bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Effects of Ciliary Neurotrophic Factor on the Hypothalamo‐Pituitary Gonadal Axis In Vitro in Female Rats
Authors: Stanley S. A. , Todd J. F. , Small C. J. , Kim M. S. , Heath M. M. , Anand P. , Ghatei M. A. , Bloom S. R. 
Published: March 2003

AbstractCiliary neurotrophic factor (CNTF) is a member of the neuropoietic family of cytokines. CNTF exerts its actions through activation of a receptor complex, which shows similarity of sequence, second messenger systems and distribution to the leptin receptor. Leptin has been demonstrated to exert profound effects on the hypothalamo‐pituitary gonadal axis. This study examines the in vitro effects of CNTF on hypothalamic luteinizing hormone releasing hormone release (LHRH) and pituitary luteinizing hormone (LH) release compared to those of leptin in the female. We report that CNTF stimulates LHRH release from medial basal hypothalamic explants harvested from proestrous female rats and this effect is of similar magnitude to that seen with leptin. In contrast, CNTF suppresses LHRH‐stimulated LH release from dispersed anterior pituitary cells harvested from proestrous female rats but has no effect on basal LH release. Leptin stimulates basal LH release but has no effect on LHRH‐stimulated LH release. The suppressive effect of CNTF on LHRH‐stimulated LH release has been confirmed in perifused anterior hemipituitaries. These results suggest a differential effect of CNTF on the hypothalamo‐pituitary gonadal axis and a possible role in the modulation of pituitary gonadal function.
Effect of Antisense Suppression of Transforming Growth Factor‐β3 Gene on Lactotropic Cell Proliferation
Authors: De A. , Hentges S. , Boyadjieva N. , Sarkar D. K. 
Published: March 2003

AbstractThe mechanism by which oestrogen regulates lactotropic cell proliferation is not well understood. Recently it has been shown that a transforming growth factor beta (TGF‐β) gene‐related peptide, TGF‐β3, is produced in the lactotropes and stimulates lactotropic cell proliferation in vitro. In this study, the role of this growth factor in oestrogen‐induced lactotropic cell proliferation was determined in vitro using oligonucleotide designed to inhibit TGF‐β3 gene expression. We used the oligonucleotide in an antisense orientation, which is complementary to regions in the TGF‐β3 message. Oligonucleotides in sense and missense orientation were also used. We found that the antisense sequence that was effectively incorporated into pituitary cells produced a marked inhibition of the stimulatory action of oestrogen on lactotropic cell proliferation. Sense and missense oligonucleotides produced no significant effects on oestrogen‐stimulated lactotropic cell proliferation. The growth‐inhibitory effect of antisense oligonucleotide was blocked by TGF‐β3 peptide. These results suggest that TGF‐β3 may be involved in the processes that mediate oestrogen‐regulated lactotropic cell proliferation.
Ghrelin Acts on Leptin‐Responsive Neurones in the Rat Arcuate Nucleus
Authors: Traebert M. , Riediger T. , Whitebread S. , Scharrer E. , Schmid H. A. 
Published: March 2003

AbstractLeptin decreases food intake and increases energy expenditure in rodents by inhibiting neurones in the hypothalamic arcuate nucleus. The growth hormone secretagogue (GHS) ghrelin is known to stimulate food intake and to be the endogenous ligand for the GHS‐receptor, which is strongly expressed in the arcuate nucleus, like the leptin receptor (Ob‐R). In this study, we analysed the effect of systemic ghrelin administration on Fos expression in the arcuate nucleus on neurones expressing Ob‐R. Injection of ghrelin (0.2 mg/kg, i.p) significantly increased the number of neurones expressing Fos protein in the ventromedial arcuate nucleus. Fifty‐seven percent of all Fos‐positive cells in the ventromedial arcuate nucleus were also positive for Ob‐R staining. Furthermore, we investigated electrophysiologically the effect of ghrelin and leptin on the activity of arcuate neurones in an in‐vitro slice preparation. Ghrelin stimulated the electrical activity dose‐dependently in 80% of all cells tested (n=49) with a threshold concentration of 10−11 M; only 8% were inhibited and 12% did not respond. The effect of ghrelin (10−7 M) was weakly antagonized by the peptidic GHS‐receptor antagonist (D‐Lys3)‐GHRP‐6 (10−4 M), which also showed a much weaker affinity (IC50, 0.9 × 10−6 M) to the GHS‐receptor than ghrelin (IC50, 0.3 × 10−9 M). Ghrelin increased the electrical activity in 76% of all cells which were inhibited by leptin (n=17). These data show that ghrelin interacts with the leptin hypothalamic network in the arcuate nucleus. The opposite effect of leptin and ghrelin on neurones in the arcuate nucleus may serve as a neurophysiological correlate of the orexigenic and anorectic effects of ghrelin and leptin.
In‐Vitro Study of the Effect of Adrenaline on the Functional Capacity of Human Neutrophils: Role During Exercise
Authors: Malpica M. I. , Rodríguez A. B. , Sáez M. C. , García J. J. , Barriga C. , Ortega E. 
Published: March 2003

