Plasma melatonin is reduced in Huntington's disease

This study was undertaken to determine whether the production of melatonin, a hormone regulating sleep in relation to the light/dark cycle, is altered in Huntington's disease. We analyzed the circadian rhythm of melatonin in a 24-hour study of cohorts of control, premanifest, and stage II/III Huntington's disease subjects. The mean and acrophase melatonin concentrations were significantly reduced in stage II/III Huntington's disease subjects compared with controls. We also observed a nonsignificant trend toward reduced mean and acrophase melatonin in premanifest Huntington's disease subjects. Onset of melatonin rise was significantly more temporally spread in both premanifest and stage II/III Huntington's disease subjects compared with controls. A nonsignificant trend also was seen for reduced pulsatile secretion of melatonin. Melatonin concentrations are reduced in Huntington's disease. Altered melatonin patterns may provide an explanation for disrupted sleep and circadian behavior in Huntington's disease, and represent a biomarker for disease state. Melatonin therapy may help the sleep disorders seen in Huntington's disease

Spring-damper coupling elements in the suspension of bridge cranes - a contribution to the improvement of lifting dynamics

SIGLEAvailable from TIB Hannover: DW 3735 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekDEGerman

Hormone levels in control, premanifest and stage II/III HD cohorts.

<p>P-value = p-value from linear regression of specified variable on age and gender (or else by gender as indicated), L indicates that logs were taken of the specified variable prior to linear regression; P indicates Freedman and Lane permutation tests were performed to account to non-normality, LP indicates Freedman and Lane permutation tests were performed after taking logs of the specified variable. In all cases, age and gender were adjusted for.</p><p>Data are presented as Mean ±SD for normally distributed data and as median [minimum–maximum] for skewed data.</p

Analysis of GH in control, premanifest and stage II/III HD cohorts.

<p>A: Mean GH concentrations over 24 hour sampling period in the three groups. B: FT analysis of GH plotting strength/power (%) against frequency (minutes) of GH oscillations for the three groups.</p

Analysis of ACTH and cortisol in control, premanifest and stage II/III HD cohorts.

<p>A: Mean ACTH concentrations over 24 hour sampling period in the three groups. B: Mean ACTH concentrations over 24 hour sampling period in the three groups. C: FT analysis of ACTH plotting strength/power (%) against frequency (minutes) of ACTH oscillations for the three groups. D: FT analysis of cortisol plotting strength/power (%) against frequency (minutes) of cortisol oscillations for the three groups. E: Mean molar cortisol:ACTH ratio over 24 hour sampling period in the three groups.</p

Analysis of LH in control, premanifest and stage II/III HD cohorts.

<p>A: Mean LH concentrations over 24 hour sampling period for female subjects in the three groups. B: Mean LH concentrations over 24 hour sampling period for male subjects in the three groups. C: FT analysis of LH plotting strength/power (%) against frequency (minutes) of LH oscillations for the three groups.</p