842 resultados para Talk


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The process of eliciting client language toward change (change talk [CT]) is implicated as a causal mechanism in motivational interviewing (MI) and brief motivational interventions (BMI). We investigated the articulation of counselor behaviors and CT during BMI with young men. We coded 149 sessions using the Motivational Interviewing Skill Code and summarized these codes into three counselor categories (MI-consistent [MICO], MI-inconsistent [MIIN], other) and three client categories (CT, counter CT [CCT], follow/neutral [F/N]). We then computed immediate transition frequencies and odds ratios using sequential analysis software. CT was significantly more likely following MICO behaviors, whereas MIIN behaviors only led to CCT and F/N. This strongly supports the use of MI skills to elicit CT during BMI with young men, whose speech also predicted counselor behaviors (particularly CT to MICO and CCT to MIIN). Additional analyses showed that among MICO behaviors, reflective listening may be a particularly powerful technique to elicit CT.

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Analysis of genetically engineered mice deficient in cell cycle regulators, including E2F1, cdk4, and pRB, showed that the major phenotypes are metabolic perturbations. These key cell cycle regulators contribute to lipid synthesis, glucose production, insulin secretion, and glycolytic metabolism. It has been shown that deregulation of these pathways can lead to metabolic perturbations and related metabolic diseases, such as obesity and type II diabetes. The cyclin-cdk-Rb-E2F1 pathway regulates adipogenesis in addition to its well-described roles in cell cycle regulation and cancer. It was also shown that E2F1 directly participates in the regulation of pancreatic growth and function. Similarly, cyclin D3, cdk4, and cdk9 are also adipogenic factors with strong effects on whole organism metabolism. These examples support the emerging notion that cell cycle regulatory proteins also modulate metabolic processes. These cell cycle regulators are activated by insulin and glucose, even in non-proliferating cells. Most importantly, these cell cycle regulators trigger the adaptive metabolic switch that normal and cancer cells require in order to proliferate. These changes include increased lipid synthesis, decreased oxidative metabolism, and increased glycolytic metabolism. In summary, these factors are essential regulators of anabolic biosynthetic processes, blocking at the same time oxidative and catabolic pathways, which is reminiscent of cancer cell metabolism.

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Veterans of infection, Leishmania parasites have been plaguing mammals for centuries, causing a morbidity toll second only to that of malaria as the most devastating protozoan parasitic disease in the world. Cutaneous leishmaniasis (CL) is, by far, the most prevalent form of the disease, with symptoms ranging from a single self-healing lesion to chronic metastatic leishmaniasis (ML). In an increasingly immunocompromised population, complicated CL is becoming a more likely outcome, characterized by severely inflamed, destructive lesions that are often refractory to current treatment. This is perhaps because our ageing arsenal of variably effective antileishmanial drugs may be directly or indirectly immunomodulatory and may thus have variable effects in each type and stage of CL. Indeed, widely differing immune biases are created by the various species of Leishmania, and these immunological watersheds are further shifted by extrinsic disturbances in immune homeostasis. For example, we recently showed that a naturally occurring RNA virus (Leishmania RNA virus (LRV)) within some Leishmania parasites creates hyperinflammatory cross-talk, which can predispose to ML: a case of immunological misfire that may require a different approach to immunotherapy, whereby treatments are tailored to underlying immune biases. Understanding the intersecting immune pathways of leishmaniasis and its co-infections will enable us to identify new drug targets, and thereby design therapeutic strategies that work by untangling the immunological cross-wires of pathogenic cross-talk.

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The c-Jun N-terminal kinase (JNK) is a mitogen-activated protein kinase (MAPK) activated by stress-signals and involved in many different diseases. Previous results proved the powerful effect of the cell permeable peptide inhibitor d-JNKI1 (d-retro-inverso form of c-Jun N-terminal kinase-inhibitor) against neuronal death in CNS diseases, but the precise features of this neuroprotection remain unclear. We here performed cell-free and in vitro experiments for a deeper characterization of d-JNKI1 features in physiological conditions. This peptide works by preventing JNK interaction with its c-Jun N-terminal kinase-binding domain (JBD) dependent targets. We here focused on the two JNK upstream MAPKKs, mitogen-activated protein kinase kinase 4 (MKK4) and mitogen-activated protein kinase kinase 7 (MKK7), because they contain a JBD homology domain. We proved that d-JNKI1 prevents MKK4 and MKK7 activity in cell-free and in vitro experiments: these MAPKK could be considered not only activators but also substrates of JNK. This means that d-JNKI1 can interrupt downstream but also upstream events along the JNK cascade, highlighting a new remarkable feature of this peptide. We also showed the lack of any direct effect of the peptide on p38, MEK1, and extracellular signal-regulated kinase (ERK) in cell free, while in rat primary cortical neurons JNK inhibition activates the MEK1-ERK-Ets1/c-Fos cascade. JNK inhibition induces a compensatory effect and leads to ERK activation via MEK1, resulting in an activation of the survival pathway-(MEK1/ERK) as a consequence of the death pathway-(JNK) inhibition. This study should hold as an important step to clarify the strong neuroprotective effect of d-JNKI1.

