PubMed Health⌕ Search

Biomedical subjects

F C Baker

Publications and source records attributed to F C Baker.

At least 19 recordsLinked to original sources
PubMed2005

Persistence of sleep-temperature coupling after suprachiasmatic nuclei lesions in rats.

The suprachiasmatic nucleus (SCN) regulates the circadian rhythms of body temperature (T(b)) and vigilance states in mammals. We studied rats in which circadian rhythmicity was abolished after SCN lesions (SCNx rats) to investigate the association between the ultradian rhythms of sleep-wake states and brain temperature (T(br)), which are exposed after lesions. Ultradian rhythms of T(br) (mean period: 3.6 h) and sleep were closely associated in SCNx rats. Within each ultradian cycle, nonrapid eye movement (NREM) sleep was initiated 5 +/- 1 min after T(br) peaks, after which temperature continued a slow decline (0.02 +/- 0.006 degrees C/min) until it reached a minimum. Sleep and slow wave activity (SWA), an index of sleep intensity, were associated with declining temperature. Cross-correlation analysis revealed that the rhythm of T(br) preceded that of SWA by 2-10 min. We also investigated the thermoregulatory and sleep-wake responses of SCNx rats and controls to mild ambient cooling (18 degrees C) and warming (30 degrees C) over 24-h periods. SCNx rats and controls responded similarly to changes in ambient temperature. Cooling decreased REM sleep and increased wake. Warming increased T(br), blunted the amplitude of ultradian T(br) rhythms, and increased the number of transitions into NREM sleep. SCNx rats and controls had similar percentages of NREM sleep, REM sleep, and wake, as well as the same average T(b) within each 24-h period. Our results suggest that, in rats, the SCN modulates the timing but not the amount of sleep or the homeostatic control of sleep-wake states or T(b) during deviations in ambient temperature.

Animals↗
PubMed2004

Interleukin 1beta enhances non-rapid eye movement sleep and increases c-Fos protein expression in the median preoptic nucleus of the hypothalamus.

Interleukin 1beta (IL-1) is a key mediator of the acute phase response in an infected host and acts centrally to coordinate responses to an immune challenge, such as fever and increased non-rapid eye movement (NREM) sleep. The preoptic area (POA) is a primary sleep regulatory center in the brain: the ventrolateral POA (VLPO) and median preoptic nucleus (MnPN) each contain high numbers of c-Fos protein immunoreactive (IR) neurons after sleep but not after waking. We hypothesized that IL-1 mediates increased NREM sleep through activation of these sleep-active sites. Rats injected intracerebroventricularly with IL-1 (10 ng) at dark onset spent significantly more time in NREM sleep 4-5 h after injection. This increase in NREM sleep was associated with increased numbers of Fos-IR neurons in the MnPN, but not in the VLPO. Fos IR in the rostral MnPN was significantly increased 2 h post IL-1 injection, although the percentage of NREM sleep in the preceding 2 h was the same as controls. Fos IR was also increased in the extended VLPO 2 h postinjection. Finally, Fos IR in the MnPN did not differ significantly between IL-1 and vehicle-treated rats that had been sleep deprived for 2 h postinjection, but it was increased in VLPO core. Taken together, these results suggest that Fos IR in the MnPN after IL-1 is not independent of behavioral state and may require some threshold amount of sleep for its expression. Our results support a hypothesis that IL-1 enhances NREM sleep, in part, through activation of neurons in the MnPN of the hypothalamus.

Animals↗
PubMed2001

Sleep and 24 hour body temperatures: a comparison in young men, naturally cycling women and women taking hormonal contraceptives.

