A systematic review of the effectiveness of community-based interventions aimed at improving health literacy of parents/carers of children.

AIM: The aim of this systematic review was to examine the effectiveness of community-based health literacy interventions in improving the health literacy of parents. METHODS: A systematic review of six databases - MEDLINE, PsycINFO, CINAHL, Cochrane Library, Embase, and Education Source - was conducted to identify relevant articles. Risk of bias was assessed using version two of the Cochrane risk of bias tool for randomised controlled trials or the Cochrane collaboration risk of bias in non-randomised studies of interventions. The study findings were grouped and synthesised following the synthesis without meta-analysis framework. RESULTS: Eleven community-based health literacy interventions for parents were identified. Study design included randomised controlled trials (n = 4), non-randomised studies with comparison group (n = 4), and non-randomised studies without a comparison group (n = 3). Interventions were delivered digitally, in person or a combination of the two. The risk of bias was high in over half the studies (n = 7). The main findings of the studies showed some potential for both in person and digital interventions to increase parental health literacy. Studies were heterogeneous preventing a meta-analysis. CONCLUSION: Community-based, health literacy interventions have been identified as potential methods for enhancing parental health literacy. Due to the small number of included studies and their potential for bias, these results must be interpreted with caution. This study emphasises the need for additional theory and evidence-based research on the long-term effects of community interventions.

Effect of an acute dose of omega-3 fish oil following exercise-induced muscle damage.

PURPOSE: The purpose of this double-blind, placebo-controlled study was to examine the effect of two fish oil supplements, one high in EPA (750 mg EPA, 50 mg DHA) and one low in EPA (150 mg EPA, 100 mg DHA), taken acutely as a recovery strategy following EIMD. METHODS: Twenty-seven physically active males (26 ± 4 year, 1.77 ± 0.07 m, 80 ± 10 kg) completed 100 plyometric drop jumps to induce muscle damage. Perceptual (perceived soreness) and functional (isokinetic muscle strength at 60° and 180° s-1, squat jump performance and countermovement jump performance) indices of EIMD were recorded before, and 1, 24, 48, 72, and 96h after the damaging protocol. Immediately after the damaging protocol, volunteers ingested either a placebo (Con), a low-EPA fish oil (Low EPA) or a high-EPA fish oil (High EPA) at a dose of 1 g per 10 kg body mass. RESULTS: A significant group main effect was observed for squat jump, with the High EPA group performing better than Con and Low EPA groups (average performance decrement, 2.1, 8.3 and 9.8%, respectively), and similar findings were observed for countermovement jump performance, (average performance decrement, 1.7, 6.8 and 6.8%, respectively, p = 0.07). Significant time, but no interaction main effects were observed for all functional and perceptual indices measured, although large effect sizes demonstrate a possible ameliorating effect of high dose of EPA fish supplementation (effect sizes ≥0.14). CONCLUSION: This study indicates that an acute dose of high-EPA fish oil may ameliorate the functional changes following EIMD.

Prediction of peak oxygen uptake from ratings of perceived exertion during arm exercise in able-bodied and persons with poliomyelitis.

STUDY DESIGN: Each participant completed an arm-crank ramp exercise test to volitional exhaustion. OBJECTIVE: To assess the utility of the rating of perceived exertion (RPE) to predict peak oxygen uptake (VO(2)peak) during arm ergometry in able-bodied participants and those with poliomyelitis. SETTING: University of Jordan, Amman, Jordan. PARTICIPANTS: In all, 16 able-bodied and 15 participants with poliomyelitis completed an arm-crank ramp exercise test to volitional exhaustion. MAIN OUTCOME MEASURES: The prediction of VO(2)peak is calculated by extrapolating the sub-maximal RPE and VO(2) values by linear regression to RPE 20. RESULTS: For the able-bodied participants, there were no significant differences between measured and predicted VO(2)peak from the three sub-maximal ranges of the RPE (RPEs before and including RPE 13, 15 and 17, P > 0.05). For the participants with poliomyelitis, the VO(2)peak predicted from RPEs before and including RPE 13 was significantly higher than measured VO(2)max (P < 0.05). The 95% limits of agreement of able-bodied participants for RPE 13, 15 and 17 (-3 ± 14, -1 ± 10 & 0 ± 8 ml kg(-1) min(-1), respectively) were lower than those observed for poliomyelitis participants (6 ± 19, 2 ± 12 and 1 ± 9 ml kg(-1) min(-1), respectively). CONCLUSION: This study has shown that the estimation of VO(2)peak from submaximal RPE during arm ergometry is generally more accurate in able-bodied participants in comparison with those with poliomyelitis.

