Not a Client but Still Vulnerable: Ethical & Legal Responsibilities with Non-Clients

All states have mandatory reporting of abuse of vulnerable populations for mental health professionals. However, the procedures are clear only when working with the client and having direct knowledge and information of the situation. This session will explore professional responsibilities with no direct knowledge of the situation or identifiable informatio

Examining adherence to activity monitoring devices to improve physical activity in adults with cardiovascular disease: A systematic review

Background Activity monitoring devices are currently being used to facilitate and monitor physical activity. No prior review has examined adherence to the use of activity monitoring devices amongst adults with cardiovascular disease. Methods Literature from June 2012 to October 2017 was evaluated to examine the extent of adherence to any activity monitoring device used to collect objective physical activity data. Randomized control trials comparing usual care against the use of an activity monitoring device, in a community intervention for adults from any cardiovascular diagnostic group, were included. A systematic search of databases and clinical trials registers was conducted using Joanna Briggs Institute methodology. Results Of 10 eligible studies, two studies reported pedometer use and eight accelerometer use. Six studies addressed the primary outcome. Mean adherence was 59.1% (range 39.6% to 85.7%) at last follow-up. Studies lacked equal representation by gender (28.6% female) and age (range 42 to 82 years). Conclusion This review indicates that current research on activity monitoring devices may be overstated due to the variability in adherence. Results showed that physical activity tracking in women and in young adults have been understudied

Gender differences in uptake, adherence and experiences: a longitudinal, mixed methods study of a physical activity referral scheme in Scotland, UK

Physical activity referral schemes (PARS) are implemented internationally to increase physical activity (PA) but evidence of effectiveness for population subgroups is equivocal. We examined gender differences for a Scottish PARS. This mixed-method, concurrent longitudinal study had equal status quantitative and qualitative components. We conducted 348 telephone interviews across three time points (pre-scheme, 12 and 52 weeks). These included validated self-reported PA and exercise self-efficacy measures, and open-ended questions about experiences. We recruited 136 participants, 120 completed 12-week and 92 completed 52-week interviews. PARS uptake was 83.8% (114/136) and 12-week adherence for those who started was 43.0% (49/114). Living in less deprived areas was associated with better uptake (p=0.021) and 12-week adherence (p=0.020), and with male uptake (p=0.024) in gender-stratified analysis. Female adherers significantly increased self-reported PA at 12 weeks (p=0.005) but not 52 weeks. Males significantly increased exercise self-efficacy between baseline and 52 weeks (p=0.009). Three qualitative themes and eight subthemes developed; gender perspectives, personal factors (health, social circumstances, transport and attendance benefits) and scheme factors (communication, social/staff support, individualisation and age appropriateness). Both genders valued the PARS. To increase uptake, adherence and PA, PARS should ensure timely, personalized communication, individualised, affordable PA and include mechanisms to re-engage those who disengage temporarily

Mycobacterium marinum Escapes from Phagosomes and Is Propelled by Actin-based Motility

Mycobacteria are responsible for a number of human and animal diseases and are classical intracellular pathogens, living inside macrophages rather than as free-living organisms during infection. Numerous intracellular pathogens, including Listeria monocytogenes, Shigella flexneri, and Rickettsia rickettsii, exploit the host cytoskeleton by using actin-based motility for cell to cell spread during infection. Here we show that Mycobacterium marinum, a natural pathogen of fish and frogs and an occasional pathogen of humans, is capable of actively inducing actin polymerization within macrophages. M. marinum that polymerized actin were free in the cytoplasm and propelled by actin-based motility into adjacent cells. Immunofluorescence demonstrated the presence of host cytoskeletal proteins, including the Arp2/3 complex and vasodilator-stimulated phosphoprotein, throughout the actin tails. In contrast, Wiskott-Aldrich syndrome protein localized exclusively at the actin-polymerizing pole of M. marinum. These findings show that M. marinum can escape into the cytoplasm of infected macrophages, where it can recruit host cell cytoskeletal factors to induce actin polymerization leading to direct cell to cell spread

Regulation of Cytosolic Phospholipase A 2 Activation and Cyclooxygenase 2 Expression in Macrophages by the β-Glucan Receptor

