g., Grayson, 2001, Redman, 1999 and Rick and Erlandson, 2008). Whether prehistoric peoples acted as the original conservationists (see Alcorn, 1993) or with no regard for preservation and sustainability (see Kay and Simmons, 2002 and Smith and Wishnie, 2000) – or some combination of the two (Erlandson and Rick, 2010) – is still hotly contested. One thing the papers in this issue clearly illustrate, however, is that as Europeans expanded around the globe, the landscapes, plant and animal species, and ecosystems they encountered had already been shaped and altered by humans for millennia. There is a growing

recognition of these facts among a broad array of scientists, as attested to selleck kinase inhibitor by the serious consideration being given to defining an Anthropocene epoch or an earlier and transitional Palaeoanthropocene. If the Anthropocene concept is accepted, as we believe it should be, its real power may lie in its potential to shape public opinion and policy. The Anthropocene can help provide powerful scientific legitimacy among the public for anthropogenic climate change and environmental degradation and act as a call for increased conservation efforts and global awareness. Austin and Holbrook (2012: 61) argued much the same in a recent issue of The Geological Society of America Today: this website The most important assertion

unfolding among these groups is that Anthropocene creates public awareness and formalizes the concept of human-induced environmental change. Although we acknowledge a distinct allure for the nearly term Anthropocene and recognize merit in the concept, pop culture does not have an interest in the stratigraphic implications of this debate. If there is an underlying desire to make social

comment about the implications of human-induced environmental change, Anthropocene clearly is effective. However, being provocative may have greater implications in pop culture than to serious scientific research. The use of the Anthropocene as a public communication tool should not, we believe, be seen as a negative. In many ways, this is its most important attribute. The scientific community can find countless examples of our inability to effectively communicate, explain, and package important scientific ideas to the public and the packaging of contrarian views by naysayers and pseudoscientists often seems to have greater impact. For geologists and biologists, the Intelligent Design debates might be the best example (see Behe, 2001 and Gilbert, 2003); for archaeologists and anthropologists, the ancient astronauts phenomenon (see von Däniken, 1999 and Wilson, 1972) may be most prominent. The esoteric debate over “stratigraphic nomenclature” (Austin and Holbrook, 2012: 61), then, may be less important than the message it conveys to our global community and the future of human–environmental interactions.

Pectinase is an enzyme able to degrade pectic substances by hydrolyzing the ester bond between galacturonic acid and methanol or by cleaving the glycosidic bonds of specific

polymers [22]. Indeed, Jin et al [17] used pectinase to hydrolyze ginsenosides and found that compound K is more readily absorbed from HGE compared to non-HGE in human individuals. Compound K has received increasing attention because various pharmacologic actions including anticancer [25], anti-inflammation [26], and antidiabetes [27] were shown to be mediated by this compound. Using pectinase-hydrolyzed ginseng extract, Ramesh et al [28] found an improved antioxidant status and minimized occurrence of oxidative stress-related disorders in aged rats. Moreover, Yuan et al [29] and [30] reported that pectinase-processed ginseng radix had antidiabetic and hypolipidemic effects in high http://www.selleckchem.com/products/tenofovir-alafenamide-gs-7340.html fat diet-fed ICR mice. Taken together, pectinase seems to be an effective tool to transform ginsenosides into deglycosylated ginsenosides, thereby enhancing the bioavailability and functionality of ginseng. Our data demonstrate that 8 wk of HGE supplementation causes a significant reduction in FPG (p = 0.017)

and PPG60min (p = 0.01) in IFG individuals. Such reductions may be due to one or a combination of different mechanisms, including intestinal glucose absorption [31] and [32], insulin secretion from pancreatic β-cells see more [33], or peripheral glucose utilization [34]. After the supplementation of HGE, noticeable but not significant difference was found in the glucose level at an earlier time point (PPG30min, p = 0.059) during OGTT. This result suggests that HGE slows the absorption of glucose in the intestinal lumen. Also, our findings of significant decreases in FPG and PPG60min suggest one additional possibility, in which HGE improves glucose intolerance through increasing

