1 Although widely used in clinical practice by many physiotherapists worldwide, there is little evidence about the efficacy or effectiveness of this intervention.2, 4 and 5 Five systematic reviews have evaluated the effect of Kinesio Taping on selected

outcomes in different populations. Williams et al6 assessed Kinesio Taping only in the prevention and treatment of sports injuries. Bassett et al and Mostafavifar et al7 and 8 assessed the effects of Kinesio Taping in people with musculoskeletal conditions. Morris et al and Kalron et al9 and 10 widened the musculoskeletal focus to other clinical areas, such as neurological and lymphatic conditions. Currently, new trials of Kinesio Taping are Verteporfin frequently being published. Although these five HDAC inhibitor review reviews were published recently, none of them included all of the following recent trials: 3, 11, 12, 13 and 14. Given this substantial amount of new data,

an updated systematic review was needed to inform clinicians and patients about the effects of this intervention in musculoskeletal conditions. The research questions of this systematic review were: Is Kinesio Taping more effective than no treatment or sham/placebo in people with musculoskeletal conditions for the outcomes of pain intensity, disability, quality of life, return to work and global impression of recovery? Is Kinesio Taping more effective than other interventions in people with musculoskeletal conditions for these outcomes? Is the addition of Kinesio Taping over other interventions more effective than other interventions alone in people with musculoskeletal conditions for these outcomes? Systematic searches were conducted of MEDLINE, Embase, CENTRAL, PEDro, SPORTDiscus, CINAHL, LILACS and SciELO. Papers were accepted in any language if a translation could be obtained.

Search strategies followed the recommendations of the Cochrane Back Review Group33. Detailed search strategies used in each database are described in Appendix 1 (see eAddenda for Appendix aminophylline 1). The date of the last search was 10 June 2013. All clinical trial registers were also searched and manual searches were performed by checking the reference lists of each eligible article. Studies were considered for inclusion if they met the criteria presented in Box 1. Conference abstracts were excluded. Studies that were conducted on healthy participants or that only collected outcomes relating to physical performance (eg, muscle strength, vertical jumping) were also excluded. The primary outcomes were pain intensity and disability measured by any validated outcome measure.

Keeping in view its importance, it was treated with DMSO-acetic anhydride an effective reagent which brings about a range of mechanistically interesting transformations in 4-hydroxycoumarin, dicoumarol,1 4-acyloxycoumarins2 and 3-substituted 4-hydroxycounmarins.3 In continuation with this, we now report structures of the compounds obtained from interaction of substituted dicoumarols (la–le) with this reagent and mechanism of their formation. A mixture of DMSO (6 ml), acetic anhydride (3 ml) and 3-3′-phenylmethylene-bis-4-hydroxycoumarin (200 mg) was kept at room temperature for 3 days.

Dilution with water afforded a precipitate which was filtered, washed and dried. Crystallization from benzene gave spiran (3). Data. Spiran (3): as needles (110 mg), m.p. 262–65 °C. IR (KBr): 1790, 1720, 1660 and 1600 cm−11H NMR (CDCI3, 90 MHz): δ 4.73 (lH,s,Ph–CH–); m/z 410 (M+) 333, 263, 262, 249, 205, 121 and 120 (Found C, 72.94; H, 3.56%. C25H14O6 Autophagy animal study required C, 73.17; H, 3.41%). 3,3′-phenylmethylene-bis-4-hydroxycoumarin (2.4 g) dissolved in 30 ml DMSO-acetic anhydride mixture (2:1, v/v) CT99021 was kept on boiling water bath. A yellow crystalline material starts separating after 30 min. After heating for about 6 h the solid was filtered, washed with dry benzene and was found to be pure enough for

spectral studies. It was characterized as 7-phenyl-7H-bis [1] benzopyrano [4,3-b: 3′, 4′-c] pyran-6, 8-dione (4a). The filtrate was poured into water, precipitate filtered, washed and dried. Crystallization from benzene gave 2, 3-dihydro-2- (2-hydroxybenzoyl)-3-phenyl-4H-furo [3,2-c] [1] benzopyran-4-one (6) as white prisms (579 mg), m.p 199–212 °C. Identity of this compound was confirmed through direct comparison (mmp and comparison of spectral data) with the authentic

