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PubMed1997

Characterization of the role played by antigen challenge in the suppression of in vivo humoral immunity by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

The goal of these studies was to characterize the role played by antigen challenge in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced immunosuppression. The effects of single exposure to TCDD (4.2, 14, and 42 microg/kg) in B6C3F1 mice on the reverse plaque assay (RPA; no sensitization) and the sheep red blood cell (SRBC) antibody response were compared. While the RPA was suppressed in a dose-dependent fashion with significance at the two highest doses, a much more dramatic effect was noted with the primary anti-SRBC response: a suppression was noted at the lowest dose, which was comparable to that observed with the highest dose in the RPA. Subsequent studies compared the RPA in B6C3F1 (Ah-high responder) and DBA/2 (Ah-low responder) mice after both single and repeated exposure to identical cumulative doses of TCDD (4.2, 14, and 42 microg/kg). The repeated exposures consisted of 14 consecutive daily treatments of 0.3, 1.0, and 3.0 microg/kg. The results indicated only a slight difference in the effects of TCDD in the two strains after single exposure, and even less difference after repeated exposure. Moreover, administering TCDD on different days relative to the SRBC challenge indicated a suppression in both strains when given 1, 2, or 3 days before antigen challenge, on the day of antigen challenge, or 1 or 2 days after antigen challenge. The only day of administration where the suppression was attenuated was 3 days after antigen challenge. These results confirm an important relationship between antigen challenge and TCDD exposure on immunosuppression.

Animals↗
PubMed1985

[Role playing].

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Humans↗
PubMed2003

Reactions of water-soluble alkylperoxyl radicals and superoxide with DNA, lipoproteins and phospholipid vesicles: the role played by electrostatic forces.

The role of electrostatic forces in free radical biology is very important but it is all too often overlooked. The radicals discussed in this review include positively-charged, negatively-charged and neutral water-soluble alkylperoxyls and superoxide. Important scientific insights have been gained by generating these radicals in known quantities by the thermal decomposition of simple, "clean", chemical precursors in the presence of potential bio-targets. For example, the abilities of these radicals to damage double-stranded DNA, a polyanion, are dictated by Coulombic forces with only the positively-charged peroxyls being capable of directly producing single-strand breaks. The Coulombic control of the reactions and reaction rates of water-soluble peroxyl radicals which are so evident with DNA do not manifest themselves with all electrostatically charged bio-targets, e.g., low density lipoprotein (LDL), probably because the charge on the surface of the LDL is not uniformly distributed.

DNA↗
PubMed1997

Saccharomyces cerevisiae Mpt5p interacts with Sst2p and plays roles in pheromone sensitivity and recovery from pheromone arrest.

SST2 plays an important role in the sensitivity of yeast cells to pheromone and in recovery from pheromone-induced G1 arrest. Recently, a family of Sst2p homologs that act as GTPase-activating proteins (GAPs) for G alpha subunits has been identified. We have identified an interaction between Sst2p and the previously identified Mpt5p by using the two-hybrid system. Loss of Mpt5p function resulted in a temperature-sensitive growth phenotype, an increase in pheromone sensitivity, and a defect in recovery from pheromone-induced G1 arrest, although the effects on pheromone response and recovery were mild in comparison to those of sst2 mutants. Overexpression of either Sst2p or Mpt5p promoted recovery from G1 arrest. Promotion of recovery by overexpression of Mpt5p required Sst2p, but the effect of overexpression of Sst2p was only partially dependent on Mpt5p. Mpt5p was also found to interact with the mitogen-activated protein kinase homologs Fus3p and Kss1p, and an mpt5 mutation was able to suppress the pheromone arrest and mating defects of a fus3 mutant. Because either mpt5 or cln3 mutations suppressed the fus3 phenotypes, interactions of Mpt5p with the G1 cyclins and Cdc28p were tested. An interaction between Mpt5p and Cdc28p was detected. We discuss these results with respect to a model in which Sst2p plays a role in pheromone sensitivity and recovery that acts through Mpt5p in addition to a role as a G alpha GAP suggested by the analysis of the Sst2p homologs.

