Alternatively, because the GPi lesions were not complete in KD, it is possible that his lesions led to imbalance in cross-talk between striatal regions which could be ameliorated by dopamine therapy. It has selleck compound been demonstrated that parallel corticostriatal loops through the basal ganglia need not operate in isolation but can instead communicate with each other, e.g., via spiralling striato-nigro-striatal connections (Haber et al., 2000) which allow ventral striatal regions to influence more dorsal striatal areas. Moreover,

the nigrostriatal system is not the only dopaminergic modulator of basal ganglia function; the intra-striatal dopaminergic system is complex and can alter with denervation (Smith and Kieval, 2000). Finally, it is important also to consider the possibility

that the effects of dopamine observed in KD might arise from indirect, knock-on effects on other neurotransmitter systems, e.g., there is evidence of interactions between dopaminergic and noradrenergic systems (Hara et al., 2010) as well as several other neurotransmitters (see Steiner and Tseng, 2010, for reviews). In macaques, using the directional reward saccade learn more task, Hong and Hikosaka (2008) found that saccades to the RS with shorter latency than to the US, with reward-related speeding being associated with activity in GPi neurons which project to the lateral habenula. If a homologous circuit operates in the human brain, Edoxaban it is likely to have been partially disrupted in KD in whom both GPi were damaged. However, the lateral habenula remained intact, together with the caudate and putamen. Furthermore, SPECT imaging of the DAT demonstrated that the nigrostriatal dopaminergic pathway was intact as there was good signal bilaterally in the caudate and putamen of KD. Thus one locus of dopaminergic drug action is potentially the intact caudate, putamen or even surviving parts of the GP complex. Another potential site of action of dopamine

is prefrontal cortex. The OFC, in concert with basal ganglia structures, is considered to have a special role in the processing of reward signals (Schultz, 2000; Kringelbach and Rolls, 2004; Wallis, 2007). Projection of KD’s lesion onto the known topography of the pallidal trans-thalamic connections to the cortex, determined using diffusion-weighted tractography (Draganski et al., 2008), suggests that the connections to the VMPFC and OFC have most likely been disrupted (Fig. 2). OFC neurons not only respond selectively to reward or aversive stimuli, but also signal relative preference for rewards and may integrate different types of information to compute a representation of value (Thorpe et al., 1983; Tremblay and Schultz, 1999; Padoa-Schioppa and Assad, 2006; Wallis and Kennerley, 2010).

peptides; type of antigen as RD1 vs. purified protein derivative (PPD)], and the study cohort characteristics (i.e. low endemic Cyclopamine supplier countries vs. high endemic countries for TB; comparison with subjects at different stages of TB and/or HIV infection/disease). 16, 19 and 21 Qualitative analysis of cytokine production

showed different subsets of bi-functional RD1-specific CD4+ T-cells among the two groups. HIV–TB were characterized by CD4+ T-cells co-producing IFNγ and TNFα, as previously reported in HIV-uninfected subjects,12, 13, 16 and 32 whereas HIV–LTBI were characterized by CD4+ T-cells co-producing TNFα and IL2. This cytokine profile is probably due to the main role that IFNγ and TNFα play, containing Mtb growth, 38 and 39 and the high frequency of these cytokines produced by the CD4+ T-cells of HIV–TB patients find more ( Fig. 4 A-C). In HIV–LTBI, in addition to TNFα, IL2 has the important task of inducing T-cell proliferation which is required for the subsequent differentiation of T-cells in effectors which are crucial for Mtb control. 40 and 41 The phenotypic characterization

of RD1 antigen-specific T-cells showed an effector memory involvement in association with active TB disease in both the CD4+42 and CD8+ T-cell subsets. Interestingly, the RD1 antigen-specific CD4+ T-cells had an EM and CM phenotype whereas the CD8+ T-cell subset presented mainly an EM phenotype with a limited contribution of the CM response. In this study, we did not observe any correlation between CM phenotype and LTBI status, as shown in HIV-uninfected subjects.13 and 43 This is likely due to the reduction of the Mtb-memory response by the HIV infection that may be eventually restored after ART. 44 We also found an increased proportion of the terminally

