The experience of facilitators and participants of long term condition self-management group programmes: a qualitative synthesis

Objective: Our aim was to systematically review the qualitative literature about the experiences of both facilitators and participants in a range of group-based programmes to support the self-management of long-term conditions. Methods: We searched 7 databases using the terms ‘self-management’, ‘group’ and ‘qualitative’. Full text articles meeting the inclusion criteria were retrieved for review. A thematic synthesis approach was used to analyse the studies. Results: 2126 articles were identified and 24 were included for review. Group participants valued being with similar others and perceived peer support benefits. Facilitators (HCP and lay) had limited group specific training, were uncertain of purpose and prioritised education and medical conformity over supportive group processes and the promotion of self-management agency and engagement. Overall, studies prioritised positive descriptions. Conclusion: Group programmes’ medical self-management focus may reduce their ability to contribute to patient-valued outcomes. Further research is needed to explore this disconnect. Practice implications: This review supports broadening the scope of group-based programmes to foreground shared learning, social support and development of agency. It is of relevance to developers and facilitators of group self-management programmes and their ability to address the burden of long-term conditions

Lifetime risk of prostate cancer overdiagnosis in Australia: Quantifying the risk of overdiagnosis associated with prostate cancer screening in Australia using a novel lifetime risk approach

© 2019 Author(s). Objectives To quantify the risk of overdiagnosis associated with prostate cancer screening in Australia using a novel lifetime risk approach. Design Modelling and validation of the lifetime risk method using publicly available population data. Setting Opportunistic screening for prostate cancer in the Australian population. Participants Australian male population (1982-2012). Interventions Prostate-specific antigen testing for prostate cancer screening. Primary and secondary outcome measures Primary: Lifetime risk of overdiagnosis in 2012 (excess lifetime cancer risk adjusted for changing competing mortality); Secondary: Lifetime risk of prostate cancer diagnosis (unadjusted and adjusted for competing mortality); Excess lifetime risk of prostate cancer diagnosis (for all years subsequent to 1982). Results The lifetime risk of being diagnosed with prostate cancer increased from 6.1% in 1982 (1 in 17) to 19.6% in 2012 (1 in 5). Using 2012 competing mortality rates, the lifetime risk in 1982 was 11.5% (95% CI 11.0% to 12.0%). The excess lifetime risk of prostate cancer in 2012 (adjusted for changing competing mortality) was 8.2% (95% CI 7.6% to 8.7%) (1 in 13). This corresponds to 41% of prostate cancers being overdiagnosed. Conclusions Our estimated rate of overdiagnosis is in agreement with estimates using other methods. This method may be used without the need to adjust for lead times. If annual (cross-sectional) data are used, then it may give valid estimates of overdiagnosis once screening has been established long enough for the benefits from the early detection of non-overdiagnosed cancer at a younger age to be realised in older age groups

Striped Magnetic Ground State of the Kagome Lattice in Fe4Si2Sn7O16

We have experimentally identified a new magnetic ground state for the kagome lattice, in the perfectly hexagonal Fe2+ (3d6, S = 2) compound Fe4Si2Sn7O16. Representational symmetry analysis of neutron diffraction data shows that below T_N = 3.5 K, the spins on 2/3 of the magnetic ions order into canted antiferromagnetic chains, separated by the remaining 1/3 which are geometrically frustrated and show no long-range order down to at least T = 0.1 K. Moessbauer spectroscopy confirms that there is no static order on the latter 1/3 of the magnetic ions - i.e., they are in a liquid-like rather than a frozen state - down to at least 1.65 K. A heavily Mn-doped sample Fe1.45Mn2.55Si2Sn7O16 has the same magnetic structure. Although the propagation vector q = (0, 1/2 , 1/2 ) breaks hexagonal symmetry, we see no evidence for magnetostriction in the form of a lattice distortion within the resolution of our data. We discuss the relationship to partially frustrated magnetic order on the pyrochlore lattice of Gd2Ti2O7, and to theoretical models that predict symmetry breaking ground states for perfect kagome lattices.Comment: 5 pages, 5 figure

Exact solutions of noncommutative vacuum Einstein field equations and plane-fronted gravitational waves

We construct a class of exact solutions of the noncommutative vacuum Einstein field equations, which are noncommutative analogues of the plane-fronted gravitational waves in classical gravity.Comment: 10 pages, comments adde

Why we might not need to stress about ruling out inducible myocardial ischemia

Editorial on the high-sensitivity cardiac troponin (hs-cTn) tests

Treating cisplatin-resistant cancer: a systematic analysis of oxaliplatin or paclitaxel salvage chemotherapy

