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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism for the transfer of fat-soluble vitamin D3 from the avascular basal cellular layers of the epidermis to dermal capillaries and peripheral circulation is unknown, although vitamin D-binding protein (DBP) is thought to mediate this process. To evaluate the effect of increased occupancy of vitamin D carrier(s) on vitamin D3 removal from the skin, serial serum vitamin D2 and D3 concentrations were determined in three groups of six healthy volunteers given combinations of an oral dose of vitamin D2 (50,000 IU) and a fixed dose of UVB radiation (27 mJ/cm2). Serum vitamin D3 levels increased significantly following UVB (time effect, P < .01 by ANOVA), but the response remained unchanged after pretreatment with vitamin D2, increasing from 3 +/- 1 to 14 +/- 5 ng/mL (mean +/- SEM), versus UVB alone, 5 +/- 1 to 16 +/- 5 ng/mL. Elevation of serum vitamin D2 levels was also similar in the groups given vitamin D2 alone (< 1 to 64 +/- 8 ng/mL) and vitamin D2 + UVB (< 1 to 45 +/- 8 ng/mL). There was no time or treatment effect for changes in serum levels of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, or (DBP) levels (P > .1). We conclude that vitamin D3 egress from the skin is not affected by elevated circulating vitamin D concentrations; thus, the cutaneous release of vitamin D is probably mediated by a protein such as DBP with a high carrying capacity for the vitamin.
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PMID:Elevation of blood vitamin D2 levels does not impede the release of vitamin D3 from the skin. 133 3

Oxytocin infusions were initiated on day 10 of the oestrous cycle in ewes, and luteal regression was induced by injection of 100 micrograms cloprostenol on day 12. Blood samples were collected at frequent intervals via an indwelling jugular vein cannula to measure concentrations of progesterone and luteinizing hormone (LH) during the luteal and follicular phases in saline (n = 6) and oxytocin (n = 5) infused animals. The oxytocin infusion maintained peripheral plasma concentrations of 53 +/- 3.2 pg oxytocin ml-1 (mean +/- SEM) compared with values of about 1 pg ml-1 during oestrus in control ewes. Oxytocin infusion had no effect on luteal phase progesterone concentrations, the timing of luteolysis, basal luteinizing hormone (LH) secretion, LH pulse frequency, or the timing or height of the LH surge. Treated ewes came into oestrus significantly earlier than controls (P < 0.05) but ovulated normally. Uterine samples collected 96 h after cloprostenol injection (approximately day 2 of the cycle) showed that oxytocin receptor concentrations were significantly higher in the endometrium in ewes that had been given a 5 day oxytocin infusion than in control animals (556 and 262 fmol mg-1 protein, respectively: geometric means from ANOVA, P < 0.001), whereas myometrial receptor concentrations were not affected (113 and 162 fmol mg-1 protein, respectively). We conclude that the previously reported delay in luteal development caused by oxytocin infusion (Wathes et al., 1991) is not due to the inhibition or delay of ovulation, but must instead occur via a direct influence on the developing corpus luteum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of oxytocin infusion on secretion of progesterone and luteinizing hormone and the concentration of uterine oxytocin receptors during the periovulatory period in cloprostenol-treated ewes. 133 45