CDC28 Protein Kinase, S cerevisiae↗
PubMed1996

[Henry Foley and the discovery in 1908 of the role played by the louse in the transmission of relapsing fever].

The author recalls the very fine clinical, epidemiological and experimental work undertaken since 1907 at Beni Ounif de Figuig, south of Oran near the algerian-moroccan border which led Henry Foley and Edmond Sergent to suspect and later demonstrate the exclusive role played by the louse (Pediculus corporis or more precisely P. vestimenti) in the transmission of relapsing fever of which they studied an important epidemic occurring there between 1907-1910. This discovery led them to incriminate also the louse in the transmission of exanthematic typhus of which the epidemiology is practically similar. On the occasion of a tunisian epidemic of relapsing fever Charles Nicolle resumed Sergent's and Foley's work which he contested without any justification. Trying to attribute to himself all the merit of the discovery of the role of the louse in the transmission of relapsing fever, Charles Nicolle quotes Sergent's and Foley's works contesting them with a certain bad faith. In 1912 he mentions only Sergent's and Foley's 1910 works (posterior of only one year to his confirmation of the role of the louse in the transmission of exanthematic typhus) and ignores totally their 1908 preliminary paper. One must therefore give full credit to Henry Foley associated with Edmond Sergent for this essential discovery of the role of the louse in human pathology in which they occupy the first place.

Animals↗
PubMed1995

Hyperinsulinemia in offspring of non-insulin-dependent diabetes mellitus patients: the role played by abnormal clearance of insulin.

Insulin resistance and hyperinsulinemia are often found in first-degree relatives of non-insulin-dependent diabetes mellitus (NIDDM) patients, and are currently considered a familial trait of this population at increased risk for diabetes. This study was undertaken to determine the role played by the metabolic clearance rate (MCR) of insulin (MCR-I) in the hyperinsulinism of these subjects. The proband population, consisting of 48 subjects aged 29.2 +/- 4.4 (mean +/- SD) years (18 men and 30 women; body mass index, 24.6 +/- 0.8 kg/m2; fasting plasma glucose, 4.54 +/- 0.37 mmol/L), was assigned in random order to four groups (I, II, III, and IV), each receiving a double insulin/glucose infusion (I, 0.025/2.0; II, 0.050/3.5; III, 0.100/6.0; and IV, 0.200/8.0 U/kg.h and mg/kg.min, respectively) to calculate MCR-I and MCR of glucose (MCR-G). Forty (14 men and 26 women) age- and body mass index-matched healthy individuals served as controls. All subjects had a normal response to an oral glucose tolerance test (75 g) according to World Health Organization criteria. Basal plasma insulin and C-peptide levels in probands were significantly (P < .05) higher than in controls in each study group; similarly, MCR-I was significantly (at least P < .05) lower in probands than in controls in all groups. MCR-G was significantly (at least P < .05) decreased in probands as compared with controls of groups III and IV.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

The active role played by xenogeneic endothelial cells in the indirect presentation pathway is not lymphocyte trans-co-stimulation.

The human CD4+ T lymphocyte response to major histocompatibility complex (MHC) class II-negative porcine endothelial cells is dependent on the presence of human monocytes through a human leukocyte antigen (HLA) class II-restricted indirect presentation pathway. Because the role of porcine endothelial cells had been previously shown to do more than simply supply xenopeptides, co-stimulatory signals were analysed. Endothelial cells were shown to express the CD54, CD58, CD59 and CD86 transcripts; however, no membrane B7 molecule could be detected. Blocking experiments in a direct pathway model confirmed that porcine endothelial cells could provide co-stimulatory signals to human T cells through the CD2 and LFA-1 pathways. Nevertheless, the proliferation achieved in the indirect presentation model required co-stimulation by LFA-1, CD2 and CD28, engaged by co-stimulation molecules expressed in the cis-form by the human monocytes. These results clearly show that the active role played by the endothelial cells in the indirect pathway is not lymphocyte trans-co-stimulation and suggest that cis-co-stimulation dominates trans-co-stimulation when both are present.

