Regulation of expression of interleukin-6. Molecular and clinical studies.
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Base Sequence↗
Biomedical subjects
A Ray
Publications and source records attributed to A Ray.
Interactions of thyrotropin-releasing hormone (TRH) with neurotensin and dopamine in the central nucleus of the amygdala during stress ulcer formation in rats.
Bilateral microinjections of thyrotropin-releasing hormone (TRH; 1, 3 and 10 micrograms) into the central nucleus of the amygdala produced a dose-related aggravation of cold restraint-induced gastric ulcers in rats. TRH (10 micrograms) also induced gastric erosions in non-stressed animals. Pretreatment with atropine methyl nitrate attenuated the TRH-induced ulcers in both stress and non-stress situations. TRH (10 micrograms) also antagonized the gastric cytoprotection of intra-amygdalar neurotensin (10 micrograms) and was ineffective in altering the stress ulcer-attenuating effects of dopamine (10 micrograms). Pretreatment with i.p. clozapine, however, prevented the inhibitory effects of dopamine on the TRH-induced aggravation of the gastric stress pathology. The results suggest an interaction of TRH, neurotensin and dopamine in the central amygdalar nucleus during stress, and indicate peripheral cholinergic pathways in the mediation of the ulcerogenic effects of TRH.
Amygdala↗
Nucleotide sequence of cDNA encoding rabbit ferritin L chain.
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Amino Acid Sequence↗
Intra-chromosomal gene conversion induced by a DNA double-strand break in Saccharomyces cerevisiae.
We have stimulated mitotic and meiotic gene conversion between non-tandem direct repeats of ADE4 by a defined double-strand break imparted in vivo to one of two copies of the gene. The experimental design permitted us to distinguish unambiguously between reciprocal intra-chromosomal crossing over and non-reciprocal break-join events that could accompany the induced conversions. We observed that (1) less than 10% of the induced conversion events are accompanied by intra-chromosomal crossing over in both mitosis and meiosis; (2) non-reciprocal break-join is not stimulated by the double-strand breaks; (3) a double-strand break in meiosis is repaired off intra-chromosomal homology (if available) with approximately sevenfold preference over repair off the homologous chromosome. Our observations, analyzed in the light of previous investigations of spontaneous inter and intra-chromosomal crossing over and gene conversion, lead to the view that chromosomal configuration constrains intra-chromosomal crossing over accompanying conversion between closely spaced repeated genes during resolution of the conversion intermediate.
Chromosomes↗
Opiate mechanisms in the central amygdala and gastric stress pathology in rats.
Bilateral microinjections of the opiate antagonist naloxone (0.1, 1.0 and 10.0 micrograms) into the central nucleus of the amygdala (CEA) produced a significant potentiation of cold restraint-induced gastric pathology in rats. The opiate agonist, beta-endorphin (0.1, 1.0 and 10.0 micrograms), on the other hand, inhibited stress ulcer formation in a dose-related manner. Stress ulcer-attenuating effects were also seen with intra-CEA injections of the enkephalin analogs [D-Ala2,D-Leu5]enkephalin (10.0 micrograms) and [D-Ala2]Met-enkephalinamide (10.0 micrograms). Pretreatment of rats with naloxone (1.0 microgram) completely antagonized and even reversed the gastric cytoprotective effects of beta-endorphin (1.0 and 10.0 micrograms). The results indicate that the CEA is important in the gastric cytomodulatory effects of endogenous opiates during stressful experiences.
Amygdala↗
Effects of intra-amygdalar dopamine agonists and antagonists on gastric stress lesions in rats.
Microinjections of dopamine (DA, 3 and 30 micrograms) or its agonist apomorphine (3 micrograms) into the central amygdala (CEA) attenuated cold restraint (3 h at 4 degrees C)-induced gastric ulcer formation in rats. Pretreatment with DA antagonists, haloperidol and metoclopramide (both i.p. and intra-amygdalar) reversed the stress ulcer attenuating effect of DA. It is suggested that the CEA is one of the central sites for this DA cytoprotection and that D2 receptors are possibly involved in this effect.
