This could be due to removal of most proteases during the two consecutive PEG6000 precipitations of FMDV antigen. We could also detect FMDV antigen after

addition of the adjuvant by oil emulsification. Such analysis is often difficult to perform by other methods due to the difficulty in extracting the antigen from the vaccine for subsequent analysis. As a result there are only few publications about stability of vaccine antigens after addition of adjuvant. Several model protein antigens Selleckchem INK1197 may be structurally altered and have reduced thermal stability upon absorption to aluminium hydroxide adjuvant [22] and [23]. Here we have shown that VP4 remains associated with FMDV virions after emulsification with oil adjuvant, indicating that virions do not substantially dissociate into 12S particles due to the inclusion in an oil emulsion. This is important for vaccine efficacy since 12S particles have a 100-fold Lenvatinib mw reduced potency as compared to 146S particles [8]. It is known that

oil-adjuvanted FMDV O1 Manisa vaccines have reduced potency upon storage for 2 or 4 months and a complete loss of potency after 7 months storage [4]. The ability to determine various aspects of FMDV antigen integrity by SELDI-TOF-MS in oil emulsions now enables studies towards the molecular mechanism underlying such instability of FMD antigen after prolonged storage of oil emulsion vaccines. This work Calpain was supported financially by The Netherlands Ministry of Agriculture, Nature and Food Quality. We thank Jolanda Meijlis, Peter van Bavel, Marianne Krikken, Anna Oosterbaan and Corrie van der Bijl (all Lelystad Biologicals bv.) for supplying FMDV antigens and vaccines and for valuable discussions. “
“Glioblastoma multiforme (GBM) is a devastating

primary brain tumor that causes death in ∼73% of individuals within 2 years of diagnosis despite treatment with surgery, radiation, and chemotherapy [1]. This tumor presents clinically as either primary GBM or progresses from a lower grade (WHO II or III) glioma leading to secondary GBM. Both primary and secondary GBM are WHO grade IV tumors with a similar prognosis [2]. Secondary GBM often arises from WHO grade II astrocytomas that are characterized by low cellularity, low mitotic index and a diffuse pattern of infiltration into normal brain. Due to the disseminated nature of the neoplasm, surgery and adjuvant therapies are frequently inadequate and the tumor evolves into secondary GBM within 5–10 years [2]. Gemistocytic astrocytoma (GemA) is a histological variant of astrocytoma that has been defined in an arbitrary fashion by the presence of at least 20% gemistocytes within the tumor mass [3]. Neoplastic gemistocytes are characterized by their plump appearance, slightly eosinophilic cytoplasm and eccentric nuclei. The classification of GemA has been controversial.

This group also demonstrated a late asthmatic response between 8 and 9 h. The mean peak response during this period was − 19.9 ± 4.9%

compared to protocol 4, 1.3 ± 2.6%. No significant bronchoconstriction to histamine was observed in any experimental animal 24 h before Ova or saline challenge (Fig. 2). Small changes were observed in some groups which represent the normal variation in sensitivity to a threshold concentration of histamine. In animals challenged with saline, no histamine-induced bronchoconstriction was observed 24 h after saline (Fig. 2A). Animals sensitised with 2 injections of 100 μg/ml Ova and 100 mg Al(OH)3 and challenged with 100 μg/ml Ova (protocol 1, Fig. 2B) also lacked histamine-induced bronchoconstriction, indicating the absence of AHR. Increasing the Ova challenge

concentration to 300 μg/ml (protocol 2, Fig. 2C) caused a significant bronchoconstriction CH5424802 cost to histamine 24 h after Ova challenge (− 38.5 ± 7.9% compared to pre- − 4.1 ± 2.3%) which resolved within 10 min. Increasing the Al(OH)3 concentration (protocol 5, Fig. 2D), increasing Ova sensitisation concentration (protocol 4) and the number of injections (protocol 3) did not further alter the nature of this response (data not shown). Increasing the time between Ova sensitisation and challenge (protocol 6, Fig. 2E) increased the size of the immediate bronchoconstriction to histamine 24 h post-challenge (− 53.9.4 ± 11.4%) compared to pre-Ova challenge, (− 10.1 ± 2.4%). The duration of the bronchoconstriction was also increased, at 10 min into the response, the bronchoconstriction was − 26.7 ± 11.4% selleck kinase inhibitor compared to the pre-Ova challenge level of 1.6 ± 2.7%. 100 μg/ml Adenosine Ova challenge significantly increased total lavage cells (protocol 1, Fig. 3A, 3.2 ± 0.5 × 106/ml) compared to saline (1.6 ± 0.13 × 106/ml). Eosinophils (Fig. 3C) made up most of this increase (1.3 ± 0.3 × 106/ml) compared to saline (0.05 ± 0.01 × 106/ml). Increasing the Ova challenge concentration (protocol 2) significantly increased the total cell numbers (5.3 ± 0.4 × 106/ml) compared to protocol 1 (3.2 ± 0.5 × 106/ml).