Abatacept↗
PubMed1986

A role played by dopamine and opioid neuronal systems in stress-induced motor suppression (conditioned suppression of motility) in mice.

Mice exhibited a marked suppression of motility (conditioned suppression of motility, which is one of stress-induced motor suppressions) when placed in the same chamber where they had previously received an electric footshock. In the present study the role played by dopamine and opioid neuronal systems in the conditioned suppression of motility has been investigated. In conditioned suppression group, the contents of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and methionine-enkephalin (Met-enk) did not change in the hypothalamus, cerebral cortex and medulla oblongata/pons, while a decrease in the contents of striatal DOPAC were induced compared to that in the control group, which was accompanied by reduction in the contents of Met-enk. In addition, the contents of DA were increased in the midbrain. The ratio of DA metabolites/DA contents in the striatum of the conditioned suppression group was decreased. In the striatum, moreover, the depletion of DA induced by alpha-methyl-p-tyrosine (alpha-MT) in the conditioned suppression group was significantly lower than that in the control group but not in the midbrain. These results suggest that the DA turnover rate and Met-enkergic activity decrease in the striatum of conditioned suppression group.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

Change in coordination across phases of psychotherapy and outcome: two mechanisms for the role played by patients' contribution to the alliance.

This article investigated the mechanisms underlying associations between patients' contribution to the alliance and outcome by examining relations between change in the alliance over the course of treatment and improvement in Short-Term Dynamic Psychotherapy (STDP) and Brief Adaptive Psychotherapy (BAP). Findings for STDP were consistent with 1 model about the role played by the alliance, according to which change in the alliance over the course of therapy is the vehicle for overall improvement. Results for BAP were consistent with the other main position proposed in the literature, which argues that a positive alliance provides the foundation for successful treatment. Discussion includes suggesting that it might prove useful in future research to group therapy approaches in terms of these 2 models and that this idea may explain 2 apparently contradictory sets of findings from previous studies on relations between change in the alliance and outcome.

Adult↗
PubMed2005

The role played by tumor necrosis factor during localized and systemic infection with Streptococcus pneumoniae.

Tumor necrosis factor (TNF) has been proposed as a major mediator of host resistance in murine models of Streptococcus pneumoniae infection; in humans, anti-TNF therapies have been implicated in increased susceptibility to pneumococcal infection. Here, we use nonlethal (serotype 6B) and lethal (serotype 3) S. pneumoniae, neutralizing monoclonal antibodies to TNF, and TNF gene-deficient mice to reexamine the role played by TNF in antistreptococcal responses. After nonlethal challenge, primary resistance and all examined parameters of the cellular inflammatory response occurred independently of TNF activity. After lethal challenge, TNF deficiency resulted in more-rapid death but did not affect lung inflammation. However, the livers of the TNF gene-deficient mice, but not of the control mice, exhibited extensive signs of systemic disease. TNF, therefore, is dispensable for a complete cellular pulmonary inflammatory response to S. pneumoniae infection but enhances survival from disseminated lethal infection, at least in part by delaying systemic organ damage.

Animals↗
PubMed2002

How laminin-1 can be recognized by the protozoan parasite Tritrichomonas foetus: possible role played by the extracellular matrix glycoprotein in both cytoadhesion and cytotoxicity exerted by the parasite.

The isoform 1 of the extracellular matrix glycoprotein Laminin is known to be an important ligand for some parasitic protozoa including Trichomonas vaginalis. The bovine parasite Tritrichomonas foetus seems to display a similar recognition process to laminin-1, as some amino acid sequences found in the LNS module of laminin-1 can also be recognized by this parasite. Which of the laminin-1 residing adhesion sequences are recognized by T. foetus, and the role played by such a protein-cell recognition process in both cytoadhesion and cytotoxicity exerted by the parasite are the subjects briefly reviewed and discussed here.