Body temperature has a circadian rhythm, and in women with ovulatory cycles, also a menstrual rhythm. Body temperature and sleep are believed to be closely coupled, but the influence on their relationship of gender, menstrual cycle phase and female reproductive hormones is unresolved. We investigated sleep and 24 h rectal temperatures in eight women with normal menstrual cycles in their mid-follicular and mid-luteal phases, and in eight young women taking a steady dose of oral progestin and ethinyl oestradiol (hormonal contraceptive), and compared their sleep and body temperatures with that of eight young men, sleeping in identical conditions. All subjects maintained their habitual daytime schedules. Rectal temperatures were elevated throughout 24 h in the luteal phase compared with the follicular phase in the naturally cycling women, consistent with a raised thermoregulatory set-point. Rectal temperatures in the women taking hormonal contraceptives were similar to those of the naturally cycling women in the luteal phase. Gender influenced body temperature: the naturally cycling women and the women taking hormonal contraceptives attained their nocturnal minimum body temperatures earlier than the men, and the naturally cycling women had blunted nocturnal body temperature drops compared with the men. Sleep architecture was essentially unaffected by either menstrual cycle phase or gender. The women taking hormonal contraceptives had less slow wave sleep (SWS), however, than the naturally cycling women. Gender, menstrual cycle phase and hormonal contraceptives significantly influenced body temperature, but had only minor consequences for sleep, in the young men and women in our study.

Body Mass Index↗
PubMed2001

Oral contraceptives alter sleep and raise body temperature in young women.

Female reproductive steroids, oestrogen and progesterone, not only affect reproductive function, but also thermoregulation and sleep. Chronic administration of synthetic steroids, as occurs in women taking oral contraceptives, may affect these regulatory systems differently from endogenous oestrogen and progesterone. We therefore investigated body temperature and sleep in ten young women taking oral contraceptives, in the active and placebo phases of the contraceptive pack, and compared them to a group of nine women with ovulatory cycles, in the mid-follicular and mid-luteal phases. Body temperature was raised throughout 24 h in the women taking oral contraceptives in the active phase, and in the naturally cycling women in the luteal phase, compared to the follicular phase. The women taking oral contraceptives in the placebo phase, however, continued to have raised body temperatures, similar to those in the active phase, indicating a prolonged action of synthetic reproductive steroids on body temperature. Sleep also was influenced by the endogenous and synthetic reproductive steroids, but independently of body temperature. The women taking oral contraceptives had more stage-2 non-rapid eye movement sleep in the active phase, both compared to their placebo phase and the naturally cycling women. The naturally cycling women, however, had more slow wave sleep in the luteal phase compared to the contraceptive group of women. Exogenous reproductive steroids therefore influence body temperature and sleep differently from endogenous progesterone and oestrogen.

Adult↗
PubMed1999

A comparison of subjective estimates of sleep with objective polysomnographic data in healthy men and women.

Twenty healthy men and women had their sleep recorded objectively, using polysomnography on 3 nonconsecutive nights. Following each night, the subjects assessed their sleep onset latency and number of awakenings, subjectively. Self-ratings were compared with objective measures of sleep onset latency (SOL), calculated as the time from lights-out to the first continuous minute of stage 2 sleep, and the number of awakenings which lasted 1 minute or longer on the polysomnograms. Apart from the first night, the subjects overestimated the time that it took them to fall asleep, despite sleep onset being scored as the latency to stage 2, rather than stage 1 sleep. On all 3 nights, the subjects underestimated the number of awakenings when compared to objective criteria. Although the subjects were consistent in their errors of estimation of their sleep compared to polysomnographic assessments over the three nights, the between-individual variation was large, so that objective and subjective ratings of SOL and awakenings were not correlated. The young men and women in our study, who were free of medication or sleep complaints, perceived their sleep inaccurately when compared to objective polysomnographic recordings.

Adult↗
PubMed1999

High nocturnal body temperatures and disturbed sleep in women with primary dysmenorrhea.

