Publications by authors named "Lapp W"

Background: Motivation to change substance use behavior is an important component of the recovery process that has usually been studied at entry into treatment. Less studied, but equally important, is the measurement of motivation over time and the role motivation plays in subsequent substance use.

Objectives: The present study sought to examine longitudinal motivation toward sobriety among residents of sober living houses.

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Protein tyrosine phosphatase 1B (PTP-1B) is a ubiquitously expressed cytosolic phosphatase with the ability to dephosphorylate JAK2 and TYK2, and thereby down-regulate cytokine receptor signaling. Furthermore, PTP-1B levels are up-regulated in certain chronic myelogenous leukemia patients, which points to a potential role for PTP-1B in myeloid development. The results presented here show that the absence of PTP-1B affects murine myelopoiesis by modifying the ratio of monocytes to granulocytes in vivo.

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We investigated the association of peri-operative myocardial ischaemia with activation of coagulation and endogenous fibrinolysis in patients undergoing vascular surgery. In 50 patients, continuous Holter monitoring was performed to assess peri-operative myocardial ischaemia and 12-lead electrocardiography was recorded preoperatively and 72 h postoperatively to assess myocardial infarction. Serial blood samples were drawn peri-operatively to determine the concentrations of fibrin monomers (for activation of coagulation), D-dimer (for endogenous fibrinolysis) and cardiac troponin T and I.

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The deregulation of the immune response is a critical component in inflammatory disease. Recent in vitro data show that T-cell protein tyrosine phosphatase (TC-PTP) is a negative regulator of cytokine signaling. Furthermore, tc-ptp(-/-) mice display immune defects and die within 5 weeks of birth.

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Unlabelled: Isolated systolic blood pressure has not been sufficiently studied in the perioperative setting and may contribute to morbidity and mortality after coronary artery bypass grafting (CABG) surgery. Our objective was to determine the prevalence of isolated systolic hypertension among patients who had CABG surgery and to assess whether isolated systolic hypertension is associated with perioperative and postoperative in-hospital morbidity or mortality. Patients who underwent CABG were selected from a prospective epidemiological study involving 2417 patients in 24 medical centers.

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In recent years, the T-cell protein tyrosine phosphatase (TC-PTP) has become an important member of the protein-tyrosine phosphatase (PTP) family in two aspects. Firstly, TC-PTP has been reported to act on downstream signalling events initiated by the epidermal growth receptor, suggesting that it may act as an important modulator of receptor tyrosine kinases and mitogenic signalling. Secondly, the finding of immune deficiency and lethality observed in TC-PTP null mice emphasizes the importance of this small PTP in the hematopoietic system.

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During acute graft-versus-host disease (GVHD) the activation of macrophages (Mphi) is mediated by 2 signals, interferon (IFN)-gamma and bacteria-derived lipopolysaccharide (LPS). A cascade of inflammatory responses that includes the release of mediators of tissue injury follows Mphi activation. Among the tissues characteristically targeted during acute GVHD are epithelial tissues of the skin and gastrointestinal tract that normally undergo continuous proliferation and are therefore sensitive to cytostatic processes.

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We have previously shown that both priming and triggering signals were needed for nitric oxide production by decidual macrophages and that nitric oxide was responsible for embryo wastage. In this study, we investigated the role of IFN-gamma as the primary signal for macrophage activation in early embryo loss. IFN-gamma-deficient (GKO) and heterozygous F1 control mice were injected with lipopolysaccharide (LPS) at day 7 of gestation.

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The T cell protein tyrosine phosphatase (TC-PTP) is one of the most abundant mammalian tyrosine phosphatases in hematopoietic cells; however, its role in hematopoietic cell function remains unknown. In this report, we investigated the physiological function(s) of TC-PTP by generating TC-PTP-deficient mutant mice. The three genotypes (+/+, +/-, -/-) showed mendelian segregation at birth (1:2:1) demonstrating that the absence of TC-PTP was not lethal in utero, but all homozygous mutant mice died by 3-5 wk of age, displaying runting, splenomegaly, and lymphadenopathy.

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In early embryo loss, the activation of maternal immune effector mechanisms play a critical role in determining the success or failure of a pregnancy. We have previously shown that increased nitric oxide production by decidual macrophages is involved in early embryo loss occurring at day 12 of gestation. In this study, using reverse transcription-PCR and Southern blotting, the expression of inducible nitric oxide synthases (iNOS) and TNF-alpha mRNA was determined to quantify macrophage activation in individual murine embryos in a model of spontaneous early embryo loss.

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In a previous report the authors demonstrated that acute graft-versus-host disease (GVHD) was associated with pathologic amounts of tumour necrosis factor alpha (TNF-alpha) and the appearance of lipopolysaccharide (LPS) in the blood of GVH reactive mice just prior to death. In this study the authors have investigated the kinetics of LPS accumulation in different organs during the course of acute GVHD using a murine model. Unirradiated C57BL/6 x AF1 (B6AF(1)) mice were transplanted with C57BL/6 (B6) lymphoid cells and killed at predetermined times after transplantation for LPS analysis.

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The onset of acute graft-vs-host disease (aGVHD) is accompanied by macrophage (M phi) priming and the presence of bacteria-derived LPS in the sera of transplanted animals. Priming of M phi occurs during aGVHD despite the suppression of T cell function. We have investigated whether IL-12 mediates the continued production of IFN-gamma during the state of T cell immunosuppression that accompanies aGVHD.