Eosinophils were significantly elevated (2.0 ± 0.2 × 106/ml) compared to protocol 1 (1.3 ± 0.3 × 106/ml). Increasing the number of 100 μg Ova sensitisation injections (protocol 3) had no effect on any cell type measured. Increasing the Ova sensitisation concentration to 150 μg (protocol 4) significantly increased total cells (8.3 ± 0.9 × 106/ml) compared to protocol 3 (4.8 ± 0.4 × 106/ml). Eosinophils (3.9 ± 0.3 × 106/ml compared to 2.4 ± 0.3 × 106/ml) and macrophages (Fig. 3B, 3.5 ± 0.3 × 106/ml compared to 2.2 ± 0.2 × 106/ml) were also significantly increased. Increasing the Al(OH)3 sensitisation concentration to 150 mg (protocol 5) significantly increased eosinophils (6.9 ± 0.8 × 106/ml) compared to protocol 4 (4.6 ± 0.5 × 106/ml). Lymphocytes (Fig. 3D) were also significantly increased (0.15 ± 0.02 × 106/ml) compared to protocol 4 (0.3 ± 0.

The amount of the MMF present in analysed formulations was presented in Table 6. The stability of drug towards the degradation conditions was explained UMI-77 in vitro in terms of percent of drug obtained after time of degradation. In the present investigation

the stability of the drug was studied under 0.1 HCl, 0.1 N NaOH, 1% H2O2, photolytic and thermal conditions at three spike levels. At each condition three replicate measurements were taken, the percent of drug found after the period of degradation was calculated and mean percent of drug was determined. In acid, base and peroxide degradation studies, MMF stock solutions at LQC, MQC and HQC concentrations were taken into three microcentrifuge tubes; 100 μL of 0.1 N HCl, 0.1 N NaOH or 100 μL of 1% H2O2 solution was added in each tube and then kept a side for 24 h. The same amount of MMF stock solutions at LQC, MQC and HQC concentrations were taken into three microcentrifuge tubes methanol was added to the samples to keep the equality amount of the sample content for the analysis. Further the analysis was done as per the optimized procedure and the percent of degradation was calculated comparing the response (peak area) of the

degraded compound and freshly prepared solutions. The percent of drug found in between 91.18 and 96.70, 93.27 and 98.72 and 90.15 and 96.01 in 0.1 HCl, 0.1 N NaOH and 1% H2O2 respectively. In case of photo stability MMF samples (LQC and HQC) should be exposed to light providing an overall illumination of not less than 1.2 million lux h and an integrated near

ultraviolet Vorinostat mw energy of not less than 200 W h/m2 to allow direct comparisons to be made between the substance and product. Samples may be exposed side-by-side with a validated GPX6 chemical actinometric system to ensure the specified light exposure is obtained, or for the appropriate duration of time when conditions have been monitored using calibrated radiometers/lux meters. The percent of drug found in between 91.45 and 96.45 in photolytic conditions. In thermal stability, samples were placed in two test tubes, two thermocouples are inserted into the tubes and one in the oven. Thermocouples and the covered tubes are placed in the oven. The temperature difference between test samples is measured for 4 h after the sample reach 55 °C. Evidence of decomposition of the sample is determined by the samples compare with 0 h–4 h. The percent of drug found in between 93.90 and 98.19 in thermal conditions. The results were presented in Table 7(a)–(e). The developed LS/MS/MS method was found to be very simple, highly precise and accurate; therefore this may be suggested as an alternative method for routine quality control. All authors have none to declare. One of the authors TVBR wishes to convey his gratitude to T.G.

