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D Mason

Publications and source records attributed to D Mason.

At least 19 recordsLinked to original sources
PubMed2005

Response of the hypothalamic-pituitary-adrenal axis to psychological stress in patients with psoriasis.

BACKGROUND: Psoriasis may, in some patients, be triggered and/or exacerbated by stress. OBJECTIVES: As activation of the hypothalamic-pituitary-adrenal (HPA) axis is critical to a successful stress response we investigated this in patients with psoriasis. METHODS: Forty patients with chronic plaque psoriasis and 40 age-matched normal controls experienced three randomly presented acute psychological stressors (cognitive, emotional and social). Serial serum cortisol, pulse rate and blood pressure assessments were undertaken at baseline and following each of the stressors. Salivary cortisol samples were collected at 09.00 h on the day of testing. RESULTS: In control subjects there was a significant (r = 0.38; P < 0.05) correlation between pulse rate and serum cortisol level following the social performance stressor; this was not evident in the psoriasis group (r = 0.07; not significant). Patients who believed that their psoriasis was highly stress responsive had significantly lower salivary cortisol levels at baseline (P < 0.01) and lower serum cortisol levels following the social performance stressor (P = 0.016) than patients with nonstress-responsive disease who believed that stress had no impact. In contrast, there was no difference between the groups for change in pulse rate poststressor. CONCLUSIONS: This study shows that patients with psoriasis, and in particular those whose disease appears to be stress responsive, exhibit an altered HPA response to acute social stress. The implication is that such patients may perhaps be primed to flares of their psoriasis. Whether this is genetically predetermined and/or a consequence of the distress of living with psoriasis remains to be determined.

Adolescent↗
PubMed2005

Mechanisms of desensitization of the adrenocorticotropin response to arginine vasopressin in ovine anterior pituitary cells.

Arginine vasopressin (AVP) stimulates adrenocorticotropin (ACTH) secretion from corticotroph cells of the anterior pituitary via activation of the V1b vasopressin receptor, a member of the G protein-coupled receptor (GPCR) family. Recently, we have shown that treatment of ovine anterior pituitary cells with AVP for short periods results in reduced responsiveness to subsequent stimulation with AVP. The aim of this study was to investigate mechanisms involved in this desensitization process. Among the GPCR family, rapid desensitization is commonly mediated by receptor phosphorylation, with resensitization being mediated by internalization and subsequent dephosphorylation of the receptors by protein phosphatases. Since desensitization of V1a vasopressin receptors is mediated by protein kinase C-mediated receptor phosphorylation, we investigated the involvement of this enzyme in desensitization of the ACTH response to AVP. Treatment of perifused ovine anterior pituitary cells with the specific protein kinase C (PKC) activator 1,2-dioctanoyl-sn-glycerol (300 microM) did not induce any reduction in response to a subsequent 5-min stimulation with 100 nM AVP, despite potently stimulating ACTH secretion. Likewise, the results obtained using the PKC inhibitor Ro 31-8220 were not consistent with involvement of PKC in AVP desensitization: 2 microM Ro 31-8220 did not reduce the ability of a 10 nM AVP pretreatment to induce desensitization to a subsequent stimulation with 100 nM AVP. Pharmacologic blockade of receptor internalization by treatment with 0.25 mg/ml concanavalin A significantly impaired the ability of a 15-min pretreatment with 10 nM AVP to induce desensitization, rather than affecting resensitization. Treatment with 10 nM okadaic acid, an inhibitor of protein phosphatase 1 and 2A, had no effect on either resensitization or desensitization. In contrast, inhibition of protein phosphatase 2B (PP2B) with 1 microM FK506 decreased the rate of resensitization: complete recovery from desensitization took 40 min, whereas in controls recovery was complete 20 min after termination of the pretreatment. These results indicate that desensitization of the ACTH response to AVP is not mediated by PKC-catalyzed phosphorylation, suggesting subtype-specific differences in the regulation of V1a and V1b vasopressin receptors. The data demonstrate that desensitization was dependent, at least in part, upon receptor internalization and that resensitization was dependent upon PP2B-mediated receptor dephosphorylation.

Adrenocorticotropic Hormone↗
PubMed2003

Desensitization of the adrenocorticotrophin responses to arginine vasopressin and corticotrophin-releasing hormone in ovine anterior pituitary cells.