the insulin action on the target tissues responsible for glucose uptake. Moreover, FPI (p = 0.063) and PPI60min (p = 0.077) showed a tendency to improve in the HGE group compared to the placebo group. In supporting this possibility, ginsenosides CK and Rg1 have been reported to enhance insulin-mediated glucose uptake in 3T3-L1 adipocytes, which is related to the increased BCKDHA GLUT4 translocation [27] and [35]. Similarly, administration of HGE improves glucose homeostasis and insulin resistance state (or glucose and lipid parameters) in high fat diet-fed mice via activation of AMP-dependent protein kinase in muscle tissue [29] and [30]. In this study, however, there was no significant difference in HOMA-β, suggesting no effect on insulin secretion. In contrast to our results, studies reveal that ginseng significantly stimulates insulin release from pancreatic β-cells [36] and [37]. These discrepancies could be due to the differences in designs (human studies vs. animal studies) and materials (hydrolyzed ginseng vs. nonhydrolyzed ginseng) used in the studies.

Experimentos com agonistas dos receptores 5‐HT4 demonstraram que estímulos nestes receptores promovem aceleração de trânsito colônico25, iniciam o reflexo peristáltico26 e aumentam a velocidade de propulsão ao longo do cólon27. Este trabalho foi realizado durante 15 dias consecutivos no laboratório de fisiologia da Universidade Federal de Juiz de Fora. O objetivo desse estudo foi mostrar através da avaliação cintilográfica, a distância percorrida pelo traçador radioativo ao longo do intestino delgado, a partir de administração gástrica (gavagem). Amemiya et al.28 revelaram, em estudos in vitro, a presença

do receptor 5‐HT4 nos nervos colinérgicos em faixas de musculatura do fundo do estômago de ratos. Coelho et al.29 estudaram em ratos o limiar

da dor durante distensão colorretal e concluiram que BYL719 o tegaserode possui propriedade antinociceptiva ao ativar o receptor 5‐HT4. Hicks et al.30 mostraram os efeitos do tegaserode no receptor agonista 5‐HT4 estimulando o trânsito do intestino delgado de ratos, mas não observaram ação antinociceptiva visceral. AZD2281 nmr James et al.31 estudaram segmentos de estômago de camundongos normais e diabéticos sob ação de serotonina e tegaserode e mediram a tensão da contração muscular do antro, fundo e piloro nestes 2 grupos experimentais. Observaram que a contração no fundo e no piloro, em ambos os grupos, foi maior com o efeito da serotonina. No antro dos camundongos normais a contração dos que usaram serotonina foi maior. O contrário ocorreu no antro dos camundongos diabéticos, onde a contração muscular com o tegaserode foi mais intensa. Jiao et al.32 estudaram os efeitos do tegaserode na distensão retal e expressão c‐Fos no sistema límbico em 2 grupos de ratos (48 animais com hipersensibilidade colônica obtida pela injeção via anal de ácido acético e 24 animais do grupo controle recebendo apenas administração via anal de solução salina). A estimulação do cólon foi feita por balões inflados no reto. A contagem de

células Fos imunorreativas foi realizada através de programação por computador. Mostraram que o tegaserode inibe resposta à distensão PIK3C2G nociva, sendo que o efeito foi mais evidente no grupo hipersensível, e atenua a expressão Fos no sistema límbico, podendo ser usado para o alívio de dores viscerais. Sun et al.33 investigaram os mecanismos do tegaserode na redução da sensibilidade visceral por meio de observação de Fos, da substância P e da expressão do peptídeo relacionado ao gene calcitonina (CGRP) na medula espinhal lombo‐sacral induzida por inflamação colônica por instilação intraluminal de ácido trinitrobenzenosulfônico (TNBS) em 24 ratos, durante 7 dias. Fos serve como um marcador quantificável para identificar populações neuronais ativadas por estímulos nocivos somático e visceral.

However, this reduction was much more marked in arteries obtained from lead-treated Bcl-2 inhibitor rats. The residual relaxation to ACh in high-KCl precontracted vessels was abolished by L-NAME indicating an additional effect of NO, independent of K+ channel activation, on ACh-induced relaxation. TEA was initially used to evaluate the overall contribution of K+ channels to the basal tone and ACh-induced relaxation. TEA increased basal tone more in preparations from the lead-treated rats compared to the untreated rats and reduced the relaxation induced by ACh more in aortic segments from the lead-treated

than untreated group; these results suggest a greater contribution of K+ channels in both basal tone and ACh-induced relaxation after lead treatment. Accordingly, Fiorim et al.

