Sleep-promoting material from human urine and its relation to factor S from brain

1980 ◽  
Vol 238 (2) ◽  
pp. E116-E123
Author(s):  
J. M. Krueger ◽  
J. Bacsik ◽  
J. Garcia-Arraras
Keyword(s):  
Ion Exchange ◽  
Slow Wave ◽  
High Voltage ◽  
Human Urine ◽  
Time Course ◽  
Slow Wave Sleep ◽  
Gel Filtration ◽  
Chemical Properties ◽  
Intraventricular Infusion ◽  
High Voltage Electrophoresis

A sleep-promoting factor was extracted from human urine. Intraventricular infusion of the purified material induced excess slow-wave sleep in rats and rabbits for 5--10 h after the infusion. Chemical properties of the urinary factor were similar to those of factor S derived from whole brains of sleep-deprived goats, sheep, and rabbits. The behavior of the urinary factor in two ion exchange chromatographic steps, high voltage electrophoresis, gel-filtration, and ultrafiltration was similar to that of factor S. Effects of the purified urinary factor on slow-wave sleep of rats and rabbits were similar in time-course and duration to those of factor S from brain. However, the factor obtained from human urine did not increase the amplitude of cortical slow waves to the same extent as did factor S from brains of sleep-deprived animals.

Effects of sleep-promoting factor from human urine on sleep cycle of cats

1981 ◽  
Vol 241 (4) ◽  
pp. E269-E274
Author(s):  
J. E. Garcia-Arraras
Keyword(s):  
Cerebrospinal Fluid ◽  
Eye Movement ◽  
Slow Wave ◽  
Human Urine ◽  
Slow Wave Sleep ◽  
Sleep Cycle ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Artificial Cerebrospinal Fluid ◽  
Normal Sleep

Slow-wave sleep (SWS) and rapid-eye-movement sleep (REM) were recorded in cats for 32 h a) under control conditions, b) following intraventricular infusions of artificial cerebrospinal fluid (CSF), and c) following infusions of sleep-promoting factor S prepared from human urine (SPU). During the first 12 h after receiving artificial CSF, the cats slept 4.9 +/- 0.2 h in slow-wave sleep (SWS) and 1.4 +/- 0.1 h in REM. Similar values were obtained from the same cats under control conditions. After infusions of SPU, the duration of SWS in the same cats increased to an average of 6.9 +/- 0.5 h with no significant change in REM averaged over 12 h; a transient decrease of REM in the first 4 h was fully compensated in subsequent hours. The increased SWS induced by the sleep-promoting factor from human urine subsided after 12 h, and there was no compensatory increase in wakefulness during the subsequent 20 h. The normal sleep cycle was not affected. In cats, therefore, the primary effect of SPU is to increase normal SWS, with little effect on REM.

scholarly journals Peptidoglycans as promoters of slow-wave sleep. I. Structure of the sleep-promoting factor isolated from human urine.

1984 ◽  
Vol 259 (20) ◽  
pp. 12652-12658
Author(s):  
S A Martin ◽  
M L Karnovsky ◽  
J M Krueger ◽  
J R Pappenheimer ◽  
K Biemann
Keyword(s):  
Slow Wave ◽  
Human Urine ◽  
Slow Wave Sleep

Time course of EEG power density during long sleep in humans

1990 ◽  
Vol 258 (3) ◽  
pp. R650-R661 ◽  
Author(s):  
D. J. Dijk ◽  
D. P. Brunner ◽  
A. A. Borbely
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Time Course ◽  
Slow Wave Sleep ◽  
Nrem Sleep ◽  
Sleep Stages ◽  
Base Line ◽  
Sleep Regulation ◽  
Recovery Sleep ◽  
Electroencephalogram Eeg

In nine subjects sleep was recorded under base-line conditions with a habitual bedtime (prior wakefulness 16 h; lights off at 2300 h) and during recovery from sleep deprivation with a phase-advanced bedtime (prior wakefulness 36 h; lights off at 1900 h). The duration of phase-advanced recovery sleep was greater than 12 h in all subjects. Spectral analysis of the sleep electroencephalogram (EEG) revealed that slow-wave activity (SWA; 0.75-4.5 Hz) in non-rapid-eye-movement (NREM) sleep was significantly enhanced during the first two NREM-REM sleep cycles of displaced recovery sleep. The sleep stages 3 and 4 (slow-wave sleep) and SWA decreased monotonically over the first three and four NREM-REM cycles of, respectively, base-line and recovery sleep. The time course of SWA in base-line and recovery sleep could be adequately described by an exponentially declining function with a horizontal asymptote. The results are in accordance with the two-process model of sleep regulation in which it is assumed that SWA rises as a function of the duration of prior wakefulness and decreases exponentially as a function of prior sleep. We conclude that the present data do not provide evidence for a 12.5-h sleep-dependent rhythm of deep NREM sleep.

Brain temperature changes coupled to sleep states persist during interleukin 1-enhanced sleep

1986 ◽  
Vol 250 (1) ◽  
pp. R96-R103 ◽  
Author(s):  
J. Walter ◽  
D. Davenne ◽  
S. Shoham ◽  
C. A. Dinarello ◽  
J. M. Krueger
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Temperature Changes ◽  
Arousal State ◽  
Intraventricular Infusion ◽  
Sleep Cycles

The effects of human interleukin 1 (IL 1) on the architecture of rabbit sleep-wake cycles and brain temperature (Tbr) changes coupled to states of vigilance were examined. Cerebral intraventricular infusion of IL 1 induced increased slow-wave sleep (SWS), increased electroencephalographic slow-wave (0.5-4 Hz) amplitudes, and fever. Heat-inactivated IL 1 failed to elicit these responses. IL 1 also significantly inhibited rapid-eye-movement (REM) sleep; however, inactivated IL 1 also reduced REM sleep; thus some of the IL 1-induced REM reduction may be related to the infusion process. The duration and number of sleep cycles (REM-to-REM interval) were unaffected by IL 1. Similarly, Tbr changes that normally occur during the transition from one arousal state to another remained unchanged after IL 1 infusion, even though rabbits were simultaneously febrile. We conclude that IL 1 selectively enhances SWS while leaving sleep cycles and Tbr changes coupled to states of vigilance undisturbed.