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Background: Patient change talk (CT) during brief motivational interventions (BMI) has been linked with subsequent changes in drinking in clinical settings but this link has not been clearly established among young people in non-clinical populations. Objective: To determine which of several CT dimensions assessed during an effective BMI delivered in a non-clinical setting to 20-year old men are associated with drinking 6 months later. Methods: Of 125 individuals receiving a face-to-face BMI session (15.8 ± 5.4 minutes), we recorded and coded a subsample of 42 sessions using the Motivational Interviewing Skill Code 2.1. Each patient change talk utterance was categorized as `Reason´, `Ability´, `Desire´, `Need´, `Commitment´, `Taking steps´, or `Other´. Each utterance was graded according to its strength (absolute value from 1 to 3) and direction (i.e. towards (positive sign) or away (negative sign) from change/in favor of status quo). `Ability´, `Desire´, and `Need´ to change (`ADN´) were grouped together since these codes were too scarce to conduct analyses. Mean strength scores over the entire session were computed for each dimension and later dichotomized in towards change (i.e. mean core > 0) and away from change/in favor of status quo. Negative binomial regression models were used to assess the relationship between CT dimensions and drinking 6 months later, adjusting for drinking at baseline. Results: Compared to subjects with a `Taking steps´ score away from change/in favor of status quo, subjects with a positive `Taking steps´ score reported significantly less drinking 6 months later (Incidence Rate Ration [IRR] for drinks per week: 0.56, 95% Confidence Interval [CI] 0.31, 1.00). IRR (95%CI) for subjects with a positive `ADN´ score was 0.58, (0.32, 1.03). For subjects with a positive `Reason´, `Commitment´, and `Other´ scores, IRR (95%CI) were 1.28 (0.77; 2.12) 1.63 (0.85; 3.14) and 1.03 (0.61; 1.72), respectively. Conclusion: A change talk dimension reflecting steps taken towards change (`Taking steps´) is associated with less drinking 6 months later among young men receiving a BMI in a non-clinical setting. Encouraging patients to take steps towa change may be a worthy objective for clinicians and may explain BMI efficacy.

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The peroxisome proliferator-activated receptors (PPAR) and thyroid hormone receptors (TR) are members of the nuclear receptor superfamily, which regulate lipid metabolism and tissue differentiation. In order to bind to DNA and activate transcription, PPAR requires the formation of heterodimers with the retinoid X receptor (RXR). In addition to activating transcription through its own response elements, PPAR is able to selectively down-regulate the transcriptional activity of TR, but not vitamin D receptor. The molecular basis of this functional interaction has not been fully elucidated. By means of site-directed mutagenesis of hPPAR alpha we mapped its inhibitory action on TR to a leucine zipper-like motif in the ligand binding domain of PPAR, which is highly conserved among all subtypes of this receptor and mediates heterodimerization with RXR. Replacement of a single leucine by arginine at position 433 of hPPAR alpha (L433R) abolished heterodimerization of PPAR with RXR and consequently its trans-activating capacity. However, a similar mutation of a leucine residue to arginine at position 422 showed no alteration of heterodimerization, DNA binding, or transcriptional activation. The dimerization deficient mutant L433R was no longer able to inhibit TR action, demonstrating that the selective inhibitory effect of PPAR results from the competition for RXR as well as possibly for other TR-auxiliary proteins. In contrast, abolition of DNA binding by a mutation in the P-box of PPAR (C122S) did not eliminate the inhibition of TR trans-activation, indicating that competition for DNA binding is not involved. Additionally, no evidence for the formation of PPAR:TR heterodimers was found in co-immunoprecipitation experiments. In summary, we have demonstrated that PPAR selectively inhibits the transcriptional activity of TRs by competition for RXR and possibly non-RXR TR-auxiliary proteins. In contrast, this functional interaction is independent of the formation of PPAR:TR heterodimers or competition for DNA binding.