Statistical Power Calculations for Clustered Continuous Data.

To calculate the sample size for a research study it is important to take into account several aspects of the study design. In particular, one needs to take into account the hypotheses being tested, the study design, the sampling design, and the method to be used for the analysis. In this paper we propose a simple method to calculate sample size for clustered continuous data under various scenarios of study design.

Genetic modification of the manganese superoxide dismutase/glutathione peroxidase 1 pathway influences intracellular ROS generation in quiescent, but not contracting, skeletal muscle cells.

Increased amounts of reactive oxygen species (ROS) are generated by skeletal muscle during contractile activity, but their intracellular source is unclear. The oxidation of 2',7'-dichlorodihydrofluorescein (DCFH) was examined as an intracellular probe for reactive oxygen species in skeletal muscle myotubes derived from muscles of wild-type mice and mice that were heterozygous knockout for manganese superoxide dismutase (Sod2(+/-)), homozygous knockout for glutathione peroxidase 1 (GPx1(-/-)), or MnSOD transgenic overexpressors (Sod2-Tg). Myoblasts were stimulated to fuse and loaded with DCFH 5-7 days later. Intracellular DCF epifluorescence was measured and myotubes were electrically stimulated to contract for 15 min. Quiescent myotubes with decreased MnSOD or GPx1 showed a significant increase in the rate of DCFH oxidation whereas those with increased MnSOD did not differ from wild type. Following contractions, myotubes from all groups showed an equivalent increase in DCF fluorescence. Thus the oxidation of DCFH in quiescent skeletal muscle myotubes is influenced by the content of enzymes that regulate mitochondrial superoxide and hydrogen peroxide content. In contrast, the increase in DCFH oxidation following contractions was unaffected by reduced or enhanced MnSOD or absent GPx1, indicating that reactive oxygen species produced by contractions were predominantly generated by nonmitochondrial sources.

Free radical generation by skeletal muscle of adult and old mice: effect of contractile activity.

Oxidative modification of cellular components may contribute to tissue dysfunction during aging. In skeletal muscle, contractile activity increases the generation of reactive oxygen and nitrogen species (ROS). The question of whether contraction-induced ROS generation is further increased in skeletal muscle of the elderly is important since this influences recommendations on their exercise participation. Three different approaches were used to examine whether aging influences contraction-induced ROS generation. Hind limb muscles of adult and old mice underwent a 15-min period of isometric contractions and we examined ROS generation by isolated skeletal muscle mitochondria, ROS release into the muscle extracellular fluid using microdialysis techniques, and the muscle glutathione and protein thiol contents. Resting skeletal muscle of old mice compared with adult mice showed increased ROS release from isolated mitochondria, but no changes in the extracellular levels of superoxide, nitric oxide, hydrogen peroxide, hydroxyl radical activity or muscle glutathione and protein thiol contents. Skeletal muscle mitochondria isolated from both adult and old mice after contractile activity showed significant increases in hydrogen peroxide release compared with pre-contraction values. Contractions increased extracellular hydroxyl radical activity in adult and old mice, but had no significant effect on extracellular hydrogen peroxide or nitric oxide in either group. In adult mice only, contractile activity increased the skeletal muscle release of superoxide. A similar decrease in muscle glutathione and protein thiol contents was seen in adult and old mice following contractions. Thus, contractile activity increased skeletal muscle ROS generation in both adult and old mice with no evidence for an age-related exacerbation of ROS generation.

Role of mitochondrial superoxide dismutase in contraction-induced generation of reactive oxygen species in skeletal muscle extracellular space.

