The seasonal change in the duration of the night time release of melatonin is responsible for activating the hypothalamic gonadtrophin-releasing hormone (GnRH) pulse generator in seasonal breeding animals. Paul Mullen and I considered that it might also be responsible for the activation of the child's GnRH pulse generator at the onset of human puberty. The real conundrum, though, is why this should happen when it does.
View Article and Find Full Text PDFThe influence of culture chamber capacity, medium volume and culture density on the growth yields of lettuce (Lactuca sativa L.) and spearmint (Mentha spicata L.) shoots were determined in an environment containing either 350 or 10,000 μmol mol CO after 8 weeks of incubation.
View Article and Find Full Text PDFIn humans 6-sulphatoxy melatonin (SaMT) is the principal metabolite of endogenous and exogenous melatonin. 5-sulphatoxy N-acetyl-serotonin (SNAS) is a minor metabolite of exogenous melatonin, but it has not been established whether the levels of endogenous SNAS in plasma derives principally from endogenous melatonin. We have developed the first radioimmunoassay (RIA) for SNAS and used it (together with RIAs for melatonin and SaMT) to determine whether endogenous SNAS derives from endogenous melatonin or from platelet serotonin.
View Article and Find Full Text PDFElevated nocturnal melatonin is found in women with idiopathic hypogonadotropic hypogonadism (IHH), but it is not known whether this is implicated in the etiology of their GnRH deficiency. It is unlikely that nocturnal melatonin can be implicated in the etiology of the GnRH deficiency of Kallmann's syndrome (KS), because this condition is caused by defective neuronal migration in embryonic life. We therefore measured nocturnal melatonin in women with IHH and KS to determine whether it was elevated in one or both conditions and thereby to determine whether it was implicated as cause or consequence of GnRH deficiency.
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