PubMed Health⌕ Search

Biomedical subjects

A Ray

Publications and source records attributed to A Ray.

At least 73 records · Page 4Linked to original sources
PubMed1989

Biochemical and pharmacological evidence for central cholinergic regulation of shock-induced aggression in rats.

Acetylcholinesterase (AChE) activity was estimated in brain and heart homogenates and plasma of 'aggressive' and 'nonaggressive' rats. Brain homogenates of 'nonaggressive' rats hydrolyzed significantly more substrate when compared to the 'aggressive' rats. Such differences were not seen in the heart homogenates or plasma of these two groups of rats. Acute DFP (0.1, 0.3 and 1.0 mg/kg) attenuated shock-induced aggression (SIA) 2 hr after treatment but facilitated SIA 24 hr and 48 hr after drug administration. Long-term DFP (0.3 mg/kg x 10 days), on the other hand, induced a significant enhancement in the SIA score, whereas atropine (1.0 and 5.0 mg/kg) produced a dose-related attenuation of the same. Pretreatment of rats with atropine (5 mg/kg) antagonized the long-term DFP-induced facilitation of SIA. These results are discussed in the light of an inhibitory central cholinergic mechanism in the regulation of SIA.

Acetylcholinesterase↗
PubMed1989

The GABA/benzodiazepine receptor complex in the central amygdalar nucleus and stress ulcers in rats.

The effects of bilateral microinjections of chlordiazepoxide and GABA into the central amygdalar nucleus on gastric ulcer formation induced by cold-restraint were examined in chronically implanted Wistar rats. Higher doses of chlordiazepoxide (20 and 30 micrograms/amygdala) significantly reduced stress ulcer development, whereas a lower dose (2.5 micrograms) produced a nonsignificant increase in ulcer severity. A similar dose/response pattern was observed following GABA administration. The benzodiazepine receptor antagonist Ro15-1788, applied to the amygdala, abolished the protective effects of both chlordiazepoxide and GABA. In addition, when Ro15-1788 (10 micrograms) was injected into the amygdala by itself, it aggravated the gastric stress pathology. However, a lower dose (5 micrograms) had an attenuating effect, opposite to the pattern of effects produced by chlordiazepoxide and GABA. The role of the amygdalar GABA-benzodiazepine receptor complex in stressful conditions is discussed.

Amygdala↗
PubMed1989

A DNA double chain break stimulates triparental recombination in Saccharomyces cerevisiae.

Mitotic recombination between his3 heteroalleles on heterologous chromosomes is stimulated by a DNA double chain break delivered in vivo at a site 8.6 kilobase pairs distant from one his3 allele and unlinked to the other. The induced recombination at his3 is accompanied by gap repair at the break site using the uncut homolog as a template. The DNA between the break site and his3 is not deleted in most of the His+ recombinants.

DNA, Fungal↗
PubMed1989

Reappearance of CD1a antigenic sites after endocytosis on human Langerhans cells evidenced by immunogoldrelabeling.

We show evidence of the reappearance of CD1a antigenic sites on the surface of human isolated Langerhans cells after internalization of CD1a antigen/CD1a monoclonal antibody (BL6) complexes. The internalization was visualized by immunogoldlabeling, and the reappearance of CD1a binding sites was shown by immunogoldrelabeling. The relabeling was distinguished from the labeling either by using two sizes of gold granules (15 and 5 nm) or by quantitative estimation with one size of gold granules, before and after the relabeling. This reappearance of sites is cycloheximide insensitive, and is evidenced, even if the transfer of gold particles to lysosomes is blocked by the monensin. These results suggest that the reexpression of CD1a antigens is due to antigens stored in the cytoplasm or to recycling of internalized sites. Some immunolabeled Birbeck granules were observed in continuity with the plasma membrane, which demonstrates their membrane origin and their involvement in the endocytosis process. However, the weak labeling of these organelles makes us believe that they are not specialized CD1a endocytosis structures.

Antigens↗
PubMed1989

A multiple cytokine- and second messenger-responsive element in the enhancer of the human interleukin-6 gene: similarities with c-fos gene regulation.

