865 resultados para Psychiatric phenotypes


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Psychiatric nurses have been facilitating therapeutic groups in acute psychiatric inpatient units for many years; however, there is a lack of nursing research related to this important aspect of care. This paper reports the findings of a study which aimed to gain an understanding of service users' experiences in relation to therapeutic group activities in an acute inpatient unit. A qualitative descriptive study was undertaken with eight service users in one acute psychiatric inpatient unit in Ireland. Data were collected using in-depth semi-structured interviews and analysed using Burnard's method of thematic content analysis. Several themes emerged from the findings which are presented in this paper.

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Purpose: The purpose of this study was toinvestigate moral distress in Irish psychiatric nurses. Design: A qualitative descriptive methodology was used. Findings: The study confirmed the presence of moral distress and the situations that gave rise to moral distress within psychiatric nurses working in acute care settings. Practice Implications: The findings indicate that while multidisciplinary teams appear to function well on the surface, situations that give rise to moral distress are not always acknowledged or dealt with effectively. Furthermore, unresolved moral conflict impacts upon the quality of clinical decision-making by not allowing open and transparent discussions that allow clinicians the opportunity to address their concerns adequately.

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The mechanisms responsible for increased cardiovascular risk associated with HIV-1 infection are incompletely defined. Using flow cytometry, in the present study, we examined activation phenotypes of monocyte subpopulations in patients with HIV-1 infection or acute coronary syndrome to find common cellular profiles. Nonclassic (CD14(+)CD16(++)) and intermediate (CD14(++)CD16(+)) monocytes are proportionally increased and express high levels of tissue factor and CD62P in HIV-1 infection. These proportions are related to viremia, T-cell activation, and plasma levels of IL-6. In vitro exposure of whole blood samples from uninfected control donors to lipopolysaccharide increased surface tissue factor expression on all monocyte subsets, but exposure to HIV-1 resulted in activation only of nonclassic monocytes. Remarkably, the profile of monocyte activation in uncontrolled HIV-1 disease mirrors that of acute coronary syndrome in uninfected persons. Therefore, drivers of immune activation and inflammation in HIV-1 disease may alter monocyte subpopulations and activation phenotype, contributing to a pro-atherothrombotic state that may drive cardiovascular risk in HIV-1 infection.

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This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette's syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader-Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies.

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BACKGROUND: The role of the microbiome has become synonymous with human health and disease. Bile acids, as essential components of the microbiome, have gained sustained credibility as potential modulators of cancer progression in several disease models. At physiological concentrations, bile acids appear to influence cancer phenotypes, although conflicting data surrounds their precise physiological mechanism of action. Previously, we demonstrated bile acids destabilised the HIF-1α subunit of the Hypoxic-Inducible Factor-1 (HIF-1) transcription factor. HIF-1 overexpression is an early biomarker of tumour metastasis and is associated with tumour resistance to conventional therapies, and poor prognosis in a range of different cancers. METHODS: Here we investigated the effects of bile acids on the cancer growth and migratory potential of cell lines where HIF-1α is known to be active under hypoxic conditions. HIF-1α status was investigated in A-549 lung, DU-145 prostate and MCF-7 breast cancer cell lines exposed to bile acids (CDCA and DCA). Cell adhesion, invasion, migration was assessed in DU-145 cells while clonogenic growth was assessed in all cell lines. RESULTS: Intracellular HIF-1α was destabilised in the presence of bile acids in all cell lines tested. Bile acids were not cytotoxic but exhibited greatly reduced clonogenic potential in two out of three cell lines. In the migratory prostate cancer cell line DU-145, bile acids impaired cell adhesion, migration and invasion. CDCA and DCA destabilised HIF-1α in all cells and significantly suppressed key cancer progression associated phenotypes; clonogenic growth, invasion and migration in DU-145 cells. CONCLUSIONS: These findings suggest previously unobserved roles for bile acids as physiologically relevant molecules targeting hypoxic tumour progression.

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Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.

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Recent studies suggest that lung cancer stem cells (CSCs) may play major roles in lung cancer development, metastasis and drug resistance. Therefore, identification of lung CSC drivers may provide promising targets for lung cancer. TAZ (transcriptional co-activator with PDZ-binding motif) is a transcriptional co-activator and key downstream effector of the Hippo pathway, which plays critical roles in various biological processes. TAZ has been shown to be overexpressed in non-small cell lung cancer (NSCLC) and involved in tumorigenicity of lung epithelial cells. However, whether TAZ is a driver for lung CSCs and tumor formation in vivo is unknown. In addition, the molecular mechanism underlying TAZ-induced lung tumorigenesis remains to be determined. In this study, we provided evidence that constitutively active TAZ (TAZ-S89A) is a driver for lung tumorigenesis in vivo in mice and formation of lung CSC. Oncogenes upregulated in TAZ-overexpressing cells were identified with further validation. The most dramatically activated gene, Aldh1a1 (Aldehyde dehydrogenase 1 family member a1), a well-established CSC marker, showed that TAZ induces Aldh1a1 transcription by activating its promoter activity through interaction with the transcription factor TEA domain (TEAD) family member. Most significantly, inhibition of ALDH1A1 with its inhibitor A37 or CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) gene knockout in lung cancer cells suppressed lung tumorigenic and CSC phenotypes in vitro, and tumor formation in mice in vivo. In conclusion, this study identified TAZ as a novel inducer of lung CSCs and the first transcriptional activator of the stem cell marker ALDH1A1. Most significantly, we identified ALDH1A1 as a critical meditator of TAZ-induced tumorigenic and CSC phenotypes in lung cancer. Our studies provided preclinical data for targeting of TAZ-TEAD-ALDH1A1 signaling to inhibit CSC-induced lung tumorigenesis and drug resistance in the future.