(2011) observed that TEA potentiated the phenylephrine response more strongly in aortic rings from lead-treated rats compared to untreated rats. In addition, patch clamp observations of K+ currents in human erythrocytes showed that lead exposure activates K+ channels (Kempe et al., 2005). Different K+ channels are involved in cardiovascular disorders, such as atherosclerosis, hypertension and stroke (Nelson and Quayle, 1995, Callera et al., 2004 and Ledoux Selleckchem ICG-001 et al., 2006). Lead treatment increased NO bioavailability in the rat aorta (Fiorim et al., 2011) and as mentioned NO could open K+ channels. Therefore, we investigated the participation of diverse K+ channels in regulating basal tone and in NO-mediated ACh-induced relaxation in lead-treated Methocarbamol rats. It has been shown that aortic tone is strongly dependent on the activity of Kv channels (Tammaro et al., 2004). In addition, Cheong et al. (2002) also has shown the participation of Kv channel currents in small blood vessels. Our results showed that 4-aminopyridine, a selective inhibitor of Kv channel, induced a greater increase in basal tone in aortic segments from lead-treated than in untreated rats. Furthermore, this inhibitor reduced the relaxation induced by ACh to a greater extent in preparations

from lead-treated compared to untreated rats. These results suggest that Kv channels contribute to the regulation vascular tone in the rat aorta and that channels contribute more to the basal tone and ACh-induced relaxation in the lead-treated rats. Several studies have shown that BKCa plays a key role in regulating vascular tone in different beds (Cheong et al., 2002, Eichhorn and Dobrev, 2007 and Briones et al., 2009), and the activation of these channels is an important component of the EDHF response in several vascular beds (Ledoux et al., 2006). Our results show that both charybdotoxin (KCa and Kv blocker) and apamin (selective SKCa blocker) did not modify basal tone in aortic segments from both groups.

Many WAKs have been shown to be involved in hormonal signals. Arabidopsis WAK1 is induced by both SA and the SA analog 2,2-dichloroisonicotinic acid (INA), and ectopic expression of the entire WAK1 or the kinase domain alone was shown to provide resistance to lethal SA levels [36]. According to cDNA microarray analysis in Arabidopsis, AtWAK1 is induced by MeJA and ethylene [37]. In this study,

Seliciclib in vivo qRT-PCR analyses revealed that TaWAK5could be induced by application of exogenous SA, ABA, and MeJA. Although an antagonistic interaction between SA- and JA-dependent signaling has been suggested [38], [39] and [40], in some cases, SA does not inhibit JA biosynthesis and may even contribute to JA-mediated signaling pathway function [41]. In Arabidopsis, concentrations of both SA and JA and the timing of initiation of SA and JA signaling are important for the outcome of the complex SA-JA signal interaction [42] and [43]. ABA has been shown to interact with the SA-JA network. ABA has been suggested to affect JA biosynthesis and resistance against the JA-inducing, necrotrophic pathogen Pythium irregular [23] and [24], and to suppress SA-dependent disease resistance [44]. Related to the role

of phyto-hormones in WAK expression, the region upstream of the start codon (1000 bp) of TaWAK5 was analyzed in this study. The promoter region contained one ABRE-like motif (ACGTG), but no SA-, or JA-responsive elements (shown in Table S3). Several studies have suggested that modulation of gene expression is accomplished through the interaction of induced regulatory proteins and specific DNA regions [45], [46] and [47]. For instance, the induction of a dehydration-responsive gene, rd22, Dabrafenib supplier is mediated by ABA. MYC and MYB recognition sites in the rd22 promoter region function as cis-acting elements that interact specifically with AtMYC2 and AtMYB2; transgenic plants overexpressing AtMYC2 and/or AtMYB2 cDNAs have higher sensitivity to ABA [47]. In this study, TaWAK5 promoter had five binding sites of an ABA-regulated protein, two of a SA-regulated protein, and one of a JA-regulated protein ( Fig. S1), suggesting that TaWAK5 was also regulated possibly through SA-, ABA-, and MeJA-hormones.

In this study, VIGS, which has been an efficient tool for rapidly analyzing the functions of plant genes [48], [49], [50] and [51], below was also used to evaluate the disease resistance role of TaWAK5. In wheat, infection with barley stripe mosaic virus (BSMV) constructs carrying a fragment of the resistance gene Lr21 caused conversion of incompatible interactions of wheat and leaf rust pathogen to compatible reactions after the gene silencing, whereas infection with a control construct or one that silences phytoene desaturase gene had no effect on resistance or susceptibility [33]. Knocking down the transcript levels of three wheat RLK genes TaRLK-R1, TaRLK-R2, or TaRLK-R3 individually or all together by VIGS and the suppression of TaHsp90.2 or TaHsp90.

