We are what we (think we) eat: The effect of expected satiety on subsequent calorie consumption.

Varying expected satiety (ES) for equi-calorie portions of different foods can affect subsequent feelings of hunger and fullness and alter consumption. To our knowledge, no study has manipulated ES for an equal portion of the same solid food, subsequent appetite has not been measured >3 h and studies have not consistently measured later consumption. Further, it is not clear whether any changes in hunger, fullness or later consumption that stem from differing ES are the result of a psychological or physiological response. The aims of this study were to manipulate ES for the same solid food on two occasions in order to compare participants' appetitive responses over a 4-h inter-meal period, to measure later consumption, and to assess whether any effect of ES on these measures was related to a physiological (i.e. total ghrelin) response. Using a within-subjects design, 26 healthy participants had their ES for omelettes manipulated experimentally, believing that a 3-egg omelette contained either 2 (small condition) or 4 (large condition) eggs. When ES was higher (large condition) participants ate significantly fewer calories at a lunchtime test meal (mean difference = 69 kcal [± 95% CI 4-136]) and consumed significantly fewer calories throughout the day (mean difference = 167 kcal [± 95% CI 26-309]). The results show that there was a significant main effect of time on hunger and fullness, but no main effect of 'portion size' (p > .05). There was also a significant interaction between time and portion size for hunger. There was no evidence for any significant differences in appetite or consumtpion resulting from changes in total ghrelin. Overall, the data suggest that ES for a solid food can be manipulated and that, when given at breakfast, having a higher ES for a meal significantly reduces lunchtime and whole day caloric consumption.

Effects of hunger state on the brain responses to food cues across the life span.

The abundant exposure to food cues in our environment is one of the main drivers of overconsumption. Food evaluation is important for the regulation of food intake by the brain and it's interaction with hunger state. Children are especially susceptible to food cues. Understanding the mechanisms behind this regulation in healthy individuals across the life span can help to elucidate the mechanisms underlying overconsumption and aid the development of future obesity prevention strategies. Few functional neuroimaging studies have been done in children and elderly. Furthermore, it is unknown how hunger state affects neural food cue reactivity in these groups, since this has not been examined consistently. We examined the effects of hunger state and age on the brain responses to low- and high calorie foods. On two mornings, 122 participants (17 children; 38 teens; 36 adults; 31 elderly) performed a food image viewing task while being scanned using fMRI, either fasted or sated. Hunger induced greater activation during high versus low calorie food image viewing than satiety in the bilateral dorsomedial (dmPFC) and in the right dorsolateral prefrontal cortex (dlPFC) across all age groups. There was no significant main effect of age group on high versus low calorie food image viewing and no interaction between age group and hunger state. The greater activation of the dlPFC across all age groups during high calorie food image viewing in a fasted state might reflect increased inhibitory control in response to these foods. This may underlie the ability to resist overconsumption of high calorie foods. Furthermore, increased medial prefrontal cortex activation during hunger might reflect increased reward value of high calorie foods, which declines with satiation. Further studies are needed to better understand these results. Notably, overweight and obese individuals should be included to examine whether these responses are altered by weight status across the life span.

The validity of wireless iButtons and thermistors for human skin temperature measurement.

Skin temperature is a fundamental variable in human thermo-physiology, and yet skin temperature measurement remains impractical in most free-living, exercise and clinical settings, using currently available hard-wired methods. The purpose of this study was to compare wireless iButtons and hard-wired thermistors for human skin temperature measurement. In the first of two investigations, iButtons and thermistors monitored temperature in a controlled water bath (range: 10-40 degrees C) and were referenced against a certified, mercury thermometer. In the second investigation, eight healthy males completed three randomized trials (ambient temperature = 10 degrees C, 20 degrees C and 30 degrees C) while both devices recorded skin temperature at rest (in low and high wind velocities) and during cycle-ergometry exercise. The results are as follows. Investigation 1: both devices displayed very high validity correlation with the reference thermometer (r > 0.999). Prior to correction, the mean bias was +0.121 degrees C for iButtons and +0.045 degrees C for thermistors. Upon calibration correction the mean bias for iButtons and thermistors was not significantly different from zero bias. Interestingly, a typical error of the estimate of iButtons (0.043 degrees C) was 1.5 times less than that of thermistors (0.062 degrees C), demonstrating iButtons' lower random error. Investigation 2: the offset between iButton and thermistor readings was generally consistent across conditions; however, thermistor responses gave readings that were always closer to ambient temperature than those given by iButtons, suggesting potential thermistor drift towards environmental conditions. Mean temperature differences between iButtons and thermistors during resting trials ranged from 0.261 degrees C to 1.356 degrees C. Mean temperature differences between iButtons and thermistors during exercise were 0.989 degrees C (ambient temperature = 10 degrees C), 0.415 degrees C (ambient temperature = 20 degrees C) and 0.318 degrees C (ambient temperature = 30 degrees C). Observed error estimates were within the acceptable limits for the skin temperature method comparison, with typical errors <0.3 degrees C, correlation coefficients >0.9 and CV <1% under all conditions. These findings indicate that wireless iButtons provide a valid alternative for human skin temperature measurement during laboratory and field investigations particularly when skin temperature measurement using other currently available methods may prove problematic.