Phagocytosis of non-opsonized microorganisms by macrophages initiates innate immune responses for host defense against infection. Cytosolic phospholipase A(2) is activated during phagocytosis, releasing arachidonic acid for production of eicosanoids, which initiate acute inflammation. Our objective was to identify pattern recognition receptors that stimulate arachidonic acid release and cyclooxygenase 2 (COX2) expression in macrophages by pathogenic yeast and yeast cell walls. Zymosan- and Candida albicans-stimulated arachidonic acid release from resident mouse peritoneal macrophages was blocked by soluble glucan phosphate. In RAW264.7 cells arachidonic acid release, COX2 expression, and prostaglandin production were enhanced by overexpressing the beta-glucan receptor, dectin-1, but not dectin-1 lacking the cytoplasmic tail. Pure particulate (1, 3)-beta-D-glucan stimulated arachidonic acid release and COX2 expression, which were augmented in a Toll-like receptor 2 (TLR2)-dependent manner by macrophage-activating lipopeptide-2. However, arachidonic acid release and leukotriene C(4) production stimulated by zymosan and C. albicans were TLR2-independent, whereas COX2 expression and prostaglandin production were partially blunted in TLR2(-/-) macrophages. Inhibition of Syk tyrosine kinase blocked arachidonic acid release and COX2 expression in response to zymosan, C. albicans, and particulate (1, 3)-beta-D-glucan. The results suggest that cytosolic phospholipase A(2) activation triggered by the beta-glucan component of yeast is dependent on the immunoreceptor tyrosine-based activation motif-like domain of dectin-1 and activation of Syk kinase, whereas both TLR2 and Syk kinase regulate COX2 expression

Regulation of Cytosolic Phospholipase a\u3csub\u3e2\u3c/sub\u3e Activation and Cyclooxygenase 2 Expression in Macrophages by the β-Glucan Receptor

Phagocytosis of non-opsonized microorganisms bymacrophages initiates innate immune responses for host defense against infection. Cytosolic phospholipase A2 is activated during phagocytosis, releasing arachidonic acid for production of eicosanoids, which initiate acute inflammation. Our objective was to identify pattern recognition receptors that stimulate arachidonic acid release and cyclooxygenase 2 (COX2) expression in macrophages by pathogenic yeast and yeast cell walls. Zymosan- and Candida albicans-stimulated arachidonic acid release from resident mouse peritoneal macrophages was blocked by soluble glucan phosphate. In RAW264.7 cells arachidonic acid release, COX2 expression, and prostaglandin production were enhanced by overexpressing the β-glucan receptor, dectin-1, but not dectin-1 lacking the cytoplasmic tail. Pure particulate (1, 3)-β-D-glucan stimulated arachidonic acid release and COX2 expression, which were augmented in a Toll-like receptor 2 (TLR2)-dependent manner by macrophage-activating lipopeptide-2. However, arachidonic acid release and leukotriene C4 production stimulated by zymosan and C. albicans were TLR2-independent, whereas COX2 expression and prostaglandin production were partially blunted in TLR2-/- macrophages. Inhibition of Syk tyrosine kinase blocked arachidonic acid release and COX2 expression in response to zymosan, C. albicans, and particulate (1, 3)-β-D-glucan. The results suggest that cytosolic phospholipase A2 activation triggered by the β-glucan component of yeast is dependent on the immunoreceptor tyrosine-based activation motif-like domain of dectin-1 and activation of Syk kinase, whereas both TLR2 and Syk kinase regulate COX2 expression

UV irradiation of skin regulates a murine model of Multiple Sclerosis

Objective: The prevalence of multiple sclerosis follows a latitude gradient, with increased disease at higher latitudes. Previous studies have focused on a vitamin D hypothesis; although recent evidence suggests that exposure to ultraviolet radiation (UVR) itself may be important. In this study, the effects of UVR on the development of experimental autoimmune encephalomyelitis (EAE) were examined. Methods: C57BL/6 mice were irradiated with a single erythemal dose of UVR (8 kJ/m2), or 4 daily sub-erythemal doses (1 kJ/m2), before sensitisation to myelin oligodendrocyte glycoprotein peptide. The UV irradiation protocols used do not increase 25-hydroxyvitamin D concentrations in serum of vitamin D-sufficient mice. The onset of EAE was recorded and mice were clinically monitored for 40 days. Results: A single dose of erythemal UVR (8 kJ/m2) significantly suppressed EAE onset and severity. Four daily exposures of sub-erythemal UVR (1 kJ/m2) also significantly delayed disease onset but was less effective than the erythemal dose. Conclusion: UV irradiation delayed the onset and reduced the severity of EAE. Continued administration of lower dose UVR following disease onset may be necessary to achieve similar results to a single higher dose delivered pre-sensitisation. Our results give further weight to suggestions that UVR exposure may delay MS onset and progression and UVB phototherapy may provide an option for treatment of MS