Objective: To examine the pre-clinical and clinical evidence for the use of oxaliplatin or paclitaxel salvage chemotherapy in patients with cisplatin-resistant cancer. Methods: Medline was searched for 1) Cell models of acquired resistance reporting cisplatin, oxaliplatin and paclitaxel sensitivities and 2) Clinical trials of single agent oxaliplatin or paclitaxel salvage therapy for cisplatin/carboplatin-resistant ovarian cancer. Results: Oxaliplatin - Oxaliplatin is widely regarded as being active in cisplatin-resistant cancer. In contrast, data in cell models suggests that there is cross-resistance between cisplatin and oxaliplatin in cellular models with resistance levels which reflect clinical resistance (<10 fold). Oxaliplatin as a single agent had a poor response rate in patients with cisplatin-resistant ovarian cancer (8%, n=91). Oxaliplatin performed better in combination with other agents for the treatment of platinum-resistant cancer suggesting that the benefit of oxaliplatin may lie in its more favourable toxicity and ability to be combined with other drugs rather than an underlying activity in cisplatin resistance. Oxaliplatin therefore should not be considered broadly active in cisplatin-resistant cancer. Paclitaxel – Cellular data suggests that paclitaxel is active in cisplatin-resistant cancer. 68.1% of cisplatin-resistant cells were sensitive to paclitaxel. Paclitaxel as a single agent had a response rate of 22% in patients with platinum-resistant ovarian cancer (n = 1918), a significant increase from the response of oxaliplatin (p<0.01). Paclitaxel-resistant cells were also sensitive to cisplatin, suggesting that alternating between agents may be beneficial. Studies of single agent paclitaxel in platinum-resistant ovarian cancer where patients had previously received paclitaxel had an improved response rate of 35.3% n=232 (p<0.01), suggesting that pre-treatment with paclitaxel improves the response of salvage paclitaxel therapy. Conclusions: Cellular models reflect the resistance observed in the clinic as the cross resistant agent oxaliplatin has a lower response rate compared to the non-cross resistant agent paclitaxel in cisplatin-resistant ovarian cancer. Alternating therapy with cisplatin and paclitaxel may therefore lead to an improved response rate in ovarian cancer

Research based criteria for the design and selection of literacy and thinking tools

This paper describes criteria for the design and selection of literacy and thinking tools. The criteria are that tools should be: (i) teaching focused (ii) learner focused, (iii) thought linked (iv) neurologically consistent, (v) subject specific, (vi) text linked, (vii) developmentally appropriate, (viii) culturally responsive, and (ix) assessment linked

An integrated general practice and pharmacy-based intervention to promote the use of appropriate preventive medications among individuals at high cardiovascular disease risk: protocol for a cluster randomized controlled trial

Background: Cardiovascular diseases (CVD) are responsible for significant morbidity, premature mortality, and economic burden. Despite established evidence that supports the use of preventive medications among patients at high CVD risk, treatment gaps remain. Building on prior evidence and a theoretical framework, a complex intervention has been designed to address these gaps among high-risk, under-treated patients in the Australian primary care setting. This intervention comprises a general practice quality improvement tool incorporating clinical decision support and audit/feedback capabilities; availability of a range of CVD polypills (fixed-dose combinations of two blood pressure lowering agents, a statin ± aspirin) for prescription when appropriate; and access to a pharmacy-based program to support long-term medication adherence and lifestyle modification. Methods: Following a systematic development process, the intervention will be evaluated in a pragmatic cluster randomized controlled trial including 70 general practices for a median period of 18 months. The 35 general practices in the intervention group will work with a nominated partner pharmacy, whereas those in the control group will provide usual care without access to the intervention tools. The primary outcome is the proportion of patients at high CVD risk who were inadequately treated at baseline who achieve target blood pressure (BP) and low-density lipoprotein cholesterol (LDL-C) levels at the study end. The outcomes will be analyzed using data from electronic medical records, utilizing a validated extraction tool. Detailed process and economic evaluations will also be performed. Discussion: The study intends to establish evidence about an intervention that combines technological innovation with team collaboration between patients, pharmacists, and general practitioners (GPs) for CVD prevention. Trial registration: Australian New Zealand Clinical Trials Registry ACTRN1261600023342

Prevention of infection and disruption of the pathogen transfer chain in elective surgery

The COVID-19 pandemic has caused us all to stop our normal activities and consider how we can safely return to caring for our patients. There are many common practices (such as an increased use of personal protective equipment) which we are all familiar with that can be easily incorporated into our daily routines. Other actions, such as cleaning more surfaces with solutions such as dilute povidone iodine or changing the air filtration systems used within operating room theaters, may require more extensive efforts on our behalf. In this article, we have attempted to highlight some of the changes that arthroplasty surgeons may need to instigate when we are able to resume elective joint arthroplasty procedures in an effort to disrupt the chain of pathogen transfer

Understanding cisplatin resistance using cellular models

Many mechanisms of cisplatin resistance have been proposed from studies of cellular models of resistance including changes in cellular drug accumulation, detoxification of the drug, inhibition of apoptosis and repair of the DNA adducts. A series of resistant models were developed from CCRF-CEM leukaemia cells with increasing doses of cisplatin from 100 ng/ml. This produced increasing resistance up to 7-fold with a treatment dose of 1.6 μg/ml. Cisplatin resistance in these cells correlated with increases in the antioxidant glutathione, yet treatment with buthionine sulphoximine, an inhibitor of glutathione synthesis, had no effect on resistance, suggesting that the increase in glutathione was not directly involved in cisplatin resistance. Two models were developed from H69 SCLC cells, H69-CP and H69CIS200 using 100 ng/ml or 200 ng/ml cisplatin respectively. Both cell models were 2-4 fold resistant to cisplatin, and have decreased expression of p21 which may increase the cell’s ability to progress through the cell cycle in the presence of DNA damage. Both the H69-CP and H69CIS200 cells showed no decrease in cellular cisplatin accumulation. However, the H69-CP cells have increased levels of cellular glutathione and are cross resistant to radiation whereas the H69CIS200 cells have neither of these changes. This suggests that increases in glutathione may contribute to cross-resistance to other drugs and radiation, but not directly to cisplatin resistance. There are multiple resistance mechanisms induced by cisplatin treatment, even in the same cell type. How then should cisplatin-resistant cancers be treated? Cisplatin-resistant cell lines are often more sensitive to another chemotherapeutic drug paclitaxel (H69CIS200), or are able to be sensitised to cisplatin with paclitaxel pre-treatment (H69-CP). The understanding of this sensitisation by paclitaxel using cell models of cisplatin resistance will lead to improvements in the clinical treatment of cisplatin resistant tumours