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\"What does your body language say about you? From strangers on the street, to your closest friends and family - even if you're not speaking, you're saying a lot with your body. Body Language explores the way we use our bodies to communicate, the way we hold ourselves, the way we sit, stand, and point our hands, feet and eyes can all reveal how we are feeling in any given situation. This book explores the body language we use in a wide-range of business and personal-life scenarios, from delivering a presentation at work to how you should act on a first date! Packed with images to clearly demonstrate each of the scenarios discussed, Body Language will help you understand the way others around you choose to communicate and also what you are saying with your own body. These valuable skills will improve your day to day communication, helping you to judge situations and understand how others around you are feeling. Use Body Language to: Harness the power of your own body language Communicate confidently to all of those around you Dip in and out of useful scenarios to find the best advice for you Understand people's hidden emotions and learn what you are hiding yourself Tackle those important life events, such as interviews, first dates, important meetings and more!\"-- Provided by publisher.

Osteoporosis is associated with increased fragility of bone and a subsequent increased risk of fracture. The diagnosis of osteoporosis is intimately linked with the imaging and quantification of bone and BMD. Scanning modalities, such as dual-energy X-ray absorptiometry or quantitative CT, have been developed and honed over the past half century to provide measures of BMD and bone microarchitecture for the purposes of clinical practice and research. Combined with fracture prediction tools such as Fracture Risk Assessment Tool (FRAX) (which use a combination of clinical risk factors for fracture to provide a measure of risk), these elements have led to a paradigm shift in the ability to diagnose osteoporosis and predict individuals who are at risk of fragility fracture. Despite these developments, a treatment gap exists between individuals who are at risk of osteoporotic fracture and those who are receiving therapy. In this Review, we summarize the epidemiology of osteoporosis, the history of scanning modalities, fracture prediction tools and future directions, including the most recent developments in prediction of fractures.This Review highlights various medical imaging techniques and fracture prediction tools that are used to diagnosis osteoporosis and discusses the potential importance of screening in at-risk populations.

Calcium, magnesium and strontium have all been implicated in both musculoskeletal and cardiovascular health and disease. However, despite these three elements being closely chemically related, there is marked heterogeneity of their characteristics in relation to cardiovascular outcomes. In this narrative review, we describe the relevant evidential landscape, focusing on clinical trials where possible and incorporating findings from observational and causal analyses, to discern the relative roles of these elements in musculoskeletal and cardiovascular health. We conclude that calcium supplementation (for bone health) is most appropriately used in combination with vitamin D supplementation and targeted to those who are deficient in these nutrients, or in combination with antiosteoporosis medications. Whilst calcium supplementation is associated with gastrointestinal side effects and a small increased risk of renal stones, purported links with cardiovascular outcomes remain unconvincing. In normal physiology, no mechanism for an association has been elucidated and other considerations such as dose response and temporal relationships do not support a causal relationship. There is little evidence to support routine magnesium supplementation for musculoskeletal outcomes; greater dietary intake and serum concentrations appear protective against cardiovascular events. Strontium ranelate, which is now available again as a generic medication, has clear anti-fracture efficacy but is associated with an increased risk of thromboembolic disease. Whilst a signal for increased risk of myocardial infarction has been detected in some studies, this is not supported by wider analyses. Strontium ranelate, under its current licence, thus provides a useful therapeutic option for severe osteoporosis in those who do not have cardiovascular risk factors.

Osteoporosis care has evolved markedly over the last 50 years, such that there are now an established clinical definition, validated methods of fracture risk assessment and a range of effective pharmacological agents. Currently, bone-forming (anabolic) agents, in many countries, are used in those patients who have continued to lose bone mineral density (BMD), patients with multiple subsequent fractures or those who have fractured despite treatment with antiresorptive agents. However, head-to-head data suggest that anabolic agents have greater rapidity and efficacy for fracture risk reduction than do antiresorptive therapies. The European Society for Clinical and Economic Aspects of Osteoporosis, Osteoarthritis and Musculoskeletal Diseases (ESCEO) convened an expert working group to discuss the tools available to identify patients at high risk of fracture, review the evidence for the use of anabolic agents as the initial intervention in patients at highest risk of fracture and consider the sequence of therapy following their use. This position paper sets out the findings of the group and the consequent recommendations. The key conclusion is that the current evidence base supports an “anabolic first” approach in patients found to be at very high risk of fracture, followed by maintenance therapy using an antiresorptive agent, and with the subsequent need for antiosteoporosis therapy addressed over a lifetime horizon.