Postnatal thermogenesis in sheep is associated with increased sympathoadrenal activities, a T3 surge and an enhanced brown adipose tissue (BAT) type II 5'-monodeiodinating (5'-MDI) activity. The latter peaks 3-4 days after birth and is known to be important in generating intracellular T3 for nuclear receptor binding. In order to further investigate the mechanism(s) responsible for neonatal thermogenesis, thyroid hormone nuclear receptor (T3NR) binding characteristics were quantified in lamb BAT from newborn (NB) to 30d of postnatal age. Maximal binding capacities (MBC, mean +/- SEM fmoles T3/mg DNA) in BAT showed a decrease as studied by ANOVA during the first 11 days (NB to 1d, 148 +/- 24 [N = 5, p < 0.01, cf. 3-5d group]; 3-5 d, 61 +/- 5.5 [N = 5]; 10-11d, 72 +/- 9.1 [N = 4]). Afterwards, MBC increased at 30d (196 +/- 32, N = 4, p less than 0.01, cf. 3-5d group). BAT T3NR binding affinities (10(9) M-1) were comparable in all age groups studied (NB-1d, 2.8 +/- 0.3; 3-5d, 3.4 +/- 0.3; 10-11d, 4.0 +/- 1.1; 30d, 2.4 +/- 0.4). The data suggest that the postnatal surge in T3 and type II 5'-MDI is accompanied with a concurrent decrease in MBC of BAT T3NR. The latter may represent a down-regulation of T3NR presumably in an attempt to regulate the overall effect of thyroid hormone in neonatal thermogenesis.
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PMID:Analysis of nuclear 3,3',5-triiodothyronine receptor in the brown adipose tissue (BAT) of the postnatal lamb. 142 12

The normal microvascular permeability of the ascending colon in horses and the microvascular permeability of that segment after ischemia and reperfusion were investigated. Microvascular permeability was estimated by the ratio of lymphatic protein to plasma protein concentration (Cl/Cp) at high lymph flow rates in 8 adult horses in 2 equal groups: normal and ischemic (2-hour period). Lymphatic flow rates and lymph and plasma protein concentrations were determined. Intestinal biopsy specimens were obtained at the end of each experiment. Flow independent values were selected and compared by one-way ANOVA, and the mean and SEM of these values were determined. The mean Cl/Cp ratios for the flow independent part of each data set were as follows: normal = 0.36 +/- 0.08; ischemic = 0.70 +/- 0.08. These groups were significantly different (P < or = 0.0001). Microscopic evaluation revealed mild congestion and edema in the normal group. The ischemic group had mild to moderate mucosal degeneration, with moderate to severe congestion and edema. We concluded that ischemia of the ascending colon, when followed by reperfusion, results in a significant increase in microvascular permeability.
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PMID:Microvascular permeability changes in ischemia/reperfusion injury in the ascending colon of horses. 142 57

Isolated rat hearts perfused with hyperosmotic Krebs-Henseleit buffer containing 60 mmol/L NaCl lose 10% of their tissue water. Perfusion of the rat hearts with Krebs-Henseleit buffer containing polyethylene glycol 8000 caused a concentration-dependent reduction in tissue water. In a study of the effect of different cryoprotectants on cardiac preservation, isolated rat hearts were flushed with a cardioplegic solution (CP-14), or CP-14 with either 50 mmol/L glycerol (CP-15), or 5% polyethylene glycol (CP-16) and frozen at -1.4 degrees C for 5 hours. Thawed hearts were reperfused in working mode to assess function. There was no recovery in CP-14 hearts. Hearts treated with CP-15 recovered 39.3% +/- 2.9% (mean +/- SEM) of control cardiac output. CP-16 boosted the recovery of cardiac output to 54.4% +/- 5.7% (p less than 0.05 vs CP-15). Glycerol significantly reduced tissue ice content; PEG further decreased the ice content to 31.7% +/- 0.6%, which was distinctively lower than that in CP-14 (44.7% +/- 1.1%) and in CP-15 hearts (34.6% +/- 1.1%). Tissue water content of CP-14 and CP-15 hearts was similar (3.83 and 3.87 gm H2O/gm dry weight). Polyethylene glycol reduced the tissue water content to 3.24 +/- 0.04 gm H2O/gm dry (p less than 0.01 vs CP-14 and CP-15 by ANOVA). Thus both glycerol and polyethylene glycol offered cryoprotection to the heart explant by reducing tissue ice formation. Polyethylene glycol was superior to glycerol by dehydrating myocardial tissue and further minimizing freezing damage.
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PMID:Freezing preservation of the mammalian heart explant. III. Tissue dehydration and cryoprotection by polyethylene glycol. 149 24