sample obtained earlier.4 Chromatography of the mother liquor gave further 500 mg of (6) (combined yield 1.079 g), 2,3-dihydro-2-hydroxymethyl-2- (α-2-hydroxybenzoyl)-3-α-phenyl-4H-furo [3,2-c] [I] benzopyran-4-one (7) as gummy mass (500 mg) and 2,3-dihydro-2-hydroxymelhyl-2- (α-2-hydroxybenzoyl)-3-β-phenyl-4H-furo [3,2-c] [1] benzopyran-4-one (8) also next as a gummy mass (390 mg). Data. 7-phenyl-7H-bis [1] benzopyrano [4,3-b: 3', 4'-c] pyran-6, 8-dione (4a): (300 mg), m.p 312–20 °C (decomposition). IR (KBr) 1720, 1655 and 1600 cm−1. 1H NMR (FT, CDCI3, 90 MHz): δ 5.17 (lHs Ph–CH-); m/z 394 (M+) 317, 173, 145, 121 and 120. 2,3-dihydro-2-hydroxymethyl-2- (α-2-hydroxybenzoyl)-3-α-phenyl-4H-furo [3,2-c] [I] benzopyran-4-one (7): IR (KBr) 3300, 1720 (broad) 1620 cm−11H NMR (CDCl3, 100 MHz): δ 5.35 (1H, s, Ph–CH–), 4.05 (2H, d, -CH2–OH, J = 11.4 Hz). m/z 414 (M+ missing), 396, 384, 279, 263, 251, 250, 249, 222 and 221. 2,3-dihydro-2-hydroxymelhyl-2- (α-2-hydroxybenzoyl)-3-β-phenyl-4H-furo [3,2-c] [1] benzopyran-4-one (8): IR (KBr) 3300, 1720, and 1620 cm−1; 1H NMR (CDCl3, 100 MHz): δ 4.8 (1H, s, Ph–CH–), 4.

Therefore, this systematic review focuses on the efficacy of mechanically assisted walking for improving walking speed and distance in ambulatory people with stroke. Comparisons between mechanically assisted walking and overground walking were also examined in order to assist clinicians to decide the most appropriate intervention for adults with stroke. The specific research questions for this review were, in ambulatory people after stroke: 1. Does mechanically assisted walking result in immediate improvements learn more in walking speed and distance compared with no intervention or a non-walking intervention? In order to make recommendations based on the highest level

of evidence, this review included only randomised or quasi-randomised trials. Searches

for relevant studies were conducted of the following databases: Medline (1946 to April Week 1 2012, CINAHL (1986 to April Week 1 2012), EMBASE (1980 to April Week 1 2012) and PEDro (to April Week 1 2012), without language or date restrictions. Search terms included words relating to stroke, mechanically assisted walking, and locomotion (see Appendix 1 on the eAddenda for the full search strategy). In addition, we contacted authors about trials that we knew were in progress from trial registration. Entinostat Titles and abstracts were displayed and screened by one reviewer to identify relevant studies. Only peer-reviewed papers were included. Full paper copies of relevant studies were retrieved and hand searching of reference lists was carried out to identify further relevant studies. The methods

and abstracts of the retrieved papers were extracted so that reviewers were blinded to authors, journal, and outcomes. Two independent reviewers examined the papers for inclusion against predetermined criteria (Box 1). Conflict was resolved after discussion with a third reviewer. Design • Randomised or quasi-randomised trial Participants • Adults (> 18 yr) Interventions • Experimental. Mechanically assisted walking training (eg, treadmill training or a gait trainer) without body weight support Outcomes measured • Walking speed Quality: and The quality of included studies was determined using PEDro scale scores extracted from the Physiotherapy Evidence Database (www.pedro.org.au). The PEDro scale rates the methodological quality of randomised trials with a score between 0 and 10 ( Maher et al 2003). Where a study was not included on the PEDro database, it was scored by a reviewer following the PEDro guidelines. Participants: Participants had to be ambulatory adults in the subacute or chronic phase after stroke. Ambulatory was defined as a score of at least 3 on the Functional Ambulatory Category ( Holden et al 1984) or a walking speed of at least 0.2 m/s at baseline or when the included participants were able to walk without help, with or without walking aids. Studies were included when at least 80% of sample comprised ambulatory participants.