Amygdala↗
T- and B-cell-derived supernatant factors enhance IgE synthesis by a myeloma cell line (U-266).
IgE synthesis by the human myeloma line U-266 was enhanced 3- to 15-fold in the presence of supernatants from cultures of mononuclear cells (MNC). The enhancing activity was concentration-dependent and was derived from cells that were cultured in the absence of serum and received no in vitro stimulation by exogenous mitogens or lymphokines. T- and B-lymphocyte-enriched populations isolated from MNC were found to generate the enhancing activity, but no enhancing activity was produced by monocytes. MNC from atopic and nonatopic donors were equally effective as sources for this activity. The enhancement of IgE synthesis was proportionally greater than the effect of the activity on cell proliferation. Furthermore, this enhancement of IgE synthesis was demonstrated to be isotype-specific in that the factor(s) had no effect on IgM- and IgG-secreting cell lines. It is suggested that augmentation of IgE synthesis by B cells at a late stage of differentiation may be accomplished by lymphokines constantly present in the cells' milieu and that the U-266 model may be useful for testing putative IgE regulatory factors.
Antibody Specificity↗
Central dopamine systems and gastric stress pathology in rats.
Acute treatments with haloperidol (1 mg/kg), clozapine (10 mg/kg) and metoclopramide (10 mg/kg) significantly facilitated cold-restraint-induced gastric ulcer formation in rats. In addition, haloperidol and clozapine also produced gastric mucosal erosions in non-stressed rats. Bilateral lesions of the ventral tegmental area (VTA) and substantia nigra also aggravated stress ulcerogenesis--VTA lesions also being effective in inducing gastric ulcers in non-stressed rats. Long-term treatment with dopaminergic blockers showed variable effects. Clozapine potentiated the gastric stress pathology, whereas no significant facilitation was observed with haloperidol or metoclopramide. In addition, withdrawal from haloperidol did not influence the gastric ulcer formation when compared to controls. The role of central dopaminergic involvement in gastric stress pathology is discussed in light of the present results.
Animals↗
The effects of buspirone, a selective anxiolytic, on stress ulcer formation in rats.
The effects of buspirone hydrochloride were investigated on the formation of cold-immobilization gastric stress ulcers. Low doses significantly attenuated, while higher doses greatly potentiated gastric stress pathology. The dopamine antagonist haloperidol, and the agonist apomorphine respectively, reversed the buspirone effects. The role of dopamine in the expression of buspirone's effects is discussed, although other transmitter systems may mediate some of the actions of buspirone.
Animals↗
The human "interferon-beta 2/hepatocyte stimulating factor/interleukin-6" gene: DNA polymorphism studies and localization to chromosome 7p21.
The human interferon-beta 2 gene (IFNB2) product is identical to that for the B-cell stimulation factor-2 (BSF-2), the hybridoma growth factor (HGF) ("interleukin-6"), and the hepatocyte stimulating factor (HSF). Proteins derived from this gene mediate the plasma protein response to tissue injury (acute-phase response) and regulate the growth and differentiation of both B and T cells. By using the enzymes MspI, BstNI, and BglI, three polymorphic systems were detected with probes for the IFNB2 gene. The MspI and BglI polymorphisms are likely to be due to base pair substitutions; the BstNI polymorphism was revealed by nine other enzymes and is likely to be due to DNA insertions within 1 kb of the 3' flanking region of the gene. This region is rich in AT dinucleotides, and slippage at DNA replication may generate the insertions of between 0.07 and 0.23 kb that were observed. The polymorphic MspI site also lies within the vicinity of the fifth exon. The BglI polymorphic site is likely to lie in 5' flanking DNA. The three polymorphisms are separate, and a variety of haplotypes was observed. A low level of linkage disequilibrium exists between the MspI and the BglI alleles. MspI and BstNI polymorphisms were observed in Caucasoids, CAR Pygmies, Zaire Pygmies, Melanesians, and Chinese but at differing frequencies, and not all alleles were present in all populations. The BglI polymorphism was observed in Caucasoids and Africans only. Linkage studies involving the IFNB2 gene and 27 other chromosome 7 markers have localized it to between D7S135 and D7S370 at 7p22-p21.(ABSTRACT TRUNCATED AT 250 WORDS)
Alleles↗
Activation of the human "beta 2-interferon/hepatocyte-stimulating factor/interleukin 6" promoter by cytokines, viruses, and second messenger agonists.