differentiated effector memory Mtb-specific CD4+ and CD8+ T-cells Cyclin-dependent kinase 3 in HIV–LTBI, as described in the HIV-uninfected subjects. 11 and 15 These findings are consistent with the observation that TNF-inhibitors decrease the terminally differentiated effector memory CD8+ T-cells, suggesting that these cells have a protective role in the control of Mtb infection. 45 In this study, we compared the response elicited by the RD1 antigen with that elicited by HIV–GAG, CMV and SEB stimuli, with the aim of defining the specificity of our results. We found that the frequency of response to HIV–GAG and SEB was not dependent on TB status. The higher frequency of response to CMV in HIV–LTBI is probably linked to the lower CD4+ T-cell counts and higher HIV-loads in the HIV–TB group compared to the HIV–LTBI, in agreement with the literature.46 A potential limitation of the present study is the relatively small number of subjects analyzed. However, it is important to consider that our intent was to enroll only those patients who were recently diagnosed with HIV infection (ART-naïve by definition) but since these patients are a minority of the total patients evaluated at INMI, few patients were available for enrollment.

A proper iron chelator should fulfill certain requirements such as high affinity for Fe(III), oral activity, low toxicity and penetration ability through biological membranes. Deferoxamine (DFO, DFB, desferrioxamine B, known also as Desferal) (Fig. 6) is a bacterial siderophore produced by a gram-positive bacteria Streptomyces species ( Henretig et al., 1983 and Imbert et

al., 1995). It is hexadentate and the most frequently used chelator proved to be very effective in the treatment of a number of diseases originating in excess body iron. Deferoxamine can bind iron both oxidation states ( Kell, 2010). Ferriprox (deferiprone) is a bidentate chelator with a high affinity for iron acting at molecular, cellular, tissue and organ levels ( Kell, 2009). Another effective chelator used in the treatment of neurological disorders is clioquinol (CQ, 5-chloro-7-iodoquinolin-8-ol) a hydroxyquinoline antibiotic containing the 8-hydroxy quinoline Z-VAD-FMK order motif. CQ was found to be an effective high-affinity chelator of iron in blocking the formation of hydrogen peroxide by Amyloid beta ( Bush, 2008). Various copper chelators, such as d-Penicillamine (d-pen), dimercaprol, trientine,

tetrathiomolybdate and clioquinol have been used in cancer treatment, especially in inhibiting angiogenesis both in vitro and in vivo (Brem et al., 1990, Gooneratne and Christensen, 1997 and Pan et Staurosporine research buy al., 2002). Brem et al. (1990) observed a reduced tumour growth following a low copper diet and d-pen treatment in glioma implanted intracerebrally in rabbits. d-pen and triente are chelators used to remove excess copper associated with Wilson’s disease. Trientine is another copper chelator, Rapamycin mw acting primarily by enhancing urinary copper excretion. A decreased tumour growth and lowered production of IL-8 with trientine treatment in hepatocellular carcinoma has been observed (Moriguchi et al., 2002). Copper

deficiency induced by tetrathiomolybdate resulted in impairment of tumour growth and angiogenesis in two animal models of breast cancer. A number of clinical trials with copper chelators such as d-pen and tetrathiomolybdate to determine their anti-angiogenic activity have also been conducted (Brewer, 2005). A phase II trial of copper depletion and penicillamine as anti-angiogenesis therapy for glioblastoma reported an effective ceruloplasmin depletion after two months of combination therapy of penicillamine and a low copper diet. However, the achievement of hypocupremia was reported not to significantly increase survival in glioblastoma patients. Polyphenolic compounds represent one of the most commonly occurring groups of plant metabolites (Melidou et al., 2005, Flora, 2009 and Perron et al., 2010). Their structure consists of a diphenyl-propane moiety containing aromatic rings linked through three carbon atoms that form an oxygenated heterocycle.

As regards to the reactive species involved in Orn and Hcit pro-oxidant effects, it is feasible that the peroxyl radical, which is scavenged by α-tocopherol whose active form is regenerated (reduced) by ascorbic acid, may underlie at least in part these oxidative

effects. However, considering that NAC also prevented these effects, we cannot exclude the possibility that a shortage of GSH could be responsible for lipid and especially protein oxidative damage provoked by Hcit and Orn. In fact, we found that Hcit ICV administration gave rise Selleckchem Talazoparib to a decrease of GSH concentrations, besides significantly inhibiting the activity of the antioxidant enzymes CAT and GPx with no effect on SOD. In contrast, Orn did not significantly affect any of these antioxidant defenses. Furthermore, it is unlikely that reactive nitrogen species participated in the pro-oxidant effects of Orn and Hcit since these compounds did not elicit nitrate and nitrite synthesis. Considering that endogenous GSH is Cyclopamine supplier considered the major naturally occurring brain antioxidant and that GPx and CAT activities are important enzymatic antioxidant

