Promoting Team-Based Exercise Among African American Breast Cancer Survivors

Physical activity benefits the health and well-being of breast cancer survivors (BCS). Yet, many African American survivors do not routinely exercise and have increased risk of poor outcomes. The purpose of this mixed-method study was to identify motivational factors compelling African American BCS to participate in a 14-week team walking program and to intend to continue exercise after the intervention concluded. Focus groups were held with participants (n = 12) before and after training. Content analysis discovered themes before the intervention: Not wanting to go at it alone, exercise not a life or treatment priority, cancer treatment affected activity, advocates to exercise, and can exercise really help? Four themes postintervention themes included: In the same boat, changed mind-set, improved weight and activity, and overcoming barriers. Physical data verified improvements. Results suggest that a team-based exercise training program may assist in overcoming a sedentary behavior tendency and subsequently improve health among survivors

Survivors Speak: A Qualitative Analysis of Motivational Factors Influencing Breast Cancer Survivors’ Participation in a Sprint Distance Triathlon

Aims and Objectives To examine motivational factors influencing breast cancer survivors to participate in triathlon training, complete a triathlon and maintain an exercise thereafter. Background Routine exercise has been shown to improve quality of life and reduce recurrence for breast cancer survivors. Yet physical and psychological factors present barriers for initiating and maintaining an exercise routine. Research is limited in exploring factors of exercise motivation from the survivor\u27s perspective. Design Qualitative design using focus groups and individual follow-up phone interviews to explore motivation for exercise initiation and maintenance. Methods One to two weeks after completing a triathlon, 11 breast cancer survivors who trained together participated in one of three focus groups to discuss their experience. Five months post triathlon 6 of the 11 participants were successfully contacted and phone interviews were conducted to explore exercise maintenance. Focus groups and interviews were analysed using content and thematic analysis. Results Five themes emerged (1) Champion for Exercise, (2) Part of a Team, (3) Everyone Had a Story, (4) Not Really Exercise and (5) What Do We Do Now? Overall, survivors recognised their need for lifestyle change (e.g. moving from a sedentary lifestyle to a more active one). More importantly, they identified the team approach to exercise initiation was crucial in their success in sustaining a behavioural change. Conclusions Emphasis needed on developing team exercise training programmes for survivors. Nurses can play a critical role in discussing with survivors, the benefits of exercise initiation and maintenance. Relevance to clinical practice Breast cancer survivors are hesitant to initiate routine exercise. Training with women who share a common lived experience increases the likelihood of success. Nurses are in a position to encourage breast cancer survivors to participate in group exercise programmes as a way to improve quality of life

The transcription factor STAT6 plays a critical role in promoting beta cell viability and is depleted in islets of individuals with type 1 diabetes

This is the final version. Available on open access from Springer Verlag via the DOI in this recordAims/hypothesis: In type 1 diabetes, selective beta cell loss occurs within the inflamed milieu of insulitic islets. This milieu is generated via the enhanced secretion of proinflammatory cytokines and by the loss of anti-inflammatory molecules such as IL-4 and IL-13. While the actions of proinflammatory cytokines have been well-studied in beta cells, the effects of their anti-inflammatory counterparts have received relatively little attention and we have addressed this. Methods: Clonal beta cells, isolated human islets and pancreas sections from control individuals and those with type 1 diabetes were employed. Gene expression was measured using targeted gene arrays and by quantitative RT-PCR. Protein expression was monitored in cell extracts by western blotting and in tissue sections by immunocytochemistry. Target proteins were knocked down selectively with interference RNA. Results: Cytoprotection achieved with IL-4 and IL-13 is mediated by the early activation of signal transducer and activator of transcription 6 (STAT6) in beta cells, leading to the upregulation of anti-apoptotic proteins, including myeloid leukaemia-1 (MCL-1) and B cell lymphoma-extra large (BCLXL). We also report the induction of signal regulatory protein-α (SIRPα), and find that knockdown of SIRPα is associated with reduced beta cell viability. These anti-apoptotic proteins and their attendant cytoprotective effects are lost following siRNA-mediated knockdown of STAT6 in beta cells. Importantly, analysis of human pancreas sections revealed that STAT6 is markedly depleted in the beta cells of individuals with type 1 diabetes, implying the loss of cytoprotective responses. Conclusions/interpretation: Selective loss of STAT6 may contribute to beta cell demise during the progression of type 1 diabetes.Diabetes UKJDR

Effects of a walking program in the psychiatric in-patient treatment setting: a cohort study.

