This book is a collection of talks presented at the International Symposium on Exotic Nuclei, held at Lake Baikal, Russia, on 24 - 28 July 2001. The talks were given by the leading scientists in the physics of exotic nuclei.Among the topics of the Symposium were the following: production and study of properties of nuclei in extreme states, strongly deformed nuclei, highly excited nuclei and nuclei far from the line of stability as well as nuclei having large angular momenta.New results of investigations are presented in the book — in particular, the data on new nuclei with proton or neutron haloes, on the changes in the shell structure of nuclei near the drip lines, and on the structure of exotic nuclei, including information on the island of inversion. The latest results on the synthesis of new superheavy elements are also provided, and existing detecting devices and accelerators of exotic nuclei, as well as future projects for the creation of similar set-ups, are presented.
G protein-coupled receptors (GPCRs) are integral membrane proteins forming the fourth largest superfamily in the human genome. Many of these receptors play key physiological roles and several pathologies have been associated with receptor functional abnormalities. GPCRs therefore represent important goals for drug design in pharmaceutical companies since they constitute the target of about one third of the drugs currently on the market. However, endogenous GPCRs are most often difficult to study because of a lack of tools to target them specifically and single out their response to physiological or drug-elicited stimulations. Hence, studies mostly focused on recombinant receptors expressed in a variety of cellular models that do not always closely reflect the receptor natural environment and often deal with levels of expression exceeding by far physiological ranges. Recent technological developments combining for example genetically modified animals and advanced imaging approaches have improved our ability to visualize endogenous GPCRs. To date, trailing receptor activation, subsequent intracellular redistribution, changes in signaling cascade up to integrated response to a drug-elicited stimulation is at hand though the impact of a physiological challenge on receptor dynamics remains a major issue. Data however suggest that the receptor may embrace a different fate depending on the type of stimulation in particular if sustained or repeated. This suggests that current drugs may only partially mimic the genuine response of the receptor and may explain, at least in part, their secondary effects. Commonalities and specificities between physiological and drug-induced activation can thus represent valuable guidelines for the design of future drugs.
Although interest in evolutionary novelties can be that these different mechanisms cooperate in the mak traced back to the time of Darwin, the appreciation ing of new genes. In the second phase of new gene evolution, conventional models of new gene evolution, and systematical experimental pursuit of the origin and evolution of new gene functions did not appear for example by gene duplication, held that the muta until the early years of last decade. Since the 1970s, tions fixed in the early stages of the new genes are Susumu Ohno, Walter Gilbert, and others from the assumed to be neutral or nearly neutral. However, it area of evolutionary genetics have made pioneer ef appears that the force of Darwinian positive selection has been detectably strong from the outset in avail forts to elaborate possibilities for major biological mechanisms, for example, gene duplication and exon able population genetic studies of young genes created through the process of exon recombination. This may shuffling, by which new gene functions could arise. However, the problem of new gene evolution did not account for a common phenomenon in phylogenetic catch significant attention among biologists generally analyses of genes with changed functions: the early even recently. One of the reasons was the lack of ex stages of such genes are usually associated with accel perimental or observational systems for investigating erated substitution rates. Nonetheless, a more general factual details of the 'birth' process of new genes.
