Patterns and Drivers of Egg Pigment Intensity and Colour Diversity in the Ocean: A Meta-Analysis of Phylum Echinodermata.

Egg pigmentation is proposed to serve numerous ecological, physiological, and adaptive functions in egg-laying animals. Despite the predominance and taxonomic diversity of egg layers, syntheses reviewing the putative functions and drivers of egg pigmentation have been relatively narrow in scope, centring almost exclusively on birds. Nonvertebrate and aquatic species are essentially overlooked, yet many of them produce maternally provisioned eggs in strikingly varied colours, from pale yellow to bright red or green. We explore the ways in which these colour patterns correlate with behavioural, morphological, geographic and phylogenetic variables in extant classes of Echinodermata, a phylum that has close phylogenetic ties with chordates and representatives in nearly all marine environments. Results of multivariate analyses show that intensely pigmented eggs are characteristic of pelagic or external development whereas pale eggs are commonly brooded internally. Of the five egg colours catalogued, orange and yellow are the most common. Yellow eggs are a primitive character, associated with all types of development (predominant in internal brooders), whereas green eggs are always pelagic, occur in the most derived orders of each class and are restricted to the Indo-Pacific Ocean. Orange eggs are geographically ubiquitous and may represent a 'universal' egg pigment that functions well under a diversity of environmental conditions. Finally, green occurs chiefly in the classes Holothuroidea and Ophiuroidea, orange in Asteroidea, yellow in Echinoidea, and brown in Holothuroidea. By examining an unprecedented combination of egg colours/intensities and reproductive strategies, this phylum-wide study sheds new light on the role and drivers of egg pigmentation, drawing parallels with theories developed from the study of more derived vertebrate taxa. The primary use of pigments (of any colour) to protect externally developing eggs from oxidative damage and predation is supported by the comparatively pale colour of equally large, internally brooded eggs. Secondarily, geographic location drives the evolution of egg colour diversity, presumably through the selection of better-adapted, more costly pigments in response to ecological pressure.

Progressive neurodegeneration after intracerebroventricular kainic acid administration in rats: implications for schizophrenia?

BACKGROUND: Intracerebroventricular (ICV) administration of kainic acid to rats produces limbic-cortical neuronal damage that has been compared to the neuropathology of schizophrenia. METHODS: Groups of adult rats were administered ICV kainic acid and then assessed for neuronal loss and the expression of proteins relevant to mechanisms of neuronal damage after one and fourteen days. Neuronal loss was assessed by two-dimensional cell counting and protein expression was assessed by immunohistochemistry. RESULTS: ICV kainic acid administration was associated with both immediate (day 1) and delayed (day 14) neuronal loss in the dorsal hippocampus. The immediate injury was largely limited to the CA3 hippocampal subfield, while the delayed injury included the CA1 subfield. Multiple mechanisms of cell death appeared to be involved in the delayed neuronal loss, as evidenced by changes in the expression of glutamate receptor subunits, heat shock protein and jun protein. CONCLUSIONS: ICV kainic acid administration to adult rats produces progressive damage to limbic-cortical neurons, involving both fast and slow mechanisms of cell death. Given the evidence for clinical deterioration, cognitive deficits and hippocampal neuropathy in some cases of schizophrenia, this animal model may be relevant for hypotheses regarding mechanisms of neurodegeneration in that disorder.

Leiomyosarcoma of renal vein.

Primary leiomyosarcoma of the renal vein has not been previously reported in the urologic literature. A case report with long-term survival is described and the literature reviewed.

Delayed neuronal loss after administration of intracerebroventricular kainic acid to preweanling rats.

Excitotoxins, such as kainic acid (KA), have been shown to produce both immediate and delayed neuronal degeneration in adult rat brain. While preweanling rats have been shown to be resistant to the immediate neurotoxicity of KA, the presence of delayed neuronal loss has not been investigated in such animals. To determine whether intracerebroventricular (i.c.v.) administration of KA would produce delayed neuronal loss, preweanling rats were administered 5 nmol or 10 nmol KA i.c.v. on postnatal day 7 (P7) and then examined at P14, P45, and P75. Using three-dimensional, non-biased cell counting, neuronal loss was observed in the CA3 subfield of the hippocampal formation at P45 and P75 in animals administered 10 nmol KA, as compared to animals administered 5 nmol KA or artificial cerebrospinal fluid. Further, the amount of immunoreactivity to jun, the protein product of the immediate early gene, c-jun, adjusted for the number of remaining neurons was increased in the same brain areas. Antibody labeling of inducible heat shock protein and glial fibrillary acidic protein was not similarly increased in animals administered i.c.v. KA. The data suggest that while i.c.v. KA does not produce immediate neuronal loss in preweanling rats, the hippocampus is altered so that neuronal loss occurs after a delay, perhaps through apoptosis. These findings may be relevant to the pathogenesis of neuropsychiatric disorders, such as schizophrenia, that are characterized by early limbic-cortical deficits but onset of illness in young adulthood.

Methods for inducing neuronal loss in preweanling rats using intracerebroventricular infusion of kainic acid.

Excitotoxins, such as kainic acid (KA), have been shown to produce neuronal degeneration in the adult rat brain. While preweanling rats have been shown to be relatively resistant to the neurotoxicity of lower doses of KA, the presence of neuronal loss at higher doses (of KA) has only begun to be investigated in such animals. A reliable method of producing neuronal loss in preweanling rats is to administer nmol concentrations of KA via intracerebroventricular (i.c.v.) injections on postnatal day 7 (P7). Using a three-dimensional, non-biased cell counting technique, we have shown that neuronal loss is observed in the CA3 subfield of the hippocampal formation at P45 and P75. Further, immunohistochemical studies of markers for cell death may be useful to examine the types of cellular processes associated with such neuronal loss. Data from our own experiments suggest the activation of immediate-early genes in the neuronal loss produced by KA administration at P7. This developmental animal model of neuronal loss may be useful in studying neurodevelopmental disorders where the onset of symptoms or cognitive deficits is thought to follow an early developmental insult.

Retroperitoneal iliac fossa abscess presenting as primary disease of the genitourinary tract.

An iliac fossa abscess is a clinical entity that has not been described in the urologic literature. Three patients presenting with urologic symptoms were evaluated and found to have iliac fossa abscesses. It is important for the urologist to be aware of the existence, diagnosis and treatment of this entity.