Following repeated or prolonged exposure to either corticotrophin-releasing hormone (CRH) or arginine vasopressin (AVP), pituitary adrenocorticotrophin (ACTH) responsiveness is reduced. This study compared the characteristics of desensitization to CRH and AVP in perifused ovine anterior pituitary cells. Desensitization to AVP occurred at relatively low AVP concentrations and was both rapid and readily reversible. Treatment for 25 min with AVP at concentrations greater than 2 nM caused significant reductions in the response to a subsequent 5 min 100 nM AVP pulse (IC(50)=6.54 nM). Significant desensitization was observed following pretreatment with 5 nM AVP for as briefly as 5 min. Desensitization was greater following a 10 min pretreatment, but longer exposures caused no further increase. Resensitization was complete within 40 min following 15 min treatment with 10 nM AVP. Continuous perifusion with 0.01 nM CRH had no effect on AVP-induced desensitization. Treatment with 0.1 nM CRH for either 25 or 50 min caused no reduction in the response to a subsequent 5 min stimulation with 10 nM CRH. When the pretreatment concentration was increased to 1 nM significant desensitization was observed, with a greater reduction in response occurring after 50 min treatment. Recovery of responsiveness was progressive following 50 min treatment with 1 nM CRH and was complete after 100 min. Our data show that in the sheep AVP desensitization can occur at concentrations and durations of AVP exposure within the endogenous ranges. This suggests that desensitization may play a key role in regulating ACTH secretion in vivo. If, as has been suggested, CRH acts to set corticotroph gain while AVP is the main dynamic regulator, any change in responsiveness to CRH may significantly influence the overall control of ACTH secretion.

Adrenocorticotropic Hormone↗
PubMed2002

Search for nu(mu)-->nu(e) and nu(mu)-->nu(e) oscillations at NuTeV.

Limits on nu(mu)-->nu(e) and nu(mu)-->nu(e) oscillations are extracted using the NuTeV detector with sign-selected nu(mu) and nu(mu) beams. In nu(mu) mode, for the case of sin(2)2alpha = 1, Delta(m)(2)>2.6 eV(2) is excluded, and for Delta(m)(2)>>1000 eV(2), sin(2)2alpha>1.1 x 10(-3). The NuTeV data exclude the high Delta(m)(2) end of nu(mu)-->nu(e) oscillation parameters favored by the LSND experiment without the need to assume that the oscillation parameters for nu and nu are the same. We present the most stringent experimental limits for nu(mu)(nu(mu))-->nu(e)(nu(e)) oscillations in the large Delta(m)(2) region.

Journal Article↗
PubMed2002

Precise determination of electroweak parameters in neutrino-nucleon scattering.

The NuTeV Collaboration has extracted the electroweak parameter sin(2)theta(W) from the measurement of the ratios of neutral current to charged current nu and (-)nu cross sections. Our value, sin(2)theta((on-shell))(W) = 0.2277 +/- 0.0013(stat) +/- 0.0009(syst), is 3 standard deviations above the standard model prediction. We also present a model independent analysis of the same data in terms of neutral-current quark couplings.

Journal Article↗
PubMed2002

Acute and chronic regulation of pituitary receptors for vasopressin and corticotropin releasing hormone.

At least two hypothalamic peptides, corticotropin releasing hormone (CRH) and vasopressin (VP), are important in regulating adrenocorticotropin (ACTH) release from the anterior pituitary. Both are secreted in a pulsatile manner and stimulate ACTH secretion by interacting with G protein-coupled receptors (GPCRs), namely the type 1 CRH receptor and V1b receptor, respectively. Repeated or prolonged stimulation with either peptide can cause reduced ACTH responsiveness or desensitisation, both in vivo and in vitro. Desensitisation of perifused sheep anterior pituitary cells to VP was found to be rapid and occurred following treatment with 5 nM VP for 5 min. This is within the range of concentrations and durations of VP pulses seen in sheep portal blood during acute stress. In contrast, significant desensitisation of the ACTH response to CRH required pre-treatment for longer than 25 min with a CRH concentration of 1 nM, suggesting that endogenous pulses may not elicit desensitisation. Although rapid GPCR desensitisation involves uncoupling of receptors from their G proteins, commonly mediated by receptor phosphorylation, and internalisation of receptors, desensitisation of neither the CRH nor VP receptor was mediated by PKA or PKC, respectively. Desensitisation of the response to VP was found to be dependent upon receptor internalisation, and resensitisation could be delayed by treatment with a protein phosphatase 2B inhibitor. The rapid kinetics of desensitisation of the ACTH response to VP suggest that this process is important in regulating the response to acute rather than chronic stress. If, as has been suggested, CRH acts in a permissive way to set corticotrope gain, desensitisation to CRH could also be important in long term regulation of ACTH secretion.

Adrenal Glands↗
PubMed2001

Extraction of R = sigma(L)/sigma(T) from CCFR nu(mu)-Fe and nu(mu)-Fe differential cross sections.

