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S Doré

Publications and source records attributed to S Doré.

35 records · Page 2Linked to original sources
PubMed1997

Experimental correlation-based identification of X-ray CT point spread function. Part 1: Method and experimental results.

Knowledge of the point spread function (PSF) of an imaging system is important when studying the characteristics of the blur present in the images. Published experimental PSF identification techniques adapt classical one-dimensional linear system identification strategies using impulse, step function or periodic input signals. This study proposes and successfully applies a correlation method based on the Wiener-Hopf equation to identify the PSF of a CT scanner. The input consists of a series of pseudorandomly located holes. Results are found to be statistically equivalent to those obtained with the impulse method at a 90% two-sided confidence interval. Like the impulse method, it readily yields two-dimensional estimate, but the larger input circumvents the major objection to the use of a wire input. Furthermore, it is relatively immune to output noise, offering an advantage over edge methods. This resistance to noise may prove helpful for nuclear medicine imaging techniques, for which the signal-to-noise ratio is much lower than that X-ray for CT.

Electricity↗
PubMed1997

Experimental correlation-based identification of X-ray CT point spread function. Part 2: Simulation and design of input signal.

The preferred signals for non-parametric correlation-based point spread function identification are white noise or pseudo-random binary sequences (PRBSs). Given the difficulty of building a phantom based on either of these signals, a new input is devised that corresponds to pseudo-randomly located holes. The positions of the holes correspond to zeros in a 2-D PRBS. To optimise the design of the phantom and to ensure proper imaging procedure, a number of simulations are conducted. The effects of the following parameters on identification quality are investigated: the size of the holes and their minimum separation, the period of the PRBS, input-output translational and rotational mis-registration, pixel size and the presence of cupping. The factors affecting identification quality the most are rotational alignment, hole size and separation, as well as sequence length. During simulations, a point spread function offering characteristics similar to the Philips Tomoscan CX is identified. Optimal results are obtained when the signal consists of 0.6 mm holes, separated by 0.9 mm, whose position is based on a 32 x 32 PRBS generated with a ten-stage shift-register. When adequate rotational alignment is provided, it is shown that the pseudo-randomly located holes signal is a good substitute for a purely white signal when identifying the PSF of a CT scanner.

Humans↗
PubMed1997

Rediscovering an old friend, IGF-I: potential use in the treatment of neurodegenerative diseases.

Insulin-like growth factor-I (IGF-I) is a pleiotropic protein that acts on many tissues and organs. As it is one of the major trophic factors in the circulation, its actions in peripheral tissues are well established. It has been used for the treatment of several diseases, including growth deficiency, osteoporosis, catabolic disorders and diabetes. Recent evidence supports the significance of IGF-I in the maintenance of the integrity and homeostasis of the nervous system. The widespread distribution of its receptor allows IGF-I to affect the survival of numerous populations of neurones and glial cells in both the CNS and the PNS. Most recently, a clinical trial has revealed the beneficial effects of IGF-I in amyotrophic lateral-sclerosis (ALS), a degenerative disease of the motoneurones. We review briefly here experimental and clinical information that suggests the potential usefulness of IGF-I in the treatment of certain neurodegenerative diseases, including ALS, Alzheimer's disease, various neuropathies and brain trauma. The rather unique propensity of IGF-I to act on a variety of neuronal cells might provide a general means of reducing or slowing down neuronal losses that occur following various brain insults.

Humans↗
PubMed1997

Presence and differential internalization of two distinct insulin-like growth factor receptors in rat hippocampal neurons.