Results indicate that during isometric adduction in the scapular plane, the three rotator cuff muscles examined were activated at low levels with DZNeP nmr no significant difference in activity levels in these muscles when isometric adduction was performed at 30°, 60°, or 90° abduction. At maximum (100%) load, supraspinatus activity was negligible while infraspinatus and subscapularis had activity that was only about one-quarter of their maximal activation. In contrast, high mean activation levels were recorded in teres major, latissimus dorsi, and rhomboid major under the same load. These levels were significantly higher than the rotator cuff activation levels. The results

of the current study, therefore, do not support the clinical observation that adduction preferentially recruits the rotator cuff muscles or activates them at substantial levels. The high level of latissimus dorsi and teres

major activity recorded in the current study support the results of force studies (Hughes and An 1996, Kuechle et al 1997) and electromyographic studies (Broome and Basmajian 1971, Jonsson et al 1972), which indicate these muscles are major contributors to adduction torque. However, although force studies have indicated that subscapularis (Kuechle et al 1997) and infraspinatus (Hughes and An 1996) have favourable moment arms to contribute to adduction torque, the results of the current study provide electromyographic evidence that this contribution is small.

Therefore, the relative increase why in the subacromial space click here occurring during adduction as shown by magnetic resonance imaging studies (Graichen et al 2005, Hinterwimmer et al 2003) is not likely to be caused by these rotator cuff muscles but rather by latissimus dorsi and teres major. The results of the current study do not support the use of shoulder adduction as an optimal exercise to strengthen the rotator cuff muscles. Reinold and colleagues (2004) have suggested that optimal strengthening exercises require high levels of activity from the target muscle while minimising surrounding muscle activity. Muscle activity levels greater than 50% of their maximum voluntary contraction have previously been categorised as high and challenging to a muscle (McCann et al 1993, Townsend et al 1991). Shoulder adduction does not generate high levels of activity in any of the rotator cuff muscles tested and it does generate very high levels of activity in latissimus dorsi and teres major as well as rhomboid major. As an exercise to strengthen the rotator cuff muscles, shoulder adduction therefore fails to meet both these criteria for an optimal strengthening exercise, regardless of the functional role the rotator cuff may be performing. In addition, the results of the current study do not support the use of an adduction manoeuvre to identify rotator cuff dysfunction.

Fecal samples were immediately frozen at home by the subjects; Dabrafenib mouse fecal extracts were subsequently prepared and stored at −70 °C [11]. Antibody levels in ALS specimens, fecal extracts and sera were analyzed by ELISA using plates coated with CFA/I, CS3, CS5, CS6, GM1 plus LTB or O78 LPS [9] and [11]. Fecal antibody levels were determined as the antigen-specific SIgA titer divided

by the total SIgA concentration of each sample [15]. LT toxin neutralization titers were determined using the Y1 adrenal cell assay [16]. Safety endpoints were defined as absence of any vaccine-related serious AEs and not significantly higher frequencies of vaccine-related severe AEs in each of the vaccine groups than in the placebo group. Primary immunogenicity endpoints

were defined as induction of immune responses in any of the vaccine groups in either of the primary assays proposed (fecal SIgA or ALS IgA) to at least four of the five primary vaccine components (CFA/I, CS3, CS5, CS6 and LTB). The magnitudes of immune responses (fold rises) were calculated as the post-immunization divided by pre-immunization antibody levels. Statistical differences were evaluated using t-test (magnitudes, ELISA results), Mann–Whitney test (magnitudes, toxin neutralization results) and Fisher’s exact test (frequencies) with Holm’s correction for multiple testing [17]. Differences between vaccine groups and the placebo group were evaluated using one-tailed statistical tests; all other statistical tests were two-tailed. P-values <0.05 were selleck chemicals llc considered significant. Of 161 subjects screened, 129 were enrolled with 30–35 subjects in each of the four study groups (Table 1 and Supplementary material; Fig. 1). The age and gender distributions were comparable in Groups A, B and C, but more males

were randomized to Group D (Table 1). Overall, MEV administered alone and in either combination with dmLT was safe and well tolerated. No serious AEs were reported and the recorded AEs were mainly mild and not significantly different among any of the vaccine groups (B, C, D) and the placebo group (A). The addition of dmLT did not alter the safety profile. Altogether 89 solicited symptoms, deemed to be possibly or probably related to treatment, were recorded (Table 2); these AEs did not differ in either frequency or intensity between the different study groups. No significant changes of other clinical parameters, including serum chemistry and hematology, were observed in any of the volunteers. ASC responses against the primary vaccine antigens were studied by counting IgA ASCs by the ELISPOT method as well as by measuring antibody levels in lymphocyte secretions by the ALS method in the initial 43 randomized subjects. Since the frequencies of responses against all antigens were comparable using the two methods (data not shown), the ALS method was used in all subsequent study subjects as the sole measure of ASC responses.