We report on the extraction of R = sigma(L)/sigma(T) from CCFR nu(mu)-Fe and nu(mu)-Fe differential cross sections. The CCFR differential cross sections do not show the deviations from the QCD expectations that are seen in the CDHSW data at very low and very high x. R as measured in nu(mu) scattering is in agreement with R as measured in muon and electron scattering. All data on R for Q(2)>1 GeV(2) are in agreement with a NNLO QCD calculation which uses NNLO parton distribution functions and includes target mass effects. We report on the first measurements of R in the low x and Q(2)<1 GeV(2) region (where an anomalous large rise in R for nuclear targets has been observed by the HERMES Collaboration).

Journal Article↗
PubMed2001

CD antigens 2001.

Explore the source record for details and available documents.

Antigens, CD↗
PubMed2001

Search for the lepton family number violating process nu(mu)e(-) --> mu(-)nu(e).

The NuTeV experiment at Fermilab has used a sign-selected neutrino beam to perform a search for the lepton number violating process nu(mu)e(-)-->mu(-)nu(e), and to measure the cross section of the standard model inverse muon decay process nu(mu)e(-)-->mu(-)nu(e). NuTeV measures the inverse muon decay asymptotic cross-section slope sigma/E to be (13.8 +/- 1.2 +/- 1.4) x 10(-42) cm(2)/GeV. The experiment also observes no evidence for lepton number violation and places one of the most restrictive limits on the cross-section ratio sigma(nu(mu)e(-)-->mu(-)nu(e))/sigma(nu(mu)e(-)-->mu(-)nu(e)) < or = 1.7% at 90% C.L. for V-A couplings and < or = 0.6% for scalar couplings.

Journal Article↗
PubMed2001

Observation of an anomalous number of dimuon events in a high energy neutrino beam.

A search for long-lived neutral particles ( N0's) with masses above 2.2 GeV/c(2) that decay into at least one muon has been performed using an instrumented decay channel at the NuTeV experiment at Fermilab. Data were examined for particles decaying into the final states mumu, mu(e), and mu(pi). Three mumu events were observed over an expected standard model background of 0.069+/-0.010 events; no events were observed in the other modes.

Journal Article↗
PubMed2001

First measurement of the low- x, low- Q(2) structure function F(2) in neutrino scattering.

A new structure function analysis of CCFR deep inelastic nu-N and nu-N scattering data is presented for previously unexplored kinematic regions down to Bjorken x = 0.0045 and Q(2) = 0.3 GeV(2). Comparisons to charged lepton scattering data from NMC and E665 experiments are made and the behavior of the structure function F(2)(nu)2 is studied in the limit Q(2)-->0.

Journal Article↗
PubMed2001

Measurements of F2 and xF(nu)(3) - xF(nu;)(3) from CCFR nu(mu)-Fe and nu;(mu)-Fe Data in a Physics Model-Independent Way.

We report on the extraction of the structure functions F2 and DeltaxF(3) = xF(nu)(3)-xF(nu;)(3) from CCFR nu(mu)-Fe and nu;(mu)-Fe differential cross sections. The extraction is performed in a physics model-independent (PMI) way. This first measurement of DeltaxF(3), which is useful in testing models of heavy charm production, is higher than current theoretical predictions. The ratio of the F2 (PMI) values measured in nu(mu) and mu scattering is in agreement (within 5%) with the predictions of next-to-leading-order parton distribution functions using massive charm production schemes, thus resolving the long-standing discrepancy between the two sets of data.

Journal Article↗
PubMed2001

GABA(A) receptors containing (alpha)5 subunits in the CA1 and CA3 hippocampal fields regulate ethanol-motivated behaviors: an extended ethanol reward circuitry.