The ovariectomy success was confirmed, after sacrifice, by the visualization of ovary absence and uterus atrophy. The rats were weighed at the beginning Bcl-2 inhibitor and at the end of the experiment. Weight changes were observed in percentage according to the formula below: (final weight−initial weight)×100initial weight The average value of solid and liquid diet consumed per rat/per day was recorded. The amount of Ca and P and the relative ratio of Ca/P, present in the alveolar bone crest, were measured using an

energy-dispersive micro X-ray fluorescence spectrometer (μEDX 1300 – 50 μm – Shimadzu®, Kyoto, Japan). After sacrifice, the mandibles were placed in a solution of 10% buffered formalin for 24 h, washed with water, then dried and frozen at −20 °C. Fixation of biological samples in formaldehyde based solutions prior to the analyses of concentrations of Ca and P in bone had already been undertaken by other authors.24, 25 and 26 To reduce possible interference to the fixation procedure in the interpretation of the results, all samples were fixed for the same period of time. The fixation in formalin was done to prevent the putrefaction of the samples during the spectrometric analysis. The region of the alveolar bone crest, right

side of the mandible, between the 1st and 2nd molar, were flattened using sandpaper no. 1200 coupled to an automatic polishing machine. This was necessary as irregularities on the surface of the sample could influence the interaction of electrons IWR-1 and the propagation of X-rays. The samples were mapped on a rectangular area, including the alveolar bone crest, which led to a window of 0.80 mm × 0.60 mm (40 × 30 points with increments of 20 μm). The voltage was set at 15 kV with automatic adjustment of the current. The time required for the mapping of each sample was approximately 260 min. The calibration of the equipment used for reference, was a commercial reagent of synthetic hydroxyapatite (Ca10(PO4)6(OH)2 – 99.999% grade – Sigma–Aldrich®, St. Louis, USA). The Ca/P ratio calculated (theoretically), in

weight percentage, used to compare the results was 2.16, calculated from the stoichiometry. The calculations selleck chemical were obtained considering 10 mol of Ca with molar mass of 40.08 g/mol and 6 mol of P with molar mass 30.97 g/mol. After obtaining the image of the map, a line of 0.3 mm was drawn at the centre of the bone crest, approximately 0.1 mm below the tip of the crest, in which the average concentrations of Ca and P were obtained. These averages were used to perform the calculation of the Ca/P ratios (Fig. 1). Data concerning the weight and diet of the rats showed non-normal distribution and were performed using non-parametric tests (Kruskal–Wallis and Mann–Whitney). No statistical adjustment was applied to the samples.

Sea Trout samples were obtained with the assistance of the National Atmospheric Oceanic Administration Research Vessel, the Oregon II and Dr. Chuck Weirich at Aqua Green. Wild alligator gar samples were collected with the assistance of Dr. Allyse Ferrara and Ricky Verrett at Nicholls State University. Control, hatchery reared juvenile alligator gar were provided

by Ricky Campbell and Carlos Echevarria of the US Fish and Wildlife Service. The authors also wish to acknowledge the assistance of Robert Ford (retired biologist), and Dr. Janice Chambers and Jenny Wagner in the MSU Center of Environmental Health Sciences. “
“While major accidental oil spills from tankers are relatively this website rare occurrences, the transportation of oil remains one of the main concerns for the various stakeholders in the protection of the marine environment (Dalton and Jin, 2010). Not only

can oil spills have a devastating effect on the marine ecosystem (Lecklin et al., 2011), they involve high acute costs through clean-up operations (Montewka et al., 2013c), Epigenetics inhibitor have a considerable impact on affected economic activities (Crotts and Mazanec, 2013 and Garcia Negro et al., 2009) and can have cultural and behavioral effects on local communities (Miraglia, 2002). As an aid in maritime transportation risk management, methods for quantitative risk assessment of maritime traffic have been developed (Özbaş, 2013). These provide insight in the spatial distribution of accidental risk of ship traffic, which can, eltoprazine when coupled to environmental sensitivity and risk analysis (Delpeche-Ellmann