AbstractWe studied the effect of adrenaline on the capacity of human neutrophils to attach, ingest and destroy Candida albicans. The neutrophils were incubated in vitro in the presence of an adrenaline concentration taken as basal (10−10 m), and another that is referred to as being reached following physical exercise (10−9 m). Two higher concentrations (10−7 m and 10−5 m), which are seldom attained in blood but which can occur at specific locations in the organism, were tested as having a possible pharmacological application. At the two high concentrations (10−7 m and 10−5 m), the capacity to attach, ingest and destroy C. albicans was greater than at the physiological concentrations (10−10 m and 10−9 m). Indeed, the capacity to attach and ingest C. albicans was significantly less after incubation with these physiological concentrations than the control values (incubation in the absence of adrenaline). Hence, high concentrations of adrenaline seem to enhance neutrophils' phagocytic capacity compared to physiological plasma concentrations, whereas small variations such as those caused by physical exercise have no effect on this functional capacity.
Nutritional Regulation of Hypothalamic Leptin Receptor Gene Expression is Defective in Diet‐Induced Obesity
Authors: Sahu A. , Nguyen L. , O'Doherty R. M. 
Published: March 2003

AbstractLeptin action in the hypothalamus plays a critical role in maintaining normal food intake and body weight. Hyperleptinaemia is associated with obesity in humans and animal models, suggesting a state of leptin resistance. Although the mechanism of leptin resistance is not clearly understood, alterations in leptin receptor (Ob‐R) gene expression have been proposed as a potential mechanism mediating modifications in leptin action in obesity and during changes in nutritional status (fed/fasted). The current study examined the effects of diet‐induced obesity (DIO) made by feeding rats a high fat diet for 9 weeks, and nutritional status on levels of long form (Ob‐Rb) and total (Ob‐Rtot) Ob‐R mRNA expression in the hypothalamus. In the fed state, hypothalamic Ob‐Rb mRNA and Ob‐Rtot mRNA levels were similar in DIO and control standard chow fed rats (SC) despite hyperleptinaemia in DIO rats. However, although an overnight fast moderately increased hypothalamic Ob‐Rb mRNA levels in SC rats, fasting did not increase Ob‐Rb mRNA levels in DIO rats. To address the possibility that elevated leptin concentration in DIO rats may mediate an alteration in OB‐R mRNA levels, we examined the effects of adenovirus‐mediated hyperleptinaemia on Ob‐R gene expression in SC rats. Despite substantially elevated plasma and cerebrospinal fluid concentrations of leptin, hypothalamic Ob‐R mRNA levels were similar in both groups. In conclusion, the current study demonstrates that DIO is associated with a loss of nutritional regulation of hypothalamic Ob‐R mRNA levels, and that hyperleptinaemia is not sufficient to alter Ob‐R mRNA expression.
Central Cholecystokinin‐Octapeptide Accelerates the Activity of the Hypothalamic Gonadotropin‐Releasing Hormone Pulse Generator in Goats
Authors: Ichimaru T. , Matsuyama S. , Ohkura S. , Mori Y. , Okamura H. 
Published: March 2003