Introduction The transradial approach for coronary artery catheterisation has increased in popularity compared to the transfemoral approach for patients undergoing percutaneous coronary interventions. However, radial artery spasm continues to be a major complication of the procedure. Current management strategies vary concerning radial artery spasm and there is limited evidence of practice in the Australian context. Aim To identify the predictors of radial artery spasm and the medications used for its prevention and management. Methods A descriptive cross-sectional study was carried out over a three-month period in two tertiary hospitals in NSW, Australia. A self-administered pre-procedural survey was completed by patients undergoing coronary artery catheterisation. This survey collected socio-demographic data and assessed anxiety using the Spielberger State-Trait Anxiety Inventory. Procedural data, including length of procedure, equipment used, occurrence of radial artery spasm, and medications given, were collected post-procedure by the interventionalist. Results Of the 169 participants, over half were male (59.8%) and aged 66 years or older (56.8%). Radial artery spasm was reported in 24 (14.2%) participants. Rates of spasm were significantly higher among females (66.6%, p  = 0.004), those aged under 65 years (62.5%, p  = 0.001) and those who reported a medical history of anxiety (33.3%, p  = 0.0004). There were no significant differences in State and Trait anxiety scores among those who had RAS and those who did not. Logistic regression identified younger age as the only statistically significant predictor of RAS (OR 0.536; 95% CI 0.171–1.684; p  = 0.005). To prevent radial artery spasm most patients received midazolam (n = 158; 93.5%), nitrates (n = 133; 78.7%) and/or fentanyl (n = 124; 73.4%) prophylactically. Nitrates were the most frequently administered medication to treat radial artery spasm (78.7%). Conclusion This study highlights that there is a need to develop a clearer understanding of the predictors of RAS, as identifying patients at risk can ensure prophylactic measures are implemented. This study identified nitrates as the preferred vasodilator as a preventative measure along with the use of sedation.

Bone forming agents, also known as anabolic therapies, are essential in managing osteoporosis, particularly for patients at very high-risk of fractures. Identifying candidates who will benefit the most from these treatments is crucial. For example, this group might include individuals with severe osteoporosis, multiple vertebral fractures, a recent fragility fracture or those unresponsive to antiresorptive treatments. Definitions of patients with a very high fracture risk vary across nations, are often based on fracture history, bone mineral density (BMD), and/or fracture risk calculated by FRAX® or other algorithms. However, for very high-risk patients, anabolic agents such as teriparatide, abaloparatide, or romosozumab are commonly recommended as first-line therapies due to their ability to stimulate new bone formation and improve bone microarchitecture, offering significant benefits in rapid fracture reduction over antiresorptive therapies. The cost-effectiveness of these agents is a critical consideration for decision-makers. Despite their higher costs, their effectiveness in significantly reducing fracture risk and improving quality of life can justify the investment, especially when long-term savings from reduced fracture rates and associated healthcare costs are considered. Additionally, after completing a course of anabolic therapy, transitioning to antiresorptive agents like bisphosphonates or denosumab is crucial to maintain the gains in bone density and minimize subsequent fracture risks. This sequential treatment approach ensures sustained protection and optimal resource utilization. In summary, the effective use of bone forming agents in osteoporosis requires a comprehensive strategy that includes accurate patient identification, consideration of cost-effectiveness, and implementation of appropriate sequential treatments, ultimately maximizing patient outcomes and healthcare efficiency.

Background Some controversy exists regarding the safety of intra-articular hyaluronic acid (IAHA) in the management of osteoarthritis (OA). Objective The objective of this study was to re-assess the safety profile of IAHA in patients with OA, through a comprehensive meta-analysis of randomized, placebo-controlled trials. Methods A comprehensive literature search was undertaken in the databases MEDLINE, Cochrane Central Register of Controlled Trials (CENTRAL), and Scopus. Randomized, double-blind, placebo-controlled, parallel-group trials that assessed adverse events (AEs) with IAHA in patients with OA were eligible for inclusion. Authors and/or study sponsors were contacted to obtain the full report of AEs. The primary outcomes were overall severe and serious AEs, as well as the following MedDRA System Organ Class (SOC)-related AEs: gastrointestinal, cardiac, vascular, respiratory, nervous system, skin and subcutaneous tissue disorders, musculoskeletal, renal and urinary disorders, infections and infestations, and hypersensitivity reaction. Results Database searches initially identified 1481 records. After exclusions according to the selection criteria, 22 studies were included in the qualitative synthesis, and nine studies having adequate data were ultimately included in the meta-analysis. From the studies excluded according to the pre-specified selection criteria, 21 with other pharmacological OA treatments permitted during the trials were a posteriori included in a parallel qualitative synthesis, from which eight studies with adequate data were finally included in a parallel meta-analysis. Since this meta-analysis was designed to assess safety, the exclusion criterion on concomitant anti-OA medication was crucial. However, due to the high number of studies that allowed mainly concomitant oral non-steroidal anti-inflammatory drugs (NSAIDs), we decided to include them in a post hoc parallel analysis in order to compare the results from the two analyses. No statistically significant difference in odds was found between IAHA and placebo for all types of SOC-related disorders, except for infections and infestations, for which significantly lower odds were found with IAHA compared with placebo, both overall (odds ratio [OR] = 0.61, 95% confidence interval [CI] 0.40–0.93; I 2  = 0%) and in studies without concomitant anti-OA medication (OR = 0.49, 95% CI 0.27–0.89). There were significant increased odds of reporting serious AEs with IAHA compared with placebo, both overall (OR = 1.78, 95% CI 1.21–2.63; I 2  = 0%) and in studies with concomitant anti-OA medication (OR = 1.78, 95% CI 1.10–2.89), but not in studies without concomitant anti-OA medication (OR = 1.78, 95% CI 0.92–3.47). Conclusions Using the available data on studies without any concomitant anti-OA medication permitted during clinical trials, IAHA seems not to be associated with any safety issue in the management of OA. However, this evidence was associated with only a “low” to “moderate” certainty. A possible association with increased risk of serious AEs, particularly when used with concomitant OA medications, requires further investigation.