Contractions of skeletal muscles produce increases in concentrations of superoxide anions and activity of hydroxyl radicals in the extracellular space. The sources of these reactive oxygen species are not clear. We tested the hypothesis that, after a demanding isometric contraction protocol, the major source of superoxide and hydroxyl radical activity in the extracellular space of muscles is mitochondrial generation of superoxide anions and that, with a reduction in MnSOD activity, concentration of superoxide anions in the extracellular space is unchanged but concentration of hydroxyl radicals is decreased. For gastrocnemius muscles from adult (6-8 mo old) wild-type (Sod2(+/+)) mice and knockout mice heterozygous for the MnSOD gene (Sod2(+/-)), concentrations of superoxide anions and hydroxyl radical activity were measured in the extracellular space by microdialysis. A 15-min protocol of 180 isometric contractions induced a rapid, equivalent increase in reduction of cytochrome c as an index of superoxide anion concentrations in the extracellular space of Sod2(+/+) and Sod2(+/-) mice, whereas hydroxyl radical activity measured by formation of 2,3-dihydroxybenzoate from salicylate increased only in the extracellular space of muscles of Sod2(+/+) mice. The lack of a difference in increase in superoxide anion concentration in the extracellular space of Sod2(+/+) and Sod2(+/-) mice after the contraction protocol supported the hypothesis that superoxide anions were not directly derived from mitochondria. In contrast, the data obtained suggest that the increase in hydroxyl radical concentration in the extracellular space of muscles from wild-type mice after the contraction protocol most likely results from degradation of hydrogen peroxide generated by MnSOD activity.

Functional development of engineered skeletal muscle from adult and neonatal rats.

A myooid is a three-dimensional skeletal muscle construct cultured from mammalian myoblasts and fibroblasts. The purpose was to compare over several weeks in culture the morphology, excitability, and contractility of myooids developed from neonatal and adult rat cells. The hypotheses tested were as follows: (1) baseline forces of myooids correlate with the cross-sectional area (CSA) of the myooids composed of fibroblasts, and (2) peak isometric tetanic forces normalized by total CSA (specific P(o)) of neonatal and adult rat myooids are not different. Electrical field stimulation was used to measure the excitability and peak tetanic forces. The proportion of the CSA composed of fibroblasts was greater for neonatal (40%) than adult (17%) myooids. For all myooids the baseline passive force normalized by fibroblast CSA (mean = 5.5 kPa) correlated with the fibroblast CSA (r(2) = 0.74). A two-element cylindrical model was analyzed to determine the contributions of fibroblasts and myotubes to the baseline force. At each measurement period, the specific P(o) of the adult myooids was greater than that of the neonatal myooids. The specific P(o) of the adult myooids was approximately 1% of the control value for adult muscles and did not change with time in culture, while that of neonatal myooids increased.

Force and power output of fast and slow skeletal muscles from mdx mice 6-28 months old.

1. Differences in the effect of age on structure-function relationships of limb muscles of mdx (dystrophin null) and control mice have not been resolved. We tested the hypotheses that, compared with limb muscles from age-matched control mice, limb muscles of 6- to 17-month-old mdx mice are larger but weaker, with lower normalised force and power, whereas those from 24- to 28-month-old mdx mice are smaller and weaker. 2. The maximum isometric tetanic force (P(o)) and power output of limb muscles from 6-, 17-, 24- and 28-month-old mdx and control mice were measured in vitro at 25 degrees C and normalised with respect to cross-sectional area and muscle mass, respectively. 3. Body mass at 6 and 28 months was not significantly different in mdx and control mice, but that of control mice increased 16 % by 17 months and then declined 32 % by 28 months. The body masses of mdx mice declined linearly with age with a decrease of 25 % by 28 months. From 6 to 28 months of age, the range in the decline in the masses of EDL and soleus muscles of mdx and control mice was from 16 to 28 %. The muscle masses of mdx mice ranged from 9 % to 42 % greater than those of control mice at each of the four ages and, even at 28 months, the masses of EDL and soleus muscles of mdx mice were 17 % and 22 % greater than control values. 4. For mdx mice of all ages, muscle hypertrophy was highly effective in the maintenance of control values for absolute force for both EDL and soleus muscles and for absolute power of soleus muscles. Throughout their lifespan, muscles of mdx mice displayed significant weakness with values for specific P(o) and normalised power approximately 20 % lower than values for control mice at each age. For muscles of both strains, normalised force and power decreased approximately 28 % with age, and consequently weakness was more severe in muscles of old mdx than in those of old control mice.