In the latter approach, the success of the work described under Assays and Correlates will be critical for this regulatory pathway to be considered acceptable. For the approval pathway

based on a single CRT, the feasibility of conducting such a study, the statistical power to conclusively demonstrate the efficacy of the vaccine, and the translation of those results to the variety of settings contemplated for introduction of an SSM-VIMT, are important questions that need to be answered. Toward identification of the preferred regulatory strategy, MVI has convened a series of technical consulting groups composed of independent experts to elucidate both of these potential CDP and regulatory pathways, considering overall feasibility, specific endpoints, requisite baseline data, malaria transmission levels, scale, and cost. The reports generated by these technical groups will be used to Dasatinib prepare a briefing document for consultation with regulatory authorities on the preferred approach, which will impact other areas of vaccine development, from ethics to policy to assays (see Table 1). Finalizing a CDP/regulatory pathway will require coordination with those assessing the measures of transmission and epidemiological data needs of SSM-VIMT trials.

Alongside the efforts selleck to finalize a regulatory pathway and CDP, progress must continue in the strengthening Histone demethylase of clinical and regulatory capacity of endemic countries, where clinical trial sites will be selected in accordance with the CDP. The level of efficacy required for an SSM-VIMT to have an impact on transmission and contribute to achieving elimination has not yet been determined. In 2010, the draft TPP presented at the MVI TBV workshop targeted ≥85% transmission-blocking efficacy, defined as the percent reduction in infection in mosquitoes [26]. However, there were not yet robust data to support a specific target efficacy.

Furthermore, as the ultimate goal is to prevent incidence in the human population, a measure of efficacy that reflects vaccine effect on a human endpoint must be utilized. Initial evidence was recently reported using a population-based, non-clinical model of malaria transmission indicating that interventions with lower efficacy levels may contribute to elimination [20]. Just as targeting antigens from multiple parasite stages may create synergies, the use of a vaccine and drug together could maximize the impact on transmission. For example, a drug could be used to clear the parasites from an infected individual at the same time as administration of a SSM-VIMT, which would prevent transmission for a longer period than a drug could. Coordination of development strategies between the drug and vaccine communities through the alignment of TPPs will ensure the most efficient progress toward common goals.

05). However, T cells from both treated and nontreated mice showed similar reactivates to ConA, thus indicating that there was no general inhibition of T cell reactivity induced by HSP65-6 × P277 vaccination. The results suggested that prevention of diabetes was associated with down-regulation of spontaneous proliferative T cell responses to the peptide P277. To test whether

HSP65 serves as carrier for P277 will enhance the Th2-like immune response by mucosal administration, the amount of IL-10, IL-4, IL-2 and IFN-γ secreted by spleen cells after P277 stimulation in vitro were assayed. Hydroxychloroquine As shown in Fig. 4, immunization of mice with the fusion protein HSP65-6 × P277 elicited much higher levels of Th2-type cytokines and lower Th1-type cytokines than the control mice (Fig. 4, *P < 0.05, compared with HSP65 and P277). The present study was undertaken to investigate whether HSP65 serves as an immunogenic carrier for a diabetogenic peptide P277 will induce anti-inflammatory response in NOD mice by mucosal administration. The prevention of diabetes was associated with a decrease in the degree of insulitis and with down-regulation

of spontaneous proliferative T cell responses to the peptide P277, and the pattern of cytokine secretion ISRIB in HSP65-6 × P277 treated mice, showed an increase in IL-10, IL-4 and a decrease in IL-2, IFN-γ secretion, compatible with a shift from a Th1-like toward a Th2-like autoimmune response. HSP60 belongs to a family of chaperone molecules highly conserved throughout evolution. A role for HSP60 as facilitators of immune responses to proteins and peptides has now been widely documented both in vivo and in vitro [21], [22] and [23]. Vaccination with tumor and viral Ags complexed to HSP65 induces strong immunity to tumors and viral infections in the murine model [10], [12] and [24], suggesting that these agents may be useful in vaccine development. The peptide P277 has been identified as an ideal target antigen to develop secondly type 1 diabetes vaccines [25].

Unfortunately, peptide P277 has low immunogenicity, so ways to improve the immunogenicity is a major goal for designing P277 vaccines. One of the most promising approaches is to use vaccine carriers. We directed our attention to HSP65 as carriers because HSP65 could have a dual role in vaccine development against type 1 diabetes. Firstly, HSP65 could be exploited as vaccine antigens against type 1 diabetes [18]. Secondly, HSP65 could be exploited as adjuvants [26]. In the present study, the dual functions of anti-type 1 diabetes were obtained (Table 1). It has been established that a Th1 response to autoantigen was necessary for type 1 diabetes development [27], [28] and [29] and the induction of autoantigen-specific Th2 responses would prevent disease development [30], [31], [32], [33] and [34].