Tubulins in the primate retina: evidence that xanthophylls may be endogenous ligands for the paclitaxel-binding site.

The xanthophylls-lutein, zeaxanthin, and meso-zeaxanthin (L&Z)-are found in the central region of the primate retina, which is called the macula lutea (yellow spot). How they are anchored there and what their function is has been debated for over 50 years. Here, we present evidence that they may be bound to the paclitaxel (Taxol) binding site of the beta-tubulin subunit of microtubules and that a major function may be to modulate the dynamic instability of microtubules in the macula. Also, we compare nucleic acid and amino acid sequences of tubulins that are in human brain with those we have isolated from human-retina and monkey-macula cDNA libraries. In so doing, we suggest that in primates, class I beta-tubulin consists of at least two subtypes (beta(Ia) and beta(Ib)). Alignment analysis of the sequences of the genes for beta(Ia) and beta(Ib) indicates that the corresponding mRNAs may have other functions in addition to that of coding for proteins. Furthermore, we show that there are at least five different types of beta-tubulin in the macula lutea of rhesus monkey.

Neurocirculatory consequences of intermittent asphyxia in humans.

We examined the neurocirculatory and ventilatory responses to intermittent asphyxia (arterial O(2) saturation = 79-85%, end-tidal PCO(2) =3-5 Torr above eupnea) in seven healthy humans during wakefulness. The intermittent asphyxia intervention consisted of 20-s asphyxic exposures alternating with 40-s periods of room-air breathing for a total of 20 min. Minute ventilation increased during the intermittent asphyxia period (14.2 +/- 2.0 l/min in the final 5 min of asphyxia vs. 7.5 +/- 0.4 l/min in baseline) but returned to the baseline level within 2 min after completion of the series of asphyxic exposures. Muscle sympathetic nerve activity increased progressively, reaching 175 +/- 12% of baseline in the final 5 min of the intervention. Unlike ventilation, sympathetic activity remained elevated for at least 20 min after removal of the chemical stimuli (150 +/- 10% of baseline in the last 5 min of the recovery period). Intermittent asphyxia caused a small, but statistically significant, increase in heart rate (64 +/- 4 beats/min in the final 5 min of asphyxia vs. 61 +/- 4 beats/min in baseline); however, this increase was not sustained after the return to room-air breathing. These data demonstrate that relatively short-term exposure to intermittent asphyxia causes sympathetic activation that persists after removal of the chemical stimuli. This carryover effect provides a potential mechanism whereby intermittent asphyxia during sleep could lead to chronic sympathetic activation in patients with sleep apnea syndrome.

An induced blood pressure rise does not alter upper airway resistance in sleeping humans.

Sleep apnea is associated with episodic increases in systemic blood pressure. We investigated whether transient increases in arterial pressure altered upper airway resistance and/or breathing pattern in nine sleeping humans (snorers and nonsnorers). A pressure-tipped catheter was placed below the base of the tongue, and flow was measured from a nose or face mask. During non-rapid-eye-movement sleep, we injected 40- to 200-microgram i.v. boluses of phenylephrine. Parasympathetic blockade was used if bradycardia was excessive. Mean arterial pressure (MAP) rose by 20 +/- 5 (mean +/- SD) mmHg (range 12-37 mmHg) within 12 s and remained elevated for 105 s. There were no significant changes in inspiratory or expiratory pharyngeal resistance (measured at peak flow, peak pressure, 0.2 l/s or by evaluating the dynamic pressure-flow relationship). At peak MAP, end-tidal CO2 pressure fell by 1.5 Torr and remained low for 20-25 s. At 26 s after peak MAP, tidal volume fell by 19%, consistent with hypocapnic ventilatory inhibition. We conclude that transient increases in MAP of a magnitude commonly observed during non-rapid-eye-movement sleep-disordered breathing do not increase upper airway resistance and, therefore, will not perpetuate subsequent obstructive events.

