PubMed Health⌕ Search

Biomedical subjects

K J Reid

Publications and source records attributed to K J Reid.

9 recordsLinked to original sources
PubMed2005

Stability of melatonin and temperature as circadian phase markers and their relation to sleep times in humans.

Circadian rhythms of core body temperature and melatonin are commonly used as phase markers of the circadian clock. Melatonin is a more stable marker of circadian phase when measured under constant routine conditions. However, little is known about the variability of these phase markers under less controlled conditions. Moreover, there is little consensus about the preferred method of analysis. The objective of this study was to assess various methods of calculating melatonin and temperature phase in subjects with regular sleep schedules living in their natural environment. Baseline data were analyzed from 42 healthy young subjects who were studied on at least two occasions. Each hospital admission was separated by at least 3 weeks. Subjects were instructed to maintain a regular sleep schedule, which was monitored for 1 week before admission by sleep logs and actigraphy. Subjects spent one habituation night under controlled conditions prior to collecting baseline temperature and melatonin measurements. The phase of the melatonin rhythm was assessed by 9 different methods. The temperature nadir (Tmin) was estimated using both Cleveland and Cosine curve fitting procedures, with and without demasking. Variability between admissions was assessed by correlation analysis and by the mean absolute difference in timing of the phase estimates. The relationship to sleep times was assessed by correlation of sleep onset or sleep offset with the various phase markers. Melatonin phase markers were more stable and more highly correlated with the timing of sleep than estimates of Tmin. Of the methods for estimating Tmin, simple cosine analysis was the least variable. In addition, sleep offset was more strongly correlated with the various phase markers than sleep onset. The relative measures of melatonin offset had the highest correlation coefficients, the lowest study-to-study variability, and were more strongly associated with sleep timing than melatonin onsets. Concordance of the methods of analysis suggests a tendency for the declining phase of the melatonin profile to be more stable and reliable than either markers of melatonin onset or measures of the termination of melatonin synthesis.

Adult↗
PubMed2003

The amount of sleep obtained by locomotive engineers: effects of break duration and time of break onset.

AIMS: To determine the effects of break duration and time of break onset on the amount of sleep that locomotive engineers obtain between consecutive work periods. METHODS: A total of 253 locomotive engineers (249 male, 4 female, mean age 39.7 years) participated. Data were collected at 14 rail depots, where participants drove electric or diesel locomotives; worked with another engineer or drove alone; carried passengers, freight, or coal; and operated in rural or urban areas. Participants completed sleep diaries and work diaries for a two week period while working their normal roster patterns. RESULTS: For breaks that began at similar times of day, total sleep time (TST) increased with break duration. For breaks of similar duration, TST was greater for those that occurred during the night-time than for those that occurred during the daytime. An average of 3.1-7.9 hours sleep was obtained in 12 hour breaks (minimum break requirement in the Australian rail industry), depending on when the break began. CONCLUSIONS: The duration and timing of breaks are both important factors in determining the amount of sleep that locomotive engineers obtain between consecutive work periods. Consequently, minimum length break requirements that do not include a time of day component may not provide locomotive engineers with the opportunity to obtain a sufficient amount of sleep prior to resuming work.

Adult↗
PubMed2001

Familial advanced sleep phase syndrome.

