bluuebunny/crossref_metadata_2025_split huggingface dataset:
Localization of the Endogenous Benzodiazepine Receptor Ligand Octadecaneuropeptide and Peripheral Type Benzodiazepine Receptors in the Rat Pituitary
Authors: Tong Yiai , Tonont Marie‐Christine , Désy Louise , Nicolast Pierre , Vaudryt Hubert , Pelletier Georges 
Published: January 2007

AbstractAn association of octadecaneuropeptide, an endogenous ligand at the benzodiazepine receptor, with the peripheral type benzodiazepine receptor has been reported in brain as well as a few peripheral tissues. In order to verify whether or not such an association occurs in the rat pituitary gland, we have proceeded to the immunocytochemical localization of octadecaneuropeptide as well as the autoradiographic localization of peripheral type benzodiazepine receptors in rat pituitary, octadecaneuropeptide immunoreactive material was found in high concentrations in the posterior lobe, whereas only a very few cells were labelled in the intermediate lobe. The anterior lobe did not show any specific staining. Immunoelectron microscopy revealed that in the posterior lobe labelling was restricted to pituicytes. Autoradiographic studies demonstrated a strong and uniform labelling in the posterior lobe after incubation with [3H] PK11195, a ligand selective for peripheral type benzodiazepine receptors. In the intermediate lobe, the autoradiographic reaction was restricted to a narrow band adjacent to the hypophysial cleft. No labelling was detected in the anterior lobe. These results demonstrate a close association between octadecaneuropeptide and peripheral type benzodiazepine receptors in the intermediate and posterior lobes of the rat pituitary gland.
The Effect of an Osmotic Stimulus on the Release of Neurohypophysial Hormones in the Cat: Preferential Release of Vasopressin with a Possible Involvement of the Area Postrema
Authors: Bissett G. W. , Chowdreyt H. S. , Feldberg W. 
Published: January 2007

AbstractIn cats anaesthetized with intravenous chloralose, the injection of 0.05 to 0.4 ml 1.54 M NaCl solution (hypertonic saline, HS) into a lateral cerebral ventricle caused a large release of vasopressin. The concentration of vasopressin greatly exceeded that of oxytocin in the same samples of plasma.Vasopressin was also released when HS was injected into the fourth ventricle and into the cisterna magna from which there is no access in the cat to the ventricles, but it was less effective by these routes than when injected into a lateral ventricle in the same cat. This suggests a possible action of HS on circumventricular organs related to the third ventricle but also indicates an additional site of action reached from the subarachnoid space which would give access to the ventral and dorsal surfaces of the brainstem.Vasopressin was not released on topical application of HS to the ‘nicotine sensitive area’ on the ventral surface of the brainstem where nicotine acts to release vasopressin without oxytocin.Vasopressin, however, was released without detectable oxytocin on topical appliction of HS to the dorsal surface of the brainstem either outside the fourth ventricle or to the floor of the ventricle at its distal extremity, in the region of the obex.A possible site where HS acts to cause a preferential release of vasopressin on injection into a lateral ventricle is the area postrema, a circumventricular organ which impinges on the walls of the fourth ventricle at the obex. Preferential release of vasopressin might then be mediated by a selective neural input, possibly through the nucleus of the tractus solitarius, from osmoreceptors in the area postrema to the vasopressin‐secreting cells in the supraoptic and paraventricular nuclei.
Galanin Interacts with Serotonin in Stimulating Prolactin Secretion in the Rat
Authors: Koshiyama Hiroyuki , Shimatsu Akira , Assadian Hossein , Hattori Naoki , Ishikawa Yasuhiro , Tanoh Tsutomu , Yanaihara Noboru , Kato Yuzuru , Imura Hiroo 
Published: January 2007

AbstractThe interaction of galanin (GAL) with serotonin (5‐HT) in the regulation of prolactin (PAL) secretion was investigated in urethaneanesthetized male rats. Intracerebroventricular administration of 5‐HT (1 and 10 μ g) and GAL (1 μ g) caused an increase in plasma PRL levels, but co‐administration of GAL did not show any additive effect on 5‐HT‐induced PRL secretion. Pretreatment with methysergide (0.25 mg/kg), a nonselective 5‐HT1 and 5‐HT2 receptor antagonist, partially inhibited the PRL increase induced by GAL. On the other hand, neither ketanserin (0.25 mg/kg), a selective 5‐HT2 receptor antagonist, nor ICS 205–930 (0.25 mg/kg), a selective 5‐HT3 receptor blocker, had any effect on GAL‐induced increase in PRL secretion. Parachlorophenylalanine (300 mg/kg), a 5‐HT synthesis inhibitor, however, caused a marked enhancement of PRL release induced by GAL, which was partially inhibited by a 5‐HT neurotoxin, 5, 6‐dihydroxytryptamine. Parachlorophenylalanine also caused a potentiation of 5‐HT‐induced PRL release, possibly by sensitizing 5‐HT receptors. These findings suggest that 5‐HT receptors are, at least partly, involved in GAL‐induced PRL release in the rat.
Gamma‐Aminobutyric Acid Modulation of Corticotrophin‐Releasing Factor‐41 Secretion from the Rat Hypothalamus in vitro
Authors: Tsagarakis S. , Rees L. H. , Besser G. M. , Grossman A. 
Published: January 2007