Severity of contraction-induced injury is affected by velocity only during stretches of large strain.

Our purpose was to investigate the effect of velocity of stretch on contraction-induced injury to whole skeletal muscles. Single stretches provide an effective method for studying factors that initiate contraction-induced injury. We tested the null hypothesis that the severity of injury is not dependent on the velocity of the stretch. From the plateau of maximum isometric contractions, extensor digitorum longus muscles of mice were administered single stretches in situ of 30--50% strain relative to muscle fiber length (L(f)) at rates of 1--16 L(f)/s. The magnitude of injury was represented by the isometric force deficit 1--10 min after the stretch. Although the null hypothesis was not supported because the force deficit was affected by velocity (r(2) = 0.09), the effect was relatively weak and was not significant except at the largest strain. Velocity had no effect on peak or average force or work input, factors established to have significant relationships with the force deficit. Velocity may play a minor role in contraction-induced injury, but its importance is negligible relative to that of strain.

Growth and development of homograft tracheal transplants in the piglet model.

OBJECTIVE: To determine the growth characteristics of homograft tracheal transplants in piglets. DESIGN: Prospective controlled animal study. SETTING: Clinical animal laboratory. SUBJECTS: Seventeen Yorkshire swine piglets. INTERVENTIONS: The tracheae of adult Yorkshire swine were harvested and treated with formaldehyde, thimerosal, and acetone to remove immunogenic major histocompatibility complexes. Eleven piglets had these chemically treated homografts transplanted into 6-cm surgically created tracheal defects. The transplants were stented. Three control piglets had a 6-cm anterior tracheofissure, no transplant, and surgical placement of the stent. Three other control piglets had no transplant, and the stent was placed endoscopically. MAIN OUTCOME MEASURES: Growth outcome measurements were tracheal length and diameter. Functional outcome measurements were lumen patency and graft viability indicated by cartilage retention. RESULTS: The mean diameter of the tracheae in the stented tracheal transplant group was 11.7 mm before transplantation and 6.6 mm 2 months after transplantation. The transplanted segments were significantly malacic 2 months after transplantation. The mean diameter of the tracheae in the tracheofissure group was 9.0 mm before surgery and 11.0 mm 2 months after surgery. The mean diameter of the tracheae in the endoscopically stented group was 11.0 mm before surgery and 14.0 mm 2 months after stent placement. All homografts showed evidence of extensive resorption of the graft cartilage. The graft cartilage was replaced by collagen, with minimal evidence of neochondrification. There was no evidence of host-vs-graft rejection. All grafted trachea had severe tracheomalacia with granulation tissue. CONCLUSIONS: Homograft tracheal transplantation results in a tracheal segment that is replaced with collagen. The transplanted cartilage is resorbed, leaving a significantly malacic segment. Homograft tracheal transplantation might result in a small malacic airway with little potential for growth when performed in children.

Motor unit properties of nerve-intact extensor digitorum longus muscle grafts in young and old rats.

Impaired reinnervation has been implicated as the cause of the threefold disparity in the recovery of maximum force (P0) of standard muscle grafts in old compared with young rats. The specific, null hypothesis of this study is that compared with age-matched control extensor digitorum longus (EDL) muscles, nerve-intact EDL muscle grafts in young and old rats show no evidence of an age-related impairment in reinnervation. Nerve-intact grafts were performed in 3-month-old and 23-month-old rats and were evaluated 60 days postoperatively. Compared with age-matched control EDL muscles, nerve-intact grafts in young and old rats showed no difference in muscle mass or motor unit numbers. The mean motor unit P0 for nerve-intact graft muscles in both age groups was significantly lower than that of age-matched control muscles. These data support our hypothesis that if axons are allowed to regenerate in an endoneurial environment, there is no evidence of an age-related impairment in muscle reinnervation.

Conditioning of skeletal muscles in adult and old mice for protection from contraction-induced injury.

