The term “sickness behavior” refers to a series of behavioral and physiological changes that occur after exposure to an inflammatory or infectious agent, or after administration of recombinant proinflammatory cytokines. Symptoms of sickness behavior include social withdrawal, anhedonia, cognitive impairment, anorexia, fever, and other symptoms. Behavioral changes associated with sickness behavior are transient in nature and serve adaptive purposes that help the individual mount an effective immune response.
Considerable attention has focused on the role of centrally acting cytokines in mediating sickness behavior. As might be expected, abnormal increases in cytokines appear to result in psychopathological outcomes. Indeed, sickness behavior and clinical depression (among other psychiatric disturbances) are evident in patients receiving cytokine therapy. Increased proinflammatory cytokine activity has been implicated in the etiology of depression, schizophrenia, and other psychiatric disorders.
Cancer-related symptoms are strikingly similar to the symptoms associated with cytokine-induced sickness behavior. On the basis of this observation and coupled with evidence that behavioral disturbances in patients with cancer may occur coincident with abnormal increases in proinflammatory cytokines, it has been suggested that common cytokine-related signaling pathways underlie sickness-related and cancer-related symptoms. In this chapter, we will discuss similarities between cancer-related symptoms and sickness behavior, and we will examine potential common mediators and mechanisms, including proinflammatory cytokines and subsequent interactions with neurotransmitter and molecular signaling pathways.
Cancer-related symptoms refer to physical and psychiatric manifestations produced by the disease process or treatment (including chemotherapy, radiotherapy, immunotherapy, and surgical procedures). Cancer-related symptoms may be categorized as physical, cognitive, or affective.
The effects of genetic erosion on the viability of small populations following habitat fragmentation are understood in theory but the critical early stages of the process have gone undocumented as the changes are rapid and difficult to monitor. We found it is possible to monitor genetic erosion in recently fragmented populations by genotyping with panels of 6–7 hypervariable nuclear microsatellite loci as markers of variability. We studied changes in variability in populations of three small mammals isolated on forest fragments in Thailand when the creation of Chiew Larn reservoir flooded the forested KhlongSaeng valley in 1987 and left about 100 rainforest fragments as islands in the lake. Mark-recapture surveys in years 5–8 post-fragmentation on island and matched undisturbed mainland sites showed that habitat fragmentation led to the onset of genetic erosion in surviving populations of a forest rat, Maxomys surifer, tree mouse, Chiropodomys gliroides, and tree shrew, Tupaia glis. Demographic and genetic responses to fragmentation were species-specific, reflecting differences in life history and behaviour. Allelic variation was invariably lost faster than heterozygosity and, in C. gliroides, genetic erosion preceded demographic decline. We found that small, recently isolated populations lose variation faster than allowed for in current conservation practice and that genetic erosion may commence before the onset of obvious demographic decline. The project has great generality throughout the increasingly fragmented humid tropics and the methods may be used to monitor genetic erosion in isolated populations of the larger mammals that are typically the focus of conservation efforts. The policy implications of our research are that populations in fragmented forests may require both ecological and genetic management if they are to survive and provide ecological services.
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