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Private law courts in the UK have maintained the de minimis threshold as a condition precedent for a successful claim for the infliction of mental harm. This de minimis threshold necessitates the presence of a ‘recognised psychiatric illness’ as opposed to ‘mere emotion’. This standard has also been adopted by the criminal law courts when reading the Offences Against the Person Act 1861 to include non-physical injury. In determining the cut-off point between psychiatric injury and mere emotion, the courts have adopted a generally passive acceptance of expert testimony and the guidelines used by mental health professionals to make diagnoses. Yet these guidelines were developed for use in a clinical setting, not a legal one. This article examines the difficulty inherent in utilising the ‘dimensional’ diagnostic criteria used by mental health professionals to answer ‘categorical’ legal questions. This is of particular concern following publication of the new diagnostic manual, DSM-V in 2013, which will further exacerbate concerns about compatibility. It is argued that a new set of diagnostic guidelines, tailored specifically for use in a legal context, is now a necessity.

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In this article I introduce the therapeutic potential that the psychodrama gives to the treatment of the patients with severe mental disorder. I propose the specific characteristics that, from the clinic practice in a Psychiatric Day Hospital of Madrid, have specially revealed fertile to the persons that participate in and also to the community framing and its assembly in the framework of a transdisciplinary work.

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RNA ligases function pervasively across the three kingdoms of life for RNA repair, splicing and can be stress induced. The RtcB protein (also HSPC117, C22orf28, FAAP and D10Wsu52e) is one such conserved ligase, involved in tRNA and mRNA splicing. However, its physiological role is poorly described, especially in bacteria. We now show in Escherichia coli bacteria that the RtcR activated rtcAB genes function for ribosome homeostasis involving rRNA stability. Expression of rtcAB is activated by agents and genetic lesions which impair the translation apparatus or may cause oxidative damage in the cell. Rtc helps the cell to survive challenges to the translation apparatus, including ribosome targeting antibiotics. Further, loss of Rtc causes profound changes in chemotaxis and motility. Together, our data suggest that the Rtc system is part of a previously unrecognised adaptive response linking ribosome homeostasis with basic cell physiology and behaviour.

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Objectives: Elevated shame and dissociation are common in dissociative identity disorder (DID) and chronic posttraumatic stress disorder (PTSD) and are part of the constellation of symptoms defined as complex PTSD. Previous work examined the relationship between shame, dissociation, and complex PTSD and whether they are associated with intimate relationship anxiety, relationship depression, and fear of relationships. This study investigated these variables in traumatized clinical samples and a nonclinical community group.

Method: Participants were drawn from the DID (n = 20), conflict-related chronic PTSD (n = 65), and nonclinical (n = 125) populations and completed questionnaires assessing the variables of interest. A model examining the direct impact of shame and dissociation on relationship functioning, and their indirect effect via complex PTSD symptoms, was tested through path analysis.

Results: The DID sample reported significantly higher dissociation, shame, complex PTSD symptom severity, relationship anxiety, relationship depression, and fear of relationships than the other two samples. Support was found for the proposed model, with shame directly affecting relationship anxiety and fear of relationships, and pathological dissociation directly affecting relationship anxiety and relationship depression. The indirect effect of shame and dissociation via complex PTSD symptom severity was evident on all relationship variables.

Conclusion: Shame and pathological dissociation are important for not only the effect they have on the development of other complex PTSD symptoms, but also their direct and indirect effects on distress associated with relationships.

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Introduction: While it is recommended that mental health professionals engage in family focused practice (FFP), there is limited understanding regarding psychiatric nurses’ practice with parents who have mental illness, their children and families in adult mental health services.

Methods: This study utilized a mixed methods approach to measure the extent of psychiatric nurses’ family focused practice and factors that predicted it. It also sought to explore the nature and scope of high scoring psychiatric nurses’ FFP and factors that affected their capacity to engage in FFP. Three hundred and forty three psychiatric nurses in 12 mental health services throughout Ireland completed the Family Focused Mental Health Practice Questionnaire (FFMHPQ). Fourteen nurses who achieved high scores on the FFMHPQ also participated in semi-structured interviews.

Results: Whilst the majority of nurses were not family focused a substantial minority were. High scoring nurses’ practice was complex and multifaceted, comprising various family focused activities, principles and processes. Nurses’ capacity to engage in FFP was determined by their knowledge and skills, working in community settings and own parenting experience.

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The transition of Psychiatric Medical Institutions for Children (PMIC) into the Iowa Plan occurred on July 1, 2012, without substantive changes as recommended by the PMIC Transition Committee. As a result, some PMICs have increased their ability to provide flexible services while retaining the ability for longer term residential capacity for children with high end mental health needs. As part of the Iowa Plan, PMICs have been able to include more services and discussion among clinical professionals in determining how to best meet the needs of a child.