Interaction of hope and optimism with anxiety and depression in a specific group of cancer survivors: a preliminary study

<p>Abstract</p> <p>Background</p> <p>Anxiety and depression have been identified as a common psychological distress faced by the majority of cancer patients. With the increasing number of cancer cases, increasing demands will be placed on health systems to address effective psychosocial care and therapy. The objective of this study was to assess the possible role of hope and optimism on anxiety and depression. We also wanted to investigate if there is a specific component of hope that could play a role in buffering anxiety and depression amongst cancer patients.</p> <p>Methods</p> <p>A retrospective cross sectional study was conducted in the outpatient station of the Oral and Maxillofacial Surgery at the University of Hong Kong, Hong Kong SAR, PR-China. Fifty patients successfully treated for OC cancer were recruited after their informed consents had been obtained during the review clinic. During their regular follow-up controls in the outpatient clinic the patients compiled the hospital anxiety and depression scale (HADS), hope scale (HS) and the life orientation scale-revised (LOT-R).</p> <p>Results</p> <p>Hope was negatively correlated with depression (<it>r </it>= -.55, <it>p </it>< .001) and anxiety (r = -.38, <it>p </it>< .05). Similar pattern was found between optimism and the latter adjustment outcomes (depression: <it>r </it>= -.55, <it>p </it>< .001; anxiety: <it>r </it>= -.35, <it>p </it>< .05). Regression analyses indentified that both hope and optimism were significant predictors of depression. Hope and optimism had equal association with depression (hope: <it>β </it>= .40 versus optimism: <it>β </it>= .38). Hope and optimism together were significantly predictive of anxiety, whereas neither hope nor optimism alone was significant individual predictors of anxiety.</p> <p>Conclusions</p> <p>Hope and optimism both negatively correlated with patients' level of anxiety and depression. Besides theoretical implications, this study brings forward relevant findings related to developing specific clinical psychological care in the field of oncology that to date has not been researched specifically in the field of oncology. The results of this study will help guide the direction of future prospective studies in the field of oncology. This will contribute significantly to increasing patients quality of life as well enabling health care facilities to provide all cancer patients a more holistic cancer care.</p

Responsiveness of the EQ-5D in breast cancer patients in their first year after treatment

<p>Abstract</p> <p>Background/aim</p> <p>The EQ-5D is a generic health-related quality of life (HRQoL) measure that is used for the purpose of economic evaluations of health interventions. Therefore, it has to be responsive to meaningful changes in health in the patient population under investigation. The aim of this study was to investigate the responsiveness of the EQ-5D in breast cancer patients in their first year after treatment.</p> <p>Methods</p> <p>The subscale global health of the disease-specific HRQoL measure EORTC QLQ-C30 was used as a reference instrument to determine meaningful changes in health and identify subgroups of patients: patients reporting a moderate-large deterioration, small deterioration, a small improvement, moderate-large improvement, or no change in health status. Responsiveness was evaluated by calculating standardized response means (SRMs) in the five subgroups of patients and performing analysis of variance procedures. The two HRQoL measures were filled out two weeks and one year after finalizing curative treatment for breast cancer (n = 192).</p> <p>Results</p> <p>The EQ-5D was able to capture both improvements and deteriorations in HRQoL. SRMs of the EQ VAS and EQ-5D Index were close to zero in the subgroup reporting no change and increased and decreased adequately in the subgroups reporting small and moderate changes. Additional analysis of variance procedures showed that the EQ-5D was able to differentiate between subgroups of patients with no change and moderate-large deterioration or improvement in health.</p> <p>Conclusion</p> <p>The EQ-5D seems an appropriate measure for the purpose of economic evaluations of health intervention in breast cancer patients after treatment.</p> <p>Trial registration</p> <p>Current Controlled Trials ISRCTN74071417.</p

Pressure Load: The Main Factor for Altered Gene Expression in Right Ventricular Hypertrophy in Chronic Hypoxic Rats

BACKGROUND: The present study investigated whether changes in gene expression in the right ventricle following pulmonary hypertension can be attributed to hypoxia or pressure loading. METHODOLOGY/PRINCIPAL FINDINGS: To distinguish hypoxia from pressure-induced alterations, a group of rats underwent banding of the pulmonary trunk (PTB), sham operation, or the rats were exposed to normoxia or chronic, hypobaric hypoxia. Pressure measurements were performed and the right ventricle was analyzed by Affymetrix GeneChip, and selected genes were confirmed by quantitative PCR and immunoblotting. Right ventricular systolic blood pressure and right ventricle to body weight ratio were elevated in the PTB and the hypoxic rats. Expression of the same 172 genes was altered in the chronic hypoxic and PTB rats. Thus, gene expression of enzymes participating in fatty acid oxidation and the glycerol channel were downregulated. mRNA expression of aquaporin 7 was downregulated, but this was not the case for the protein expression. In contrast, monoamine oxidase A and tissue transglutaminase were upregulated both at gene and protein levels. 11 genes (e.g. insulin-like growth factor binding protein) were upregulated in the PTB experiment and downregulated in the hypoxic experiment, and 3 genes (e.g. c-kit tyrosine kinase) were downregulated in the PTB and upregulated in the hypoxic experiment. CONCLUSION/SIGNIFICANCE: Pressure load of the right ventricle induces a marked shift in the gene expression, which in case of the metabolic genes appears compensated at the protein level, while both expression of genes and proteins of importance for myocardial function and remodelling are altered by the increased pressure load of the right ventricle. These findings imply that treatment of pulmonary hypertension should also aim at reducing right ventricular pressure

