Given an abstract, generate a keyword (a noun phrase) that best describes the focus or contribution of the paper. Such keywords can be directly from the given abstract or outside it.

Ex Input:
Abstract: I have suggested that the X-linked gene Tabby (Ta) and its autosomal mimics in the mouse may be homologous with the genes for sex-linked anhidrotic (hypohidrotic) ectodermal dysplasia (Christ-Siemens-Touraine syndrome, CST) and its apparent autosomal mimics in the human. In the present study, I examined whether anhidrosis, a cardinal feature of CST, is present in the putative mouse sex-linked model, Tabby. The results demonstrate that whereas normal mice perspire on the volar and plantar surfaces of their paws, hemizygous Ta/Y male mice show anhidrosis and absence of sweat glands, as do human hemizygous male sufferers of CST. This result is strongly supportive of the hypothesis that Ta is homologous to the gene for CST.

Ex Output:
Animal

Ex Input:
Abstract: The steady state levels of the prodynorphin-derived opioid peptides, dynorphin A, dynorphin B, and alpha-neo-endorphin, have been extensively studied in the magnocellular/posterior pituitary system of the rat. To determine whether the rat system serves as a general model for prodynorphin processing in the mammalian posterior pituitary, we examined the steady state levels of prodynorphin-derived opioid peptides in the posterior pituitary systems of representatives of three diverse orders of mammals: guinea pig (order Rodentia), pig (order Artiodactyla), and rhesus monkey (order Primates). In each species studied there was evidence for species-specific deviations from the rat model. The most pronounced differences were observed with respect to the conversion of dynorphin A-(1-17) to dynorphin A-(1-8). In rodents, rats, and guinea pigs, under steady state conditions, the molar ratios of these forms are approximately 1:2 and 2.5:1, respectively. However, in the pig and rhesus monkey, the molar ratios of these forms are 10:1 and 14:1, respectively. Thus, under steady state conditions, the conversion of dynorphin A-(1-17) to dynorphin A-(1-8) appears to be a minor event in porcine and rhesus monkey posterior pituitary. Species-specific variations were also observed with respect to the steady state levels of alpha-neo-endorphin and dynorphin B-(1-13). In addition, the results of these studies suggest that the conversion of prodynorphin-derived opioids to leu-enkephalin probably represents a minor event in the species studied.

Ex Output:
Animal

Ex Input:
Abstract: Half-hourly sampling of plasma TSH was done across 3 days in four normal young men. Sleep was denied for 64 h from 0700 h on awakening from accommodation sleep until polygraphic sleep was resumed at 7100 h of the third day (D3) such that 2 consecutive nights of usual 2300-0700 h sleep were missed. This protocol allowed examination of any modulatory effects on the daily patterns in TSH concentrations during sleep deprivation on D1-2 (1100-3500, 3500-5900 h) or during resumption of usual nightly sleep on D3 (5900-8300) compared to that of a previously studied group of normal young men. The circadian nature of the daily TSH waveform was evidenced by its daily repetition within a subject both basally and during D1-2 sleep deprivation and by its synchronization within the basal, deprived, or resumed sleep days. The peaks in each subject's daily TSH patterns on D1-2 were consistently longer, and the daily maxima and cosine acrophases on D1-2 were consistently later than those on D3 when basal sleep was resumed. About half the daily TSH concentration maxima and daily cosinor amplitudes on D1-2 were greater than those of the respective sleep-resumed TSH patterns of D3. Both the group mean TSH patterns and the cosinor 95% confidence ellipses also indicated the daily peak in the TSH waveform to be significantly longer, later, and larger during D1-2 sleep deprivation than during the basal or D3 periods. These results indicate that significant alteration of the daily TSH waveform can occur in response to absence of sleep and are compatible with the existence of an inhibitory effect in early nightly sleep on TSH release. The TSH patterns during the 1700-2300 h intervals of rising TSH levels were congruent in the basal, deprived, and resumed sleep periods. Prompt reversion to the basal TSH pattern also occurred when sleep was resumed on D3. Both of these observations suggest the alteration in TSH waveform during sleep deprivation to have arisen from an inhibitory effect in sleep rather than from a change in period or phase of a generating oscillator.

Ex Output:
Adult