Three quantitative intervention studies were randomised controlled trials (RCTs), six were non-randomised controlled

trials (nRCTs), one was a prospective cohort study and two were non-comparative studies (case series). Fifteen qualitative studies were evaluations of interventions (including seven evaluations of included interventions) and 11 were stand-alone qualitative studies investigating beliefs, attitudes and practice relating to dietary BIBW2992 manufacturer and physical activity behaviours. Two quantitative intervention studies were rated ++, eight were rated + and two were rated −. The main limitations to quality were poor description of the source population, lack of sufficient power or power calculations and lack of reported effect sizes PLX4032 in vivo (Supplementary Table 2). Eight qualitative studies were rated ++, 18 were rated + and none were rated −. The main quality limitations were reporting of participant characteristics and researcher/participant interaction, as well as data collection and analysis methods (Supplementary Table 3). Quantitative intervention studies were categorised as: dietary/nutritional; food retail; physical

activity; and multi-component interventions. The most common duration for an intervention was one year (Ashfield-Watt et al., 2007+; Bremner et al., 2006+; Cochrane and Davey, 2008+; Cummins et al., 2005+). Other interventions lasted between two weeks (Steptoe et al., 2003++) and six months (Lindsay et al., 2008+). One intervention lasted four years (Baxter

et al., 1997+). Intervention duration varied across different types of interventions. Two dietary/nutritional community-level interventions aimed to increase fruit and vegetable intake in deprived communities (Ashfield-Watt et al., 2007+; Bremner et al., 2006+) and four interventions involved enabling people to choose and cook healthy food (Kennedy et al., 1998−; McKellar et al., 2007+; Steptoe et al., 2003++; Wrieden et al., 2007+), one of which focused on promoting a Mediterranean-type diet (McKellar et al., 2007+). Overall, findings demonstrated mixed effectiveness (Supplementary Table 6). There was evidence of mixed 17-DMAG (Alvespimycin) HCl effectiveness on fruit and vegetable intake, consumption of high fat food, physiological measurements and nutrition knowledge. Evidence suggested no significant impact on weight control or other eating habits, such as intake of starchy foods, fish or fibre. Two interventions involved the introduction of a large-scale food retailing outlet in the intervention area (Cummins et al., 2005+; Wrigley et al., 2003−), and findings were mixed in terms of effectiveness (Supplementary Table 6). One study found a positive effect on psychosocial variables. Both studies indicated mixed effectiveness on fruit and vegetable intake, and evidence suggested no significant impact on health outcomes.

Quantification of apoptotic cells was done using Image J software (NIH, Bethesda MD). Formalin-fixed, paraffin-embedded lung sections mounted on slides were deparaffinized with xylene and dehydrated through graded concentrations of alcohol, and then incubated with 3% hydrogen peroxidase for 20 min to block endogenous peroxidase activity. Following antigen retrieval for VEGF, the sections were incubated overnight at 4 °C with primary antibody for VEGF consequent to incubation with biotinylated secondary antibody, followed by streptavidin.

Following addition of substrate-chromogen and counterstaining with hematoxylin, VEGF expression were identified by the brown cytoplasmic staining. Immunostaining Tofacitinib in vitro for TR3 was carried out following the same protocol using primary antibody for TR3 (Santa Cruz Biotechnology, Santa Cruz CA). Established (VEGF or TR3) immunoreactive lung tissue sections and primary antibody-null sections were included as positive and negative controls respectively. Areas showing immunoreactivity for VEGF or TR3 coupled with evidence of tissue remodeling as evidence of tumor growth were selected; and five random fields (under a combined magnification of ×400) were selected for scoring. Scoring of VEGF or TR3 immunopositivity was carried out by calculating the immunohistochemical score (IHS) as the sum of the quantity and staining

Ruxolitinib mw intensity scores as demonstrated by Saponaro et al.