The hallmark of "beta 2-interferon (IFN-beta 2)/hepatocyte-stimulating factor/interleukin 6" gene expression is its inducibility in different types of human cells (fibroblasts, monocytes, epithelial cells, and endothelial cells) by different stimuli, which include cytokines such as tumor necrosis factor, interleukin 1 (IL-1) and platelet-derived growth factor, different viruses, and bacterial products such as endotoxin. The activation by cytokines, viruses, and second messenger agonists of the IFN-beta 2 promoter linked to the bacterial chloramphenicol acetyltransferase (CAT) gene was studied after transfection into HeLa cells. A chimeric gene containing IFN-beta 2 DNA from -1180 to +13 linked to the CAT gene was inducible approximately 10-fold by phorbol 12-myristate 13-acetate (PMA), followed, in decreasing order, by pseudorabies and Sendai viruses (7- to 11-fold each); serum (6- to 9-fold); the cytokines tumor necrosis factor, IL-1, and epidermal growth factor (3- to 5-fold each); the cAMP agonists BrcAMP and forskolin and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (2- to 6-fold each); poly(I).poly(C) (2- to 4-fold); 1,2-diacylglycerol and the calcium ionophore A23187 (1.5- to 2-fold each). Bacterial endotoxin did not activate this IFN-beta 2/CAT fusion gene in HeLa cells. Deletion of the 5' boundary of the IFN-beta 2 DNA from -1180 to -596 in the fusion gene preserved its activation by IL-1, tumor necrosis factor, epidermal growth factor, serum, pseudorabies, and Sendai viruses and by PMA, Br-cAMP, and forskolin; deletion to -225 led to a small reduction (by a factor of 1.5-2) in the responsiveness to serum, PMA, and Sendai virus but not to the other inducers; a further deletion to -112 greatly reduced all responsiveness. Thus, the region between -225 and -113 in IFN-beta 2, which contains DNA motifs similar to the regulatory elements in the human c-fos gene, appears to contain the major cis-acting regulatory elements responsible for the activation of the IFN-beta 2 promoter by several different cytokines, viruses, and second messenger agonists.
Base Sequence↗
Prolactin and thyroid status in prepubertal children with mild to moderate obesity.
Prolactin (PRL) response to thyrotropin releasing hormone (TRH) in 21 prepubertal children with mild to moderate obesity was compared with that in 21 normal prepubertal children (controls). Basal PRL levels were normal but the mean peak PRL response and mean increment in PRL levels following TRH administration were significantly lower in prepubertal obese children (p less than 0.001). The mean PRL responses to TRH were significantly impaired at all time intervals in prepubertal obese boys and girls compared to the control subjects. Linear regression and correlation coefficient analysis did not reveal any significant relation between the percent overweight and PRL response. Basal T4, T3 levels and T3 and TSH response to TRH were similar in both groups. The findings suggest that neuroendocrine regulation of prolactin is impaired in prepubertal children even with mild to moderate obesity. This could be secondary to altered neurotransmitter status at the hypothalamic level. Further studies are needed to determine whether the defect is innate or acquired, primary or secondary.
Child↗
Effect of aldrin on spermatogenesis, plasma gonadotrophins and testosterone, and testicular testosterone in the rat.