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Previously, we demonstrated that immature CD4+8+ and mature CD4+ thymocyte populations were selectively eliminated during murine graft-versus-host disease (GVHD) as a consequence of elevated levels of endogenous glucocorticoids. In this report, we investigated whether the marked reduction of CD4+8+ and CD4+ thymocyte populations would affect host CD4+ and CD8+ T cell populations in the spleens and lymph nodes (LN) of mice undergoing GVHD. GVHD was induced in (C57BL/6 x A)F1 (B6AF1) mice by injecting A strain parental lymphoid cells.

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GVHD in animal models induces severe thymic atrophy as a result of prolonged secretion of high concentrations of adrenal glucocorticoids. In this study we investigated the mechanism responsible for the persistent stimulation of the adrenal glands to secrete glucocorticoids in mice undergoing GVHD. GVHD was induced across the major and multiple minor histocompatibility antigen difference in unirradiated C57Bl/6 x AF1 hybrid mice by the intravenous injection of A strain parental lymphoid cells.

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Studies have shown that graft-vs-host disease (GVHD) in animal models induces persistent elevated levels of circulating adrenal glucocorticoids. In this report, we investigated the effects of endogenous glucocorticoids on the outcome of GVHD by adrenalectomizing (ADX) unirradiated (C57BL/6 x A)F1 (B6AF1) mice before GVHD induction. GVHD was induced by injection of 20 x 10(6) A strain parental lymphoid cells into B6AF1 mice.

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The graft-versus-host reaction (GVHR) results in profound, long-lasting immunosuppression characterized by T cell unresponsiveness to antigenic and mitogenic stimuli. In this report, the roles of the protein tyrosine kinases p56lck and p59fyn in GVHR-induced T cell anergy were investigated. GVHR was induced by the intravenous transfer of parental lymphoid cells into F1 hybrid recipient mice.

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The nature of the effector cell(s) responsible for the depression of B-cell genesis in the bone marrow of mice undergoing systemic graft-versus-host disease (GVHD) has been examined. Donor C57BL/6 (B6) mice were treated in vivo with either a single injection of anti-asialo GM1 antibody (anti-ASGM1) to eliminate naturally occurring (endogenous) ASGM1+ cells or B6xAF1 (B6AF1) lymphoid cells followed by anti-ASGM1 to eliminate both endogenous and "induced" ASGM1+ cells. Lymphoid cells from donor mice after the elimination of endogenous ASGM1+ cells produced severe GVHD and concomitant depression of B-cell genesis when injected into B6AF1 recipients.

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The limit violation effect (LVE) was studied by inducing male social drinkers to consume either more or less beer than their prestated limit on alcohol intake. Affective and behavioral reactions to the violation of drinking limits were mediated by attributional style and aspects of drinking restraint. Subjects who reported greater than average levels of self-blaming attributions, restrictions on alcohol intake and cognitive preoccupation with alcohol became depressed and angry after the violation of drinking limits.

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In this report, the relationship between irradiation and graft-versus-host disease (GVHD)-induced cutaneous injury was investigated. Unirradiated F1 hybrid mice were grafted with irradiated skin and then injected with parental strain lymphoid cells to induce GVHD. Although low grade dermal lymphoid infiltrates were observed in unirradiated skin grafts of some GVH-reactive mice, and irradiated grafts of normal animals showed occasional fibrosis, only the irradiated grafts of GVH-reactive mice developed lesions consisting of vacuolar degeneration of the epidermal-dermal junction and necrotic keratinocytes accompanied by pronounced epidermal infiltrates, characteristic of clinical cutaneous GVHD.

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Time perception is affected by the pharmacological action of many drugs, but the contribution of expected effects of drugs has not been considered. A new design, the extended balanced placebo design (EBPD), is presented to study both the pharmacological and expected effects of alcohol on time perception. The EBPD makes it possible to examine the effects of alcohol across a broad range of expected and pharmacological doses.

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Creative individuals may use psychoactive drugs to enhance their ability to produce creative works, but it is difficult to differentiate the pharmacological effects from other influences. Part of the problem is that creativity defies any simple definition, making it hard to determine when or how much creativity is evident. The other major obstacle is that life circumstances are confounded with the propensity to use drugs (including alcohol), so the causal relation of drugs to creativity is uncertain.

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One way of scoring the Ways of Coping Checklist is to compute relative1 proportional scores in which the mean score for each scale is divided by the sum of the means for all of the scales. The proportional scoring method reportedly sets the score on each scale relative to the score for the whole scale. Using the proportional scores, direct comparisons can be made for the profiles of subjects who differ in term of the sheer magnitude of their responses.

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The graft-vs.-host reaction (GVHR) results in damage to the epithelial and lymphoid compartments of the thymus and thus in abnormal maturation and function of thymocytes in mice undergoing GVHR. In this report, the effects of GVHR on thymic T cell receptor (TCR) expression and usage have been investigated.

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In the present study, the measurement of drinking restraint was broadened by developing new items that better characterized its cognitive nature as well as by testing a factor structure which represents restraint as including both the regulation and the failure to regulate alcohol intake. A previously observed (Collins, George & Lapp, 1989) three-component structure of the Restrained Drinking Scale (RDS; Ruderman & McKirnan, 1984) was confirmed. In addition, two factors were extracted from the new set of cognitive items, which when combined with the RDS clusters formed a new measure of drinking restraint, the Temptation and Restraint Inventory (TRI).

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In this report we have investigated macrophage (M phi) activity and tumor necrosis factor alpha (TNF-alpha) production during graft-vs.-host disease (GVHD). TNF-alpha production by M phi requires two signals: priming of M phi by interferon followed by triggering of TNF-alpha production and release by lipopolysaccharide (LPS).

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