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Client change talk (CT) during motivational interviewing and brief motivational interventions (BMIs) have been described as predictors of behavior change, but these links have not been clearly evaluated in research on young people. Within 127 BMIs with 20-year-old men with at-risk alcohol consumption, each CT utterance was categorized and given a strength rating using the Motivational Interviewing Skill Code 2.1. Several ways of categorizing and measuring CT were tested using stepwise regression procedures. Overall CT measures were not significantly related to changes in drinking at 6-month follow-up. Regarding CT sub-dimensions, the frequency of ability/desire/need to change and of ability/desire/need not to change, as well as the average strength of ability/desire/need, predicted significant change in the expected direction. CT length was not significantly linked to outcome. The frequency and strength with which some CT sub-dimensions are expressed during BMI seemed to be important predictors of change in drinking among young men and might thus be especially important for clinicians to notice.

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The performance of Pseudomonas biocontrol agents may be improved by applying mixtures of strains which are complementary in their capacity to suppress plant diseases. Here, we have chosen the combination of Pseudomonas fluorescens CHA0 with another well-characterized biocontrol agent, P. fluorescens Q2-87, as a model to study how these strains affect each other's expression of a biocontrol trait. In both strains, production of the antimicrobial compound 2,4-diacetylphloroglucinol (DAPG) is a crucial factor contributing to the suppression of root diseases. DAPG acts as a signaling compound inducing the expression of its own biosynthetic genes. Experimental setups were developed to investigate whether, when combining strains CHA0 and Q2-87, DAPG excreted by one strain may influence expression of DAPG-biosynthetic genes in the other strain in vitro and on the roots of wheat. DAPG production was monitored by observing the expression of lacZ fused to the biosynthetic gene phlA of the respective strain. Dual-culture assays in which the two strains were grown in liquid medium physically separated by a membrane revealed that Q2-87 but not its DAPG-negative mutant Q2-87::Tn5-1 strongly induced phlA expression in a DeltaphlA mutant of strain CHA0. In the same way, phlA expression in a Q2-87 background was induced by DAPG produced by CHA0. When coinoculated onto the roots of wheat seedlings grown under gnotobiotic conditions, strains Q2-87 and CHA0, but not their respective DAPG-negative mutants, were able to enhance phlA expression in each other. In summary, we have established that two nonrelated pseudomonads may stimulate each other in the expression of an antimicrobial compound important for biocontrol. This interpopulation communication occurs in the rhizosphere, i.e., at the site of pathogen inhibition, and is mediated by the antimicrobial compound itself acting as a signal exchanged between the two pseudomonads.

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Catalonia is a bilingual country where the presence of English in the social context is small; the amount of input received by the primary education pupils is very little and this input mainly comes from the English lessons at school. Consequently, this situation combined with the increasing demand for English and the fact that the new generations want to become communicatively competent in English place the role of English teachers in a relevant position. This research project analyses the role of the English teacher talk; in particular, the study focuses on the teacher’s oral productions in foreign language lessons (EFL) and in content-based lessons (CLIL).

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OBJECTIVE: Client change talk has been proposed as a mechanism of change in motivational interviewing (MI) by mediating the link between therapist MI-consistent behaviors (MICO) and client behavioral outcomes. We tested under what circumstances this mechanism was supported in the context of a clinical trial of brief MI for heavy drinking among nontreatment seeking young men. METHOD: We conducted psycholinguistic coding of 174 sessions using the MI Skill Code 2.1 and derived the frequency of MICO and the strength of change talk (CTS) averaged over the session. CTS was examined as a mediator of the relationship between MICO and a drinking composite score measured at 3-month follow-up, controlling for the composite measure at baseline. Finally, we tested therapist gender and MI experience as well as client readiness to change and alcohol problem severity as moderators of this mediation model. RESULTS: CTS significantly predicted outcome (higher strength related to less drinking), but MICO did not predict CTS. However, CTS mediated the relationship between MICO and drinking outcomes when therapists had more experience in MI and when clients had more severe alcohol problems (i.e., significant conditional indirect effects). CONCLUSIONS: The mechanism hypothesized by MI theory was operative in our brief MI with heavy drinking young men, but only under particular conditions. Our results suggest that attention should be paid to therapist selection, training, and/or supervision until they reach a certain level of competence, and that MI might not be appropriate for nontreatment seeking clients drinking at a lower level of risk. (PsycINFO Database Record