Kirjahaku

With over 525 images and photos that focus on his career from age 45 to 60, American still-life painter Jackson reveals his work methods, inspirations, and development. Featuring more than 525 paintings in Robert C. Jackson's iconic style of realism with a slyly irreverent twist, this beautiful book thoughtfully covers his midcareer works. Many of his signature themes are recognizable but now treated more deeply, the compelling nature of his art is intensified, and larger canvases prevail. Known especially for his realistic still-life paintings featuring objects such as soda crates, balloon dogs, and foods, Jackson creates playful, exuberant art that often makes impossible situations believable, one reason for its wide appeal. Learn more about: • His final college semester when he took Painting 101 to fill out his schedule. • The first time he ever quit anything. (It was a career as an engineer.) • How the concept of "seriously funny" motivates him. • The cleansing and growth that occurs with aging as a painter. • Zippy, the clown he keeps on retainer to make balloon dogs. Jackson's paintings have been featured in five solo museum exhibitions to date, and are in private, corporate, and museum collections worldwide, ranging from the Delaware Art Museum to the South Dakota Art Museum. Jackson's conversational insights begin each section and address how he built a successful art career. Jackson offers specific details of interest to collectors as well as to artists also striving for a full-time career in painting. For example, coming up with new source material year after year requires effort, and Jackson explains his processes for doing just that. He also shares how embracing commissioned artwork as a collaborative art process can be fulfilling for both the artist and client. Candid black-and-white photos of Jackson at work and play express the spirit he brings to his art. Understand why new fans and established collectors alike respond to this artist who has found his unique and identifiable voice within contemporary art.

It is estimated that 80 to 90% of drugs under development never make it to the marketplace due to insufficient clinical activity, unacceptable toxicity, rapid appearance of drug resistance, or other factors that should be, at least partially, predictable from preclinical testing. This new text asks the question, "How can we use computational methods to improve the success rate in drug development?" Computer Techniques in Preclinical and Clinical Drug Development shows how modeling makes it possible to extract the maximum amount of information and predictive value from preclinical data. Computer modeling methods from the areas of pharmacokinetics, pharmacodynamics, cytokinetics, and inhibition kinetics of multi-enzyme pathways are all discussed in this unique reference source.

Most art books are not in the first person, so while there is some truth to the analyses, some things are always off. Robert C. Jackson set out to interview 20 contemporary representational artists (himself included) and showcase their artwork within the context of their interviews. Here you will meet Steven Assael, Bo Bartlett, Debra Bermingham, Margaret Bowland, Paul Fenniak, Scott Fraser, Woody Gwyn, F. Scott Hess, Laurie Hogin, Robert C. Jackson, Alan Magee, Janet Monafo, John Moore, Charles Pfahl, Scott Prior, Stone Roberts, Sandra Mendelsohn Rubin, Daniel Sprick, Will Wilson, and Jerome Witkin. Each of these artists has a very elusive quality–a unique voice. Seeing their work from across a room they are all recognizable. Their artworks are showcased in this large book with more than 140 images of their paintings as well as photographs of the artists in their studios and an epilogue by Pamela Sienna.

It is estimated that 80 to 90% of drugs under development never make it to the marketplace due to insufficient clinical activity, unacceptable toxicity, rapid appearance of drug resistance, or other factors that should be, at least partially, predictable from preclinical testing. This new text asks the question, "How can we use computational methods to improve the success rate in drug development?" Computer Techniques in Preclinical and Clinical Drug Development shows how modeling makes it possible to extract the maximum amount of information and predictive value from preclinical data. Computer modeling methods from the areas of pharmacokinetics, pharmacodynamics, cytokinetics, and inhibition kinetics of multi-enzyme pathways are all discussed in this unique reference source.

Advances in cancer genomics are transforming our understanding of cancer, and have profound implications for its prevention, diagnosis, and treatment. Evolutionary dynamics suggests that as few as two mutations can cause transformation of normal cells into cancer stem cells. A process of Darwinian selection, involving a further three or more mutations, taking place over a period of years, can then result in progression to a life-threatening tumour. In many cases the immune response can recognise and eliminate the mutant cells, but most advanced tumours have mutations that activate immune checkpoints and enable the tumour to hide from the immune system. For the most hard-to-treat tumours, future progress will require molecular diagnostics to detect cancer-causing mutations in healthy subjects, and new drugs or vaccines that prevent the progression process. Chapters of this book deal with the signalling pathways that control cell division, and changes in these pathways in cancer cells. Three cell cycle checkpoints that are often mutated in cancer are analysed in detail. A discussion of chronic myeloid leukaemia illustrates the role of reactive oxygen species in driving progression from a chronic to an acute condition. A single drug that suppresses reactive oxygen can prevent disease progression and turn an otherwise deadly disease into a condition that can be managed to enable many years of normal life. Another chapter discusses chronic myelomonocytic leukaemia, a disease that involves both genetic and epigenetic change. Tumour progression is discussed as a multi-stage process in which cancer stem cells evolve into genetically unstable, invasive, metastatic, drug-resistant growths. Each of these stages can act as targets for drugs or immunomodulators, but the future of cancer treatment lies in understanding tumour dynamics, and arresting malignancy at the earliest possible stage. Evolutionary dynamics is a primarily mathematical technique, but the target readership will be tumour biologists, clinicians, and drug developers. Computational detail is provided in an online supplement, but the main text emphasises the implications of the dynamics for an understanding of tumour biology and does not require mathematical expertise.

Advances in cancer genomics are transforming our understanding of cancer, and have profound implications for its prevention, diagnosis, and treatment. Evolutionary dynamics suggests that as few as two mutations can cause transformation of normal cells into cancer stem cells. A process of Darwinian selection, involving a further three or more mutations, taking place over a period of years, can then result in progression to a life-threatening tumour. In many cases the immune response can recognise and eliminate the mutant cells, but most advanced tumours have mutations that activate immune checkpoints and enable the tumour to hide from the immune system. For the most hard-to-treat tumours, future progress will require molecular diagnostics to detect cancer-causing mutations in healthy subjects, and new drugs or vaccines that prevent the progression process. Chapters of this book deal with the signalling pathways that control cell division, and changes in these pathways in cancer cells. Three cell cycle checkpoints that are often mutated in cancer are analysed in detail. A discussion of chronic myeloid leukaemia illustrates the role of reactive oxygen species in driving progression from a chronic to an acute condition. A single drug that suppresses reactive oxygen can prevent disease progression and turn an otherwise deadly disease into a condition that can be managed to enable many years of normal life. Another chapter discusses chronic myelomonocytic leukaemia, a disease that involves both genetic and epigenetic change. Tumour progression is discussed as a multi-stage process in which cancer stem cells evolve into genetically unstable, invasive, metastatic, drug-resistant growths. Each of these stages can act as targets for drugs or immunomodulators, but the future of cancer treatment lies in understanding tumour dynamics, and arresting malignancy at the earliest possible stage. Evolutionary dynamics is a primarily mathematical technique, but the target readership will be tumour biologists, clinicians, and drug developers. Computational detail is provided in an online supplement, but the main text emphasises the implications of the dynamics for an understanding of tumour biology and does not require mathematical expertise.