Chromatographie and Electrophoretic Properties of Synthetic Human Fibrinopeptides

1974 ◽  
Vol 32 (02/03) ◽  
pp. 651-658
Author(s):  
Robin McKenzie ◽  
D. S Pepper ◽  
A. B Kay
Keyword(s):  
Thin Layer ◽  
High Voltage ◽  
Low Voltage ◽  
Gel Filtration ◽  
Paper Electrophoresis ◽  
Molecular Weights ◽  
Electrophoretic Mobilities ◽  
Rf Values ◽  
Layer Chromatography ◽  
High Voltage Electrophoresis

SummarySome properties of synthetic human fibrinopeptides were studied by thin-layer chromatography, thin-layer electrophoresis and low voltage and high voltage paper electrophoresis. The Rf values and electrophoretic mobilities of the peptides in these systems were determined. In high voltage electrophoresis synthetic and natural (fibrinogen-derived) peptides migrated in an identical fashion.When gel filtration was performed in 0.05 M pyridine or 0.1 N ammonia, synthetic fibrinopeptides A and B appeared to be aggregated. In contrast, when filtration was performed in 1.3 M formic acid, the peptides eluted in positions corresponding to their monomeric molecular weights.In addition it was possible to quantitate synthetic fibrinopeptides by two colorimetric assays, the Sakaguchi reaction and the Folin-Ciocalteu method. Ultraviolet extinction coefficients for each peptide were also determined.

scholarly journals Initiation of sleep-dependent cortical-hippocampal correlations at wakefulness-sleep transition

2014 ◽  
Vol 112 (7) ◽  
pp. 1763-1774 ◽  
Author(s):  
Daniel C. Haggerty ◽  
Daoyun Ji
Keyword(s):  
Slow Wave ◽  
High Voltage ◽  
Memory Consolidation ◽  
Slow Wave Sleep ◽  
Brain Area ◽  
Neuronal Firing ◽  
Gradual Process ◽  
Voltage Spike ◽  
Sleep Transition ◽  
Spike Wave

Sleep is involved in memory consolidation. Current theories propose that sleep-dependent memory consolidation requires active communication between the hippocampus and neocortex. Indeed, it is known that neuronal activities in the hippocampus and various neocortical areas are correlated during slow-wave sleep. However, transitioning from wakefulness to slow-wave sleep is a gradual process. How the hippocampal-cortical correlation is established during the wakefulness-sleep transition is unknown. By examining local field potentials and multiunit activities in the rat hippocampus and visual cortex, we show that the wakefulness-sleep transition is characterized by sharp-wave ripple events in the hippocampus and high-voltage spike-wave events in the cortex, both of which are accompanied by highly synchronized multiunit activities in the corresponding area. Hippocampal ripple events occur earlier than the cortical high-voltage spike-wave events, and hippocampal ripple incidence is attenuated by the onset of cortical high-voltage spike waves. This attenuation leads to a temporary weak correlation in the hippocampal-cortical multiunit activities, which eventually evolves to a strong correlation as the brain enters slow-wave sleep. The results suggest that the hippocampal-cortical correlation is established through a concerted, two-step state change that first synchronizes the neuronal firing within each brain area and then couples the synchronized activities between the two regions.

scholarly journals Slow-Wave Sleep in Daytime and Nocturnal Sleep: An Estimate of the Time Course of "Process S"

1986 ◽  
Vol 1 (4) ◽  
pp. 303-308 ◽  
Author(s):  
John B. Knowles ◽  
Alistair W. MacLean ◽  
Laura Salem ◽  
Charles Vetere ◽  
Margot Coulter
Keyword(s):  
Slow Wave ◽  
Time Course ◽  
Slow Wave Sleep ◽  
Nocturnal Sleep

Fractionation of Urine to Allow Desmosine Analysis by Radioimmunoassay

1992 ◽  
Vol 29 (1) ◽  
pp. 72-78 ◽  
Author(s):  
Barry Starcher ◽  
Marti Scott
Keyword(s):  
Ion Exchange ◽  
Affinity Chromatography ◽  
Human Urine ◽  
Gel Filtration ◽  
Ion Exchange Chromatography ◽  
Exchange Chromatography ◽  
The Other ◽  
Normal Adult ◽  
Average Adult

The present study was designed to re-evaluate the radioimmunoassay for desmosine in urine, which is currently used as a measure of elastin metabolism. Using ion exchange chromatography, gel filtration and affinity chromatography it was shown that at least five other compounds in hydrolysates of human urine competed for desmosine in the RIA. Fractionating the urine prior to hydrolysis with acetone removed one of the major contaminants. The other contaminants could subsequently be removed by extracting the urine hydrolysate with a mixture of chloroform/ethanol (60:40). Samples from nine normal adult urines showed that an average of 45% of the RIA competing material in unfractionated urine was not desmosine. The final extracted residue retained all of the desmosine and only 16% of the original solids. The average adult urine contains approximately 50 pmol desmosine/mg creatinine, reflecting a daily turnover of between 3 and 4 mg of elastin per day.

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