The weakest pulse of light a human can detect sends about 100 photons through the pupil and produces 10-20 rhodopsin isomerizations in a small retinal area. It has been postulated that we cannot see single photons because of a retinal noise arising from randomly occurring thermal isomerizations. Direct recordings have since demonstrated the existence of electrical 'dark' rod events indistinguishable from photoisomerization signals. Their mean rate of occurrence is roughly consistent with the 'dark light' in psychophysical threshold experiments, and their thermal parameters justify an identification with thermal isomerizations. In the retina of amphibians, a small proportion of sensitive ganglion cells have a performance-limiting noise that is low enough to be well accounted for by these events. Here we study the performance of dark-adapted toads and frogs and show that the performance limit of visually guided behaviour is also set by thermal isomerizations. As visual sensitivity limited by thermal events should rise when the temperature falls, poikilothermous vertebrates living at low temperatures should then reach light sensitivities unattainable by mammals and birds with optical factors equal. Comparison of different species at different temperatures shows a correlation between absolute threshold intensities and estimated thermal isomerization rates in the retina.

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We used MRI to study the lesions in a consecutive group of 64 patients with an acute trauma of the knee and normal plain radiography during the winter season. Bone bruise was present in 35 of the patients, and these were referred to subsequent MRI 4 and 12 months later. After 4 months bone bruise was still present in 69% of the patients and after 12 months in 12%. Soft tissue lesions, for example, lesion in the meniscus, ACL rupture, or MCL lesion was present in 94% of the patients with bone bruise. Interobserver agreement varied from good to excellent. Soft tissue lesions are found in almost all patients with bone bruise, and these generally resolve 4-12 months after the injury. In the patients with no bone bruise the number of ligament injuries was lower.

In this review I have attempted to define (1) how the genetic program responsible for migration, sexual maturation, and death after spawning is implemented via the endocrine system, and (2) to what extent environmental factors influence the implementation of the genetic program. The time of upstream migration and the body size at migration may vary enormously (e.g. in Lampetra fluviatilis). Whether the differences reflect different genetic backgrounds in different populations or different environmental conditions in previous stages is unknown. Migration is correlated with lack of food intake, loss of marine osmoregulatory capacity, and atrophy of the intestine. The possible endocrine control of this phase is not clear. Development of secondary sex characters, final maturation of the gonads, spermiation, and ovulation seem to depend on a gonadotropic factor secreted by the pro- and meso-adenohypophysis, but gonadotropin is not as important as in higher vertebrates. Increases in day length or in temperature do not appear to be important clues for initiating sexual maturation; rather this may depend on a metabolic signal related to starvation. The period of natural starvation, from upstream migration until death after spawning, involves atrophy or degeneration in most organs and tissues at the same time as the gonads are developing. With the exception of the intestine and the size of the liver in males, degeneration is generally slow during upstream migration. Upon sexual maturation, the changes are rapid. Energy expenditure and gonadal growth are based on mobilization of lipid and protein, mainly from the body wall. The mobilization of lipid and of protein runs in parallel, both being slow before and rapid during sexual maturation. The possible role of gonadotropin, sex hormones, and insulin in the metabolism of the starving lamprey is discussed. Other hormones seem of little importance. Little is known about the role of the autonomic nervous system in the catabolic processes. Death after spawning can be delayed considerably by hypophysectomy and seems to depend on gonadotropin in females and on some pituitary factor different from gonadotropin in males. Treatment with estradiol surprisingly prolongs life. In all cases of prolonged life induced experimentally, the rate of reduction in body length is slow, probably reflecting a reduced intensity of starvation.Key words: physiology, starvation, reproduction, death, metabolism, migration