Aarupcurran6773

ention. This contrasts previous research that has suggested wearable activity tracker may increase youth physical activity levels in the short-term. Lower engagement in MVPA 6-months post-intervention was observed for males but not for females, though it is unclear why this finding was observed. The results suggest wearable activity trackers, in combination with supporting materials, may not be effective for increasing physical activity levels in adolescents.

ACTRN12616000899448 . Australian and New Zealand Clinical Trials Registry. Registered 7 July 2016.

ACTRN12616000899448 . Australian and New Zealand Clinical Trials Registry. Registered 7 July 2016.

Measurement of patients' healthcare experiences is increasingly used as an indicator of quality of care, but there are concerns that existing measures omit information that is meaningful to patients and that results may not be used systematically to inform service improvement. Further, current approaches may be inadequate for some population groups, such as Indigenous people in Australia, whose healthcare experience is impacted by the context of colonisation and discordance between Indigenous understandings of health and the Western biomedical health system. This study aimed to assess the extent to which existing patient experience measures used in Australia collect information about critical aspects of cancer care, as previously identified by Indigenous people affected by cancer and their health care providers.

A two-stage process was used to examine the adequacy of existing patient experience measures for Indigenous people in Australia (1) relevant tools and measures were identified and assessed, and fole.

Existing tools are likely to miss key aspects of Indigenous peoples' experiences of cancer care in Australia. Failure to adequately assess care experiences related to cultural safety may compromise efforts to improve health outcomes. Addressing gaps requires development of experience measures that are strengths-based, reflect an Indigenous worldview and measure aspects of experience relevant to Indigenous people.

Alcohol harms are rising globally, and alcohol policies, where they exist, are weak or under-developed. Limited progress has been made since the formulation of the World Health Organisation (WHO) Global Strategy in 2010. WHO is seeking to accelerate progress in implementing international efforts to reduce the harmful use of alcohol. The threat to global health posed by tobacco is well understood by policy communities and populations globally; by contrast alcohol is much less so, despite available evidence.

Global alcohol corporations have sought to become trusted sources of advice for policy makers and consumers, while continuing to grow their markets. Evidence-informed public health messaging faces formidable competition from transnational corporations as the worlds of corporate and political communications, social and mainstream media become increasingly linked, presenting new opportunities for corporate actors to shape global health governance. Alcohol messaging that uses means of persuasion tied to innion on alcohol and policy issues varies across time and place and can be influenced by dedicated public health interventions. Alcohol marketing dominates people's thinking about alcohol because we currently allow this to happen. Greater ambition is needed in developing countermarketing and other interventions to promote evidence-informed ideas with the public. Alcohol policies need to be further developed, and implemented more widely, in order to arrest the growing burden of alcohol harms across the world.

Structured RNAs play varied bioregulatory roles within microbes. To date, hundreds of candidate structured RNAs have been predicted using informatic approaches that search for motif structures in genomic sequence data. The human microbiome contains thousands of species and strains of microbes. Yet, much of the metagenomic data from the human microbiome remains unmined for structured RNA motifs primarily due to computational limitations.

We sought to apply a large-scale, comparative genomics approach to these organisms to identify candidate structured RNAs. With a carefully constructed, though computationally intensive automated analysis, we identify 3161 conserved candidate structured RNAs in intergenic regions, as well as 2022 additional candidate structured RNAs that may overlap coding regions. We validate the RNA expression of 177 of these candidate structures by analyzing small fragment RNA-seq data from four human fecal samples.

This approach identifies a wide variety of candidate structured RNAs, including tmRNAs, antitoxins, and likely ribosome protein leaders, from a wide variety of taxa. Overall, our pipeline enables conservative predictions of thousands of novel candidate structured RNAs from human microbiomes.

This approach identifies a wide variety of candidate structured RNAs, including tmRNAs, antitoxins, and likely ribosome protein leaders, from a wide variety of taxa. Overall, our pipeline enables conservative predictions of thousands of novel candidate structured RNAs from human microbiomes.

A high-salt diet (HSD) is one of the major risk factors for acute ischemic stroke (AIS). Zongertinib chemical structure As a potential mechanism, surplus salt intake primes macrophages towards a proinflammatory phenotype. In this study, whether HSD could blunt the efferocytic capability of macrophages after ischemic stroke, thus exacerbating post-stroke neural inflammation, was investigated.

Wild-type male C57BL/6 mice were fed with fodder containing 8% sodium chloride for 4 weeks and subjected to transient middle cerebral occlusion (tMCAO). Disease severity, macrophage polarization as well as efferocytic capability were evaluated. Bone marrow-derived macrophages were cultured in vitro, and the impact of high salinity on their efferocytic activity, as well as their expression of phagocytic molecules, were analyzed. The relationships among sodium concentration, macrophage phenotype, and disease severity in AIS patients were explored.

HSD-fed mice displayed increased infarct volume and aggravated neurological deficiency. Mice fed with HSD suffered exacerbated neural inflammation as shown by higher inflammatory mediator expression and immune cell infiltration levels.