defenses ( Halliwell and Gutteridge, 2007), we presume that the rat cortical antioxidant defenses were compromised by in vivo administration of Hcit. Furthermore, it is also conceivable that the reduction of GSH levels may reflect increased reactive MAPK inhibitor species generation elicited by Hcit. In this context, it may be presumed that Orn did not reduce GSH levels probably because it induced less reactive species formation compared to Hcit, reflected by its lower oxidative effects. Our present data strongly indicate that in vivo administration of the major amino acids

accumulating in HHH syndrome induces oxidative stress in rat cerebral cortex since this deleterious cell condition results from an imbalance between the total antioxidant defenses and the reactive species generated in a tissue ( Halliwell and Gutteridge, 2007). It should be emphasized that the brain has low cerebral antioxidant defenses compared with other tissues ( Halliwell and Gutteridge, 1996), a fact that makes this tissue more vulnerable to increased reactive species. With respect to the parameters of energy metabolism, Orn and Hcit compromised the aerobic glycolytic pathway and the CAC activity since they significantly decreased CO2 formation from labeled glucose and acetate, respectively. It is therefore possible that Orn and Hcit may have inhibited the activity of one or more glycolytic enzymes, one or more reactions of the CAC, and/or the respiratory chain.

Sample (25 μl) was added to the corresponding well in a 96-well filter plate containing 25 μl of anti-caspase-3 or PARP conjugated beads. The plate was incubated at 4 °C overnight. After washing, 25 μl of detection antibody was added to each well and the plate was incubated for 1 h at RT. Detection antibody was removed by vacuum filtration and 25 μl of pre-diluted streptavidin-conjugated

phycoerythrin was added to each well. The plate was incubated for 15 min at RT on a shaker. After vacuum filtration, 120 μl of assay buffer was added to each well. The plate was shaken for 1 min and analyzed with the Bio-Plex 100 Array System (Bio-Rad, Hercules, CA). Cells were seeded onto coverslips in a 12-well ABT-199 concentration plate overnight and grown to 80% confluency. After cells were treated with CdTe-QDs and positive controls, cells were washed with PBS and incubated with annexin V solution containing 1 μg/ml of annexin V-phycoerythrin in annexin V binding buffer (R&D Systems, Minneapolis, MN) for 10 min at 37 °C. Cells were

washed twice with PBS and fixed with 4% paraformaldehyde click here containing 0.1% Triton X-100 for 10 min. After that, cells were washed twice with PBS and incubated with sytox red (1:1000) for 15 min. After washing, cover slips were mounted on slides and dried overnight before being observed with a Nikon TE2000 microscope attached to a C1 confocal unit. Fas level was measured using a Fas ELISA assay kit from Promokine (PromoCell GmbH, Heidelberg, Germany). Briefly, after treatments, cells were homogenized in lysis buffer (20 mM Tris, pH 7.4, 137 mM NaCl, 1% NP-40) containing protease inhibitors. Cell lysates were vortexed and centrifuged at 12,000 rpm

for 15 min at 4 °C. The supernatants were collected, measured for protein concentration and used in the ELISA assay, following the manufacturer’s instructions. Caspase-8 activity was measured using a caspase-8 enzymatic assay kit from Abcam (Cambridge, MA). Briefly, after treatments, cells were resuspended in chilled cell lysis buffer and incubated on ice Glutathione peroxidase for 10 min. Cell lysates were centrifuged for 1 min at 10,000 × g. Supernatants were collected, measured for protein concentration and placed on ice until analysis. For each sample, 100 μg of protein was used and diluted in 50 μl of cell lysis buffer. To each sample, 50 μl of provided 2× reaction buffer and 5 μl of the 4 mM acetyl-Ile-Glu-Thr-Asp p-nitroaniline (IETD-pNA) substrate were added. The samples were incubated at 37 °C for 1 h, transferred to a microtiter plate and read at 405 nm in a microplate reader. Bcl2 level was measured using bead plex assay kit from EMD Millipore Corporation (Billerica, MA) according to the manufacturer’s protocol. After treatments, cells were homogenized in the lysis buffer provided and centrifuged at 12,000 rpm for 20 min at 4 °C. The supernatants were collected and diluted in assay buffer.

