Shallow genetic and morphological divergence among seaperches in the South Pacific (family Scorpaenidae; genus Helicolenus).

The phylogenetic relationships among populations of seaperch, Helicolenus spp., in the south-west Pacific were examined with mtDNA markers. Parts of the cytochrome b gene [459 base pair (bp)] and the control region (448 bp) were sequenced in 58 specimens from the south-west Pacific and four specimens of Helicolenus lengerichi from Chile. Only one clade was recognized in New Zealand coastal waters, despite a wide range of colour morphs. This clade also occurred in the mid Tasman Sea on the Norfolk Ridge and around Tasmania and Victoria. A second sympatric clade was identified around Tasmania and Victoria and to the west of New Zealand. A third allopatric clade was identified to the north of New Zealand and in deep water on the Chatham Rise and a fourth clade on the Foundation Seamounts and the Louisville Ridge. Helicolenus lengerichi from Chile formed a fifth clade. Assuming a molecular clock, the clades were estimated to have diverged c. 0.7-2.6 million years ago. Only two clades, around Tasmania and Victoria, were separated using morphology, colour (in live) and dorsal-fin soft ray counts and were confirmed as Helicolenus percoides and Helicolenus barathri. Two characters, orbit diameter and colour variation, previously used to identify two species in New Zealand waters were unreliable characters for species discrimination. Principle component analyses of 11 morphological measures from 67 individuals did not delineate the clades. A canonical discriminant analysis was able to separate four of the five clades, but mean discriminate probabilities were low (77.6%), except for the five Chilean specimens of H. lengerichi (100%).

Long-term auxologic effects of human growth hormone.

Seventy-eight children with idiopathic growth hormone deficiency treated with human growth hormone continuously for up to 5 years were studied; 58 were prepubertal at the start of treatment, and remained so throughout the treatment period, and 20 were showing pubertal signs at the start of treatment. Height velocity increased markedly in the prepubertal group over the first year of therapy, with a gradual decrease in the following years. The increased growth rate of the first treatment year continued in the pubertal group. Height standard deviation score for chronologic age increased significantly throughout all treatment years, but for bone age did not change in either group. The more frequent the treatment regimen, the better was the growth response; a dose effect independent of frequency was identified. Thus human growth hormone treatment cannot make up a deficit in height prognosis already present at diagnosis, but prevents further loss of stature, which is why early diagnosis is important.