Ventilatory response to induced auditory arousals during NREM sleep.

Sleep state instability is a potential mechanism of central apnea/hypopnea during non-rapid eye movement (NREM) sleep. To investigate this postulate, we induced brief arousals by delivering transient (0.5 second) auditory stimuli during stable NREM sleep in eight normal subjects. Arousal was determined according to American Sleep Disorders Association (ASDA) criteria. A total of 96 trials were conducted; 59 resulted in cortical arousal and 37 did not result in arousal. In trials associated with arousal, minute ventilation (VE) increased from 5.1 +/- 1.24 minutes to 7.5 +/- 2.24 minutes on the first posttone breath (p = 0.001). However, no subsequent hypopnea or apnea occurred as VE decreased gradually to 4.8 +/- 1.5 l/minute (p > 0.05) on the fifth posttone breath. Trials without arousal did not result in hyperpnea on the first breath nor subsequent hypopnea. We conclude that 1) auditory stimulation resulted in transient hyperpnea only if associated with cortical arousal; 2) hypopnea or apnea did not occur following arousal-induced hyperpnea in normal subjects; 3) interaction with fluctuating chemical stimuli or upper airway resistance may be required for arousals to cause sleep-disordered breathing.

Retinyl palmitate in macaque retina-retinal pigment epithelium-choroid: distribution and correlation with age and vitamin E.

Retinyl palmitate (RP) and retinyl stearate (RS) are of central importance in the visual cycle because they are the major storage molecules for retinol. In some tissues (e.g. liver) the amount of vitamin A (mostly in the form of retinyl ester) is positively correlated with both the amount of alpha-tocopherol (alpha-T) and age. Furthermore, alpha-T is a noncompetitive inhibitor of the hydrolysis of RP. We measured RP, RS, alpha-T and beta+gamma-tocopherol (beta+gamma-T) as functions of distance from the foveal center (eccentricity) in the retina-RPE-choroid (NRC) of rhesus monkeys using high-pressure liquid chromatography. It was found that the central and peripheral NRC differed with respect to these parameters. The concentration (pmoles sq mm-1) of RP was higher in the central NRC than in the peripheral NRC and was at a maximum in the region of the fovea. Furthermore, although in the peripheral NRC. RP was well correlated with age and alpha-T (similar to other tissues), in the central NRC, RP per sq mm was more clearly related to photoreceptor density. These differences imply that the central NRC controls the concentration of RP within it, while the concentration of RP in the peripheral NRC is determined by its environment (e.g. nutrients available from blood) and the age of the individual.

Is beta-carotene an antioxidant?

An hypothesis is presented that is opposed to the conventional viewpoint that beta-carotene is an in vivo free-radical scavenger. It is suggested that there are biochemical reasons why beta-carotene, other carotenoids, and especially their metabolites may be harmful to mammalian systems. Finally, the hypothesis that the macular pigment carotenoids, lutein and zeaxanthin, are free-radical scavengers is challenged.

A retrospective clinical study of resin-bonded cingulum rest seats.

PURPOSE: The purpose of this study was to evaluate the success of the resin-bonded cingulum rest seats (RBCRS) supporting removable partial dentures. MATERIALS AND METHODS: Twenty-six patients who had been treated with RBCRSs were recalled and examined. RESULTS: None of the patients who had RBCRSs placed on their teeth experienced debonding, and none of the teeth showed clinically significant signs of wear to the rest seats. CONCLUSIONS: The use of RBCRSs to support removable partial dentures is a highly successful method of treatment.

Neurocirculatory consequences of abrupt change in sleep state in humans.