Quantitative evaluation of the different varieties of germ cells at stage VII of the seminiferous epithelium cycle, namely type-A spermatogonia (ASg), preleptotene spermatocytes (pLSc), mid-pachytene spermatocytes (mPSc) and step 7 spermatids (7Sd), along with radioimmunoassay of plasma gonadotrophins (FSH and LH), testosterone and testicular testosterone were performed in Wistar rats following treatment with aldrin (polycyclic chlorinated hydrocarbon insecticide) for approximately one (13 days) or two cycles (26 days) of the seminiferous epithelium. Extensive degeneration of all varieties of germ cells at stage VII, reduction in the sperm count and significant reductions in plasma concentrations of LH and testosterone were observed following aldrin treatment. The reduction in plasma concentrations of FSH was statistically significant only after treatment for two cycles. The inhibitory effect of aldrin on plasma gonadotrophins, testosterone levels, testicular testosterone content and numbers of 7Sd and ASg was maximum after treatment for two cycles. Administration of human chorionic gonadotrophin along with aldrin treatment for two cycles partially prevented the degeneration of germ cells and enhanced testosterone production. The results indicate that aldrin may have a direct inhibitory influence on gonadotrophin release, but the possibility of a direct action of the insecticide at the level of the testes is also discussed.
Aldrin↗
[Langerhans cell: CD1 antigens and the Birbeck granule].
Langerhans cells are characterized by two types of markers: an ultrastructural marker, the Birbeck granule and different membrane markers: HLA-D antigens, T4 antigen, and some of the CD1 antigens. These antigens which are specific for the epidermal Langerhans cells, are not expressed by the other epidermal cells. Three CD1 antigens are biochemically defined on human thymocytes, they display a glycoprotein chain non covalently attached to beta-2-microglobulin. Only two of these glycoproteins: the T6 and M241 molecules have been detected on Langerhans cells. The presence of these CD1 antigens on Langerhans cells enhances their relationships to thymocytes, in contrast, Langerhans cells cannot be any more easily associated with the macrophage-monocyte lineage. The physiology of the ultrastructural marker is not well known. Its membrane origin has been experimentally proved since T6 antigen has been found closely associated to newly formed Birbeck granules.
Animals↗
The central amygdala and immobilization stress-induced gastric pathology in rats: neurotensin and dopamine.
Bilateral microinjections of neurotensin (3, 10 and 30 micrograms) into the central amygdala had a dose-related attenuating effect on cold-restraint gastric ulcers in rats. Similar inhibitory effects were also observed with intra-amygdalar dopamine (3, 10 and 30 micrograms). Pretreatment with 6-hydroxydopamine (10 micrograms) or haloperidol (1 mg/kg), however, reversed the ulcer attenuating effect of neurotensin. The results indicate that the central amygdala is important in the mediation of the cytoprotective effects of neurotensin and dopamine.
Amygdala↗
Adaptors, linkers, and methylation.
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Base Sequence↗
Involvement of brain transmitters in the modulation of shock-induced aggression in rats by propranolol and related drugs.
(+/-)Propranolol (1, 3, 10 and 30 mg/kg) exhibited a differential effect on footshock aggression (FSA) in rats. Lower doses (1 and 3 mg/kg) of the drug facilitated FSA, whereas an inhibitory effect was observed with higher doses (10 and 30 mg/kg) of the same. (+)Propranolol (30 mg/kg) and UM-272 (1 and 10 mg/kg) as well as physostigmine (0.1 and 0.5 mg/kg) all produced inhibition of FSA. Similar FSA inhibitory effects were also observed with salbutamol (1 and 5 mg/kg). Pretreatment with atropine and not methylatropine attenuated the anti-aggressive effect of (+/-)propranolol (10 mg/kg) without appreciably altering the facilitatory effect (1 mg/kg) of the drug on FSA. In addition, at the anti-aggressive doses, (+/-)propranolol (10 mg/kg) and UM-272 (10 mg/kg), significantly inhibited brain cholinesterase enzyme activity when compared to saline controls. (+/-)Propranolol (10 mg/kg) also inhibited significantly the aggression induced by reserpine-apomorphine treatment. It is inferred that a central cholinergic and dopaminergic mechanism is involved in the anti-aggressive effect of (+/-)propranolol, whereas the low dose induced facilitation of affective aggression could be attributed to central beta-adrenoceptor blockade.
Acetylcholinesterase↗
Sustained B-lymphocyte immunodeficiency attributed to phenytoin therapy.
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Adolescent↗