PCV-7 has been shown in many studies to be highly immunogenic and effective against IPD [5], [15], [16] and [17], with the vaccine efficacy of 97.4% against vaccine serotypes in the US [5]. In the large trial in South Africa and Gambia, the efficacy of PCV-9 was 83% and 77% against IPD caused by vaccine serotypes [18] and [19]. Twice as many IPD cases were indirectly prevented due to herd immunity after the PCV-7 implementation in the US [8]. Due to serotype specific efficacy of the vaccine, serotype coverage of IPD implies and predicts the efficacy of the vaccine. In this region, the serotype coverage of 70.3% by PCV-7 in IPD in children under five years of age in our study was less than the 78% coverage found in Singapore

[15], but higher than in a study in China in 2008 which found 63.6%, 64.8% and 79.6% coverage by PCV-7, PCV-10 and PCV-13, respectively [20].

The serotype coverage of IPD isolates by PCV-7 in children ≤14 years Veliparib cell line old in Taiwan was 85%, somewhat higher than in our study [21]. WHO reported the overall serotype coverage of PCV-7 ranged from 60 to 85% worldwide [22]. There has been a concern about the increased proportion of nonvaccine serotypes reported in the US and Spain after introduction of PCV-7 vaccination program [8], [23] and [24]. The widely use of PCV-7 may contributed to the emergence of nonvaccine serotypes, especially serotype 19A [8], [23] and [24]. However, a study in Korea reported an increase in serotype 19A even before the introduction GPX6 of Selleck Forskolin PCV-7 [25]. It is probable that both selective vaccine pressure and clonal spread were contributing factors to the circulating serotypes in the community. In Thailand, we reported the serotype coverage of PCV-7, PCV-9, PCV-11, and PCV-13 of 73.9%, 77.4%, 77.4%, and 87.8%, respectively, in children younger than 5 years of age during 2001–2005 [11]. The serotype coverage found in this study was somewhat lower than that report, but was still within the 95% confidential interval. Although PCV-7 has been available in Thailand since June 2006, the vaccine has been

used mainly in private settings with an estimated 55,000 doses sold each year, representing less than 5% of children <5 years of age. This low vaccine uptake did not seem to affect the serotype distribution in this relatively small study. The top seven serotypes of invasive isolates found in our study were different in rank of order and frequency (%) in each age groups, as well as whether the sites were sterile or non-sterile. Although the top seven serotypes of isolates from sterile sites in children younger than 5 years of age were not completely match with other studies reported earlier in Thailand [11], [26], [27] and [28], they were quite consistent. The common serotypes found in those and our studies were 6B, 14, 19A, 19F, 23F. The PCV that included all these serotypes, i.e. PCV-13, would be the most appropriate for large scale use in Thailand.

Our health intent and aim is, for pregnancies complicated by a HDP, to improve short- and long-term maternal, perinatal, and paediatric outcomes, and related cost-effectiveness of interventions. The expected benefit of using this guideline is improved outcomes for mother, baby, and child, through evidence-advised practice. The target users are multidisciplinary maternity care providers from primary to tertiary levels

of health care. learn more The questions that this guideline seeks to address are: • How, and in what setting, should blood pressure (BP) be measured in pregnancy and what is an abnormal BP? The guideline was developed by a methodologist and maternity care providers (from obstetrics, internal medicine, anaesthesia, and paediatrics) knowledgeable about the HDP and guideline development. The literature reviewed included the previous (2008) SOGC HDP guideline and INCB28060 cell line its references [3] covering articles until July 2006, as well as updated literature from January 2006 until March 2012, using a search strategy similar to that for the 2008 guideline (and available upon request); a notable addition was exploration of the perspective and interests of patients with a HDP [4]. Literature reviews were conducted

by librarians of the College of Physicians and Surgeons of British Columbia and University of British Columbia, restricting articles to those published in English and French. We prioritized randomized controlled trials (RCTs) and systematic reviews (if available) for therapies