Thymidine kinase (2013). Here, the quantity score (percentage immunopositive cells; 0 = immunonegative, 1 = 25% immunopositive cells, 2 = 26–50% immunopositive cells, 3 = 51–75% immunopositive cells, and 4 = 76–100% immunopositive cells) and staining intensity score (0 = no intensity, 1 = weak intensity, 2 = moderate intensity, and 3 = strong intensity) were combine to give a minimum-to-maximum IHS of 0–7. Scoring was done by two researchers independently at three different times and the data collated and the mean IHS computed. Staining for each marker was done in triplicates and the experiments were repeated three times. Tissue sections (4–5 μm thick) mounted on poly-L-lysine–coated slide were deparaffinized and blocked for peroxidase activity. After washing with PBS, the sections were pretreated in citrate buffer in a microwave oven for 20 min at 92–98 °C. After washing (2×) with PBS, specimens were incubated in 10% normal goat serum for 20 min. Subsequently, the sections were incubated with a 1:500 diluted mouse CD31 monoclonal antibody at room temperature for 1 h, followed by a 30 min treatment with rabbit anti-mouse antibody. After washing (3×) with PBS, the section was developed with diaminobenzidene-hydrogen peroxidase substrate, and counterstained with hematoxylin. To calculate microvessel density (MVD), three most vascularised areas of the tumor (‘hot spots’) were selected and mean values obtained by counting vessels.

3 (Beckman Coulter, USA) or Flowjo v7.6.5 (Tree Star, USA) software. All analyses were gated on a minimum of 100,000 live lymphocytes. All data were analyzed with GraphPad Prism 5 software (GraphPad, USA) using un-paired student’s two-sided t-test (2 treatment groups) or one- or two-way ANOVA with Bonferroni post-test (3 treatment groups). Mycobacterial counts were log10 transformed before comparison. A Two-tailed correlation analysis was used to obtain coefficient of determination (r2) from the Pearson correlation coefficient (r).

Differences LY2157299 solubility dmso with a p value <0.05 were considered significant and denoted with *, <0.01 with ** and <0.001 with ***. To establish the long-term persistence of viable BCG bacilli, groups of mice were immunized at week 0 with a standard dose (2 × 105 CFU) of the licensed human vaccine BCG Danish 1331. At sequential monthly time-points, the BCG burden of individual mice was determined in pooled draining lymph nodes (d.LNs), spleen and lungs; plating the entire organs/tissues to maximise detection. Fig. 1A demonstrates that viable BCG bacilli were cultured from the d.LNs throughout the experimental duration of 16 months. The burden was highest and most consistent at 6 weeks post immunization (p.i.) at 3.0 log10 CFU ABT-199 order (±0.5), decreasing

to 2.4 log10 CFU (±0.5) at 16 months p.i. BCG were cultured from the majority of spleen samples, although with large replicate variability. CFU counts increased from 1.7 log10 CFU (±1.7) at 6 weeks p.i. to 2.3 log10 CFU (±2.3) at 17 weeks p.i., decreasing to 0.0 log10 CFU (±2.0) by 16 months p.i. Culture of BCG from the lungs was sporadic and only possible in

1 or 2 replicates at each time point up to 22 weeks p.i., after which it was undetected. Given the established importance of IFN-γ producing CD4 T cells in protection against TB, the frequency of BCG-specific IFN-γ secretors in the spleen was evaluated by ex vivo ELISPOT using defined protein cocktail at defined time-points following BCG immunization. Etomidate Fig. 1B shows that whilst IFN-γ secreting cell frequency was maximal at 6 weeks p.i. (1197 SFU/million cells) and declined thereafter; substantial frequencies of IFN-γ secreting cells (478 SFU/million cells) were present 16 months p.i., as previously described [9]. Regression analyses between the mean spleen IFN-γ ELISPOT frequency and the mean bacterial burden in d.LNs showed a statistically significant correlation, demonstrating a clear link between antigen load (from the most reliable tissue indicator) and IFN-γ responses circulating through the spleen (Fig. 1C). To establish the minimum treatment regimen to clear persistent bacilli after BCG immunization, groups of mice were immunized with BCG for 6 weeks (previously shown to induce protection) [9] and [28].

Other ingredients for the formulations were collected from a local Ayurvedic vendor and identified by Ayurvedic practitioner. Both the formulations Brahmi Ghrita (BG) and Saraswatarishta (SW) were prepared

and standardized in accordance with Ayurvedic Formulary of India. 15 and 16 Phenytoin and Tetramethoxypropane (TMP) was procured from Sigma Aldrich Co., St. Louis, USA used MG-132 in vitro as positive control and standard respectively. All the other chemicals used for biochemical estimation like Potassium chloride (KCl), Thiobarbituric acid (TBA), Trichloroacetic acid (TCA), Hydrochloric acid (HCl) and Butylated hydroxytoluene (BHT) were of analytical grade, obtained from Qualigen fine chemicals Pvt. Ltd. Mumbai. Wistar (Albino) rats of either selleckchem sex (140–200 g) were procured from National Toxicology Center, Pune. The animals were allowed to acclimatize