We tested the hypothesis that enhanced resting metabolic rate (RMR) in highly trained endurance athletes is an acute effect of prior exercise induced by catecholamines and not serum thyroxine. RMR and energy-regulating hormones were studied in nine highly trained women runners during habitual training (period I), and suspension of training (period II). Data were collected during the follicular phase of two consecutive menstrual cycles, confirmed by serum progesterone and estradiol. Subjects maintained training between the two periods. Total energy intake and diet composition, body weight, and oral temperature did not change from period I to period II (P greater than 0.05). With suspension of training, urinary epinephrine and nonrepinephrine excretion dropped (P less than 0.022) while serum TSH rose (P = 0.011) and free T4 did not change (P = 0.182). RMR (mean +/- SEM) was 274 +/- 6.2 and 252 +/- 7.8 kJ.h-1 for periods I and II, respectively, with repeated measures ANOVA indicating a drop in RMR occurred with cessation of exercise (P = 0.048). The augmentation of RMR by exercise lasted more than 15 h but less than 39 h post-exercise. The results suggest that the drop in catecholamines may partly explain the lower RMR following suspension of training.
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PMID:Effect of suspending exercise training on resting metabolic rate in women. 154 97

Alterations in arterial oxygen and carbon dioxide influence cerebrovascular resistance and therefore cerebral blood flow (CBF), but the magnitude of these CBF responses have not been well defined in normal humans. Duplex scanning (B-mode imaging and pulsed Doppler shift analysis) was used to measure internal carotid blood flow (ICBF) as an indicator of CBF in 20 normal subjects during alterations of arterial O2 and CO2. End-tidal PCO2 (PETCO2) was measured by mass spectrometry, arterial oxygen saturation by pulse oximetry, and unilateral (right) ICBF by duplex scanning. A variety of gas mixtures were administered to achieve hypoxemia (FIO2 = 0.075-0.10) and hypercapnia (FICO2 = 0.05) or the subject was asked to hyperventilate to PETCO2 = 16-24 mm Hg. The ICBF was determined five times in each of six conditions: (1) normoxia/normocapnia; (2) normoxia/hypercapnia; (3) normoxia/hypocapnia; (4) hypoxia/normocapnia; (5) hypoxia/hypercapnia; and (6) hypoxia/hypocapnia. During normoxia and normocapnia, the mean ICBF was 330 +/- 19 (SEM) mL/min. Specific CO2 reactivity was 7.4 +/- 0.7 mL/min/mmHg, which is equivalent to 2.3% +/- 0.1% of normocapnic blood flow per mm Hg change in CO2. During normocapnia, ICBF increased by 2.9 +/- 0.9 mL/min for each percentage decrease in oxygen saturation. Using an ANOVA with repeated measures to fit the responses, the following statistically significant relationship was found: ICBF (mL/min) = 333 + 6.3.(PETCO2 - 40) + 2.7 DSO2 +/- 81 where DSO2 is arterial desaturation (100 - arterial saturation). An additional "between subject" variation had a mean of 0 and a standard deviation of 82 mL/min. There was no statistically significant evidence of an interaction between O2 and CO2 response. Our data suggest that hypoxia and carbon dioxide changes will alter CBF simultaneously and additively. Duplex scanning of the internal carotid artery, which can be performed at the bedside, is sufficiently sensitive to detect changes in ICBF and internal carotid artery oxygen delivery.
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PMID:Human cerebrovascular response to oxygen and carbon dioxide as determined by internal carotid artery duplex scanning. 158 51