g. http://www.guardian.co.uk/environment/2010/oct/20/spending-review-cuts-environment). In various cases this cutting of budgets has reduced

the number of sampling locations ( De Jonge et al., 2006), frequency of sampling ( Abramic et al., 2012, or required looking for cheaper assessment methods ( Lampadariou et al., 2005). We accept that all fields include the ‘law of diminishing returns’, what may be called the 80/20 rule – in the first 20% of the time studying a problem then you obtain 80% of the information required, but to obtain the remaining 20% information then requires a disproportionate amount of time and energy. However, our fear here is that rather than scientific criteria learn more being used to define the level of monitoring, it is economics – i.e. the ‘bean-counters’ are now dictating the science to be undertaken such that we will reach a stage where monitoring is not longer fit-for-purpose or even, paradoxically, value-for-money. Biological/ecological monitoring is often centered on measuring the community composition of an area and detecting whether that has changed, for example due to pollution of the arrival of alien and invasive species (Gray and Elliott, 2009). One of the

ways proposed for saving money is to use presence/absence of Metformin an ecological component instead of Ion Channel Ligand Library abundance (Bates et al., 2007) and another relates to the taxonomic sufficiency i.e. the use of high taxonomic levels (e.g. family instead of species), since its first formulation by Warwick (1988). This suggests that samples could be analysed

to higher taxonomic levels, detecting the pollution effects on marine communities with similar statistical accuracy, and saving money because of the higher cost of identifying organisms at the species level (Dauvin et al., 2003 and Dimitriou et al., 2012). In this way, it is interesting to note that the analysis to family level is only cheaper if you are skilled to species level; if you do not train taxonomists (which is the current trend in all countries) then even family level identification is difficult and expensive. We are also amazed that managers are willing to spend thousands of euros/dollars on chemical analyses but then complain about biological samples (which require people with skills instead of machines) costing money. Secondly, while it has long been accepted that analytical quality assurance/quality control (AQC/QA) is required in chemistry laboratories, which may commit up to 40% of their time and budget to this, there has been resistance to adopting this in biological analyses (Elliott, 1993 and Gray and Elliott, 2009).

U dzieci otrzymujących probiotyk było mniej dodatnich wyników testów skórnych, zwłaszcza wśród dzieci matek z objawami alergii. Miniello i wsp. [47], stwierdzili, że obecność L. reuteri w przewodzie pokarmowym wpływa na skład cytokin w płucach u pacjentów z atopią. Badacze ci mierzyli stężenie INF gamma i IL-4 w wydychanym powietrzu u dzieci z atopowym i niealergicznym zapaleniem skóry, którym doustnie

podawano L. reuteri ATCC 55730 lub placebo przez 8 tygodni. Autorzy wykazali, że poziom tych cytokin zmienia się tylko u dzieci z atopią otrzymujących verum. Rosenfeldt i wsp. [48] przeprowadzili badanie z randomizacją, w którym podawali L. rhamnosus i L. reuteri DSM równocześnie dzieciom w wieku 1–13 lat z wypryskiem atopowym, PD332991 przez 6 tygodni. Wykazano znaczącą różnicę w odsetku pacjentów, u których stwierdzono poprawę w zakresie objawów klinicznych, pomiędzy grupą otrzymującą probiotyki a grupą otrzymującą placebo (56% vs 15%). Poprawa dotyczyła szczególnie pacjentów, u których wcześniej wykazano przynajmniej jedną pozytywną reakcję w punktowych testach skórnych

lub podwyższone INCB024360 stężenie IgE. U pacjentów otrzymujących probiotyki uzyskano większą redukcję poziomu eozynofilowego białka kationowego. U tych pacjentów odnotowano także znaczącą redukcję objawów ze strony przewodu pokarmowego [49]. W badaniach na zwierzętach wykazano ponadto potencjalną rolę L. reuteri w hamowaniu reakcji zapalnej w Niclosamide obrębie drzewa oskrzelowego w przebiegu astmy [50, 51]. Niektórzy autorzy podnoszą również wpływ L. reuteri na zmniejszenie zapadalności na choroby infekcyjne, zarówno u dzieci, jak i u dorosłych. I tak Weizman i wsp. [52] wykazali, że dzieci otrzymujące L. reuteri rzadziej chorują, wymagają mniej wizyt lekarskich, rzadziej w ich przypadku w porównaniu z dziećmi otrzymującymi placebo zachodzi konieczność absencji w żłobku. Tubelius