AbstractThere is increasing evidence for a centrally mediated inhibitory effect of the amino‐acid neurotransmitter y‐aminobutyric acid (GABA) on the hypothalamo‐pituitary‐adrenal axis. In the present study, the direct effect of GABA in modulating the release of the 41‐residue corticotrophin‐releasing factor (CRF‐41), the major CRF identified so far, was investigated in acute hypothalamic explants by utilizing previously validated incubation and assay techniques. While GABA (10‐7’to 10‐5 M) had no effect on basal CRF‐41 release (P > 0.05), it significantly suppressed K ‐ (28 mM)‐stimulated release in a dose‐dependent manner (P < 0.01). A similar inhibitory effect was observed with the GABA agonist muscimol (10‐7 to 10‐5 M). Noradrenaline (10‐6 M) ‐induced CRF‐41 release was also significantly inhibited by GABA 10‐6 M. The inhibitory effect of GABA on K+‐stimulated CRF‐41 secretion was completely. reversed by the GABA antagonists bicuculline and picrotoxin (10‐6 to 10‐5 M) in a dose‐dependent fashion. Both bicuculline and picrotoxin stimulated basal and K+ (28 mM)‐stimulated CRF‐41 release, indicating the presence of tonic inhibition by endogenous GABA in the basal state. Finally, GABA 10‐5 M was able to significantly inhibit the stimulated release of CRF‐41 from the isolated median eminence.In summary, the present data provide strong evidence that GABA‐induced inhibition of the hypothalamo‐pituitary‐adrenal axis is mediated, at least in part, through an inhibitory action on CRF‐41 secretion. It is likely that these GABA receptors are located directly on CRF‐41 neurons, probably on nerve terminals in the median eminence.
Influence of Ovarian Steroids on the Ultrastructural Plasticity of the Adult Rat Supraoptic Nucleus Induced by Central Administration of Oxytocin
Authors: Montagnese Catherine , Poulain Dominique A. , Theodosis Dionysia T. 
Published: January 2007

AbstractIn earlier studies, we showed that continuous intracerebroventricular infusion of oxytocin, for several days, into the third ventricle of normally hydrated, non‐lactating adult female rats significantly reduced glial coverage of magnocellular oxytocinergic neurons in the hypothalamus. It also induced synaptic remodelling whereby many oxytocinergic neurons became synaptically contacted by the same presynaptic terminals (shared synapses). Such changes were closely similar to those observed in the oxytocinergic system when it is physiologically activated, as during parturition and lactation.We now report that central oxytocin does not act alone to modify the ultrastructure of the magnocellular nuclei, but requires the concomitant action of sex steroids. Intracerebroventricular infusion of oxytocin was effective in inducing neuronal‐glial and synaptic changes only in supraoptic nuclei of female rats undergoing a prolonged diestrus, or in castrated female rats treated during the infusion period with daily intramuscular injections of progesterone for 4 days followed by 17β‐estradiol for 2 days. Infusion of oxytocin in rats with regular estrous cycles, or in castrated rats treated with progesterone or estrogen alone had no effect on the ultrastructure of the nucleus. Our observations also indicate that the action of oxytocin on the anatomy of its own neurons is very specific: only 4‐threonine‐oxytocin, a closely related oxytocin analogue, had an effect similar to that of oxytocin; vasopressin, 4‐threonine‐7‐glycine oxytocin and cholecystokinin left the magnocellular nuclei structurally unaltered.
Ontogeny of Diabetes Insipidus in the Brattleboro Rat: Morphological and Physiological Correlates
Authors: Pow D. V. , Morris J. F. 
Published: January 2007