This study investigated whether pretreatment with glycopyrronium can attenuate the hypotension caused by anaesthesia of the elderly with propofol. Twenty elderly patients (77.1 +/- 2.44 years, mean +/- SEM) of ASA physical status 2 or 3 scheduled for elective urological procedures were given glycopyrronium 0 (n = 10) or 5 micrograms.kg-1 (n = 10) in a randomised, double-blind manner, 5 min before induction of anaesthesia with propofol infused at 600 ml.h-1 (average induction dose 1.7 +/- 0.06 mg.kg-1, mean +/- SEM) followed by maintenance with a propofol infusion at 10 mg.kg-1.h-1. Although glycopyrronium significantly increased heart rate (p less than 0.01, ANOVA), the decrease in blood pressure 2 and 5 min after induction was similar in both groups. The study had a power of 80% to detect a 20 mmHg difference in systolic arterial pressure between treatment groups with p less than 0.05.
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PMID:The effect of pre-induction glycopyrronium on the haemodynamic response of elderly patients to anaesthesia with propofol. 162 80

We investigated whether fatigue of the expiratory muscle, that is, the abdominal muscle, may account for a change in the respiratory effort sensation in normal subjects during expiratory threshold loading. The respiratory effort sensation was scored using a modified Borg scale. Expiratory muscle fatigue was assessed both from changes in the maximal static expiratory pressure and in the centroid frequency (fc) of the abdominal muscle electromyogram (EMG). Expiratory threshold loading (magnitude of threshold; 40 to 60% of the maximal expiratory pressure at FRC, breathing frequency = 15/min, and duty cycle = 0.5) was continued until exhaustion or for 30 min. Loading was repeated following a 15-min recovery period after the end of the first expiratory loading. The maximal static expiratory pressure during loading (Pmmax) decreased initially and then remained decreased. Decreases were smaller with the 40% load (22 +/- 6%, SEM) than with the 60% load (37 +/- 3%) (p less than 0.05). The decrease during the second run of the 60% load was greater than during the first (p less than 0.01 by ANOVA). The maximal expiratory pressure at TLC before the second run of the 60% load was decreased by 9 +/- 3% compared with the control (p less than 0.02) but that with the 40% load was not. The fc with the 60% load decreased initially by 8 +/- 1% and then remained constant, although no change was observed with the 40% load.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship of respiratory effort sensation to expiratory muscle fatigue during expiratory threshold loading. 173 58

A three-dimensional analysis to evaluate structural changes in cultured cardiac myocytes following adrenergic innervation was performed using stereological techniques formerly limited to cells in tissue and organs. Cell volumes were calculated for two groups of cells at 96 hours in culture: isolated myocytes and myocytes innervated with adrenergic neurons. Relative and absolute volumes of the nucleus, cytoplasm, and cell were quantified by systematically sampling sections throughout the cell and by point count sampling techniques. Volumetric estimates were similarly determined for the mitochondria, sarcomeres, and other cellular components in the cytoplasm. Data were analyzed with ANOVA and randomized block design to control for variation among the cultures. Adrenergic innervation produced a 44% increase in cell volume, X +/- SEM, (3,344 +/- 196 microns3 to 4,816 +/- 400 microns3, P = 0.007). The absolute volume of mitochondria significantly increased after innervation (521 +/- 42 microns3 to 744 +/- 54 microns3, P less than 0.01). Absolute sarcomere volume did not change significantly (750 +/- 92 microns3 to 642 +/- 1061 microns3, P = 0.14). Other cellular components, defined as all cytoplasmic components except mitochondria and sarcomeres, significantly increased with innervation (1,739 +/- 166 microns3 to 3,097 +/- 338 microns3, P = 0.02). The relative volume of the nucleus and the cytoplasm in the cell remained unchanged following innervation. However, the relative volume of mitochondria decreased by 6%, the percent of the cytoplasm occupied by the sarcomeres decreased by 44%, and the volume occupied by the other cellular components increased by 22%. These findings support the use of stereological analysis as a means to quantify cell volumes of cultured myocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Application of stereological analysis of cell volume to isolated myocytes in culture with and without adrenergic innervation. 174 21


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