The pharmacological characteristics, localization and process of internalization of the insulin-like growth factor I and II receptors were studied in rat primary hippocampal cultured neurons grown under serum-free conditions. [125I]insulin-like growth factor-I binding was specific with an apparent affinity (Kd) of 0.1 nM and IC50 values of 0.1, 2.9 and 99.7 nM for insulin-like growth factor-I, insulin-like growth factor-II and insulin, respectively. The competition by insulin suggests the presence of genuine insulin-like growth factor-I receptors and not insulin-like growth factor binding proteins. In contrast, [125I]insulin-like growth factor-II binding showed a Kd of 0.1 nM and IC50 values of 0.2 and 20.5 nM for insulin-like growth factor-II and insulin-like growth factor-I while insulin was inactive, a well established characteristic of the insulin-like growth factor-II receptor. Using emulsion autoradiography, specific binding sites for [125I]insulin-like growth factor-I and -II were over the whole cultured neurons. The use of selective insulin-like growth factor-I and -II receptor antibodies further confirmed the existence of these receptors in rat hippocampal cultured neurons. To investigate the respective internalization profile of [125I]insulin-like growth factor-I and [125I]insulin-like growth factor-II receptor-ligand complexes in neurons, a technique of acid stripping was used. The apparent rate of endocytosis was found to be greater for the insulin-like growth factor-II than for the insulin-like growth factor-I receptor complexes. The internalization of [125I]insulin-like growth factor-I and [125I]insulin-like growth factor-II ligand-receptor complexes was confirmed using phenylarsine oxide which significantly blocked both internalization processes. In order to eliminate possible receptor recycling, monensin was used and shown to have no effect on the internalization of either ligand. Since the insulin-like growth factor-I receptor is coupled to tyrosine kinase activity, tyrphostin 47, a specific tyrosine kinase inhibitor. was used and shown to decrease [125I]insulin-like growth factor-I but not the [125I]insulin-like growth factor-II receptor internalization profile. Accordingly, insulin-like growth factor-I is apparently internalized mostly via the insulin-like growth factor-I tyrosine kinase type receptor, while insulin-like growth factor-II is not. The insulin-like growth factor-II receptor ligand complex is likely internalized via a pathway possibly related to mannose-phosphorylated residues as the insulin-like growth factor-II/mannose-6-phosphate receptor has been implicated in the intracellular targeting of lysosomal proteins containing glycosylated residues. Taken together, our results indicate that primary hippocampal cultured neurons represent a unique model for investigating the differential role and intracellular trafficking of both insulin-like growth factor-I and insulin-like growth factor-II receptor ligand complexes and their relevance to the respective functional role of these two-related trophic factors in the central nervous system.

Animals↗
PubMed1997

Distribution and levels of [125I]IGF-I, [125I]IGF-II and [125I]insulin receptor binding sites in the hippocampus of aged memory-unimpaired and -impaired rats.

The insulin-like growth factors (IGF-I and IGF-II) and insulin are localized within distinct brain regions and their respective functions are mediated by specific membrane receptors. High densities of binding sites for these growth factors are discretely and differentially distributed throughout the brain, with prominent levels localized to the hippocampal formation. IGFs and insulin, in addition to their growth promoting actions, are considered to play important roles in the development and maintenance of normal cell functions throughout life. We compared the anatomical distribution and levels of IGF and insulin receptors in young (five month) and aged (25 month) memory-impaired and memory-unimpaired male Long Evans rats as determined in the Morris water maze task in order to determine if alterations in IGF and insulin activity may be related to the emergence of cognitive deficits in the aged memory-impaired rat. In the hippocampus, [125I]IGF-I receptors are concentrated primarily in the dentate gyrus (DG) and the CA3 sub-field while high amounts of [125I]IGF-II binding sites are localized to the pyramidal cell layer, and the granular cell layer of the DG. [125I]insulin binding sites are mostly found in the molecular layer of the DG and the CA1 sub-field. No significant differences were found in [125I]IGF-I. [125I]IGF-II or [125I]insulin binding levels in any regions or laminae of the hippocampus of young vs aged rats. and deficits in cognitive performance did not relate to altered levels of these receptors in aged memory-impaired vs aged memory-unimpaired rats. Other regions. including various cortical areas, were also examined and failed to reveal any significant differences between the three groups studied. It thus appears that IGF-I, IGF-II and insulin receptor sites are not markedly altered during the normal ageing process in the Long Evans rat, in spite of significant learning deficits in a sub-group (memory-impaired) of aged animals. Hence. recently reported changes in IGF-I receptor messenger RNA levels in aged memory-impaired rats are apparently not reflected at the level of the translated protein.