AbstractThe homozygous Brattleboro rat is a mutant of the Long Evans rat which fails to produce assayable quantities of vasopressin. Somata of supraoptic magnocellular neurons from adult Brattleboro rats are hypertrophied relative to those from normally hydrated adult Long Evans rats. We have investigated, by light microscopic morphometric analysis of immunoperoxidase‐labelled vibratome sections, the postnatal growth of magnocellular neurons in normal Long Evans rats, and the relative hypertrophy of these cells in Brattleboro rats.Morphometric analysis of the somata of immunoidentified oxytocinergic and vasopressinergic supraoptic magnocellular neurons from Long Evans rats aged between 1 and 140 days postnatum revealed that their somata increased rapidly in size only after 14 days; a time that coincides with the start of weaning, with a transient increase in serum osmolality, and with the onset of ability to produce hyperosmotic urine. Oxytocin‐ and vasopressin‐containing neurons in Long Evans rats achieved adult dimensions by 45 days postnatum. By contrast, somata of oxytocin neurons in the Brattleboro rat already showed significant hypertrophy relative to those in Long Evans rats at 7 days postnatum; hypertrophy continued until at least 140 days. The hypertrophy in the Brattleboro rat at 7 days was associated with markedly raised serum osmolality relative to that of age‐matched Long Evans rats between 1 and 14 days.
Diagnostic Markers for Neonatal Sepsis: Comparing C‐reactive Protein, Interleukin‐6 and Immunoglobulin M
Authors: Khassawneh M. , Hayajneh W. A. , Kofahi H. , Khader Y. , Amarin Z. , Daoud A. 
Published: January 2007

AbstractThis clinical study was conducted to evaluate the diagnostic value of C‐reactive protein (CRP), interlekin‐6 (IL‐6) and immunoglobulin M (IgM) in the early diagnosis of neonatal sepsis. The diagnostic values of each marker separately or in combinations were evaluated. The optimal cut‐off values of each marker in the diagnosis of neonatal sepsis were defined. Between December 2004 and March 2005, a total of 78 neonates at different ages with different diagnoses in a neonatal intensive care unit in North Jordan were enrolled. Patients were classified into ‘sepsis’ group, ‘probable sepsis’ group and ‘no sepsis’ group. Blood samples were collected for CRP, IL‐6 and IgM determination. A CRP value of 5 mg/l was the best among the three parameters with 95% sensitivity and 98% negative predictive value. Combination between parameters was helpful in enhancing the ability to diagnose sepsis. The best combination was CRP ≥ 5 mg/l and/or IgM of ≥20 mg/dl. We conclude that CRP, IL‐6 and IgM are helpful in the early diagnosis of Gram‐negative neonatal sepsis. However, CRP continues to be the best single test. The use of both CRP and IgM in combination was the most helpful in predicting Gram‐negative neonatal sepsis. We speculate a significant role of this combination in making decisions regarding antibiotics treatment and upgrading the level of medical care and observation in a setting where Gram‐negative micro‐organisms are causing the majority of neonatal infections.
Induction of CD16+ CD56bright NK Cells with Antitumour Cytotoxicity not only from CD16− CD56bright NK Cells but also from CD16− CD56dim NK Cells
Authors: Takahashi E. , Kuranaga N. , Satoh K. , Habu Y. , Shinomiya N. , Asano T. , Seki S. , Hayakawa M. 
Published: January 2007

AbstractThe aim of this study was to examine the effect of cytokines on different subsets of NK cells, while especially focusing on CD16− CD56dim cells and CD16− CD56bright cells. When human peripheral blood mononuclear cells (PBMC) were cultured with a combination of IL‐2, IL‐12 and IL‐15 for several days, a minor population of CD56bright NK cells expanded up to 15%, and also showed potent cytotoxicities against various cancer cells. Sorting experiments revealed that unconventional CD16− CD56+ NK cells (CD16− CD56dim NK cells and CD16− CD56bright NK cells, both of which are less than 1% in PBMC) much more vigorously proliferated after cytokine stimulation, whereas predominant CD16+ CD56dim NK cells proliferated poorly. In addition, many of the resting CD16− CD56bright NK cells developed into CD16+ CD56bright NK cells, and CD16− CD56dim NK cells developed into CD16− CD56bright NK cells and also further into CD16+ CD56bright NK cells by the cytokines. CSFE label experiments further substantiated the proliferation capacity of each subset and the developmental process of CD16+ CD56bright NK cells. Both CD16− CD56dim NK cells and CD16− CD56bright NK cells produced large amounts of IFN‐γ and Fas‐ligands. The CD16+ CD56bright NK cells showed strong cytotoxicities against not only MHC class I (−) but also MHC class I (+) tumours regardless of their expression of CD94/NKG2A presumably because they expressed NKG2D as well as natural cytotoxicity receptors. The proliferation of CD16+ CD56bright NK cells was also induced when PBMC were stimulated with penicillin‐treated Streptococcus pyogenes, thus suggesting their role in tumour immunity and bacterial infections.
Digestion, Absorption and Tissue Distribution of Ovalbumin and Palmitoyl‐ovalbumin: Impact on Immune Responses Triggered by Orally Administered Antigens
Authors: Oliveira F. M. , Dos Santos E. M. , Alves A. C. , Campana‐Pereira M. A. , Ramaldes G. A. , Cardoso V. N. , Ruiz‐de‐Souza V. , Gontijo C. M. 
Published: January 2007

