humanizes the effects of legal histories and leaves space for local particularities. A focus on literary texts and the affordances enabled by the variances in form and aesthetics demonstrates the necessity of incorporating multiple stories, histories, and traumas into our accounts of the past.

Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.