AbstractTo clarify central actions of cholecystokinin‐octapeptide (CCK‐8) on reproduction, effects of an intracerebroventricular (i.c.v.) administration of CCK‐8 on the activity of the gonadotropin‐releasing hormone (GnRH) pulse generator were examined in ovariectomized (OVX) goats in the absence or presence of oestradiol. Goats were chronically fitted with recording electrodes in the mediobasal hypothalamus, and electrophysiological manifestations of the GnRH pulse generator were monitored as characteristic increases in the multiple‐unit activity (MUA volleys). In OVX goats, a bolus i.c.v. injection of as little as 0.01 nmol of CCK‐8 induced a MUA volley with a short latency, which resulted in a significant decrease in the post‐treatment volley interval compared to that in the saline injected control. Administration of higher doses of CCK‐8 (0.1 and 2 nmol) did not further accelerate the occurrence of the MUA volley, but stimulatory effects were observed for a longer period than that after the 0.01 nmol injection. When goats were treated with oestradiol, while a bolus i.c.v. injection of 0.01 nmol CCK‐8 had no effect, an injection of 0.1 nmol of the peptide significantly decreased the post‐treatment volley interval. On continuous i.c.v. infusion of CCK‐8 at 3 nmol per 200 µl/h for 3 h, MUA volleys with shorter intervals than those in the control were successively induced without any apparent change in basal plasma luteinizing hormone levels in OVX goats. These results demonstrate that central CCK‐8 strongly accelerates the activity of the GnRH pulse generator in goats.
Inducible Nitric Oxide Synthase is Responsible for Nitric Oxide Release from Murine Pituicytes
Authors: Kjeldsen T. H. , Rivier C. , Lee S. , Hansen E. W. , Christensen J. D. , Moesby L. 
Published: March 2003

AbstractThis study investigated whether pituicytes were able to produce and release nitric oxide (NO), and which type of nitric oxide synthase (NOS) would be responsible for this phenomenon. Lipopolysaccharide (LPS) 1 µg/ml was used as inflammatory mediator. Because pituicytes are known to secrete interleukin (IL)‐6 upon stimulation with LPS, this parameter was also investigated. Cultured pituicytes, from 4‐week‐old male mice, were stimulated with LPS for 6 h or 24 h. At 24 h, there was a significant increase in accumulated nitrite indicating NO formation. In contrast, IL‐6 release was already significantly higher 6 h after stimulation and further increased at 24 h. The correlation between accumulated nitrite and secreted IL‐6 was 0.84 after 24 h of incubation with LPS. The expression of inducible NOS (iNOS) mRNA in the pituicytes was significantly higher than the control level after 6 h and 24 h of exposure to LPS, with levels at 6 h being significantly higher than those at 24 h. There was no detected expression of endothelial NOS or neuronal NOS mRNA. Cultured pituicytes were also subjected to immunocytochemistry for iNOS protein at 6, 12, and 24 h after stimulation with LPS. Most cells were positive for iNOS, but there were no observable differences with the time points that we used. Collectively, these results show that pituicytes are able to produce NO, and that the inducible form of NOS is responsible for this production. Furthermore, there is a weak correlation between NO and IL‐6 released from pituicytes after 24 h of stimulation with LPS.
Growth Hormone‐Releasing Hormone‐Producing and Dopaminergic Neurones in the Mouse Arcuate Nucleus Are Independently Regulated Populations
Authors: Phelps C. J. , Romero M. I. , Hurley D. L. 
Published: March 2003

AbstractDifferentiation of hypophysiotropic neurones that regulate the secretion of growth hormone (GH) and prolactin is influenced by GH and prolactin. Genetic GH and prolactin deficiency in mutant rodent models such as the Ames dwarf (df/df) mouse results in an increase in the number of GH‐stimulatory GH‐releasing hormone (GHRH) neurones and a reduction of prolactin‐inhibitory tuberoinfundibular dopaminergic (TIDA) neurones in the arcuate nucleus during postnatal development. The present study tested the hypothesis that these concomitant changes in numbers of tyrosine hydroxylase (TH)‐ and GHRH‐immunoreactive neurones in df/df hypothalamus might represent a neuronal population of fixed number that undergoes a partial change in phenotype during postnatal development. To evaluate this possibility, the postnatal reduction of the df/df TIDA population was prevented by administering prolactin neonatally to preserve TH phenotype; dwarf and normal sibling mice were treated with daily injections of ovine prolactin or vehicle starting at postnatal day 12 and continuing for 30 days. Following this treatment, numbers of arcuate neurones containing GHRH or TH, or both, were quantified using immunocytochemistry. It was hypothesized that prolactin preservation of TH‐immunoreactive cell number would be accompanied by either a decrease in the GHRH‐producing population or an increase in numbers of cells producing both TH and GHRH. In prolactin‐treated normal (DF/df) mice, numbers of arcuate TH‐immunoreactive neurones were similar to those in vehicle‐treated normals. Numbers of TH‐positive neurones in prolactin‐treated dwarfs were higher than in vehicle‐treated dwarfs, and did not differ from numbers in DF/df. Numbers of GHRH‐immunoreactive cells in vehicle‐treated df/df were higher than in vehicle‐treated DF/df, and were not different in prolactin‐treated groups of either dwarf or normal mice. Neurones containing both TH and GHRH constituted 15% of the TH population, and 76% of the GHRH population, in control normal mice; in control dwarfs, double‐labelled cells were 9.3% of TH and 9.9% of GHRH. Numbers of cells immunoreactive for both TH and GHRH were not affected by prolactin treatment in either mouse type. These results demonstrate that the increase in number of GHRH‐expressing neurones in the df/df arcuate nucleus does not occur at the expense of the TH phenotype, and that this increase is not influenced by prolactin feedback. Although coexpression of TH and GHRH in a subpopulation indicates that TIDA and GHRH populations are not exclusive, they appear to be influenced independently by prolactin and GH signals during development.
NFκB Activation in Mouse Pituitary: Comparison of Response to Interleukin‐1β and Lipopolysaccharide
Authors: Parnet P. , Pousset F. , Laye S. 
Published: March 2003