Animals↗
PubMed1952

Role playing.

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Education, Nursing↗
PubMed2006

Exploring cyclosporine A-side effects and the protective role-played by antioxidants: the morphological and immunohistochemical studies.

Cyclosporine A (CsA) is the immunosuppressor most frequently used in transplant surgery and in the treatment of autoimmune diseases, because of its specific inhibiting effect on the signal transduction pathways of cell T receptor. It has been shown that CsA is able to generate reactive oxygen species and lipid peroxidation, which are directly involved in the CsA nephrotoxicity, hepatotoxicity and cardiotoxicity. So, the use of antioxidants seems to be a useful tool in attempting to reduce CsA adverse effects. The aim of this review is to summarise the general aspect of CsA, the classification of antioxidants, their mechanism of action and their administration for improving CsA side effects. The protective role of different antioxidants has been evaluated on CsA-induced nephrotoxicity. It has been shown that the antioxidants, improved the morphological renal cytoarchitecture, increased the antioxidant enzyme content, decreased lipid peroxidation and reactive species oxygen (ROS). The protective role of antioxidants was also found in CsA hepatotoxicity and was related to the increase in antioxidant capacity of hepatic tissue, which was responsible for ameliorating hepatic morphology. Recently, it has been demonstrated that CsA induces side effects on the heart but the data to this purpose are very few and also the number of results on the protective role played by antioxidants it is very limited. In conclusion, not only do these observations provide insight into the intricate mechanism of CsA adverse effects, but they also present novel opportunities for the design and development of more effective therapeutic strategies against negative effects.

Animals↗
PubMed2006

Role played by brainstem neurons in regulating testosterone secretion via a direct neural pathway between the hypothalamus and the testes.

We previously reported anatomical and functional evidence for a direct, inhibitory neural pathway that regulates testosterone (T) secretion independently of the pituitary. This pathway is activated by the intracerebroventricular (icv) administration of agents that stimulate stress responses, such as IL-1beta, corticotropin-releasing factor (CRF), and norepinephrine (NE), which results in a blunted T response to the administration of human chorionic gonadotropin (hCG). Blunting of the T response is mediated by central beta-adrenergic receptor stimulation. CRF, but not ethanol (EtOH) or IL-1beta, acts directly on the paraventricular nucleus of the hypothalamus to activate the pathway. Here we explored the role played by brain areas hypothesized to be part of this pathway, such as neurons in the dorsal pons [including the locus coeruleus (LC) of the brainstem], where NE is produced. Microinfusion of EtOH or IL-1beta, but not CRF, into these neurons activated the pathway. Electrolytic lesions of this region significantly reversed the inhibitory effect of icv-administered EtOH on hCG-induced T release, while having no effect on the ability of IL-1beta or CRF to do so. However, the icv administration of IL-1beta, EtOH, or CRF, in doses that rapidly inhibit the T response to hCG, all caused a significant depletion of NE from the LC. Collectively, these results indicate that in addition to the paraventricular nucleus, the brainstem area containing the LC is part of a neural pathway that connects the brain to the testes independently of the pituitary. We also speculate that EtOH may stimulate this pathway through NE-dependent activation of the dorsal pons.

Animals↗
PubMed2006

Evidence that Spt2/Sin1, an HMG-like factor, plays roles in transcription elongation, chromatin structure, and genome stability in Saccharomyces cerevisiae.