i wsp. [53] wykazali znaczne zmniejszenie zachorowalności na infekcje układu oddechowego lub przewodu pokarmowego, powodujące krótkotrwałe nieobecności w pracy z powodu złego samopoczucia wśród dorosłych otrzymujących codziennie L. reuteri. Tym badaniem objęto ponad 260 osób, którym losowo podawano probiotyk lub placebo przez 80 dni. Innym kierunkiem niedawno podjętych badań jest możliwość zastosowania L. reuteri w leczeniu zakażeń układu moczowego u pacjentów z pęcherzem neurogennym po uszkodzeniach rdzenia kręgowego, wymagających stałego lub okresowego cewnikowania pęcherza. Anukan i wsp. [54] wykazali, że u pacjentów z takimi problemami doustna podaż mieszaniny L. reuteri i L. rhamnosus powoduje zmniejszenie miejscowej produkcji TNF-alfa i niektórych interleukin. Czy jednak odkrycie to będzie miało istotne znaczenie kliniczne, pozostaje przedmiotem dalszych badań. Cadieux i wsp. [55] wykazali, że L. reuteri i L. rhamnosus powodują inhibicję wzrostu uropatogennych E. coli. Istotnym elementem zdrowia człowieka jest dobry stan stomatologiczny. Wykazano, że L.

This is consistent with our previous finding where H/W rats showed minimal or no change in body weight following

TCDD treatment whereas significant weight loss was observed for the sensitive L-E strain after both time points ( Boutros et al., 2011), as is a more prominent decrease in plasma glucose upon TCDD treatment in L-E than H/W rats ( Viluksela et al., 1999). Dysregulation of Slc37a4 could be involved in the differential energy and feed metabolism between sensitive and resistant strains and the selleck kinase inhibitor resulting wasting syndrome observed in the sensitive strains but not in resistant strains ( Boutros et al., 2011 and Pohjanvirta and Tuomisto, 1994). Endocrine imbalance is another acute effect that follows TCDD treatment (Pohjanvirta and Tuomisto, 1994). Some portion

of endocrine disruption may be due to altered synaptic transmission and communication from neurons to the endocrine system. Acp2, a gene that is consistently induced by 2-fold in the sensitive strains but not in the resistant strain, encodes a lysosomal acid phosphatase that catalyzes p-nitrophenyl phosphate hydrolysis. The abundance of the phosphatase in the nerve endings suggests its potential role in synaptic transmission ( Tanino et al., 1999). In other studies, Acp2 was found to play a role in acute pancreatitis ( Lakowska et al., 2001). It is difficult to evaluate the role of Acp2 in TCDD toxicity due to the insufficient characterization of its physiological functions, but the increase in Acp2 expression may have a role in the imbalance in the endocrine Bcl-2 inhibitor system of rats that are exposed to TCDD ( Pohjanvirta and Tuomisto, 1994). Long-term exposure to TCDD leads to cancer formation in liver and other organs (Viluksela et al., 2000). Prkcdbp encodes a protein kinase-binding protein that may be involved in the control of cell growth mediated by protein kinase C ( Izumi et al., 1997). Prkcdbp showed greater than 3-fold induction in the sensitive strains but did not reach statistical significant in the resistant H/W strain. Impaired control of cell growth could well

contribute to the carcinogenic effect of TCDD Immune system in sensitive animals. On the other hand, Sdc1, a mouse homolog that is found to promote cell–cell adhesion, showed significant repression by at least 3-fold in all the sensitive strains but remained unperturbed in the resistant H/W strain. Sdc1 has been previously shown to be implicated in hepatocellular cancer (HCC). Both the gene and protein expression of Sdc1 was significantly reduced in HCC with extra-hepatic metastasis in comparison with those without ( Matsumoto et al., 1997). This suggests that Sdc1 may play a role in determining metastatic potential. A highly characteristic feature of the acute toxicity of TCDD is its delayed emergence. Even after supralethal doses of TCDD, the exposed animals do not die immediately but only after 2–5 weeks (Pohjanvirta and Tuomisto, 1994).