AbstractThe mouse anterior pituitary contains both types of interleukin (IL)‐1 receptors, IL‐1 receptor type I (IL‐1RI) and IL‐1 receptor type II (IL‐1RII). These receptors are expressed mainly on somatotroph cells. In the present study, the ability of the mouse pituitary to respond in vivo to IL‐1 or to lipopolysaccharide (LPS) was demonstrated by measuring, with an electrophoretic mobility shift assay, the presence of an active NFκB complex in cell nuclei from pituitaries of mice injected intraperitoneally with recombinant rat‐IL‐1β or LPS. Using immunohistochemistry with an antibody directed against the p65 NFκB subunit, a rapid and transient NFκB response to LPS was observed. This response was present predominantly in the nuclei of glial fibrillary acidic protein (GFAP)‐positive cells and F4/80‐labelled cells of the posterior and the anterior pituitary 15 min after stimulation and became faint after 2 h. In comparison, the early and strong NFκB response to IL‐1β treatment was localized into somatotroph cells, GFAP positive cells and F4/80‐labelled cells of the posterior and anterior pituitary. Activation of NFκB in response to IL‐1β was no longer apparent in IL‐1RI knockout mice, confirming that this receptor is essential for the transduction of IL‐1 signal in the pituitary, but remained after LPS treatment. In addition, we investigated the effect of IL‐1 on target genes by measuring the mRNA and proteins synthesis of growth hormone (GH), IL‐6 and IL‐1ra in the pituitary and the plasma. IL‐1β was shown to induce a rapid and strong synthesis of IL‐6 and IL‐1ra in the pituitary but failed to regulate GH contents or release. These data suggest that the pituitary is able to respond to a systemic infection via cytokine‐mediated responses transduced by IL‐1.
The relationship between sleep apnoea, bruxism, and the time it took the patient to seek for treatment in TMD patients
Authors: KOBAYASHI Y. , SHIGA H. 
Published: March 2003

It has been suggested that the length of time from the onset of symptoms to the time the patients seek treatment and sleep disorders has a large effect on the treatment of TMD, especially in conservative treatment. In this experiment the relationship between the time it took patients to seek treatment and bruxism and sleep disorders was clarified.Twenty female TMD patients (13 arthrogenous, 7 myogenous) in their twenties were selected. The length of time it took for the patients to seek for treatment was determined from the questionnaire. Using a wireless telemeter system, the EEG, FOG, ECG, masseter EMG, mental EMG, and respirogram of subjects were recorded throughout night and the frequency of bruxism and sleep apnoea was calculated. Bruxism was defined as those burst groups associated with muscular activities that lasted more than 5 s or had more than two bursts within 5 s. The relationship among the length of time needed to seek for treatment, frequency of bruxism and sleep apnoea was investigated.Both the frequency of bruxism and sleep apnoea increased when the length of time it took for the patient to seek treatment was long (bruxism: r=0·650, apnoea: r=0·655, P < 0·01). The frequency of sleep apnoea increased as the frequency of bruxism increased (r=0·495, P < 0·05). From these results it was suggested that there was a direct correlation among the three factors, the length of time it took to seek for treatment, frequency of bruxism and frequency of sleep apnoea. and when taking natural history it was imperative to pay more attention.
The effect of change of oral sensory input accordance with the experimental occlusal interference on electroencephalogram
Authors: MUSHIMOTO E. , TANAKA H. , ICHIKAWA D. 
Published: March 2003