for eight days. Housed and maintained in standard laboratory conditions fed with standard rat pellet diet and water ad libitum. The experiment was conducted with prior permission of Institutional Animal Ethical Committee (IAEC Ref. No. 884/ac/05/CPCSEA) and according to the Committee for the Purpose of Control and Supervision on Experiments on Animals (CPCSEA) guidelines. Animals were divided into four groups (n = 6); Group I served as control group and received only water and feed ad libitum, Group II received standard drug Phenytoin (25 mg/kg IP), Group III and Group IV received Brahmi Ghrita (BG) (0.9 ml/kg) and Saraswatarishta (SW) (0.9 ml/kg) orally for eight days respectively, at a fixed time in the morning. The dose was decided according to the therapeutic human dose of the formulations extrapolated to animals. 17 MES seizures until were induced by Electro-convulsometer (Medicraft Electro Medicals P. Ltd.) as described by Swinyard18 (1985). Exactly 1 h after the drug administration, maximal electroshock seizures

were elicited by the application of electric shock (60 Hz AC, 150 mA) for 0.2 s (s) using corneal electrodes. This current intensity brought forth complete tonic extension of hind limbs in control rats. For recording various parameters, rats were placed on a clean tile, permitting full view of the animal motor responses to seizure. Duration of various phases of epileptic attacks like jerking, grooming, tail straub, extension of hind limb and recovery were observed, recorded and compared with the control and phenytoin group. Animals were sacrificed by cervical dislocation and brain tissues were isolated immediately, washed with ice cold Phosphate Buffer Saline (PBS) and stored at −80 °C until further use. Estimation of lipid peroxidation in brain tissue was measured by using the method of Ohkawa et al 1979.19 Brain homogenate was prepared in PBS (10%) and One ml of 0.15 M KCl was added to 0.5 ml of homogenate. It was incubated for 30 min at 37 °C (degree centigrade) and the reaction mixture was treated with 2 ml of TBA- TCA-HCl reagent, 0.

8). Our study had some limitations. First, there is little http://www.selleckchem.com/products/pd-0332991-palbociclib-isethionate.html consensus in the literature regarding definitions of contracture (Fergusson et al 2007). Our definitions of contracture were chosen so that they could be applied easily to many joints, but they may not concur with other definitions of contracture or have functional implications. Choosing a definition of contracture that reflects a ‘functionally significant’ loss in joint range is dificult as this will vary across individuals and across joints. As some readers may wish that contracture was defined differently, we have included

more information on the incidence of contractures defined in various ways in Appendices 1 to 3 of the eAddenda. Second, selleck products patients were recruited from only one site. As with any single-site study, the study sample may not be widely

representative because of site idiosyncrasies. Last, a small proportion of data were missing, particularly from patients who were unable to be scored on the Motor Assessment Scale or the pain rating scale because of language deicits or impaired cognition. More viable measures of function and pain, eg, proxy measures of pain (Sackley et al 2008) or multiple imputation techniques (Sterne et al 2009), could be used to reduce the potential bias caused by missing data in future studies. In conclusion, about half of all patients developed at least one contracture after stroke. Incidence of contractures across all joints ranged from 12% to 28% six months after stroke. A range of simple clinical measures do not accurately predict who will develop a contracture. eAddenda:Appendices

1, 2, 3, and available at jop.physiotherapy.asn.au Ethics: The local Human Research Ethics committee (South Eastern Sydney and Illawarra Area Health Service) approved this study. All participants or guardians gave written informed consent before data collection began. Competing interests: None. Support: The project was supported by the Physiotherapy Org 27569 Research Foundation, and by the Neurology Department of St George Hospital. Professor Herbert is supported by the Australian NHMRC. The authors thank patients and family members who were part of the study. The authors also thank the assistance of Li Na Goh and Min Jiat Teng who worked as research assistants on the project. “
“The Assessment of Physiotherapy Practice (APP) is a 20-item instrument covering professional behaviour, communication, assessment, analysis and planning, intervention, evidence-based practice, and risk management. Each item is assessed on a 5-level scale from 0 (Infrequently/rarely demonstrates performance indicators) to 4 (Demonstrates most performance indicators to an excellent standard).