Aging↗
PubMed1997

Systemic administration of kainic acid induces selective time dependent decrease in [125I]insulin-like growth factor I, [125I]insulin-like growth factor II and [125I]insulin receptor binding sites in adult rat hippocampal formation.

Administration of kainic acid evokes acute seizure in hippocampal pathways that results in a complex sequence of functional and structural alterations resembling human temporal lobe epilepsy. The structural alterations induced by kainic acid include selective loss of neurones in CA1-CA3 subfields and the hilar region of the dentate gyrus followed by sprouting and permanent reorganization of the synaptic connections of the mossy fibre pathways. Although the neuronal degeneration and process of reactive synaptogenesis have been extensively studied, at present little is known about means to prevent pathological conditions leading to kainate-induced cell death. In the present study, to address the role of insulin-like growth factors I and II, and insulin in neuronal survival as well as synaptic reorganization following kainate-induced seizure, the time course alterations of the corresponding receptors were evaluated. Additionally, using histological preparations, the temporal profile of neuronal degeneration and hypertrophy of resident astroglial cells were also studied. [125I]Insulin-like growth factor I binding was found to be decreased transiently in almost all regions of the hippocampal formation at 12 h following treatment with kainic acid. The dentate hilar region however, exhibited protracted decreases in [125I]insulin-like growth factor I receptor sites throughout (i.e. 30 days) the study. [125I]Insulin-like growth factor II receptor binding sites in the hippocampal formation were found to be differentially altered following systemic administration of kainic acid. A significant decrease in [125I]insulin-like growth factor II receptor sites was observed in CA1 subfield and the pyramidal cell layer of the Ammon's horn at all time points studied whereas the hilar region and the stratum radiatum did not exhibit alteration at any time. A kainate-induced decrease in [125I]insulin receptor binding was noted at all time points in the molecular layer of the dentate gyrus whereas binding in CA1-CA3 subfields and discrete layers of the Ammon's horn was found to be affected only after 12 h of treatment. These results, when analysed with reference to the observed histological changes and established neurotrophic/protective roles of insulin-like growth factors and insulin, suggest possible involvement of these growth factors in the cascade of neurotrophic events that is associated with the reorganization of the hippocampal formation observed following kainate-induced seizures.

Animals↗
PubMed1996

Prostaglandin E2 up-regulates insulin-like growth factor binding protein-3 expression and synthesis in human articular chondrocytes by a c-AMP-independent pathway: role of calcium and protein kinase A and C.

Insulin-like growth factor-1, IGF-1, is believed to be an important anabolic modulator of cartilage metabolism and its bioactivity and bioavailability is regulated, in part, by IGF-1 binding protein 3 (IGFBP-3). Prostaglandin E2 (PGE2) stimulates IGF-1 production by articular chondrocytes and we determined whether the eicosanoid could regulate IGFBP-3 and, as such, act as a modifier of IGF-1 action at a different level. Using human articular chondrocytes in high density primary culture, Western and Western ligand blotting to measure secreted IGFBP-3 protein, and Northern analysis to monitor IGFBP-3 mRNA levels, we demonstrated that PGE2 provoked a 3.9 +/- 1.1 (n = 3) fold increase in IGFBP-3 mRNA and protein. This effect was reversed by the Ca++ channel blockers, verapamil and nifedipine, and the Ca++/calmodulin inhibitor, W-7. The Ca+2 ionophore, ionomycin, mimicked the effects of PGE2 as did the phorbol ester PMA, which activates Ca++/-phospholipid-dependent protein kinase C (PKC). Cyclic AMP mimetics, such as forskolin, IBMX, Ro-20-1724, and Sp-cAMP, inhibited the expression and synthesis of the binding protein. PGE2 did not increase the levels of cAMP or protein kinase A (PKA) activity in chondrocytes. The PGE2 secretagogue, IL-1 beta, down-regulated control levels of IGFBP-3 which could be completely abrogated by pre-incubation with the tyrosine kinase inhibitor, erbstatin, and partially reversed (50 +/- 8%) by KT-5720, a PKA inhibitor. These observations suggested that PGE2 does not mediate the effect of its secretagogue and that IL-1 beta signalling in chondrocytes may involve multiple kinases of diverse substrate specificities. Dexamethasone down-regulated control, constitutive levels of IGFBP-3 mRNA and protein eliminating the previously demonstrated possibility of cross-talk between glucocorticoid receptor (GR) and PGE2 receptor signalling pathways. Taken together, our results suggest that PGE2 modulates IGFBP-3 expression, protein synthesis, and secretion, and that such regulation may modify human chondrocyte responsiveness to IGF-1 and influence cartilage metabolism.