BACKGROUND: The circadian rhythms of sleep propensity and melatonin secretion are regulated by a central circadian clock, the suprachiasmatic nucleus of the hypothalamus. The most common types of sleep disorders attributed to an alteration of the circadian clock system are the sleep/wake cycle phase disorders, such as delayed sleep phase syndrome and advanced sleep phase syndrome (ASPS). Advanced sleep phase syndrome is characterized by the complaint of persistent early evening sleep onset and early morning awakening. Although the complaint of awakening earlier than desired is relatively common, particularly in older adults, extreme advance of sleep phase is rare. OBJECTIVE: To phenotypically characterize a familial case of ASPS. METHODS: We identified a large family with ASPS; 32 members of this family gave informed consent to participate in this study. Measures of sleep onset and offset, dim light melatonin onset, the Horne-Ostberg morningness-eveningness questionnaire, and clinical interviews were used to characterize family members as affected or unaffected with ASPS. RESULTS: Affected members rated themselves as "morning types" and had a significant advance in the phase of sleep onset (P<.001) and offset (P =.006) times. The mean sleep onset was 2121 hours for the affected family members and 0025 hours for the unaffected family members. The mean sleep offset was 0507 hours for the affected members and 0828 hours for the unaffected members. (Times are given in military form.) In addition, the phase of the circadian rhythm of melatonin onset for the affected family members was on average 3-1/2 hours earlier than for the unaffected members. CONCLUSIONS: The ASPS trait segregates with an autosomal dominant mode of inheritance. The occurrence of familial ASPS indicates that human circadian rhythms, similar to those in animals, are under genetic regulation. Genetic analysis of familial sleep and circadian rhythm disorders is important for identifying a specific gene(s) responsible for the regulation of sleep and circadian rhythms in humans.

Adult↗
PubMed2000

Two classes of androgen receptor elements mediate cooperativity through allosteric interactions.

Genes uniquely regulated by the androgen receptor (AR) typically contain multiple androgen response elements (AREs) that in isolation are of low DNA binding affinity and transcriptional activity. However, specific combinations of AREs in their native promoter context result in highly cooperative DNA binding by AR and high levels of transcriptional activation. We demonstrate that the natural androgen-regulated promoters of prostate specific antigen and probasin contain two classes of AREs dictated by their primary nucleotide sequence that function to mediate cooperativity. Class I AR-binding sites display conventional guanine contacts. Class II AR-binding sites have distinctive atypical sequence features and, upon binding to AR, the DNA structure is dramatically altered through allosteric interactions with the receptor. Class II sites stabilize AR binding to adjacent class I sites and result in synergistic transcriptional activity and increased hormone sensitivity. We have determined that the specific nucleotide variation within the AR binding sites dictate differential functions to the receptor. We have identified the role of individual nucleotides within class II sites and predicted consensus sequences for class I and II sites. Our data suggest that this may be a universal mechanism by which AR achieved unique regulation of target genes through complex allosteric interactions dictated by primary binding sequences.

Allosteric Regulation↗
PubMed1997

Effect of atenolol on nocturnal sleep and temperature in young men: reversal by pharmacological doses of melatonin.

To examine the physiological role of melatonin in sleep, nocturnal melatonin secretion was suppressed using 100 mg oral atenolol in two studies. In Study 1, nocturnal sleep was recorded in 8 young men over 4 nights. Subjects received atenolol on one of the last 2 nights and showed significantly increased total wake time (TWT) and wakefulness after sleep onset (WASO), as well as decreased REM sleep and slow-wave sleep (SWS). When melatonin (total 5 mg) was given after atenolol on the other night, the changes in TWT, WASO, REM, and SWS were reversed. In Study 2, sleep onset latencies (SOL) and core temperature (Tc) of 10 young men were measured for 3 nonconsecutive nights. In a cross-over design, atenolol given on one night significantly suppressed urinary 6-sulphatoxymelatonin (6s-aMT) production and increased hourly measures of Tc and SOL relative to baseline night values. Oral melatonin (3 mg), administered after atenolol, reversed the changes in Tc and SOL. These results suggest that endogenous melatonin may assist in the maintenance of normal sleep architecture (Study 1) and also increase nocturnal sleep propensity by hypothermic effects (Study 2).

Adult↗
PubMed1976

Genetic counseling. An evaluation of public health genetic clinics.

The geographic distribution of County Health Department clinic facilities in the state of California has made it readily possible to establish a regionalized program for genetic counseling services, using public health nurses as a major source of case-finding. From both consumer and health professional standpoints, regionalized satellite genetic counseling clinics have been successful, and in particular, the effectiveness of public health nurses in identifying clinical genetic problems is readily apparent.Long-term follow-up reinforcement of genetic counseling appears to be an important conclusion from these studies. It is our suggestion that reinforcement of counseling would best be accomplished through the health team member (physician, nurse and so forth) following the patient or family rather than through the consulting geneticist.

Adult↗