Issue addressed: To assess the effectiveness of a walking program in a psychiatric in-patient unit. Method: In-patients at a private psychiatric unit were offered the opportunity to participate in a daily morning 40 minute walk led by an activity supervisor. After discharge, outcomes for patients who had regularly participated in the walking group (n=35) and patients who had not participated (n=49) were compared for length of stay during their period of admission and Clinical Global Impression - Severity (CGI-S) and&nbsp; Depression Anxiety Stress Scales (DASS) scores measured at admission and discharge. This was a retrospective analysis of data collected routinely. Results: There were no significant differences between the two cohorts on most primary outcome measures, including length of stay, DASS scores at admission and at discharge and CGI-S scores at admission. Patients who had not participated in the walking group had a significantly lower score on a single measure, the CGI-S, than patients who had participated (p=0.001). Conclusions: This study showed no evidence that in-patients benefited from participating in the physical activity program. However, this must be&nbsp; interpreted within the confines of a number of study limitations and, as such, the findings can neither support nor refute the effectiveness of physical activities.<br /

Detection of medically important Candida species by absolute quantitation real-time polymerase chain reaction

Background: Chronic obstructive pulmonary disease (COPD) is one of the most important causes of disability and mortality in the world. Although cigarette smoking and environmental pollutants have been recognized as the major causes of COPD, the role of infection in the pathogenesis and progression of COPD has also been reported. Objectives: The aim of the present study was to find the relationship between Helicobacter Pylori infection and COPD through anti H. pylori IgG serology, real time PCR of bronchoalveolar lavage and trans bronchial biopsy urease tests. Patients and Methods: This descriptive cross-sectional study was carried out on 60 adults with COPD. After obtaining the patient’s history, physical examination, spirometry and confirmation of COPD diagnosis by pulmonologist, subjects were selected through convenience sampling. In order to determine the severity and prognosis of disease, the global initiative for chronic obstructive lung disease (GOLD) criteria and BODE index were used. Subjects underwent bronchoscopy for obtaining bronchoalveolar lavage (BAL) samples and biopsy was performed. Biopsy and BAL samples were investigated respectively by urease test and real time PCR. Moreover, patients’ serum samples were serologically studied for detection of anti H. pylori IgG. Results: Mean age of the participants was 60.65 ± 9.15 years, and 25% were female and 75% were male. The prevalence rate of H. pylori in COPD patients was 10% according to real time PCR, 88.3% according to the serology test and 0% based on the urease test. According to the results of PCR and considering the severity of disease based on the GOLD criteria, from those with a positive PCR, one patient (16.6%) had very severe obstruction, three (50%) had severe obstruction and two patients (33.3%) had moderate obstruction. The relationship between H. pylori presence (based on PCR) and disease severity and prognosis was not statistically significant. Conclusions: These findings can justify the hypothesis of direct injury and chronic inflammation via inhalation and aspiration resulting in H. pylori colonization. In fact, it is thought that H. Pylori infection, beside the host genetic vulnerability and other environmental risk factors might make the patient susceptible to COPD or lead to COPD worsening. Although we found H. pylori infection in some patients with COPD, the results of this study, could not explain the pathogenic mechanisms of COPD

Medical Evaluation and Triage of the Agitated Patient: Consensus Statement of the American Association for Emergency Psychiatry Project BETA Medical Evaluation Workgroup

Numerous medical and psychiatric conditions can cause agitation; some of these causes are life threatening. It is important to be able to differentiate between medical and nonmedical causes of agitation so that patients can receive appropriate and timely treatment. This article aims to educate all clinicians in nonmedical settings, such as mental health clinics, and medical settings on the differing levels of severity in agitation, basic triage, use of de-escalation, and factors, symptoms, and signs in determining whether a medical etiology is likely. Lastly, this article focuses on the medical workup of agitation when a medical etiology is suspected or when etiology is unclear

Mutant Huntingtin Fragments Form Oligomers in a Polyglutamine Length-Dependent Manner \u3cem\u3ein Vitro\u3c/em\u3e and \u3cem\u3ein Vivo\u3c/em\u3e

Huntington disease (HD) is caused by an expansion of more than 35–40 polyglutamine (polyQ) repeats in the huntingtin (htt) protein, resulting in accumulation of inclusion bodies containing fibrillar deposits of mutant htt fragments. Intriguingly, polyQ length is directly proportional to the propensity for htt to form fibrils and the severity of HD and is inversely correlated with age of onset. Although the structural basis for htt toxicity is unclear, the formation, abundance, and/or persistence of toxic conformers mediating neuronal dysfunction and degeneration in HD must also depend on polyQ length. Here we used atomic force microscopy to demonstrate mutant htt fragments and synthetic polyQ peptides form oligomers in a polyQ length-dependent manner. By time-lapse atomic force microscopy, oligomers form before fibrils, are transient in nature, and are occasionally direct precursors to fibrils. However, the vast majority of fibrils appear to form by monomer addition coinciding with the disappearance of oligomers. Thus, oligomers must undergo a major structural transition preceding fibril formation. In an immortalized striatal cell line and in brain homogenates from a mouse model of HD, a mutant htt fragment formed oligomers in a polyQ length-dependent manner that were similar in size to those formed in vitro, although these structures accumulated over time in vivo. Finally, using immunoelectron microscopy, we detected oligomeric-like structures in human HD brains. These results demonstrate that oligomer formation by a mutant htt fragment is strongly polyQ length-dependent in vitro and in vivo, consistent with a causative role for these structures, or subsets of these structures, in HD pathogenesis