Cellular changes in boric acid-treated DU-145 prostate cancer cells

Epidemiological, animal, and cell culture studies have identified boron as a chemopreventative agent in prostate cancer. The present objective was to identify boron-induced changes in the DU-145 human prostate cancer cell line. We show that prolonged exposure to pharmacologically-relevant levels of boric acid, the naturally occurring form of boron circulating in human plasma, induces the following morphological changes in cells: increases in granularity and intracellular vesicle content, enhanced cell spreading and decreased cell volume. Documented increases in β-galactosidase activity suggest that boric acid induces conversion to a senescent-like cellular phenotype. Boric acid also causes a dose-dependent reduction in cyclins A–E, as well as MAPK proteins, suggesting their contribution to proliferative inhibition. Furthermore, treated cells display reduced adhesion, migration and invasion potential, along with F-actin changes indicative of reduced metastatic potential. Finally, the observation of media acidosis in treated cells correlated with an accumulation of lysosome-associated membrane protein type 2 (LAMP-2)-negative acidic compartments. The challenge of future studies will be to identify the underlying mechanism responsible for the observed cellular responses to this natural blood constituent

Lithium Decreases Glial Fibrillary Acidic Protein in a Mouse Model of Alexander Disease.

Alexander disease is a fatal neurodegenerative disease caused by mutations in the astrocyte intermediate filament glial fibrillary acidic protein (GFAP). The disease is characterized by elevated levels of GFAP and the formation of protein aggregates, known as Rosenthal fibers, within astrocytes. Lithium has previously been shown to decrease protein aggregates by increasing the autophagy pathway for protein degradation. In addition, lithium has also been reported to decrease activation of the transcription factor STAT3, which is a regulator of GFAP transcription and astrogliogenesis. Here we tested whether lithium treatment would decrease levels of GFAP in a mouse model of Alexander disease. Mice with the Gfap-R236H point mutation were fed lithium food pellets for 4 to 8 weeks. Four weeks of treatment with LiCl at 0.5% in food pellets decreased GFAP protein and transcripts in several brain regions, although with mild side effects and some mortality. Extending the duration of treatment to 8 weeks resulted in higher mortality, and again with a decrease in GFAP in the surviving animals. Indicators of autophagy, such as LC3, were not increased, suggesting that lithium may decrease levels of GFAP through other pathways. Lithium reduced the levels of phosphorylated STAT3, suggesting this as one pathway mediating the effects on GFAP. In conclusion, lithium has the potential to decrease GFAP levels in Alexander disease, but with a narrow therapeutic window separating efficacy and toxicity

Spleen transcriptome response to infection with avian pathogenic Escherichia coli in broiler chickens

<p>Abstract</p> <p>Background</p> <p>Avian pathogenic <it>Escherichia coli </it>(APEC) is detrimental to poultry health and its zoonotic potential is a food safety concern. Regulation of antimicrobials in food-production animals has put greater focus on enhancing host resistance to bacterial infections through genetics. To better define effective mechanism of host resistance, global gene expression in the spleen of chickens, harvested at two times post-infection (PI) with APEC, was measured using microarray technology, in a design that will enable investigation of effects of vaccination, challenge, and pathology level.</p> <p>Results</p> <p>There were 1,101 genes significantly differentially expressed between severely infected and non-infected groups on day 1 PI and 1,723 on day 5 PI. Very little difference was seen between mildly infected and non-infected groups on either time point. Between birds exhibiting mild and severe pathology, there were 2 significantly differentially expressed genes on day 1 PI and 799 on day 5 PI. Groups with greater pathology had more genes with increased expression than decreased expression levels. Several predominate immune pathways, Toll-like receptor, Jak-STAT, and cytokine signaling, were represented between challenged and non-challenged groups. Vaccination had, surprisingly, no detectible effect on gene expression, although it significantly protected the birds from observable gross lesions. Functional characterization of significantly expressed genes revealed unique gene ontology classifications during each time point, with many unique to a particular treatment or class contrast.</p> <p>Conclusions</p> <p>More severe pathology caused by APEC infection was associated with a high level of gene expression differences and increase in gene expression levels. Many of the significantly differentially expressed genes were unique to a particular treatment, pathology level or time point. The present study not only investigates the transcriptomic regulations of APEC infection, but also the degree of pathology associated with that infection. This study will allow for greater discovery into host mechanisms for disease resistance, providing targets for marker assisted selection and advanced drug development.</p