Mild cognitive impairment, dementia and osteoporosis are common diseases of ageing and, with the increasingly ageing global population, are increasing in prevalence. These conditions are closely associated, with shared risk factors, common underlying biological mechanisms and potential direct causal pathways. In this review, the epidemiological and mechanistic links between mild cognitive impairment, dementia and skeletal health are explored. Discussion will focus on how changes in brain and bone signalling can underly associations between these conditions, and will consider the molecular and cellular drivers in the context of inflammation and the gut microbiome. There is a complex interplay between nutritional changes, which may precede or follow the onset of mild cognitive impairment (MCI) or dementia, and bone health. Polypharmacy is common in patients with MCI or dementia, and there are difficult prescribing decisions to be made due to the elevated risk of falls associated with many drugs used for associated problems, which can consequently increase fracture risk. Some medications prescribed for cognitive impairment may directly impact bone health. In addition, patients may have difficulty remembering medication without assistance, meaning that osteoporosis drugs may be prescribed but not taken. Cognitive impairment may be improved or delayed by physical activity and exercise, and there is evidence for the additional benefits of physical activity on falls and fractures. Research gaps and priorities with the aim of reducing the burden of osteoporosis and fractures in people with MCI or dementia will also be discussed.

Background This study evaluated observational and causal relationships between rheumatoid arthritis (RA) and cardiovascular disease and imaging phenotypes in the UK Biobank. Methods RA was defined using linked hospital records, self-reported diagnostics, and medication data. Controls were participants without a record of RA. Cardiovascular diseases (CVDs) were defined using linked hospital records over an average of 14 years of prospective follow-up, including: ischaemic heart diseases (IHD), acute myocardial infarction (AMI), atrial fibrillation, any arrhythmia, non-ischaemic cardiomyopathies, pericardial disease, stroke, peripheral vascular disease, and venous thromboembolism. For participants with cardiovascular magnetic resonance (CMR) available as part of the UK Biobank Imaging Study, we considered measures of cardiac structure and function extracted using automated pipelines. Associations of RA with prevalent and incident CVDs were calculated using logistic and Cox regression. Linear regression was used to examine associations with CMR metrics. Models were adjusted for demographic, lifestyle, and clinical confounders. Causal associations were assessed using two-sample Mendelian randomisation. Genetic instruments for RA (22,350 cases and 74,823 controls), nine CVDs (FinnGen, n  = 224,737), and 11 CMR phenotypes (UK Biobank) were extracted and associations assessed using inverse-variance weighting with pleiotropy adjustments and multiple testing corrections. Results The analysis included 1,436 RA cases (mean age 59.9 years; 70.6% female) and 476,975 controls (mean age 56.5 years; 54.3% female). Participants with RA lived in more socioeconomically deprived areas (as per the Townsend Deprivation Index), had lower physical activity levels, were more likely to smoke, and had a higher baseline prevalence of CVDs. In fully adjusted models, participants with RA had a significantly higher hazard of multiple incident CVDs, with the greatest risks related to pericardial disease (HR 2.63 (1.85, 3.74)), heart failure (HR 1.68 (1.42, 1.99)), and AMI (HR 1.53 (1.20, 1.96)). Mendelian Randomisation analyses supported causal links between RA and AMI (OR 1.07 (1.02, 1.09), p  = 0.009), arrhythmias (OR 1.05 (1.02, 1.06), p  = 0.0007), and IHD (OR 1.05 (1.01, 1.06), p  = 0.036). No significant associations were identified between RA and CMR phenotypes. Conclusions People with RA have a heightened risk of multiple prevalent and incident CVDs, independent of shared risk factors, with suggestions of causal links with IHD, AMI, and arrhythmias.