The purpose of this study was to design a conditioning program that protected muscles in both adult and old mice from a protocol of contractions that previously caused a significant number of damaged fibers and a deficit in force. Hind-limb dorsiflexor muscles of adult (7 months) and old (22 months) female B6D2F1 mice were exposed once a week to a protocol of repeated forced stretches while maximally activated in vivo. By week 4, muscles of adult, but not old, mice showed no force deficit. Conditioning was continued for 6 weeks, when both age groups showed no force deficit for two consecutive weeks. Three days after the sixth contraction protocol, when morphological damage and force deficits are most severe, the numbers of damaged fibers in muscles of adult and old mice were not different from those in uninjured control muscles and the force deficits were reduced dramatically compared with unconditioned muscles. We conclude that muscles of both adult and old mice conditioned successfully, but muscles of old mice conditioned more slowly than those of adult mice.

Skeletal muscle regeneration in very old rats.

This study was undertaken to assess the regenerative capacity of skeletal muscle in rats near the end of their normal life span. Two experiments were performed. In the first, extensor digitorum longus (EDL) muscles were cross-age transplanted from 32-month-old male inbred Wistar (WI/HicksCar) rats in place of an EDL muscle in 4-month-old hosts. The other EDL muscle in the hosts was autotransplanted. After 60 days, the old-into-young muscle transplants regenerated as well as the young-into-young autotransplants. In the second experiment, EDL muscles in young adult (4 months) and old rats (32 and 34 months) of WI/HicksCar and Brown Norway (BN) were injected with a local anesthetic, bupivacaine, and allowed to regenerate for 41 days. In all cases, the masses and absolute maximum tetanic force of the regenerates equaled or exceeded those of untouched contralateral control muscles. These experiments showed that under appropriate conditions, very old muscles can regenerate to equal or exceed the contralateral control values, which in old rats are much less than those in muscles of young rats.

Force and power output of diaphragm muscle strips from mdx and control mice after clenbuterol treatment.

Based on its anabolic properties, treatment with the beta(2)-adrenoceptor agonist, clenbuterol, has been proposed as a strategy for ameliorating the symptoms of muscular dystrophy. In the dystrophic mdx mouse, only the diaphragm muscle exhibits progressive and severe degeneration in muscle structure and function similar to that observed in Duchenne muscular dystrophy. We tested the hypothesis that 20 weeks of clenbuterol treatment ( approximately 1.5-2 mg kg(-1)day(-1)) would increase the force and power output of diaphragm muscle strips of 6-month-old mdx and control mice. At this age, the diaphragm muscles of mdx mice show extensive degeneration and impaired contractility compared with control mice. Clenbuterol treatment did not increase the normalized force or power output of diaphragm strips from either mdx or control mice. The degeneration and necrosis within the diaphragm muscle of mdx mice was also not ameliorated by clenbuterol treatment. The results indicate that clenbuterol treatment does not improve the structure or function of diaphragm muscles from mdx mice.

Excitability and contractility of skeletal muscle engineered from primary cultures and cell lines.

The purpose of this study was to compare the excitability and contractility of three-dimensional skeletal muscle constructs, termed myooids, engineered from C2C12 myoblast and 10T1/2 fibroblast cell lines, primary muscle cultures from adult C3H mice, and neonatal and adult Sprague-Dawley rats. Myooids were 12 mm long, with diameters of 0.1-1 mm, were excitable by transverse electrical stimulation, and contracted to produce force. After approximately 30 days in culture, myooid cross-sectional area, rheobase, chronaxie, resting baseline force, twitch force, time to peak tension, one-half relaxation time, and peak isometric force were measured. Specific force was calculated by dividing peak isometric force by cross-sectional area. The specific force generated by the myooids was 2-8% of that generated by skeletal muscles of control adult rodents. Myooids engineered from C2C12-10T1/2 cells exhibited greater rheobase, time to peak tension, and one-half relaxation time than myooids engineered from adult rodent cultures, and myooids from C2C12-10T1/2 and neonatal rat cells had greater resting baseline forces than myooids from adult rodent cultures.

Contraction-induced injury to single permeabilized muscle fibers from mdx, transgenic mdx, and control mice.