Calcium↗
PubMed1996

Prostaglandin E2 stimulates incorporation of proline into collagenase digestible proteins in human articular chondrocytes: identification of an effector autocrine loop involving insulin-like growth factor I.

Prostaglandin E2 (PGE2) stimulates collagen gene promoter activity in transfected human chondrocytes though no canonical cyclic AMP (cAMP) response element has been yet identified. Human insulin-like growth factor-1 (IGF-1) induces an increase in collagen type II expression and synthesis in chondrocytes. Since our preliminary data suggested that PGE2 can stimulate IGF-1 release from human articular chondrocytes, we examined whether the eicosanoid could influence collagen synthesis and whether the effect was mediated by IGF-1. Incubation of primary cultures of human articular chondrocytes with increasing concentrations of PGE2 resulted in a dose-dependent (ANOVA, F= 51.62, P < 0.0001, n = 5) and saturable increase in the synthesis and release of IGF-1 and expression of IGF-1 mRNA. At relatively low concentrations (30 pmol/1 to 30 nmol/l), PGE2 stimulated an increase in the incorporation of [3H]proline into collagenase digestible protein (CDP) (P < 0.01, n = 5) whereas at high levels (300 nmol/l to 3 micromol/l) of the eicosanoid, incorporation diminished precipitously. Human IGF-1 mimicked the effects of low PGE2 concentrations by stimulating in a dose-dependent (ANOVA, F= 31.65, P < 0.001, n = 3) and saturable fashion the incorporation of [3H]proline into CDP although the magnitude of the response induced by IGF-1 was far greater (3.5-fold). An IGF-1 receptor blocking antibody completely abrogated the IGF-1 induced response suggesting that the effect was specifically IGF-1 receptor mediated. Furthermore, the PGE2-induced increase in [3H]proline incorporation into CDP was inhibited (63%, P < 0.001, n = 7) by the addition to the culture medium of an anti-IGF-1 antibody. We conclude that PGE2 may act as a secretagogue of IGF-1 and that the latter growth factor may mediate, via an autocrine loop and the IGF-1 receptor, at least some of the anabolic effects of the eicosanoid on cartilage metabolism.

Adult↗
PubMed1996

Distribution and levels of insulin-like growth factor (IGF-I and IGF-II) and insulin receptor binding sites in the spinal cords of amyotrophic lateral sclerosis (ALS) patients.

The structurally related peptides, insulin and insulin-like growth factors (IGF-I and IGF-II), have neurotrophic properties and potentially could be of therapeutic value in human neurodegenerative disorders. In this study, we compared the anatomical distribution of [125I]IGF-I, [125I]IGF-II and [125I]insulin binding sites in thoracic spinal cords from patients who died of amyotrophic lateral sclerosis (ALS) and normal controls. For these three ligands, the greatest amounts of specific binding were located in the deeper layers of the dorsal horn > intermediate zone > lamina X > ventral horn > superficial layers of the dorsal horn > white matter of the spinal cord. Highly significant (P < 0.001) increases in the density of [125I]IGF-I and [125I]IGF-II binding were apparent in various laminae of the cord of ALS patients with increased binding being particularly evident in the ventral horn and the intermediate zone. Significant (P < 0.05) increases were also seen in lamina X and in the dorsal horn. In contrast, no significant differences in [125I]insulin binding were observed between ALS and control spinal cords. Taken together, these data reveal significant increases in both [125I]IGF-I and [125I]IGF-II binding levels in the spinal cords of ALS patients albeit to different extents. These findings may be of relevance for future therapeutic strategies aimed at slowing the progression of this chronic neurodegenerative disease, as recently suggested by the beneficial therapeutic effects of an IGF-I treatment in ALS patients.