Primary dysmenorrhea is characterized by painful uterine cramps, near and during menstruation, that have an impact on personal life and productivity. The effect on sleep of this recurring pain has not been established. We compared sleep, nocturnal body temperatures, and hormone profiles during the menstrual cycle of 10 young women who suffered from primary dysmenorrhea, without any menstrual-associated mood disturbances, and 8 women who had normal menstrual cycles. Dysmenorrheic pain significantly decreased subjective sleep quality, sleep efficiency, and rapid eye movement (REM) sleep but not slow wave sleep (SWS), compared with pain-free phases of the menstrual cycle and compared with the controls. Even before menstruation, in the absence of pain, the women with dysmenorrhea had different sleep patterns, nocturnal body temperatures, and hormone levels compared with the controls. In the mid-follicular, mid-luteal, and menstrual phases, the dysmenorrheics had elevated morning estrogen concentrations, higher mean in-bed temperatures, and less REM sleep compared with the controls, as well as higher luteal phase prolactin levels. Both groups of women had less REM sleep when their body temperatures were high during the luteal and menstrual phases, implying that REM sleep is sensitive to elevated body temperatures. We have shown that dysmenorrhea is not only a disorder of menstruation but is manifest throughout the menstrual cycle. Furthermore, dysmenorrheic pain disturbs sleep, which may exacerbate the effect of the pain on daytime functioning.

Adult↗
PubMed1998

Menstrual factors in sleep.

The changing endocrine profile in premenopausal women alters aspects of sleep and circadian rhythms. Subjectively women appear to feel a greater need for sleep and report poor and insufficient sleep more often than men. This greater sleep requirement may manifest with a higher amplitude of slow-wave sleep in the EEG in women. Healthy young women, with biphasic body temperature rhythms of ovulatory menstrual cycles, have more stage 2 sleep, higher spindle frequency activity and less rapid-eye movement (REM) sleep when progesterone predominates in the luteal phase. These sleep-EEG changes may largely be caused by neurosteroids acting on the brain. Sleep regulatory mechanisms, indicated by the onset to sleep, slow-wave sleep (SWS) and slow-wave activity, appear to be unaffected by menstrual phase in women with normal cycles. Women with premenstrual mood symptoms have more stage 2 sleep and seemingly less SWS and REM sleep, a blunted circadian rhythm of melatonin and an earlier minimum body temperature than asymptomatic women. Subjective repercussions include increased daytime sleepiness, lethargy and fatigue. Treatment strategies for menstrual-associated complaints include using oral contraceptives and sleep deprivation but the physiology and pharmacology of normal menstrual changes, the disorders and their treatment need to be better understood.

Journal Article↗
PubMed1998

Different nocturnal body temperatures and sleep with forced-air warming in men and in women taking hormonal contraceptives.

We studied how forced-air warming, conventionally used to control body temperature during and after anaesthesia, affected the nocturnal rectal temperatures and sleep composition of young men and women. Seven healthy women who were taking oral or injection contraceptives, and six healthy men spent 3 nights in a controlled environment: an adaptation night followed by 2 nights when they slept under either a down duvet (baseline) or a quilt perfused with warm air (hot). Repeated analysis of variance (ANOVA) revealed significant gender differences in the body temperature responses. On the baseline night, despite sleeping under the same conditions, the women did not show a nocturnal drop in body temperature as shown by the men. Forced-air warming increased body temperature to a similar extent in the men and the women, and resulted in enhanced hyperthermia in the women, and blunted the drop in body temperature in the men, compared to their baseline nights. The significant increases in body temperature had no consequences, however, for the subjective sleep quality of either the men or women, and only minor consequences for objective sleep composition. Both men and women had increased amounts of Stage 2 sleep on the hot night (P < 0.04). In addition, the women had reduced rapid eye movement (REM) sleep when compared to their baseline night (P < 0.04). Our results confirm that in a passive thermal environment, women who are taking oral or injection contraceptives have higher nocturnal body temperatures than men. Also, as sleep architecture was minimally affected by the increases in body temperature of between 0.2 and 0.3 degree C on the hot night in the men and women, and subjective sleep quality was unaffected, our results question the existence of a tight association between sleep and body temperature.