and Soomere, 2013 and Singkran, 2013), provide input to maritime spatial planning (Frazao Santos et al., 2013) and planning of oil combating resources (Lee and Jung, 2013). Risk assessment methods can also be used to assess the effect of proposed risk control options (van Dorp and Merrick, 2011). Worldwide, ship groundings, collisions and fires are the most frequently occurring accident types (Guedes Soares and Teixeira, 2001) and also in the Gulf of Finland, groundings and collisions represent the majority of the accident types (Kujala et al., 2009). Assessing oil spills from such accidents thus is an important aspect of maritime risk assessment. In this paper, we limit the scope to cargo oil spill size assessment of a product tanker in a ship–ship collision, i.e. vessels with a deadweight between 10 k and 60 k (Evangelista, 2002). A number of oil spill models have been developed. Przywarty (2008) and Gucma and Przywarty (2008) report on an oil spill model based on the analysis of accident statistics, which cannot account for specific traffic characteristics. IMO, 2003 and IMO, 1995 presents a model for measuring the outflow performance of a particular vessel design against a reference double-hull design.

006). This suggested stronger associations between lean adjusted total fat mass and trabecular density in the male than female children. In this pre-pubertal, free-living population, fat mass, adjusted for lean mass, was associated positively with bone size but negatively with true volumetric density assessed by pQCT, across the whole fat mass distribution. We recruited children from a free-living population cohort and used objective measures of body composition and bone size and density.

However, there are several limitations to our study. We were only able to study a proportion of the original cohort. However the children who underwent the 6 year assessment did not differ at birth or 1 year old from those who did not. Mothers of children who underwent 6 year assessment were broadly similar to mothers of those children who did not, but were more likely to be of higher social class and PLX3397 mw less likely to smoke. However, as the analysis

is based on internal comparisons it is difficult to envisage how this would have spuriously selleckchem shown an association between fat mass and bone size and density. The study population included a very small number of non-white Caucasian children and therefore it is uncertain whether our findings may be generalisable across these other ethnic groups. Secondly we used DXA to measure bone mass. This technique is associated with technical limitations in children. Measurement of bone mineral ID-8 in young children is

hampered by their tendency to move and also by their low absolute BMC. However, we used specific paediatric software, and movement artefact was modest and uniform across the cohort; those few children with excessive movement were excluded from the analysis. DXA measures of bone mass have been shown to correlate well with whole body calcium content in ashing studies of piglets [13] and [14]. Finally, we used a number of adjustments in the analyses, for example adjusting fat mass for lean mass. There is a biological rationale for this approach, as described in the methods, but as a result of co-linearity between measurements, it is possible that some analyses were over-adjusted; our conclusions are supported, however, by the results from the unadjusted analyses. Children who are overweight have approximately a twofold increased risk of forearm fractures compared with controls [15]. A recent study has shown that among obese children with a history of fracture, lumbar spine bone mineral apparent density was reduced by 2–3 sd compared with non-obese children with a history of fracture [16]. Thus at least part of the increased risk of fracture in obese children may be mediated via reduced bone density rather than other factors such as increased risk of falling. Our findings are in accord with some, but not all, studies of pre-pubertal children using DXA and pQCT.

It is important to note that 80% of the HCV genotype 1-infected patients in this study had subgenotype 1a, which has reportedly been more difficult VX-809 manufacturer to treat than subgenotype 1b when using protease inhibitor-based direct-acting antiviral regimens.32, 33 and 34 Combination regimens that include ombitasvir and ABT-450/r with or without RBV have been studied in genotype 1-infected patients in other phase 2 and phase 3 studies. In a phase 2b trial evaluating various

combinations of ombitasvir, ABT-450/r, the nonnucleoside polymerase inhibitor dasabuvir, and RBV administered for 8, 12, or 24 weeks in genotype 1-infected patients, SVR24 rates up to 96.2% in treatment-naïve patients and 95.3% in prior pegIFN/RBV-null responder patients were observed.29 A phase 2 study assessing a 12-week regimen of ABT-450/r and ombitasvir without RBV in genotype 1b-infected patients reported SVR12 rates of 95.2% in treatment-naïve patients and 90.0% in Belnacasan in vivo prior pegIFN/RBV-null responder patients.30 In phase 3 trials, a regimen of ombitasvir/ABT-450/r and dasabuvir with RBV was evaluated in treatment-naïve and pegIFN/RBV treatment-experienced HCV genotype 1-infected patients with and without cirrhosis. Regimens of ombitasvir/ABT-450/r and dasabuvir with RBV achieved SVR12 rates up to 96% in each of the large patient populations evaluated in these trials.17, 21 and 31