Aged↗
PubMed1996

IGF and IGF-binding protein system in the synovial fluid of osteoarthritic and rheumatoid arthritic patients.

Various arthritic disorders result from a disruption of the equilibrium between the synthesis and degradation of tissue matrix macromolecules. Growth factors, particularly insulin-like growth factor-I (IGF-I), are believed to play an important role in maintaining this equilibrium. In this study, we determined the levels of IGF-I, IGF-II, and characterized and measured the amount of IGF-binding proteins (IGFBPs) in the synovial fluid (SF) of osteoarthritis (OA), rheumatoid arthritis (RA) patients and normal individuals. Furthermore, we characterized the IGFBP found in these SFs. The levels of IGF-I, IGF-II and IGFBP-3 were determined by specific radioimmunoassays (RIAs). IGFBP identification and measurement were carried out using the Western ligand blot (WLB) technique, and characterization performed by Western immunoblot. IGFBP-3 proteolysis was analyzed by autoradiography after incubation of SF with radiolabeled IGFBP-3. Results showed a statistically significant increase (P < 0.001) in the IGF-I level in arthritic SF vs normal controls; 75 +/- 11 ng/ml and 82 +/- 11 ng/ml were recorded for RA (N = 8) and OA (N = 10), respectively, whilst normal controls (N = 9) were at 19 +/- 7 ng/ml. No difference in the level of IGF-II was recorded between the three groups studied. Human SF demonstrated the presence of IGFBP-1, -2, -3 and -4, but not that of IGFBP-5 and -6. The level of IGFBP-3 tested either by WLB or RIA was significantly higher (P < 0.001) in RA and OA patients. Moreover, a statistical and positive correlation between the levels of IGF-I and IGFBP-3 was noted. WLB analysis indicated that the amount of IGFBP-1 did not vary among the groups. The levels of IGFBP-2 and -4 were significantly increased (P < 0.02) solely in the RA SF. Further experiments demonstrated that a limited IGFBP-3 proteolysis occurred in human SF. Moreover, the ratio of total IGF over total bioactive IGFBPs was lower in RA (P < 0.05), and to a lesser extent in OA than normal specimens. This study showed the presence of four IGFBPs (1 4) in human SF for which the IGFBP-2, -3 and -4 were enhanced in arthritic fluid. Importantly, although proteolysis occurred in the SF, an increased amount of bioactive IGFBPs were present in arthritic SF, which may affect the bioavailability of IGF-I within the articular tissues.

Aged↗
PubMed1995

Increased insulin-like growth factor 1 production by human osteoarthritic chondrocytes is not dependent on growth hormone action.

OBJECTIVE: To investigate insulin-like growth factor 1 (IGF-1) production in normal and osteoarthritis (OA) chondrocytes and to further examine the role of growth hormone (GH) in adult human cartilage and, in particular, in diseased tissue. METHODS: IGF-1 production was measured with a radioimmunoassay. Binding assay, Northern blot, and reverse transcriptase polymerase chain reaction (RT-PCR) techniques were used for GH receptor (GHR) detection. The biological response to GH was estimated via IGF-1 production. RESULTS: We observed that basal levels of IGF-1 production were significantly higher in OA chondrocytes than in normal cells (P < 0.005). Adult human chondrocytes, however, were unresponsive to GH stimulation with regard to IGF-1 production, as shown in dose-response (0-1,000 ng/ml) and time-course (days 1-8) studies. In addition, no specific 125I-GH binding was detected in either cell type. Northern blot analysis revealed a 5.5-kb GHR messenger RNA (mRNA) species, but semiquantitative RT-PCR revealed no difference in GHR mRNA expression by normal and OA chondrocytes. CONCLUSION: This study indicates that the elevated synthesis of IGF-1 by adult human OA chondrocytes occurs through a GH/GHR-independent mechanism, suggesting that other factors are capable of controlling local IGF-1 production in these cells.