The arterial pressure elevations that accompany sleep apneas may be caused by chemoreflex stimulation, negative intrathoracic pressure, and/or arousal. To assess the neurocirculatory effects of arousal alone, we applied graded auditory stimuli during non-rapid-eye-movement (NREM) sleep in eight healthy humans. We measured muscle sympathetic nerve activity (intraneural microelectrodes), electroencephalogram (EEG; C4/A1 and O1/A2), arterial pressure (photoelectric plethysmography), heart rate (electrocardiogram), and stroke volume (impedance cardiography). Auditory stimuli caused abrupt increases in systolic and diastolic pressures (21 +/- 2 and 15 +/- 1 mmHg) and heart rate (11 +/- 2 beats/min). Cardiac output decreased (-10%). Stimuli that produced EEG evidence of arousal evoked one to two large bursts of sympathetic activity (316 +/- 46% of baseline amplitude). Stimuli that did not alter EEG frequency produced smaller but consistent pressor responses even though no sympathetic activation was observed. We conclude that arousal from NREM sleep evokes a pressor response caused by increased peripheral vascular resistance. Increased sympathetic outflow to skeletal muscle may contribute to, but is not required for, this vasoconstriction. The neurocirculatory effects of arousal may augment those caused by asphyxia during episodes of sleep-disordered breathing.

Vitamin E, retinyl palmitate, and protein in rhesus monkey retina and retinal pigment epithelium-choroid.

PURPOSE: To measure the amounts of vitamin E, retinyl palmitate, and protein in the primate retina and its supporting tissues-the retinal pigment epithelium and choroid. To compare the amounts and concentrations of these materials in the central retina with those in the peripheral retina and to compare the concentration of vitamin E in the retina with that in plasma. Finally, to compare these results in rhesus monkey with existing measurements in humans. METHODS: Ocular tissues from rhesus monkeys (Macaca mulatta) were extracted with a two-phase solvent system. Components in the extract were separated by reverse-phase high-pressure liquid chromatography. Two detectors in series monitored the effluent: Vitamin E was quantified with an internal standard and fluorescence detection, whereas retinyl palmitate was quantified with an external standard and ultraviolet light detection. RESULTS: Amounts of vitamin E, retinyl palmitate, and protein in tissues from rhesus monkey compared reasonably well with those reported for humans. The content of vitamin E in the peripheral neural retina was moderately correlated with its protein content and, to a greater extent, with the concentration of vitamin E in the plasma; however, the content of vitamin E in the central neural retina correlated only with the amount of protein in the central neural retina. CONCLUSIONS: These results are consistent with rhesus monkey as a model for the use of vitamin E by human ocular tissues. The amount of vitamin E in the central neural retina appears to be more closely regulated than the amount of vitamin E in the peripheral neural retina.

Radial distribution of tocopherols in rhesus monkey retina and retinal pigment epithelium-choroid.

PURPOSE: To map vitamin E as a function of distance from the foveal center in the primate retina and retinal pigment epithelium (RPE)-choroid. METHODS: Eyecups from rhesus monkeys were dissected with circular trephines so that the innermost disc, centered on the fovea, was in the center of a series of concentric rings. Two different types of dissection were performed. For one type, the authors used circular trephines with diameters of 1, 4, 8, and 10 mm (1,4-D), whereas for the other type the diameters were 2, 5, 8, and sometimes 10 mm (2,5-D). When possible, the neural retina was separated from the RPE-choroid. Tissues were analyzed for vitamin E, retinyl palmitate, and protein. RESULTS: Surface area, volume, and protein were used as indexes of the amount of tissue analyzed. Distributions of vitamin E in neural retina were dependent on the tissue metric used and type of dissection performed. However, regardless of the tissue metric used, the central 1-mm disc of the 1,4-D was, on average, higher in vitamin E content than was the central 2-mm disc of the 2,5-D. This was particularly true when volume was the tissue metric. From the average values of vitamin E in a series of concentric discs, a composite plot of the vitamin E concentration in the neural retina was generated that took into consideration both types of dissection. That plot displayed a local maximum in the fovea and then precipitously declined to a minimum in the region between 0.5 and 1.0 mm eccentricity (near the foveal crest); at greater eccentricities, the vitamin E concentration rose to a value similar to that in the fovea, i.e., the composite plot indicated that vitamin E has a V-shaped distribution in the central neural retina. Vitamin E distribution in the RPE-choroid, with surface area as the tissue metric, also was measured. For this tissue, the foveal region displayed a local maximum. CONCLUSIONS: By combining the results of two different types of dissection, the authors found that in the neural retina, vitamin E displayed a minimum near the foveal crest. This minimum correlated anatomically with the site at which areolar (geographic) atrophy frequently occurs in retinal pigment epithelial cells in the human disease, age-related macular degeneration.

Combined hypoxia and hypercapnia evokes long-lasting sympathetic activation in humans.