and evaluated substantive clinical outcomes for mothers (death; serious morbidity, including eclampsia, HELLP syndrome, and other major end-organ complications; severe hypertension; placental abruption; preterm delivery; Caesarean delivery; maternal adverse effects of drug therapies or other interventions; and long-term health) and babies (perinatal death, stillbirth, and neonatal death; small for gestational age infants; NICU care; serious isothipendyl neonatal morbidity, and long-term paediatric health and neurodevelopment). All authors graded the quality of the evidence and their recommendations, using the Canadian Task Force on Preventive Health Care (Appendix Table A1) [5] and GRADE (Level of evidence/Strength of recommendation, Appendix Table A2) [6]. This document was reviewed by the Executive and Council of the SOGC, and the approved recommendations published on the SOGC website as an Executive Summary (www.sogc.com). 1. BP should be measured with the woman in the sitting position with the arm at the level of the heart (II-2A; Low/Strong). BP measurement in pregnancy should use non-pregnancy standardized technique [7] and [8]. BP may be measured by ambulatory BP monitoring (ABPM) or home BP monitoring (HBPM) [9], using auscultatory or automated methods [10]. Most clinics and hospitals use aneroid or automated devices.

If differences over time (from baseline to follow-up) were found, these were further explored using the Wilcoxon signed-rank test with Bonferroni-Hochberg correction (Norman and Streiner 2000). Between-group differences were analysed using a Mann-Whitney U test only at 8 weeks to avoid multiple testing. The

flow of participants through the trial is presented in Figure 2. Forty-eight patients met all eligibility criteria. One participant from the experimental group (a 68-yearold female with a right-sided ischaemic stroke who regretted participation) and one from the control group (a 62-year old male with a left-sided ischaemic stroke who was rehospitalised due to acute liver and kidney failure) dropped out the day after baseline measurement and before receiving any intervention. These participants were not selleck chemical included in the analyses because their data were missing due to unavailability for further measurements. Of the 11 patients who were lost to follow-up or discontinued their prescribed intervention during the 8-week treatment period, four (36%) complained of pain. Baseline characteristics of the 46 participants analysed are shown in Table 1. Twenty-two participants (51%, n = 43) had no clue as to which group they were allocated, but 17 participants (40%) were correct in their belief regarding allocation. The three participants who were lost to followup before 8 weeks did not provide data about allocation beliefs. The two assessors had no clue

regarding group allocation in 67% and 72% of the cases. They were correct in their belief

regarding allocation in 9 (21%) and 4 Talazoparib clinical trial (9%) of the participants, respectively. In the experimental group more participants were prescribed pain and spasticity medication, as presented in Table 2. They also received slightly more conventional therapy for the arm and adhered less to the prescribed intervention protocol. Overall, compliance in the experimental group was 68% (stretch positioning) and 67% (NMES), compared to 78% (sham positioning) and 75% (TENS) in the PDK4 control group. Non-compliance was mainly caused by drop-out and early weekend leaves. All mentioned differences between the groups were not statistically significant. All primary and secondary outcome measures are presented in Tables 3, 4 and 5. Individual participant data are presented in Table 6 (see eAddenda for Tables 4, 5 and 6). Except for elbow extension and the control participants’ wrist extension with extended fingers, both groups showed reductions in mean passive range of motion of all joints (Table 3). The multilevel regression analysis identified significant time effects for the three shoulder movements and for forearm supination. There was no significant group effect nor a significant time × group interaction. A random intercept model fitted the data best (-2log-likelihood criterion). At end-treatment, the mean between-group difference for passive shoulder external rotation was 13 deg (95% CI 1 to 24).

The activated OAg was designated OAg-oxNaIO4. For conjugation to CRM197, OAg-oxNaIO4 was added to CRM197 in NaH2PO4 100 mM pH 7.2 to give a final concentration of 10 and 5 mg/mL, respectively. NaBH3CN was added immediately after (OAg-oxNaIO4:NaBH3CN = 1:1 w/w),

and the reaction mixture stirred overnight at 37 °C. After this time, NaBH4 (OAg-oxNaIO4:NaBH4 = 1:1 w/w) was added and the mixture was stirred at 37 °C for 2 h. The conjugate was designated OAg-oxNaIO4-CRM197. OAg-oxTEMPO-CRM197: random activation of the OAg chain with TEMPO and conjugation to CRM197. OAg (3 mg/mL, corresponding to [CH2OH] of 7.69 mM) and NaHCO3 (molar ratio NaHCO3/CH2OH = 30), were added to a stirred solution of TEMPO (molar ratio TEMPO/CH2OH = 0.05) in DMF. The reaction was cooled selleck chemical to 0 °C and TCC (molar ratio TCC/CH2OH = 1.6) was added. The activated sugar was recovered from the reaction mixture by precipitation with EtOH (85 v/v% in the final mixture) after 2 h of stirring at 0 °C. The pellet was washed twice with 100% EtOH (1.5 volumes with respect to the reaction mixture volume) and lyophilized. The activated OAg was designated OAg-oxTEMPO2h. The same procedure was used for the synthesis of OAg-oxTEMPO12h, increasing the reaction time to 12 h. OAg-oxTEMPO2 h