Here, other initiatives, such as www.physiotherapyexercises.com, are useful. This website, which is appraised in detail in this issue of the journal, allows free online access to definitions of a wide array of exercises used in rehabilitation. Each exercise is described using text, diagrams, and photographs, in some cases supplemented

by video. It therefore provides comprehensive definitions of over 900 exercises. Physiotherapists wishing to describe an exercise can refer to the site knowing that the exercise they name will not be misinterpreted. Other selleck chemicals aspects (such as resistance, repetitions, and any modifications) still need to be defined, but at least the basic description can be unambiguously agreed upon by reference to the site. Other sites do much to standardise even more complex interventions, such as pulmonary rehabilitation on the Australian Lung Foundation’s Pulmonary Rehabilitation Toolkit website. Physiotherapists should consider using and supporting initiatives such as those described above. Increasing standardisation of the terms we use clinically and in research has the potential to improve communication within the profession. “
“Interest in the therapeutic alliance between clinician and patient began in the fields of medical care (Stewart 1995) and psychotherapy (Hovarth and Symonds 1991, Martin et al FG-4592 mw 2000). The therapeutic alliance, also referred to in the literature as the working

alliance, therapeutic bond, or helping alliance, is a general construct that usually includes in its theoretical definition the collaborative nature, the affective bond, and the goal and task agreement between patients

and clinicians (Martin et al 2000). Other constructs, such as trust (Hall et al 2002) Histone demethylase and empathy (Mercer et al 2004), may overlap with this definition and are also used to assess the quality of the alliance. More recently, this concept has been considered in the field of physical rehabilitation, including physiotherapy settings (Hall et al 2010). The evidence has shown that a good therapeutic alliance can positively influence treatment outcomes such as improvement in symptoms and health status and satisfaction with care (Hall et al 2010). A good example comes from musculoskeletal rehabilitation. Patients undergoing physiotherapy for chronic low back pain with a strong therapeutic alliance showed an increase as high as four points on a 0–10 scale of global perceived effect compared to those with a weak therapeutic alliance (Ferreira et al 2009). In the field of physiotherapy, the nature of most interventions is usually long-term. Hence, patients’ adherence to longterm treatment regimens is vital to achieve effective clinical practice (WHO 2003). More broadly, it has been recognised that lack of adherence to long-term therapies results in poor clinical outcomes and unnecessarily high costs of health care (WHO 2003).

Four studies reported compliance of at least 80% ( Barnard et al 2000, Feiereisen et al 2007, Pu et al 2001, Tyni-Lenné et al 2001), and one study reported’excellent’ compliance ( Beckers et al 2008). Two studies reported compliance with means of 75% and 78% respectively ( Cider et al 1997, Mandic et

al 2009) and one study did not report compliance ( Selig et al 2004). Among all of the studies, only one sudden death was reported, which occurred at home three days after Veliparib molecular weight the most recent resistance training session. One drop-out was reported in the resistance training group due to noncompliance ( Table 3). One study reported that four patients had intermittent mild musculoskeletal symptoms during resistance training with minor modification of their training protocol afterwards ( Pu et al 2001). No safety issues were reported PD173074 in vitro by either the resistance training alone or combined aerobic training studies. Interventions: Four studies ( Cider et al 1997, Pu et al 2001, Selig et al 2004, Tyni-Lenné et al 2001) compared resistance training alone with usual activity, usual care, or sham exercise. The other four studies ( Barnard et al 2000, Beckers et al 2008, Feiereisen et al 2007, Mandic et al 2009) studied combined (resistance and aerobic) training versus aerobic training groups. All the training programs

were supervised. The length of training ranged from 2 to 6 months. The intensity for resistance training was Galeterone moderate or about 50–75% of one repetition maximum

(1RM), while aerobic training on a treadmill or cycle ergometer was moderate to vigorous intensity. Two studies used high intensity exercise at 80% of 1RM, with no exercise-induced cardiac events reported (Barnard et al 2000, Pu et al 2001). The resistance training usually consisted of 2 sets of 8–12 repetitions for 5–6 exercises targeting the large muscle groups of upper limbs, trunk, and lower limbs. The exercise duration was around 30–60 minutes and exercise frequency was 2–3 times per week. One study included respiratory muscle training as one of the nine exercises (Beckers et al 2008). This was the largest number of exercises among the eight studies. We examined by separate analyses the effect of resistance training alone or in combination with aerobic training. Four studies reported cardiac function, seven reported exercise capacity, and five reported quality of life. All reported whether there were adverse events. Cardiac function: The effect of resistance training alone on cardiac function was examined in one trial ( Pu et al 2001), with no significant difference in left ventricular ejection fraction compared to control (MD 1.8%, 95% CI –5.7 to 9.3).