GABA receptors within the mesolimbic circuitry have been proposed to play a role in regulating alcohol-seeking behaviors in the alcohol-preferring (P) rat. However, the precise GABA(A) receptor subunit(s) mediating the reinforcing properties of EtOH remains unknown. We examined the capacity of intrahippocampal infusions of an alpha5 subunit-selective ( approximately 75-fold) benzodiazepine (BDZ) inverse agonist [i.e., RY 023 (RY) (tert-butyl 8-(trimethylsilyl) acetylene-5,6-dihydro-5-methyl-6-oxo-4H-imidazo [1,5a] [1,4] benzodiazepine-3-carboxylate)] to alter lever pressing maintained by concurrent presentation of EtOH (10% v/v) and a saccharin solution (0.05% w/v). Bilateral (1.5-20 microgram) and unilateral (0.01-40 microgram) RY dose-dependently reduced EtOH-maintained responding, with saccharin-maintained responding being reduced only with the highest doses (e.g., 20 and 40 microgram). The competitive BDZ antagonist ZK 93426 (ZK) (7 microgram) reversed the RY-induced suppression on EtOH-maintained responding, confirming that the effect was mediated via the BDZ site on the GABA(A) receptor complex. Intrahippocampal modulation of the EtOH-maintained responding was site-specific; no antagonism by RY after intra-accumbens [nucleus accumbens (NACC)] and intraventral tegmental [ventral tegmental area (VTA)] infusions was observed. Because the VTA and NACC contain very high densities of alpha1 and alpha2 subunits, respectively, we determined whether RY exhibited a "negative" or "neutral" pharmacological profile at recombinant alpha1beta3gamma2, alpha2beta3gamma2, and alpha5beta3gamma2 receptors expressed in Xenopus oocytes. RY produced "classic" inverse agonism at all alpha receptor subtypes; thus, a neutral efficacy was not sufficient to explain the failure of RY to alter EtOH responding in the NACC or VTA. The results provide the first demonstration that the alpha5-containing GABA(A) receptors in the hippocampus play an important role in regulating EtOH-seeking behaviors.

Animals↗
PubMed2001

T-cell-mediated control of autoimmunity.

Inflammatory responses provoked by pathogens are antigen-specific in their induction but are nonspecific in their effects. Consequently, they are potentially damaging to the host that produces them. In addition, the immune system can respond specifically to self antigens, thereby giving rise to autoimmune diseases. A number of regulatory mechanisms have evolved to prevent such adverse effects. One of these has been shown to depend on a particular subset of CD4+ T cells that appears to have evolved specifically for this protective role. These cells are termed regulatory T cells. This review summarises what is known about them.

Animals↗
PubMed2001

Human CD4(+)CD25(+) thymocytes and peripheral T cells have immune suppressive activity in vitro.

CD4(+)CD25(+) T cells in mice and rats are capable of transferring protection against organ-specific autoimmune disease and colitis and suppressing the proliferation of other T cells after polyclonal stimulation in vitro. Here we describe the existence in humans of CD4(+)CD25(+) T cells with the same in vitro characteristics. CD4(+)CD8(-)CD25(+) T cells are present in both the thymus and peripheral blood of humans ( approximately 10 % of CD4(+)CD8(-) T cells), proliferate poorly in response to mitogenic stimulation and suppress the proliferation of CD4(+)CD25(-) cells in co-culture. This suppression requires cell contact and can be overcome by the addition of exogenous IL-2. CD4(+)CD25(+) cells from thymus and blood were poor producers of IL-2 and IFN-gamma, and suppressed the levels of these cytokines produced by CD4(+)CD25(-) cells. However, CD4(+)CD25(+) PBL produced higher levels of IL-4 and similar amounts of IL-10 as CD4(+)CD25(-) cells. Regulatory CD4(+)CD25(+) T cells have an activated phenotype in the thymus with expression of CTLA-4 and CD122 (IL-2Rbeta). The fact that CD4(+)CD25(+) regulatory T cells are present with a similar frequency in the thymus of humans, rats and mice, suggests that the role of these cells in the maintenance of immunological tolerance is an evolutionarily conserved mechanism.

Autoimmunity↗
PubMed2001

Coronary angioplasty and Rotablator atherectomy trial (CARAT): immediate and late results of a prospective multicenter randomized trial.

Mechanical rotational atherectomy with the Rotablator is widely used for percutaneous coronary revascularization, but the ideal debulking strategy remains unknown. The purpose of this study was to compare the immediate and late results after Rotablator using two treatment strategies: Large burrs (burr/artery ratio of >0.7) to achieve maximal debulking (lesion debulking strategy) or small burrs (burr/artery ratio < or = 0.7) to modify lesion compliance (lesion modification strategy). Two hundred twenty-two patients at six centers were prospectively enrolled in this study and randomly assigned to large (n = 104 patients with 118 lesions) or small (n = 118 patients with 136 lesions) burrs. The primary endpoint was final diameter stenosis at the end of the procedure, and secondary endpoints included inhospital angiographic and clinical complications, and target lesion revascularization at 6 months. Baseline demographic and angiographic characteristics were similar. There were no differences in procedural success, the extent of immediate lumen enlargement, inhospital ischemic complications, or late target vessel revascularization. However, compared with small burrs, patients randomized to large burrs were more likely to experience serious angiographic complications (5.1% vs. 12.7%, P < 0.05) immediately after atherectomy. This study suggests that a routine lesion modification strategy employing small burrs (burr/artery ratio < or = 0.7) achieves similar immediate lumen enlargement and late target vessel revascularization compared with a more aggressive debulking strategy (burr/artery ratio >0.7), but with fewer angiographic complications.

Aged↗