Muscle fibers of mdx mice that lack dystrophin are more susceptible to contraction-induced injury, particularly when stretched. In contrast, transgenic mdx (tg-mdx) mice, which overexpress dystrophin, show no morphological or functional signs of dystrophy. Permeabilization disrupts the sarcolemma of fibers from muscles of mdx, tg-mdx, and control mice. We tested the null hypothesis stating that, after single stretches of maximally activated single permeabilized fibers, force deficits do not differ among fibers from extensor digitorum longus muscles of mdx, tg-mdx, or control mice. Fibers were maximally activated by Ca(2+) (pCa 4.5) and then stretched through strains of 10%, 20%, or 30% of fiber length (L(f)) at a velocity of 0.5 L(f)/s. Immediately after each strain, the force deficits were not different for fibers from each of the three groups of mice. When collated with studies of membrane-intact fibers in whole muscles of mdx, tg-mdx, and control mice, these results indicate that dystrophic symptoms do not arise from factors within myofibrils but, rather, from disruption of the sarcolemmal integrity that normally provides protection from contraction-induced injury.

Assembly of the dystrophin-associated protein complex does not require the dystrophin COOH-terminal domain.

Dystrophin is a multidomain protein that links the actin cytoskeleton to laminin in the extracellular matrix through the dystrophin associated protein (DAP) complex. The COOH-terminal domain of dystrophin binds to two components of the DAP complex, syntrophin and dystrobrevin. To understand the role of syntrophin and dystrobrevin, we previously generated a series of transgenic mouse lines expressing dystrophins with deletions throughout the COOH-terminal domain. Each of these mice had normal muscle function and displayed normal localization of syntrophin and dystrobrevin. Since syntrophin and dystrobrevin bind to each other as well as to dystrophin, we have now generated a transgenic mouse deleted for the entire dystrophin COOH-terminal domain. Unexpectedly, this truncated dystrophin supported normal muscle function and assembly of the DAP complex. These results demonstrate that syntrophin and dystrobrevin functionally associate with the DAP complex in the absence of a direct link to dystrophin. We also observed that the DAP complexes in these different transgenic mouse strains were not identical. Instead, the DAP complexes contained varying ratios of syntrophin and dystrobrevin isoforms. These results suggest that alternative splicing of the dystrophin gene, which naturally generates COOH-terminal deletions in dystrophin, may function to regulate the isoform composition of the DAP complex.

Power output of fast and slow skeletal muscles of mdx (dystrophic) and control mice after clenbuterol treatment.

The mdx mouse is the most commonly used animal model for Duchenne muscular dystrophy. We tested the null hypothesis that 20 weeks of clenbuterol treatment ( approximately 2 mg kg-1 day-1) of mdx and control mice would have no effect on the absolute and specific force (Po, kN m-2) and absolute and normalised power output (W kg-1) of extensor digitorum longus (EDL) and soleus muscles. For mdx and control mice, clenbuterol treatment produced modest increases in the mass of the two muscles but did not increase absolute or specific force or normalised power output. For absolute power output, only the EDL muscles of mdx mice showed a difference following treatment, with the power output of treated mice being 118 % that of the untreated mice. The modest effects of clenbuterol treatment on the dynamic properties of skeletal muscle provide little support for any improvement in muscle function for the dystrophic condition.

The capacity of mdx mouse diaphragm muscle to do oscillatory work.

1. Mdx mice were used as a model for Duchenne muscular dystrophy; both lack dystrophin. It was hypothesized that the mdx condition would have a marked effect on the ability of diaphragm muscle from mdx mice to do active net work and generate power. This hypothesis was tested using the work-loop technique. 2. Specific twitch force, specific tetanic force and maximum power were all significantly less in diaphragm strips from mdx mice than those from control mice. 3. In all preparations muscle length at which maximum power was achieved (Lw) was about 8% less than that at which maximum tetanic force was achieved (L0), both in mdx and control muscle. 4. The isometric force-length curve for mdx muscle was steeper on both sides of the plateau. Similarly, the curve relating net work per cycle to muscle length was steeper for mdx muscle on both sides of the plateau. 5. Maximum power of mdx muscle was achieved at a lower strain than for control muscle; maximum power occurred at a strain of 10.2% for mdx and 14.7% for control. Further increases in strain caused a marked decrease of power production in mdx muscle, whereas they caused a smaller decrease in control muscle. 6. In summary, at muscle lengths longer than Lw and at high strains, performance of mdx muscle was compromised relative to that of control muscle. Work and power were compromised more than isometric force.