Other phase 3 trials evaluated this regimen with and without RBV.18 SVR12 rates of 97.0% and 90.2% were observed in HCV subgenotype 1a-infected patients receiving ombitasvir/ABT-450/r and dasabuvir with and without RBV, respectively.18 SVR12 rates in HCV subgenotype 1b-infected patients receiving ombitasvir/ABT-450/r and dasabuvir with and without RBV were 99.0% and 99.5%, respectively.18 Response rates in this study in HCV genotype 2-infected patients were high Mirabegron despite 80% of the patients having subgenotype 2b infection, which has been identified as more difficult

to treat with pegIFN-containing regimens than subgenotype 2a.22, 35 and 36 The exploratory regimens in this study resulted in SVR in some HCV genotype 3-infected patients, but the overall SVR rates in this group of patients were low. The results of this study also indicate that the safety and tolerability of both the RBV-containing and RBV-free regimen compare favorably to pegIFN-based therapy. Patients receiving these all-oral regimens avoid the subcutaneous injections required for pegIFN therapy. Also, the rates of adverse events commonly associated with pegIFN treatment, such as fatigue, headache, nausea, and depression, were lower in patients in this study than previously reported in patients receiving pegIFN.37 One patient in this study had a grade 3 bilirubin elevation; this elevation was predominantly indirect bilirubin, consistent with the known effect of protease inhibitors on the organic anion-transporting polypeptide 1B1.

, 2006). Low self-efficacy was identified as a barrier to treatment adherence (Shaw et al., 1994, Taylor and May, 1996, Stenstrom et al., 1997, Chen et al., 1999, Oliver and Cronan, 2002 and Milne et al., 2005). Poor self-efficacy could explain a patient’s low confidence in their ability to overcome obstacles to initiating, maintaining

or recovering selleck compound from relapses in exercise (Sniehotta et al., 2005). Low self-efficacy could be identified by clinicians using simple questions such as “How confident are you that you can…” (a) “overcome obstacles to exercising?” or (b) “return to exercise, despite having relapsed for several weeks?” Strategies to address low self-efficacy should be specific to the individual’s stage of exercise behaviour or perceived obstacles (Scholz et al., 2005). The use of strategies such as agreeing realistic expectations (Jensen and Lorish, 1994), setting treatment goals (Evans and Hardy, 2002), action planning (Sniehotta et al., 2005), coping planning

and positive reinforcement (Gohner and Schlicht, 2006) may help increase patient self-efficacy and adherence. Depression (Minor and Brown, 1993, Shaw et al., 1994, Rejeski et al., 1997 and Oliver and Cronan, 2002), anxiety (Minor and Brown, 1993 and Dobkin et al., 2006) and helplessness (Sluijs et al., 1993 and Castenada et al., 1998) were barriers to treatment adherence. Physiotherapists should be sensitive to the presence of anxiety, CT99021 manufacturer depression and helplessness and ensure that these patients are referred to relevant healthcare services for appropriate management as required.

Simultaneously ensuring that pain is being effectively managed may be helpful in reducing anxiety or depression which is pain related. Additionally it may be helpful to reinforce the message that exercise is an effective way of countering both low mood and negative thoughts, whilst simultaneously improving pain and function (Lim et al., 2005). Greater social support and encouragement for exercise in this group of patients may provide motivation, role models and guidance that may be important (Castenada et al., 1998). Low levels of FAD social activity (Funch and Gale, 1986, Minor and Brown, 1993, Sluijs et al., 1993, Rejeski et al., 1997 and Oliver and Cronan, 2002) and social or familial support (Shaw et al., 1994) were barriers to treatment adherence. Some patients believe they would more readily exercise if accompanied by someone else during their activity (Milroy and O’Neil, 2000 and Campbell et al., 2001). The support provided by the physiotherapist, the development of the patient–practitioner relationship and positive feedback from the physiotherapist may also increase adherence (Sluijs et al., 1993 and Campbell et al., 2001). Clinicians could consider organising rehabilitation programmes which incorporate social contact and support.