The aim of this study is to clarify the effect of the change of oral sensory input on brain function and to confirm whether it can be detected electroencephalographically.Eight healthy dentate dental students were selected as subjects, and asked to wear the experimental occlusal interference on the right second molar for 1 week. Simultaneous recordings were made with electromyograms (EMG) and electroencephalogram (EEG) before and after maximum clenching. Evaluation by visual analogue scale (VAS) questionnaires was also done. Twelve‐session experiments were carried out over a period of 12 days. Daily changes of EMG activity of masticatory muscle, six comfort parameters (VAS), and EEG caused by premature contact were analysed statistically applying repeated measured anova and Tukey–Kramer analysis.The discomfort which was described by VAS did not disappear during the interference period. Just after applying the interference, EMG activity during clenching was decreased significantly (P < 0·01) compared with control. Significant change in EEGs between before and after clenching were observed, that is, the percentage power fraction of β wave (%β) tends to increase. On the contrary, %α in EEGs after clenching decreased significantly (P < 0·01) compared with before clenching during the interference period, as verified by VAS evaluation.In conclusion, it is suggested that the decrease of %α in EEGs after clenching may be caused by premature contact influence on the masticatory system, reflected in the presence of discomfort during occlusion, and somatosensor information from the occlusal sensation might be recognized in the higher centre of the brain, and the possibility of detecting change might be indicated electroencephalographically.
The efficacy of occlusal appliance therapy in patients with temporomandibular disorders of mainly myogenous pain. A randomized controlled trial in a short‐term perspective
Authors: EKBERG E. , NILNER M. , VALLON D. 
Published: March 2003

Aim:  In a randomized controlled trial investigate the short‐term effect of treatment with stabilization appliance compared with a control appliance in patients with temporomandibular disorders (TMD) of mainly myogenous pain.Material and methods:  Out of 926 referrals to the Department of Stomatognathic Physiology in Malmö for treatment of TMD during 2 years, 338 patients were clinically screened for possible participation in the study. Patients with mainly myogenous pain were selected from the original group of 926 patients. Sixty TMD patients with mainly myogenous pain were allocated at random into two equally sized groups: (T) treatment group given a stabilization appliance; (C) control group given a control appliance. The study was performed as a randomized controlled trial and comprised four visits. At the last visit, after 10 weeks of treatment with occlusal appliance, the treatment outcome was evaluated.Results:  There was a significant reduction of changes in overall severity of pain, reported pain during mandibular movements and reduction of changes in severity of headache in the treatment group compared with the control group. There was also a significant decreased number of tender masticatory muscles in the treatment group compared with the control group.Conclusion:  The results of this short‐term evaluation suggest that the stabilization appliance is effective in the alleviation of symptoms and signs in TMD patients of mainly myogenous pain. The stabilization appliance can therefore be recommended for TMD patients of mainly myogenous pain.
Prediction of sleep‐disordered breathing by unattended overnight oximetry
Authors: OLSON L. G. , AMBROGETTI A. , GYULAY S. G. 
Published: March 2003

SummaryBetween January 1994 and July 1997, 793 patients suspected of having sleep‐disordered breathing had unattended overnight oximetry in their homes followed by laboratory polysomnography. From the oximetry data we extracted cumulative percentage time at SaO2 < 90% (CT90) and a saturation variability index (ΔIndex, the sum of the differences between successive readings divided by the number of readings – 1). CT90 was weakly correlated with polysomnographic apnea/hypopnea index (AHI), (Spearman 𝓅=0.36, P< 0.0001) and with ΔIndex (𝓅=0.71, P< 0.0001). ΔIndex was more closely correlated with AHI (𝓅=0.59, P< 0.0001). In a multivariate model, only ΔIndex was significantly related to AHI, the relationship being AHI=18.8 ΔIndex +7.7. The 95% CI for the coefficient were 16.2, 21.4, and for the constant were 5.8, 9.7. The sensitivity of a ΔIndex cut‐off of 0.4 for the detection of AHI≥15 was 88%, for detection of AHI≥20 was 90% and for the detection of AHI≥25 was 91%. The specificity of ΔIndex ≥0.4 for AHI≥15 was 40%. In 113 further patients, oximetry was performed simultaneously with laboratory polysomnography. Under these circumstances ΔIndex was more closely correlated with AHI (𝓅=0.74, P< 0.0001), as was CT90 (𝓅=0.58, P< 0.0001). Sensitivity of ΔIndex ≥0.4 for detection of AHI≥15 was not improved at 88%, but specificity was better at 70%. We concluded that oximetry using a saturation variability index is sensitive but nonspecific for the detection of obstructive sleep apnea, and that few false negative but a significant proportion of false positive results arise from night‐to‐night variability.