Adult↗
PubMed1989

Juvenile hormone bisepoxide biosynthesis in vitro by the ring gland of Drosophila melanogaster: a putative juvenile hormone in the higher Diptera.

The in vitro production of juvenile hormone (JH) was investigated by using isolated ring glands from third instar Drosophila melanogaster. A JH-like molecule is secreted that comigrates with a synthetic sample of methyl 6,7;10,11-bisepoxy-3,7,11-trimethyl-(2E)-dodecenoate (JHB3) during TLC, liquid chromatography, and GC analysis. Purified product from farnesoic acid-stimulated ring glands was analyzed by electron impact GC/MS and gave a mass spectrum identical to synthetic JHB3. Additional structure confirmation was obtained following conversion of product from unstimulated biosynthesis to a derivative that comigrated on liquid chromatography with the derivative prepared from synthetic JHB3. Physiological studies revealed that JHB3 is produced solely by the corpus allatum portion of the ring gland in vitro. Isolated ring glands from other cyclorrhaphous dipteran larvae also produce JHB3 almost exclusively in vitro. Corpora allata from mosquito larvae, however, produce only JH III, indicating that JHB3 production may be restricted to the higher Diptera. Topically applied synthetic JHB3 caused developmental responses in newly formed D. melanogaster white puparia similar to those obtained with JH III. The data suggest that JHB3 is a fly juvenile hormone.

Animals↗
PubMed1988

Comparative metabolism of branched-chain amino acids to precursors of juvenile hormone biogenesis in corpora allata of lepidopterous versus nonlepidopterous insects.

Comparative studies were performed on the role of branched-chain amino acids (BCAA) in juvenile hormone (JH) biosynthesis using several lepidopterous and nonlepidopterous insects. Corpora cardiaca-corpora allata complexes (CC-CA, the corpora allata being the organ of JH biogenesis) were maintained in culture medium containing a uniformly 14C-labeled BCAA, together with [methyl-3H]methionine as mass marker for JH quantification. BCAA catabolism was quantified by directly analyzing the medium for the presence of 14C-labeled propionate and/or acetate, while JHs were extracted, purified by liquid chromatography, and subjected to double-label liquid scintillation counting. Our results indicate that active BCAA catabolism occurs within the CC-CA of lepidopterans, and this efficiently provides propionyl-CoA (from isoleucine or valine) for the biosynthesis of the ethyl branches of JH I and II. Acetyl-CoA, formed from isoleucine or leucine catabolism, is also utilized by lepidopteran CC-CA for biosynthesizing JH III and the acetate-derived portions of the ethyl-branched JHs. In contrast, CC-CA of nonlepidopterans fail to catabolize BCAA. Consequently, exogenous isoleucine or leucine does not serve as a carbon source for the biosynthesis of JH III by these glands, and no propionyl-CoA is produced for genesis of ethyl-branched JHs. This is the first observation of a tissue-specific metabolic difference which in part explains why these novel homosesquiterpenoids exist in lepidopterans, but not in nonlepidopterans.

Amino Acids, Branched-Chain↗
PubMed1987

Sources of propionate for the biogenesis of ethyl-branched insect juvenile hormones: Role of isoleucine and valine.

Corpora allata from adult female Manduca sexta biosynthesize the sesquiterpenoid juvenile hormone (JH) III and the unusual ethyl-branched homologue JH II in vitro. We maintained corpora allata in medium 199 using [methyl-(3)H]methionine as the source of the JH methyl ester moiety and as a mass marker. This allowed measurement of the relative contributions of (14)C-labeled precursors to the biogenesis of JH II and III carbon skeletons. We showed efficient incorporation of a propionate equivalent, from isoleucine or valine catabolism, into the ethyl-branched portion of JH II, using double-label liquid scintillation counting of isolated JHs and gas chromatography/mass spectrometry with selected ion monitoring of JH deuteromethoxyhydrin derivatives. Methionine was a poor source of propionate for JH II biosynthesis, while glucose, succinate, threonine, and beta-alanine did not contribute propionate at all. Leucine, isoleucine, and glucose incorporated into JH III and the acetate-derived portion of JH II.