and OAg-oxTEMPO12h were conjugated to CRM197, using the same conditions for OAg-oxNaIO4. The two corresponding conjugates were designated learn more OAg-oxTEMPO2h-CRM197 and OAg-oxTEMPO12h-CRM197, respectively. OAg-ADH-SIDEA-CRM197: selective

activation of the terminal KDO with ADH, followed by reaction with SIDEA and conjugation to CRM197. The synthesis of this conjugate was performed as previously first described [28] and detailed in SI. OAg-NH2-SIDEA-CRM197: selective activation of the terminal KDO with NH4OAc, followed by reaction with SIDEA and conjugation to CRM197. OAg was solubilized in 500 mM NH4OAc pH 7.0 at a concentration of 40 mg/mL. NaBH3CN was added immediately (NaBH3CN:OAg = 2:5 w/w). The solution was mixed at 30 °C for 5 days. The reaction mixture was desalted on a G-25 column and the OAg-NH2 was dried. The following steps of conjugation were performed as for OAg-ADH-SIDEA-CRM197 and the resulting conjugate was designed OAg-NH2-SIDEA-CRM197. All conjugates were purified by hydrophobic interaction chromatography (HIC) on a Phenyl HP column [GE Healthcare], loading 500 μg of protein for mL of resin in 50 mM NaH2PO4 3 M NaCl pH 7.2. The purified conjugate was eluted in water and the collected fractions were dialyzed against 10 mM NaH2PO4 pH 7.2. Total saccharide was quantified by phenol sulfuric assay [29], protein content by micro BCA (using BSA as standard and following manufacturer’s instructions [Thermo Scientifics]) and the ratio of saccharide to protein calculated. OAg-CRM197 conjugates profiles were compared with free CRM197 by HPLC-SEC and SDS-PAGE (see SI).

Therefore, the effects of resistance training, either alone or in combination with aerobic training, in people with chronic heart failure remain unclear. Therefore the following research GSK1349572 ic50 questions for this study focused on people with heart failure: 1. Does resistance training

improve heart function, exercise capacity and quality of life in people with chronic heart failure more than no intervention or usual care? Six electronic databases (PubMed, MEDLINE, EMBASE, Chinese Electronic Periodical Service [CEPS], CINAHL, and Cochrane Library Register of Controlled Trials) were searched from the earliest available date until September 2009. We hand-searched reference lists of all identified original articles, previous meta-analyses and reviews. Experts were asked to identify any other relevant trials known to them. The following keywords and Medical Subject Heading (MeSH) terms were used in our searches: heart failure, heart dysfunction, ventricular dysfunction, resistance training, strength exercise, strength training, weight-lifting, and weight

training (see Appendix 1 on the eAddenda for the full search strategy). Published randomised trials limited to human subjects were considered. Articles written in languages other Nutlin-3 order than English or Chinese were excluded. Two reviewers (CLH and CLC) reviewed the trials using predetermined criteria independently (Box 1). Reviewers were not blinded to authors, place of publication, or results. Design • Randomised trial Participants • Adults with chronic heart failure Intervention • Progressive resistance exercise training, with training defined as a structured, hospital- or home-based program with a target exercise type, intensity, duration and frequency, and with regular measurement of whether these were achieved Outcome measures • Cardiac function Comparisons • Progressive resistance exercise training versus no training or usual care or sham exercise Quality: All trials were critically appraised for methodological quality using the PEDro Scale (0 to 10, Maher et al 2003, de Morton, 2009) by two reviewers (CLH

and CLC). Any disagreements were resolved by discussion with another reviewer (YTW). Participants: Age, gender, about and cause and severity of chronic heart failure were recorded to determine the similarity of participants between groups and between trials. Intervention: The target intensity, duration, and frequency of exercise and the length of the intervention period were recorded. For the study question assessing the effect of resistance training alone, the control was categorised as no intervention, usual activity or sham exercise. For the study question assessing the effect of combined training versus aerobic training alone, the target intensity, duration, and frequency of aerobic exercise were also recorded.