Impact of an interactive workshop on specialist physiotherapists' practice when implementing a new clinical care pathway for people with musculoskeletal conditions.

BACKGROUND: A new pathway of care proposes early comprehensive assessment and targeted management by specialist musculoskeletal clinicians for people with musculoskeletal conditions at risk of poor outcomes. Adoption of this care pathway is likely to be influenced by beliefs and behaviours of specialist musculoskeletal clinicians. OBJECTIVE: To evaluate the effect of an interactive educational workshop about the proposed clinical care pathway on knowledge, beliefs and practice of specialist musculoskeletal physiotherapists. DESIGN: Mixed methods. METHODS: Fifty specialist musculoskeletal physiotherapists participated in a 2-day interactive educational workshop. Knowledge, beliefs and clinical practice behaviours were assessed immediately before the workshop and 3 months' later using surveys. RESULTS: Knowledge about key guideline messages improved and were maintained at follow-up. Most participants agreed to provide more targeted interventions to patients at risk of poor outcome (92%, 95% CI: 81%-98%) and utilise prognostic screening tools (84%, 95% CI: 71 to 93). However, only 56% (95% CI: 39%-68%) of participants believed implementing a shared care pathway was easy. At follow-up, participants' beliefs were more aligned with the proposed care pathway (i.e., shared care: 83%, 95% CI: 68%-93%). With respect to clinical practice, there were 16% more referrals back to the primary physiotherapist at 3 months than before the workshop. Barriers (practitioner, patient and system factors) to implementation of the care pathway were discussed. CONCLUSION: An interactive educational workshop influenced specialist musculoskeletal physiotherapists' knowledge, beliefs and clinical practice, but barriers need to be overcome to facilitate widespread implementation.

Effectiveness of interventions aiming at reducing sedentary behaviour in a non-surgical population with overweight or obesity: A systematic review and meta-analysis.

AIM: This systematic review and meta-analyses of randomised controlled trials (RCTs) investigated the effectiveness of interventions to reduce sedentary behaviour amongst people with overweight or obesity. Secondarily, it aimed to investigate the effectiveness of these interventions on body mass index (BMI), time spent in moderate-to-vigorous physical activity (MVPA) and health-related quality of life (HRQoL). METHODS: A search of six databases (CENTRAL, PubMed, Embase, PEDro, CINAHL and PsycINFO) was conducted from inception to July 2018. RCTs in which sedentary behaviour was measured by accelerometry or inclinometry, with participants of any age with overweight or obesity were included. Subgroup analyses were undertaken comparing studies that included adults versus children and studies with an active component (e.g., treadmill desk, physically active breaks) versus no active component to their intervention. RESULTS: Nine studies (n=1859) were included. Compared to the control group, the interventions significantly reduced time spent in sedentary behaviour (standardised mean difference [95% confidence interval] -0.33 [-0.59 to -0.08] overall; -0.53 [-0.95 to -0.11] in adults). Subgroup analyses demonstrated that only interventions that included active components reduced time spent in sedentary behaviour (-0.54 [-0.88 to -0.20]) and increased time spent in MVPA (1.29 [0.02 to 2.56]). Subgroup analyses demonstrated that interventions only reduced BMI in studies of children (-0.09 [-0.18 to -0.00]) and in those with no active component (-0.09 [-0.18 to -0.01]). There were insufficient data to investigate the effectiveness of these interventions on HRQoL. CONCLUSIONS: This novel systematic review and meta-analyses suggests interventions aiming to effectively reduce objectively-measured sedentary behaviour need to specifically include an active component.

Molecular characterization of the autophagy-related gene Beclin-1 from the olive flounder (Paralichthys olivaceus).

Autophagy is an important cellular response to starvation and stress, and plays critical roles in embryogenesis, development, cell death, cancer, and immunity. Beclin-1 is one of the central regulators of autophagy in mammals. In the present study, we isolated a PoBeclin-1 cDNA from the olive flounder (Paralichthys olivaceus) by screening a flounder gill cDNA library and rapid amplification of cDNA ends (RACE). The PoBeclin-1 cDNA we isolated encodes a 447-amino acid polypeptide containing a conserved Bcl-2-binding domain. The deduced amino acid sequence of PoBeclin-1 showed high degrees of sequence identity (80.5-95.3%) with Beclin-1 from human, frog, mouse, zebrafish, and pufferfish. PoBeclin-1 transcripts were detected from 1 day post-hatching and were found to be ubiquitously expressed in the healthy flounder. Expression of PoBeclin-1 mRNA was increased in the kidney and spleen of flounders challenged with viral hemorrhagic septicemia virus (VHSV). When infected with VHSV, PoBeclin-1-overexpressing HINAE cells had low level (about 26%) of VHSV G transcripts compared to control cells. Taken together, these results suggest that PoBeclin-1 may play a role in the innate immune response to viral infection in the flounder.

Nitric oxide induces BNIP3 expression that causes cell death in macrophages.

Nitric oxide (NO) is involved in many physiological processes and also causes pathological effects by inducing apoptosis. It can enhance or suppress apoptosis depending on its concentration and the cell type involved. In this report, we used cDNA microarray analysis to show that SNAP, an NO donor, strongly induces Bcl-2/adenovirus E1B 19kDa-interacting protein 3 (BNIP3) in macrophages. BNIP3 is a mitochondrial pro-apoptotic protein that contains a Bcl-2 homology 3 domain and a COOH-terminal transmembrane (TM) domain. Macrophages activated by LPS/IFN-gamma produce nitric oxide synthase 2 (NOS2) and release endogenous NO. Expression of BNIP3 was also induced in macrophages by LPS/IFN-gamma, and the induction was blocked by a NOS2 inhibitor, S-methyl-isothiourea. Peritoneal macrophages from NOS2-null mice failed to produce BNIP3 in response to LPS/IFN-gamma. We conclude that BNIP3 expression in macrophages is controlled by the intracellular level of nitric oxide. Overexpression of BNIP3 but not of BNIP3 deltaTM, a BNIP3 mutant without the TM domain and C-terminal tail, led to apoptosis of the cells. Promoter analysis showed that the region between -281 and -1 of the 5'-upstream enhancer region of murine BNIP3 was sufficient for NO-dependent expression of BNIP3.

Cytosolic NADP(+)-dependent isocitrate dehydrogenase protects macrophages from LPS-induced nitric oxide and reactive oxygen species.

Macrophages activated by microbial lipopolysaccharides (LPS) produce bursts of nitric oxide and reactive oxygen species (ROS). Redox protection systems are essential for the survival of the macrophages since the nitric oxide and ROS can be toxic to them as well as to pathogens. Using suppression subtractive hybridization (SSH) we found that cytosolic NADP(+)-dependent isocitrate dehydrogenase (IDPc) is strongly upregulated by nitric oxide in macrophages. The levels of IDPc mRNA and of the corresponding enzymatic activity were markedly increased by treatment of RAW264.7 cells or peritoneal macrophages with LPS or SNAP (a nitric oxide donor). Over-expression of IDPc reduced intracellular peroxide levels and enhanced the survival of H2O2- and SNAP-treated RAW264.7 macrophages. IDPc is known to generate NADPH, a cellular reducing agent, via oxidative decarboxylation of isocitrate. The expression of enzymes implicated in redox protection, superoxide dismutase (SOD) and catalase, was relatively unaffected by LPS and SNAP. We propose that the induction of IDPc is one of the main self-protection mechanisms of macrophages against LPS-induced oxidative stress.