Journal Article↗
PubMed1985

Isoprenoid synthesis in isolated embryonic Drosophila cells. Sterol-independent regulatory signal molecule is distal to isopentenyl 1-pyrophosphates.

Embryonic Drosophila cells (Kc cells) were used to further characterize sterol-independent modulation of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity. 3-Methyl-3-5-dihydroxyvalerate (mevalonate), 3-fluoromethyl-3,5-dihydroxyvalerate (fluoromevalonate), and 3-ethyl-3,5-dihydroxyvalerate (homomevalonate) were tested as modulators. Although mevalonate caused a rapid, reversible suppression of reductase activity, fluoro- and homomevalonate increased activity; fluoromevalonate was more effective than homomevalonate. Mevalonate, added simultaneously with fluoromevalonate, blocked the analogue's effect on Kc cell reductase activity. However, mevalonate did not suppress an established fluoromevalonate increase in HMG-CoA reductase activity. Fluoromevalonate blocked [1-14C, 5-3H]mevalonate conversion to 14CO2- and 3H-labeled lipids and [3H] mevalonate 5-pyrophosphate accumulated. Neither protein nor RNA synthesis were required for mevalonate-mediated suppression of reductase activity. However, fluoromevalonate's effect on reductase activity required protein synthesis. Furthermore, in the absence of protein synthesis, fluoromevalonate-stabilized Kc cell HMG-CoA reductase activity. We have concluded that mevalonate, fluoromevalonate, homomevalonate, and compactin (mevinolin) modulated HMG-CoA reductase activity because they altered isoprenoid carbon flow to a post-isopentenyl 1-pyrophosphate regulatory, signal molecule.

Animals↗
PubMed1985

Juvenile hormone titre and regulation in the cockroach Diploptera punctata.

Titres of juvenile hormone (JH) have been determined in both hemolymph and whole body extracts of female Diploptera punctata during the first gonotrophic cycle using a method employing gas chromatography/mass spectrometry for qualitative and quantitative analysis. JH III is the sole JH found in both adult and last instar D. punctata. Maximum values of approximately 1500 ng/ml (approximately 6 microM) were observed at the middle of the gonotrophic cycle, when basal oocyte growth rate was greatest. Changes in rates of JH release in vitro by corpora allata paralleled closely the changes in JH titre, suggesting that biosynthesis is a major regulator of titre. JH levels per animal were calculated from observed JH titres, and at certain time points in the gonotrophic cycle JH obtained from analysis of whole bodies were significantly greater than those predicted from hemolymph titres. These results suggest the existence of a nonhemolymph JH pool in D. punctata. Decay in JH titre after allatectomy of 5 day females has also been studied. Following a rapid initial decline, the rate of decay slowed appreciably 4 h post-operation. Thus, use of a first-order rate constant to estimate half-life of JH significantly underestimated the longevity of the hormone. The apparent persistence of JH following allatectomy may be due to the existence of a nonhemolymph JH pool.

Animals↗
PubMed1984

Detection of only JH III in several life-stages of Nauphoeta cinerea and Thermobia domestica.

We have conducted a reinvestigation into both the identification and quantification of juvenile hormone (JH) from several developmental stages of the cockroach, Nauphoeta cinerea, and the firebrat, Thermobia domestica, using a gas chromatography-mass spectrometric (GC/MS) method. We detected only JH III in these animals in contrast to prior studies in which JH I, II, and/or III had been reported using a different scheme relying on HPLC purification and subsequent GC/MS analysis under chemical ionization (CI) conditions. Very high levels (approximately 800 ng/g) of JH III were found in N. cinerea embryos at stages after dorsal closure whereas first stadium nymphs and female penultimate stadium nymphs contained only low levels (approximately 1 ng/g and approximately 7 ng/ml respectively); in adult females at the stage of rapid oocyte growth approximately 150 ng JH III per ml of hemolymph was measured. T. domestica nymphs and egg laying adults contained only low levels (approximately 1 ng/g) of JH III. The results emphasize the caution which must be used in interpreting results of procedures for analysis of JH at parts-per-billion levels, and also enforce prior observations that the higher JH homologs are not present except in the Lepidoptera.

