Proximate basis of the covariation between a melanin-based female ornament and offspring quality.

In contradiction to sexual selection theory, several studies showed that although the expression of melanin-based ornaments is usually under strong genetic control and weakly sensitive to the environment and body condition, they can signal individual quality. Covariation between a melanin-based ornament and phenotypic quality may result from pleiotropic effects of genes involved in the production of melanin pigments. Two categories of genes responsible for variation in melanin production may be relevant, namely those that trigger melanin production (yes or no response) and those that determine the amount of pigments produced. To investigate which of these two hypotheses is the most likely, I reanalysed data collected from barn owls ( Tyto alba). The underparts of this bird vary from immaculate to heavily marked with black spots of varying size. Published cross-fostering experiments have shown that the proportion of the plumage surface covered with black spots, a eumelanin composite trait so-called "plumage spottiness", in females positively covaries with offspring humoral immunocompetence, and negatively with offspring parasite resistance (i.show $132#e. the ability to reduce fecundity of ectoparasites) and fluctuating asymmetry of wing feathers. However, it is unclear which component of plumage spottiness causes these relationships, namely genes responsible for variation in number of spots or in spot diameter. Number of spots reflects variation in the expression of genes triggering the switch from no eumelanin production to production, whereas spot diameter reflects variation in the expression of genes determining the amount of eumelanin produced per spot. In the present study, multiple regression analyses, performed on the same data sets, showed that humoral immunocompetence, parasite resistance and wing fluctuating asymmetry of cross-fostered offspring covary with spot diameter measured in their genetic mother, but not with number of spots. This suggests that genes responsible for variation in the quantity of eumelanin produced per spot are responsible for covariation between a melanin ornament and individual attributes. In contrast, genes responsible for variation in number of black spots may not play a significant role. Covariation between a eumelanin female trait and offspring quality may therefore be due to an indirect effect of melanin production.

From neuroprogression to neuroprotection: implications for clinical care.

Bipolar disorder follows a staged trajectory in which persistence of illness is associated with a number of clinical features such as progressive shortening of the inter-episode interval and decreased probability of treatment response. This neuroprogressive clinical process is reflected by both progressive neuroanatomical changes and evidence of cognitive decline. The biochemical foundation of this process appears to incorporate changes in inflammatory cytokines, cortisone, neurotrophins and oxidative stress. There is a growing body of evidence to suggest that these markers may differ between the early and late stages of the disorder. The presence of a series of tangible targets raises the spectre of development of rational neuroprotective strategies, involving judicious use of current therapies and novel agents. Most of the currently used mood stabilisers share effects on oxidative stress and neurotrophins, while novel potentially neuroprotective agents are being developed. These developments need to be combined with service initiatives to maximise the opportunities for early diagnosis and intervention.

PathBeat. Number 1 (May 2000) University of Iowa Department of Pathology.

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PathBeat. Number 2 (October 2000) University of Iowa Department of Pathology.

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PathBeat. Number 3 (December 2001) University of Iowa Department of Pathology.

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PathBeat. Number 4 (December 2002) University of Iowa Department of Pathology.

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PathBeat. Number 5 (July 2003) University of Iowa Department of Pathology.

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PathBeat. Number 6 (July 2004) University of Iowa Department of Pathology.

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PathBeat. Number 7 (May 2005) University of Iowa Department of Pathology.

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PathBeat. Number 8 (Summer 2008) University of Iowa Department of Pathology.

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PathBeat. Number 9 (Winter 2008) University of Iowa Department of Pathology.

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PathBeat. Number 10 (Summer 2009) University of Iowa Department of Pathology.

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PathBeat. Number 11 (Spring 2010) University of Iowa Department of Pathology.

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PathBeat. Number 12 (Spring 2011) University of Iowa Department of Pathology.

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PathBeat. Number 13 (Winter 2012) University of Iowa Department of Pathology.

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