We studied ventilatory and neurocirculatory responses to combined hypoxia (arterial O2 saturation 80%) and hypercapnia (end-tidal CO2 + 5 Torr) in awake humans. This asphyxic stimulus produced a substantial increase in minute ventilation (6.9 +/- 0.4 to 20.0 +/- 1.5 l/min) that promptly subsided on return to room air breathing. During asphyxia, muscle sympathetic nerve activity (intraneural microelectrodes) increased to 220 +/- 28% of the room air baseline. Approximately two-thirds of this sympathetic activation persisted after return to room air breathing for the duration of our measurements (20 min in 8 subjects, 1 h in 2 subjects). In contrast, neither ventilation nor sympathetic outflow changed during time control experiments. A 20-min exposure to hyperoxic hypercapnia also caused a sustained increase in sympathetic activity, but, unlike the aftereffect of asphyxia, this effect was short lived and coincident with continued hyperpnea. In summary, relatively brief periods of asphyxic stimulation cause substantial increases in sympathetic vasomotor outflow that outlast the chemical stimuli. These findings provide a potential explanation for the chronically elevated sympathetic nervous system activity that accompanies sleep apnea syndrome.

A technique for making an esthetic maxillary complete denture surgical stent.

A technique for making an esthetic complete denture as a surgical stent to be used in conjunction with hydroxyapatite augmentation surgery of the maxillary arch is presented. The technique involves the use of an articulator, a remount jig, and duplication of a surgically prepared cast.

The transmandibular implant: prosthodontic treatment considerations.

The transmandibular implant (TMI) is a type of transosteal implant designed for use in the edentulous mandible. The implant is composed of a gold-based alloy. The TMI is a loaded implant in that the prosthesis is supported by the implant. A transitional type of prosthesis, for insertion following surgery can be made either by altering the patient's existing mandibular complete denture or by making a new denture. The completed prosthesis is retained by clips held in the mandibular denture with autopolymerizing acrylic resin. The clips engage Dolder bar segments, which are a part of the implant suprastructure, and provide the necessary retention for the mandibular complete denture.

Ocular toxicity of low-molecular-weight components of silicone and fluorosilicone oils.

Silicone oil (SiO) and fluorosilicone oil (FSiO) are injected into the vitreous cavity in difficult cases of retinal detachment surgery. SiO and FSiO contain linear and cyclic low-molecular-weight components (LMWC) that are thought to cause ocular toxicity. Using the purified oils (without LMWC) and some of the individual LMWC, the authors evaluated the relation of the LMWC to the short-term ocular toxicity of the oils. When octamethylcyclotetrasiloxane or other single small species of linear and cyclic LMWC of SiO were injected into the rabbit anterior chamber, severe inflammation and corneal edema were induced. The ocular responses to the single species of the LMWC of SiO decreased with an increase of the molecular weights. Cyclic LMWC of FSiO (a mixture of trimethyl-3,3,3-trifluoropropylcyclotrisiloxane and tetramethyl-3,3,3-trifluoropropylcyclotetrasiloxane) also induced inflammation and corneal edema. However, unpurified SiO and FSiO, as well as purified oils (via solvent fractionation), did not cause significant adverse ocular response, presumably because the amounts of LMWC (especially the smallest species) in the oils were relatively small. Using gas chromatography, the authors analyzed SiO and FSiO recovered from rabbit and human vitreous cavities up to 2 yr after injection. In most of the cases, the concentrations of LMWC in SiO decreased after injection. This is consistent with the possibility that LMWC diffused from the oils into the ocular tissues. The long-term effect of LMWC in intraocular SiO and FSiO has not been determined. However, diffusion of LMWC into ocular tissues may relate to the chronic ocular toxicity of the oils.

Analysis of strength and endurance in fast twitch skeletal muscle after an acute in vitro exposure to an anabolic steroid.

Forty extensor digitorum longus (EDL) muscles from adult rats were used in an in vitro experiment to determine the effects of an anabolic steroid on strength and endurance. Experimental muscles, exposed to a 1 x 10(-3) M testosterone propionate, were compared in strength and endurance to control muscles. Multivariate repeated measures analyses of variance and covariance, and univariate pooled variance t-tests showed the control muscles to be significantly (alpha less than or equal to 0.025) stronger and more durable than the steroid exposed muscles. The results failed to support the notion that steroids enhance contractile strength and endurance in skeletal muscle. It is speculated that steroids may block important mechanisms of muscle contraction, resulting in a decrease in force production.