Animals↗
PubMed1983

Farnesol and farnesal dehydrogenase(s) in corpora allata of the tobacco hornworm moth, Manduca sexta.

The metabolism of [3H]farnesol was studied in cell-free preparations of corpora allata from the tobacco hornworm, Manduca sexta, to assess the role of this presumed biosynthetic precursor of juvenile hormone (JH) III. A reversed-phase ion-pair liquid chromatographic (RP-IPC) procedure was devised to separate farnesol from several potential intermediates in its presumed metabolism to JH III: farnesal, farnesoic acid, 10,11-epoxyfarnesoic acid, and methyl farnesoate. Following incubation of (2E,6E)-[1,5,9-3H]farnesol with homogenates of corpora allata from fifth instar larvae or adult female M. sexta, and analysis by RP-IPC, the major radiolabeled products corresponded to farnesoic acid, farnesal, and a polar product(s) presumably derived from the tritium on C-1 of farnesol. Inclusion of NAD+ in the incubations conducted with crude homogenates resulted in enhanced [3H]farnesol metabolism, decreased accumulation of [3H]farnesal, and increased levels of [3H]farnesoic acid. Substitution of NADP+ for NAD+ was ineffective, suggesting that farnesol and/or farnesal dehydrogenase were NAD+-dependent enzymes. Pellet fractions obtained by differential centrifugation of crude homogenates exhibited both farnesol and farnesal dehydrogenase activity but only the latter was clearly stimulated by addition of NAD+. The alcohol/aldehyde dehydrogenase(s) showed some substrate specificity for the 2E isomer; nerol and (2Z,6E)-farnesol were barely metabolized under conditions in which either geraniol or (2E,6E)-farnesol were rapidly oxidized. The identity of the [3H]farnesal zone obtained from RP-IPC was further established by normal-phase liquid chromatography and by gas-liquid chromatography-mass spectrometry.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Oxidoreductases↗
PubMed1981

Biosynthesis of 3-hydroxy-3-methylglutaryl-CoA, 3-hydroxy-3-ethylglutaryl-CoA, mevalonate and homomevalonate by insect corpus allatum and mammalian hepatic tissues.

Both radioactively labeled 3-hydroxy-3-methyglutarylcoenzyme A and its homolog 3-hydroxy-3-ethylglutarylcoenzyme A are produced by a cytosolic fraction obtained from corpora allata-corpora cardiaca complexes of the moth Manduca sexta, incubated with [1-14C]acetylcoenzyme A plus unlabeled propionylcoenzyme A. A particulate fraction isolated from the same tissue was able to reduce [Me-3H]hydroxymethylglutaryl-CoA and [3-14C]hydroxyethylglutaryl-CoA to mevalonate and homomevalonate, respectively, when NADPH was used as the electron donor. These reactions are in keeping with the proposed homoisoprenoid biosynthetic pathway for certain of the insect juvenile hormones. Measurement of products produced in picomole levels was accomplished by their conversion to ultraviolet absorbing derivatives which were subsequently analyzed by thin-layer chromatography and liquid chromatography followed by collection and liquid scintillation counting of appropriate fractions. Similar assays conducted with cell-free preparations from corpora allata of the grasshopper Schistocerca nitens, the mealworm beetle Tenebrio molitor, and from rat liver, species in which homoisoprenoid compounds have not been detected, also resulted in formation of the normal and homologous products (although no hydroxymethylglutaryl-CoA/hydroxyethylglutaryl-CoA reductase activity could be demonstrated in T. molitor). The latter results indicate a rather loose substrate specificity of the enzymes leading to mevalonate formation.

Acyl Coenzyme A↗