The importance of chloride ions in cell physiology has not been fully recognized until recently, in spite of the fact that chloride (Cl-), together with bicarbonate, is the most abundant free anion in animal cells, and performs or determines fundamental biological functions in all tissues. For many years it was thought that Cl- was distributed in thermodynamic equilibrium across the plasma membrane of most cells. Research carried out during the last couple of decades has led to a dramatic change in this simplistic view. We now know that most animal cells, neurons included, exhibit a non-equilibrium distribution of Cl- across their plasma membranes. Over the last 10 to 15 years, with the growth of molecular biology and the advent of new optical methods, an enormous amount of exciting new information has become available on the molecular structure and function of Cl- channels and carriers. In nerve cells, Cl- channels and carriers play key functional roles in GABA- and glycine-mediated synaptic inhibition, neuronal growth and development, extracellular potassium scavenging, sensory-transduction, neurotransmitter uptake and cell volume control. Disruption of Cl- homeostasis in neurons underlies pathological conditions such as epilepsy, deafness, imbalance, brain edema and ischemia, pain and neurogenic inflammation. This book is about how chloride ions are regulated and how they cross the plasma membrane of neurons. It spans from molecular structure and function of carriers and channels involved in Cl- transport to their role in various diseases. The first comprehensive book on the structure, molecular biology, cell physiology, and role in diseases of chloride transporters / channels in the nervous system in almost 20 years Chloride is the most abundant free anion in animal cells. THis book summarizes and integrates for the first time the important research of the past two decades that has shown that Cl- channels and carriers play key functional roles in GABA- and glycine-mediated synaptic inhibition, neuronal growth and development, extracellular potassium scavenging, sensory-transduction, neurotransmitter uptake and cell volume control The first book that systematically discusses the result of disruption of Cl- homeostasis in neurons which underlies pathological conditions such as epilepsy, deafness, imbalance, brain edema and ischemia, pain and neurogenic inflammation Spanning topics from molecular structure and function of carriers and channels involved in Cl- transport to their role in various diseases Involves all of the leading researchers in the field Includes an extensive introductory section that covers basic thermodynamic and kinetics aspects of Cl- transport, as well as current methods for studying Cl- regulation, spanning from fluorescent dyes in single cells to knock-out models to make the book available for a growing population of graduate students and postdocs entering the field
Translation Mechanisms provides investigators and graduate students with overviews of recent developments in the field of protein biosynthesis that are fuelled by the explosive and synergic growth of structural biology, genomics, and bioinformatics. The outstanding progress in our understanding of the structure, dynamics, and evolution of the prokaryotic and eukaryotic translation machinery, as well as applications in medicine and biotechnology, are described in 26 chapters covering recent discoveries on: -the subtleties of tRNA aminoacylation with natural and unnatural amino acids. -the control of mRNA stability, a key step of gene regulation. -ribosome structure and function, in the era of the atomic-crystal resolution of the ribosome. -the regulation of the biosynthesis of the translational machinery components. -the action of a variety of inhibitors of translation and the prospect for clinical studies.
Primary liver cancer occurs when cancerous (malignant) cells begin to grow in the tissues of liver. Although many cancers are on the decline, the incidence of primary liver cancer in the United States increased over 70 percent between 1975 and 1995. The increase is linked to rising rates of hepatitis B and C infection -- the leading causes of liver cancer. Far more common than primary liver cancer, however, is cancer that occurs when tumours from other parts of the body spread (metastasize) to the liver. The liver is especially vulnerable to invasion by tumour cells and with the exception of the lymph nodes, is the most common site of metastasis. There are two main kinds of liver cancer. Hepatoma and cholangiocarcinoma. Heptoma is cancer of the hepatocytes. (The main functioning liver cell). Hepatoma is primary liver cancer. Hepatoma usually grows in the liver as a ball-like tumour, invading the normal tissue surrounding it. Cancer of the bile duct cells is called cholangiocarcinoma. Cholangiocarcinoma originates in the bile ducts and is often caused by infestation with the liver fluke Clonorchis (a parasite). The cancer grows along the bile ducts in sheets or lines, and is difficult to find on X-ray studies. This book presents the latest new research developments from around the world in the field of liver cancer.
In this book, the clinical chapters are organized into sections by defined developmental pathways or gene families, and each section is preceded by a general overview. For each disorder the authors cover the disease-causing genes, the role of these genes in development as elucidated in model organisms, the human mutations that have been identified, and the developmental pathogenesis of the condition. Clinical descriptions, along with discussions of therapy and counseling, are provided. This book will be an invaluable resource for physicians, dentists, and other health professionals and for basic scientists interested in developmental processes and genetic perturbations that affect them.