Regulation of STAT1 signalling in human pancreatic β-cells by the lysine deacetylase, HDAC6; a new therapeutic opportunity in type 1 diabetes?

This is the author accepted manuscript. The final version is available from the American Diabetes Association via the DOI in this record Data and Resource Availability: All data are available from the corresponding authors on requestType 1 diabetes arises from the selective destruction of pancreatic β-cells by autoimmune mechanisms and intracellular pathways driven by Janus (JAK)-kinase mediated STAT isoforms (especially STAT1 & STAT2) are implicated as mediators of β-cell demise. Despite this, the molecular mechanisms that regulate JAK-STAT signalling in β-cells during the autoimmune attack remain only partially disclosed and the factors acting to antagonise pro-inflammatory STAT1 signalling are uncertain. We have recently implicated Signal Regulatory Protein (SIRP)-α in promoting β-cell viability in the face of ongoing islet autoimmunity and now reveal that this protein controls the availability of a cytosolic lysine deacetylase, HDAC6, whose activity regulates the phosphorylation and activation of STAT1. We provide evidence that STAT1 serves as a substrate for HDAC6 in β-cells and that sequestration of HDAC6 by SIRPα in response to anti-inflammatory cytokines (such as interleukin-13) leads to increased STAT1 acetylation. This then impairs the ability of STAT1 to promote gene transcription in response to pro-inflammatory cytokines including interferon-gamma (IFNγ). We further find that SIRPα is lost from the β-cells of subjects with recent-onset type 1 diabetes under conditions when HDAC6 is retained and STAT1 levels are increased. On this basis, we report a previously unrecognised role for cytokine-induced regulation of STAT1 acetylation in the control of β-cell viability and propose that targeted inhibition of HDAC6 activity may represent a novel therapeutic modality to promote β-cell viability in the face of active islet autoimmunity.Diabetes UKSteve Morgan Foundation Grand Challenge Senior FellowshipEuropean Union’s Horizon 2020European Federation of Pharmaceutical Industries and Associations (EFPIA)Leona M. and Harry B. Helmsley Charitable TrustEFSD/JDRF/Lill

Effects of Sex Hormones on Ocular Blood Flow and Intraocular Pressure in Primary Open Angle Glaucoma: A Review

Primary open-angle glaucoma (POAG) is a multifactorial optic neuropathy characterized by progressive retinal ganglion cell death and visual field loss. Some speculate that gender plays a role in the risk of developing POAG and that the physiologic differences between men and women may be attributed to the variable effects of sex hormones on intraocular pressure (IOP), ocular blood flow, and/or neuroprotection. Estrogen, in the form of premenopausal status, pregnancy, and post-menopausal hormone therapy is associated with increase in ocular blood flow, decrease in IOP and neuroprotective properties. The vasodilation caused by estrogen and its effects on aqueous humor outflow may contribute. On the other hand, although testosterone may have known effects in the cardiovascular and cerebrovascular systems, there is no consensus as to its effects in ocular health or POAG. With better understanding of sex hormones in POAG, sex hormone-derived preventative and therapeutic considerations in disease management may provide for improved gender-specific patient care

Glyoxylate cycle gene ICL1 is essential for the metabolic flexibility and virulence of Candida glabrata

We would like to acknowledge Professor Karl Kuchler from Medical University of Vienna for the kind gifts of C. glabrata strains used in this study. This study was funded by Fundamental Research Grant Scheme (FRGS) from Ministry of Education (MOE), Malaysia (Grant number: 01-01-14-1456FR). S.Y. is a recipient of the MyBrain 15 Scholarship from MOE, Malaysia. A.B. was supported by the Medical Research Council Centre for Medical Mycology at the University of Aberdeen (MR/N006364/1), by a programme grant from the UK Medical Research Council (MR/M026663/1), by a Strategic Award from the Wellcome Trust (097377) and by a grant from the UK Biotechnology and Biological Sciences Research Council (BB/P020119/1).Peer reviewedPublisher PD