Aged↗
PubMed1995

Effects of exercise during normoxia and hypoxia on the growth hormone-insulin-like growth factor I axis.

The response of plasma insulin-like growth factor I (IGF I) to exercise-induced increase of total human growth hormone concentration [hGHtot] and of its molecular species [hGH20kD] was investigated up to 48 h after an 1-h ergometer exercise at 60% of maximal capacity during normoxia (N) and hypoxia (H) (inspiratory partial pressure of oxygen = 92 mmHg (12.7 kPa); n = 8). Lactate and glucose concentrations were differently affected during both conditions showing higher levels under H. Despite similar maximal concentrations, the increase of human growth hormone (hGH) was faster during exercise during H than during N[hGHtot after 30 min: 8.6 (SD 11.4) ng.ml-1 (N); 16.2 (SD 11.6) ng.ml-1 (H); P < 0.05]. The variations in plasma [hGH20kD] were closely correlated to those of [hGHtot], but its absolute concentration did not exceed 3% of the [hGHtot]. Plasma IGF I concentration was significantly decreased 24 h after both experimental conditions [N from 319 (SD 71) ng.ml-1 to 228 (SD 72) ng.ml-1, P < 0.05; H from 253 (SD 47) to 200 (SD 47) ng.ml-1, P < 0.01], and was still lower than basal levels 48 h after exercise during H [204 (SD 44) ng.ml-1, P < 0.01]. Linear regression analysis yielded no significant correlation between increase in plasma [hGHtot] or [hGH20kD] during exercise and the plasma IGF I concentration after exercise. It was concluded that the exercise-associated elevated plasma [hGH] did not increase the hepatic IGF I production. From our study it would seem that the high energy demand during and after the long-lasting intensive exercise may have overridden an existing hGH stimulus on plasma IGH I, which was most obvious during hypoxia.

Adult↗
PubMed1994

Human osteoarthritic chondrocytes possess an increased number of insulin-like growth factor 1 binding sites but are unresponsive to its stimulation. Possible role of IGF-1-binding proteins.

OBJECTIVE: To characterize the insulin-like growth factor 1 (IGF-1) receptor in human osteoarthritic (OA) and normal adult chondrocytes. The biologic response of chondrocytes to IGF-1 stimulation was examined, as was the presence and synthesis of IGF binding proteins (IGFBP) in these cells. METHODS: Binding studies, Northern blot, immunohistochemical analysis, and affinity cross-linking experiments were performed for characterization of the IGF receptor, and the latter method was also used for IGFBP determination. The biologic response was estimated via the incorporation of radiolabeled proline into a newly synthesized protein. RESULTS: Binding experiments revealed a single class of binding sites. The mean +/- SEM affinity (Kd) of normal chondrocytes was 1.4 +/- 0.4 nM, with 26.8 +/- 5.5 x 10(3) binding sites/cell. OA chondrocytes had a lower affinity (Kd 15.4 +/- 4.7 nM) and a higher density (1,178.3 +/- 299.5 x 10(3) binding sites/cell) compared with normal cells (P < 0.004 and P < 0.001, respectively). Immunohistochemical studies with a monoclonal antibody (MAb) against the type 1 IGF receptor (alpha IR3) showed increased staining in OA cartilage compared with normal tissue. Biologic responses of chondrocytes after IGF-1 stimulation revealed that OA chondrocytes were unresponsive, whereas a 2.5-fold increase in new protein synthesis was observed in normal cells. Competition studies in normal chondrocytes revealed that both IGF-1 and IGF-2 displaced radiolabeled IGF-1 in a comparable manner; however, insulin at high concentration weakly competes. Moreover, MAb alpha IR3 effectively blocked specific binding in normal chondrocytes (77%), but not in OA chondrocytes (26%). Northern blot and covalent cross-linking analyses revealed the specific band characteristic of type 1 receptor. With the latter technique, other bands corresponding to the IGFBPs were also detected. Comparison between normal and OA chondrocytes showed increased intensity of the IGFBP bands, particularly those corresponding to the IGFBP-3 doublet. CONCLUSION: It is shown that type 1 IGF receptor is expressed in human articular cartilage and that the level of binding sites is significantly increased in OA chondrocytes. Interestingly, despite the higher level of binding sites in OA cells, no response to IGF-1 stimulation was found in these cells. Our data suggest that this increase in specific binding may involve not only the type 1 IGF receptor but also IGFBP on the cell surface. The latter, by binding the IGF-1, will diminish the bioavailability of IGF-1 and thus prevent its anabolic action.