AbstractPrevious work in this laboratory has demonstrated that ovalbumin coupled to palmitoyl residues (palmitoyl‐Ova) does not induce oral tolerance. The present study sought to determine whether this coupling affects digestion, absorption and transfer of antigen. Ova and palmitoyl‐Ova were shown to be digested differently in vitro by proteolytic enzymes and presented different tissue distribution kinetics after being labelled with 99mtechnetium and orally administered to animals. Palmitoyl‐Ova remained longer in the stomach, while native Ova was quickly transferred to the gut and other organs. After 3 h, higher levels of palmitoyl‐Ova were found in the blood, Peyer's patches, mesenteric lymph nodes, liver and, especially, the spleen, which appears to be essential for immunization with palmitoyl‐Ova. In fact, splenectomized mice treated orally with palmitoyl‐Ova became tolerant, while tolerance to Ova was not affected. Thus, palmitoyl coupling was demonstrated to affect antigen digestion, absorption and transport. This is the first time that the spleen has been shown to be required for oral immunization with palmitoyl‐Ova.
TLR2 but not TLR4 Signalling is Critically Involved in the Inhibition of IFN‐γ‐induced Killing of Mycobacteria by Murine Macrophages
Authors: Arko‐Mensah J. , Julián E. , Singh M. , Fernández C. 
Published: January 2007

AbstractGamma‐interferon (IFN‐γ) plays a determinant role in activating macrophages that are critical to control Mycobacterium tuberculosis infection. However, M. tuberculosis can escape killing by attenuating the response of macrophages to IFN‐γ by blocking the transcription of a subset of IFN‐γ inducible genes. This inhibition occurs after signalling through Toll‐like receptor 2 (TLR2). While most studies have investigated the inhibition of IFN‐γ responsive genes after TLR2 signalling, the present study focuses on the functional implications of inhibition of IFN‐γ signalling in macrophages with regard to mycobacteria killing. Here, we provide evidence that exposure of the murine macrophage cell line J774 to the TLR2 ligands; 19‐kDa or zymosan, but not the TLR4 ligand LPS, inhibits IFN‐γ‐induced killing of Mycobacterium bovis Bacillus Calmette–Guérin (BCG). Moreover, exposure of bone marrow‐derived macrophages (BMM) from TLR4‐deficient and wild‐type (WT), but not from TLR2‐deficient mice to 19‐kDa lipoprotein (19‐kDa) or zymosan, results in an impairment of IFN‐γ‐mediated killing. We demonstrate that 19‐kDa and zymosan inhibit the ability of IFN‐γ to activate murine macrophages to kill BCG without inhibiting nitric oxide (NO) or tumour necrosis factor (TNF) production. Finally, we demonstrate that the inhibitory effect of 19‐kDa on IFN‐γ signalling is overcome with increasing amounts of IFN‐γ indicating that the refractoriness could be reversed at optimal IFN‐γ concentrations. The critical role of TLR2 but not TLR4 signalling in the inhibition of IFN‐γ promoted killing of mycobacteria is discussed.
Myzus persicae (green peach aphid) feeding on Arabidopsis induces the formation of a deterrent indole glucosinolate
Authors: Kim Jae Hak , Jander Georg 
Published: January 2007