Selected Toll-like Receptor Ligands and Viruses Promote Helper-Independent Cytotoxic T Cell Priming by Upregulating CD40L on Dendritic Cells

SummaryCD40L (CD154) on CD4+ T cells has been shown to license dendritic cells (DCs) via CD40 to prime cytotoxic T lymphocyte (CTL) responses. We found that the converse (CD40L on DCs) was also important. Anti-CD40L treatment decreased endogenous CTL responses to both ovalbumin and influenza infection even in the absence of CD4+ T cells. DCs expressed CD40L upon stimulation with agonists to Toll-like receptor 3 (TLR3) and TLR9. Moreover, influenza infection, which stimulates CTLs without help, upregulated CD40L on DCs, but herpes simplex infection, which elicits CTLs through help, did not. CD40L-deficient (Cd40lg−/−) DCs are suboptimal both in vivo in bone marrow chimera experiments and in vitro in mixed lymphocyte reactions. In contrast, Cd40lg−/− CD8+ T cells killed as effectively as wild-type cells. Thus, CD40L upregulation on DCs promoted optimal priming of CD8+ T cells without CD4+ T cells, providing a mechanism by which pathogens may elicit helper-independent CTL immunity

En Attendant Centiloid

Aims: Test the robustness of a linear regression transformation of semiquantitative values from different Aβ tracers into a single continuous scale. Study Design: Retrospective analysis. Place and Duration of Study: PET imaging data acquired in Melbourne and Perth, Australia, between August 2006 and May 2014. Methodology: Aβ imaging in 633 participants was performed with four different radiotracers: flutemetamol (n=267), florbetapir (n=195), florbetaben (n=126) and NAV4694 (n=45). SUVR were generated with the methods recommended for each tracer, and classified as high (Aβ+) or low (Aβ-) based on their respective thresholds. Linear regression transformation based on reported head-to-head comparisons of each tracer with PiB was applied to each tracer result. Each tracer native classification was compared with the classification derived from the transformed data into PiB-like SUVR units (or BeCKeT: Before the Centiloid Kernel Transformation) using 1.50 as a cut-off. Results: Misclassification after transformation to PiB-like SUVR compared to native classification was extremely low with only 3/267 (1.1%) of flutemetamol, 1/195 (0.5%) of florbetapir, 1/45 (2.2%) of NAV4694, and 1/126 (0.8%) of florbetaben cases assigned into the wrong category. When misclassification occurred (Conclusion: While a definitive transformation into centesimal units is being established, application of linear regression transformations provide an interim, albeit robust, way of converting results from different Aβ imaging tracers into more familiar PiB-like SUVR units

Etiology of Severe Non-malaria Febrile Illness in Northern Tanzania: A Prospective Cohort Study.

The syndrome of fever is a commonly presenting complaint among persons seeking healthcare in low-resource areas, yet the public health community has not approached fever in a comprehensive manner. In many areas, malaria is over-diagnosed, and patients without malaria have poor outcomes. We prospectively studied a cohort of 870 pediatric and adult febrile admissions to two hospitals in northern Tanzania over the period of one year using conventional standard diagnostic tests to establish fever etiology. Malaria was the clinical diagnosis for 528 (60.7%), but was the actual cause of fever in only 14 (1.6%). By contrast, bacterial, mycobacterial, and fungal bloodstream infections accounted for 85 (9.8%), 14 (1.6%), and 25 (2.9%) febrile admissions, respectively. Acute bacterial zoonoses were identified among 118 (26.2%) of febrile admissions; 16 (13.6%) had brucellosis, 40 (33.9%) leptospirosis, 24 (20.3%) had Q fever, 36 (30.5%) had spotted fever group rickettsioses, and 2 (1.8%) had typhus group rickettsioses. In addition, 55 (7.9%) participants had a confirmed acute arbovirus infection, all due to chikungunya. No patient had a bacterial zoonosis or an arbovirus infection included in the admission differential diagnosis. Malaria was uncommon and over-diagnosed, whereas invasive infections were underappreciated. Bacterial zoonoses and arbovirus infections were highly prevalent yet overlooked. An integrated approach to the syndrome of fever in resource-limited areas is needed to improve patient outcomes and to rationally target disease control efforts