Adult↗
PubMed1991

Contribution of hGH20K variant to blood hGH response in sauna and exercise.

Exercise-induced increases in blood somatotropin (hGH) have always been considered in terms of quantity of the circulating molecules. Knowing that the hypophysis can release several GH species, we investigated the differential release in blood of total hGH (hGHT) and the main hGH variant (hGH20K) molecules in six trained male swimmers exposed to three different conditions known to favor GH release in blood: 45 min--70% maximum oxygen uptake (VO2max) bicycling and swimming, and 20 min of sauna bathing. Based on the binding specificity of hGH antibodies, hGH20K was isolated then assayed using the Nichols immunoradiometric assay system. All three experimental conditions produced significant (P less than 0.001) elevations in blood hGHT and hGH20K. In all three cases, mean blood hGH20K contribution to blood hGHT was relatively constant (11.9, SE 0.7%). Rises in rectal temperature were not statistically related to the changes in blood hGHT. This demonstration of a relatively constant elevation in hGH20K during bicycling, swimming, and sauna bathing can hardly explain the large differences in blood hGHT responses reported in literature under similar conditions.

Adult↗
PubMed1991

HGH20k species and variability of GH responses to long-duration exercise in male cyclists fed different food supplements.

Exercise studies dealing with hGH have always considered this hormone as a unique molecular entity. We postulated that the well-known variability in blood total hGH response could possibly be explained, at least in part, by concomitant changes in blood hGH20k levels, variant form possibly expressing some of the hGH anti-insulinic properties. Six male trained cyclists were imposed a 2-hr long ergocycle exercise. Food supplements were given prior to and/or during exertion to exacerbate a possible contribution from hGH20k to total hGH variability by modification of substrate availability. Both blood total hGH and hGH20k levels increased with exercise, the largest increases being observed in absence of supplementation. Large variability of responses were observed in both blood total hGH and hGH20k levels, the latter variant contributing minimally to total blood hGH response (4.3 +/- 0.8%), and being closely associated with the main species (r = 0.90; p less than 0.001). It was concluded that variations associated with hGH20k increases observed in response to prolonged exercise cannot explain the large intra-and inter-individual variability measured in blood total hGH response.

Adult↗
PubMed1990

[Development of fetal semiology in North America].

A survey of the emergence of fetal semiology in the 17 editions of the Williams' Textbook of Obstetrics used by North-American medical students since 1900 was carried out. Three periods were identified: 1906-1950: the fetus, seen as a part of its mother, is ignored until birth and is of no interest to the obstetricians. From the fifties', the decrease in maternal mortality and progress in physiology and therapeutics permitted to study the fetus and a greater attention given to the care of the sick newborn. Since 1970, the availability of ultrasonography has contributed in making the fetus the second patient for obstetricians. It is now possible to study its growth, integrity, health, and well-being. Furthermore, the fetus is now accessible to establish a prenatal diagnosis.

Embryonic and Fetal Development↗