Interleukin-6 (IL-6) is a major systemic alarm signal that indicates the occurrence of tissue damage. The IL-6 gene is induced in various cell types by serum, inflammation-associated cytokines, viruses, and second-messenger agonists. There is an overall functional similarity between IL-6 and c-fos promoters, since transfection of excess amounts of either promoter DNA into intact HeLa cells modulates the function of the heterologous promoter construct. Furthermore, the transcription regulatory factor Fos transrepresses both the IL-6 and c-fos promoters. The 115-base pair (bp) region from -225 to -111 in the IL-6 5'-flanking region, which shares nucleotide sequence similarity with the c-fos serum response (SRE) and adjacent AP-1-like (the CGTCA motif) elements, confers responsiveness to several reagents, including serum, forskolin, and phorbol ester, upon the heterologous herpesvirus thymidine kinase (TK) promoter. In gel shift assays using nuclear extracts from HeLa cells, the 115-bp IL-6 enhancer formed several complexes that (i) were increased when extracts from induced HeLa cells were used and (ii) were inhibited most efficiently by the fos E DNA fragment (-700 to -100) and by c-fos oligonucleotides containing an intact AP-1-like site (the CGTCA motif). The 23-bp oligonucleotide designated AR1 from within the IL-6 enhancer region (-173 to -151) contains a CGTCA motif and bound nuclear proteins that also associated with c-fos oligonucleotides containing either an intact SRE or AP-1-like site. A single copy of AR1 inserted upstream of the herpesvirus TK promoter rendered this heterologous promoter inducible by IL-1 alpha, tumor necrosis factor, and serum as well as by activators of the protein kinase A (forskolin) and protein kinase C (phorbol ester) signal transduction pathways. Mutations in the AP-1-like site within AR1 (CGTCA----GTTCA) decreased inducibility of the chimeric IL-6/TK/chloramphenicol acetyltransferase gene by phorbol ester and by forskolin but not by serum, IL-1 alpha, or tumor necrosis factor. These data not only show that the AR1 segment from within the IL-6 enhancer binds nuclear proteins that also bind to c-fos regulatory elements but also demonstrate that a single copy of this 23-bp element is functionally sufficient to confer responsiveness to a variety of inducers and thus define a multiple-response element.

Base Sequence↗
PubMed1989

Effect of beta-adrenoceptor antagonists and some related drugs on maximal electroshock seizures in mice.

(+/-) Propranolol (1-50 mg/kg), (+) propranolol (50 mg/kg) and pindolol (10-50 mg/kg) exhibited significant protective effects against MES (maximum electroshock seizures), whereas, timolol (1 mg/kg), the propranolol analog, UM-272 (1 and 10 mg/kg), and the beta-agonist, terbutaline (1 and 10 mg/kg) were ineffective. Cholinergic agents, physostigmine (0.01-1.0 mg/kg), and atropine (1 and 10 mg/kg), the serotonin antagonist, cyproheptadine (0.05 mg/kg), and the prostaglandin synthesis inhibitor, indomethacin (10 mg/kg), were also without effect on the MES extensor phase. Further, pretreatment of mice with terbutaline, atropine, cyproheptadine or indomethacin did not influence the anti-MES effect of propranolol to any significant extent. The results indicate that the observed anticonvulsant effects of beta-adrenoceptor antagonists are unrelated to noradrenergic or other central neurotransmitter systems and that a non-specific mechanism, probably a membrane stabilizing effect is involved.

Adrenergic beta-Antagonists↗
PubMed1989

Prevalence of common infective agents of vaginitis.

A total of 100 women with vaginitis and 50 age matched healthy women were studied for common infective agents of vaginitis. The vaginal secretions collected from these women were examined for Trichomonas vaginalis, G. vaginalis, and Candida species. The prevalence of infective agents in the patients was T. vaginalis 11 per cent. Candida species 30 per cent and Gardnerella vaginalis 31 per cent. In contrast, in the control group the prevalence was Candida species 14 per cent and G. vaginalis 22 per cent. T. vaginalis was not isolated from any of the control women. Mixed infections with G. vaginalis and Candida species were seen in four cases and T. vaginalis and Candida species in one case only. Mixed infection with T. vaginalis ahd G. vaginalis was not observed in any of the patients studied.

Candidiasis, Vulvovaginal↗
PubMed1989

Role of dopaminergic mechanisms in the central amygdalar nucleus in the regulation of stress-induced gastric ulcer formation in rats.

Microinjections (i/am) of dopamine (DA) antagonists, haloperidol or clozapine (1 and 5 micrograms) into the central amygdalar nucleus (CEA) produced dose-related aggravations in cold-restraint (3 h at 4 degrees C) stress-induced gastric ulcer formation in rats. On the other hand, DA (10 micrograms, i/am), its agonist, apomorphine (5 mg/kg, ip) and its precursor, l-Dopa (100 mg/kg, ip) significantly inhibited stress ulcerogenesis. Pretreatment of rats (i/am) with clozapine antagonized or reversed the gastric cytoprotective effects of DA, apomorphine and l-Dopa. The results indicate that the CEA is important for the observed gastric cytomodulatory effects of both centrally and peripherally administered dopaminergic agents during stressful experiences.

Amygdala↗
PubMed1988

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↗
PubMed1988

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↗
PubMed1988

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↗
PubMed1988

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↗
PubMed1988

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↗
PubMed1988

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↗