SummaryCruciferous plants produce a wide variety of glucosinolates as a protection against herbivores and pathogens. However, very little is known about the importance of individual glucosinolates in plant defense and the regulation of their production in response to herbivory. When Myzus persicae (green peach aphid) feeds on Arabidopsis aliphatic glucosinolates pass through the aphid gut intact, but indole glucosinolates are mostly degraded. Although aphid feeding causes an overall decrease in Arabidopsis glucosinolate content, the production of 4‐methoxyindol‐3‐ylmethylglucosinolate is induced. This altered glucosinolate profile is not a systemic plant response, but is limited to the area in which aphids are feeding. Aphid feeding on detached leaves causes a similar change in the glucosinolate profile, demonstrating that glucosinolate transport is not required for the observed changes. Salicylate‐mediated signaling has been implicated in other plant responses to aphid feeding. However, analysis of eds5, pad4, npr1 and NahG transgenic Arabidopsis, which are compromised in this pathway, demonstrated that aphid‐induced changes in the indole glucosinolate profile were unaffected. The addition of purified indol‐3‐ylmethylglucosinolate to the petioles of cyp79B2 cyp79B3 mutant leaves, which do not produce indole glucosinolates, showed that this glucosinolate serves as a precursor for the aphid‐induced synthesis of 4‐methoxyindol‐3‐ylmethylglucosinolate. In artificial diets, 4‐methoxyindol‐3‐ylmethylglucosinolate is a significantly greater aphid deterrent in the absence of myrosinase than its metabolic precursor indol‐3‐ylmethylglucosinolate. Together, these results demonstrate that, in response to aphid feeding, Arabidopsis plants convert one indole glucosinolate to another that provides a greater defensive benefit.
Neuromodulatory effects of gonadotropin‐releasing hormone on retinotectal synaptic transmission in the optic tectum of rainbow trout
Authors: Kinoshita Masae , Kobayashi Suguru , Urano Akihisa , Ito Etsuro 
Published: January 2007

AbstractGonadotropin‐releasing hormone (GnRH) is a hypophysiotropic decapeptide that stimulates the release of gonadotropins from the pituitary. In addition, there are extra‐hypothalamic GnRH neurons that project to all regions of the brain and whose function remains unknown. Here, we investigated the effects of GnRH on retinotectal synaptic transmission, the synapses of which are formed between retinal fibers and tectal periventricular neurons that express GnRH receptor mRNA. We used rainbow trout as our study model. The excitatory postsynaptic currents (EPSCs), which were evoked by electrical stimulation of the retinal fibers and recorded in periventricular neurons, were suppressed by antagonists of ionotropic glutamate receptors. EPSCs were increased by application of each of two types of GnRH (GnRH2 and GnRH3) in the trout tectum. Such facilitation lasted for at least 10 min after application of the GnRH. To our knowledge, this is the first report of GnRH modulating conventional synaptic transmission in the brain, suggesting that tectal GnRH enhances tectal sensitivity for retinal inputs. Furthermore, such long‐lasting facilitation might occur across all the brain regions innervated by GnRH neurons, and GnRH might simultaneously switch neuronal activities in the brain regions relevant to reproductive behaviors.
Elevated cholesteryl ester transfer protein concentration is associated with an increased risk for cardiovascular disease in women, but not in men, with Type 2 diabetes: the Hoorn Study
Authors: Alssema M. , Dekker J. M. , Kuivenhoven J. A. , Nijpels G. , Teerlink T. , Scheffer P. G. , Diamant M. , Stehouwer C. D. A. , Bouter L. M. , Heine R. J. 
Published: January 2007

AbstractAims  Cholesteryl ester transfer protein (CETP) exchanges neutral lipids between lipoproteins. As the role of CETP in the atherogenic process is still not fully clarified, we studied the association of CETP concentration with the prevalence of cardiovascular disease (CVD) and with intima‐media thickness of the carotid artery (IMT) in subjects with normal glucose tolerance (NGT), impaird fasting glucose and/or impaired glucose tolerance (IFG/IGT) and Type 2 diabetes mellitus.Methods  Subjects (n = 566) were recruited from the 2000–2001 follow‐up examination of the Hoorn study. CETP concentration was determined by immunoassay. CVD was defined as self‐reported history of arterial surgery, cerebral vascular event, amputation, angina, claudication, possible infarction, measured ankle‐brachial index < 0.90 or ECG abnormalities. The right common carotid artery IMT was measured by ultrasound at 10 mm proximal to the carotid bulb.Results  In men, CETP concentration was not associated with CVD, irrespective of glucose tolerance status. In women with NGT or IGT, there was also no relationship. However, in women with Type 2 diabetes, the risk of CVD was increased in those with high CETP concentration [odds ratio = 3.34 (1.56; 7.14)]. No statistically significant association was found between CETP concentration and IMT in the entire cohort.Conclusions  In an elderly Caucasian population, associations of CETP concentration with CVD were dependent on glucose tolerance status and gender. The finding that high CETP concentration was strongly associated with increased prevalence of CVD in women with Type 2 diabetes warrants further investigation.