Spt2/Sin1 is a DNA binding protein with HMG-like domains that has been suggested to play a role in chromatin-mediated transcription in Saccharomyces cerevisiae. Previous studies have suggested models in which Spt2 plays an inhibitory role in the initiation of transcription of certain genes. In this work, we have taken several approaches to study Spt2 in greater detail. Our results have identified previously unknown genetic interactions between spt2Delta and mutations in genes encoding transcription elongation factors, including members of the PAF and HIR/HPC complexes. In addition, genome-wide and gene-specific chromatin immunoprecipitation analyses suggest that Spt2 is primarily associated with coding regions in a transcription-dependent fashion. Furthermore, our results show that Spt2, like other elongation factors, is required for the repression of transcription from a cryptic promoter within a coding region and that Spt2 is also required for repression of recombination within transcribed regions. Finally, we provide evidence that Spt2 plays a role in regulating the levels of histone H3 over transcribed regions. Taken together, our results suggest a direct link for Spt2 with transcription elongation, chromatin dynamics, and genome stability.

Chromatin↗
PubMed2006

Differential role played by the MEK/ERK/EGR-1 pathway in orthopoxviruses vaccinia and cowpox biology.

Appropriation of signalling pathways facilitates poxvirus replication. Poxviruses, as do most viruses, try to modify the host cell environment to achieve favourable replication conditions. In the present study, we show that the early growth response 1 gene (egr-1) is one of the host cell factors intensely modulated by the orthopoxviruses VV (vaccinia virus) and CPV (cowpox virus). These viruses stimulated the generation of both egr-1 mRNA and its gene product, throughout their entire replication cycles, via the requirement of MEK [mitogen-activated protein kinase/ERK (extracellular-signal-regulated kinase) kinase]/ERK pathway. We showed that, upon VV infection, EGR-1 translocates into the nucleus where it binds to the EBS (egr-1-binding site) positioned at the 5' region of EGR-1-regulated genes. In spite of both viruses belonging to the same genus, several lines of evidence, however, revealed a remarkable contrast between them as far as the roles played by the MEK/ERK/EGR-1 pathway in their biological cycles are concerned. Hence (i) the knocking-down of egr-1 by siRNA (small interfering RNA) proved that this transcription factor is of critical relevance for VV biology, since a decrease of about one log cycle in virus yield was verified, along with a small virus plaque phenotype, whereas the gene silencing did not have a detrimental effect on either CPV multiplication or viral plaque size; (ii) while both pharmacological and genetic inhibition of MEK/ERK resulted in a significant decrease in VV yield, both approaches had no impact on CPV multiplication; and (iii) CPV DNA replication was unaffected by pharmacological inhibition of MEK/ERK, but phosphorylation of MEK/ERK was dependent on CPV DNA replication, contrasting with a significant VV DNA inhibition and VV DNA replication-independence to maintain ERK1/2 phosphorylation, observed under the same conditions.

Animals↗
PubMed2002

Arf1 GTPase plays roles in the protein traffic between the endoplasmic reticulum and the Golgi apparatus in tobacco and Arabidopsis cultured cells.

Arf GTPases are known to be key regulators of vesicle budding in various steps of membrane traffic in yeast and animal cells. We cloned the Arabidopsis Arf1 homologue, AtArf1, and examined its function. AtArf1 complements yeast arf1 arf2 mutants and its GFP-fusion is localized to the Golgi apparatus in plant cells like its animal counterpart. The expression of dominant negative mutants of AtArf1 in tobacco and Arabidopsis cultured cells affected the localization of co-expressed GFP-tagged proteins in a variety of ways. AtArf1 Q71L and AtArf1 T31N, GTP- and GDP-fixed mutants, respectively, changed the localization of a cis-Golgi marker, AtErd2-GFP, from the Golgi apparatus to the endoplasmic reticulum but not that of GFP-AtRer1B or GFP-AtSed5. GFP-AtRer1B and GFP-AtSed5 were accumulated in aberrant structures of the Golgi by AtArf1 Q71L. A soluble vacuolar protein, sporamin-GFP, was also located to the ER by AtArf1 Q71L. These results indicate that AtArf1 play roles in the vesicular transport between the ER and the Golgi and in the maintenance of the normal Golgi organization in plant cells.

ADP-Ribosylation Factor 1↗