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This full color, portable guide covers all diseases and conditions commonly seen in general medical practice. This edition has been updated to reflect the latest clinical developments in medicine. Designed for quick access and employing an effective blend of concise text, bulleted key points, decision trees, and summary tables, the \"Manual\" makes it easy to find what you need at the point of care. -- From publisher's description.

Viruses cannot replicate by themselves. Instead, they rely on the host for almost all their replicative functions. Similarly, many viruses are unable to cause damage without the host immune system. Because of this, two strategies can often ameliorate disease — antivirals, which block replication, and antiinflammatories, which can limit the damage induced by infection. In the lung, this latter strategy is exemplified by the treatment of Pneumocystis jiroveci , in which treatment with glucocorticoids reduces the severity of disease and the risk of death. 1,2 However, because blocking inflammatory pathways raises the possibility of diminishing the host response and increasing replication of . . .

The Covid-19 epidemic continues to rage, especially in countries that have been unable or unwilling to institute strong public health measures. A return to normality has increasingly come to rely on the success of vaccines to prevent disease and, we hope, limit further spread of infection. However, this hope has been tempered by several unknowns. No existing vaccines have been shown to be effective against infection with any betacoronavirus, the family that includes SARS-CoV-2, which causes Covid-19. SARS, caused by another betacoronavirus, ended on its own before serious efforts at vaccine development were undertaken, and the rather small number of . . .

Macrophages are an essential component of the tumor microenvironment and have been ascribed a role in cancer-promoting inflammation. 1,2 Phagocytic cells (a component of innate immunity) mediate first-line resistance against pathogens and, when appropriately activated, can mediate extracellular killing and phagocytosis of tumor cells. 1-3 However, tumor progression is associated with subversion of immunity, and signals in the tumor microenvironment originating from cancer cells, stroma, and other immunocompetent cells set tumor-associated macrophages to a tumor-promoting mode (

On April 29, 2010, the Food and Drug Administration (FDA) approved a new immunotherapy, sipuleucel-T, for the treatment of patients with asymptomatic or minimally symptomatic castration-resistant prostate cancer. Traditionally, immune-based therapies have been categorized according to whether the agent has direct antitumor effects (so-called passive immunotherapy) or stimulates a host antitumor response (active immunotherapy) and whether the agent elicits a general increase in immune activation (nonspecific) or an immune response based on tumor recognition (specific). Sipuleucel-T is a form of active specific immunotherapy. The sipuleucel-T intervention involves harvesting the patient's peripheral-blood mononuclear cells (PBMCs), culturing them with a chimeric protein . . .

A fundamental challenge in the post-genome era is to understand and annotate the consequences of genetic variation, particularly within the context of human tissues. We present a set of integrated experiments that investigate the effects of common genetic variability on DNA methylation and mRNA expression in four human brain regions each from 150 individuals (600 samples total). We find an abundance of genetic cis regulation of mRNA expression and show for the first time abundant quantitative trait loci for DNA CpG methylation across the genome. We show peak enrichment for cis expression QTLs to be approximately 68,000 bp away from individual transcription start sites; however, the peak enrichment for cis CpG methylation QTLs is located much closer, only 45 bp from the CpG site in question. We observe that the largest magnitude quantitative trait loci occur across distinct brain tissues. Our analyses reveal that CpG methylation quantitative trait loci are more likely to occur for CpG sites outside of islands. Lastly, we show that while we can observe individual QTLs that appear to affect both the level of a transcript and a physically close CpG methylation site, these are quite rare. We believe these data, which we have made publicly available, will provide a critical step toward understanding the biological effects of genetic variation.

The results of a 23-year study of caloric restriction in rhesus macaques are reported; restricted caloric intake did not increase survival, but improved the metabolic profile of monkeys started at older ages and showed a trend towards delaying age-associated disease in monkeys started at a young age. Low-calorie diet no guarantee of longer life Restricting food intake has been shown to extend lifespan and improve health in various species. Here, the results of a 23-year study of caloric restriction in rhesus macaque monkeys are reported. When started at older ages, restricting caloric intake did not increase survival, but improved the metabolic profile of the monkeys. Young monkeys on a calorie-restricted diet showed a trend towards a delay in age-associated disease onset, but they, too, showed no increase in lifespan. Given that lifespan studies in humans are impractical, work with non-human primates is as near as we can get, and these results suggest that the effects of caloric restriction in long-lived animals are far from straightforward. Calorie restriction (CR), a reduction of 10–40% in intake of a nutritious diet, is often reported as the most robust non-genetic mechanism to extend lifespan and healthspan. CR is frequently used as a tool to understand mechanisms behind ageing and age-associated diseases. In addition to and independently of increasing lifespan, CR has been reported to delay or prevent the occurrence of many chronic diseases in a variety of animals. Beneficial effects of CR on outcomes such as immune function 1 , 2 , motor coordination 3 and resistance to sarcopenia 4 in rhesus monkeys have recently been reported. We report here that a CR regimen implemented in young and older age rhesus monkeys at the National Institute on Aging (NIA) has not improved survival outcomes. Our findings contrast with an ongoing study at the Wisconsin National Primate Research Center (WNPRC), which reported improved survival associated with 30% CR initiated in adult rhesus monkeys (7–14 years) 5 and a preliminary report with a small number of CR monkeys 6 . Over the years, both NIA and WNPRC have extensively documented beneficial health effects of CR in these two apparently parallel studies. The implications of the WNPRC findings were important as they extended CR findings beyond the laboratory rodent and to a long-lived primate. Our study suggests a separation between health effects, morbidity and mortality, and similar to what has been shown in rodents 7 , 8 , 9 , study design, husbandry and diet composition may strongly affect the life-prolonging effect of CR in a long-lived nonhuman primate.

Updated to include the newest drugs and those currently in development, this Fifth Edition is a comprehensive reference on the preclinical and clinical pharmacology of anticancer agents. Organized by drug class, the book provides the latest information on all drugs and biological agents-their mechanisms of action, interactions with other agents, toxicities, side effects, and mechanisms of resistance. The authors explain the rationale for use of drugs in specific schedules and combinations and offer guidelines for dose adjustment in particular situations. This edition's introduction includes timely information on general strategies for drug usage, the science of drug discovery and development, economic and regulatory aspects of cancer drug development, and principles of pharmacokinetics. Eight new chapters have been added and more than twenty have been significantly revised. A companion website includes the fully searchable text and an image bank.