Here,

we assess on the presence of co-isolated viruses in

Here,

we assess on the presence of co-isolated viruses in influenza virus isolates recovered from MDCK cells. This article provides more specific data about the kind and frequency of co-infecting respiratory viruses in human influenza virus-containing samples and about the fate of such co-infecting viruses during passage in MDCK cells. Nasal or pharyngeal samples from the 2007/2008 influenza season were provided by a clinical diagnostic laboratory located in Stuttgart, Germany. These samples from patients with acute respiratory tract infections were obtained by physicians mainly from Southern Germany and were sent to the diagnostic laboratory in liquid virus transport medium. Aliquots of the clinical specimens (with a laboratory number as an anonymous identifier) were sent to Novartis Vaccines in Marburg, Germany, by a weekly courier service. During transportation SKI-606 purchase the samples were stored at 2–8 °C. Directly after Quisinostat datasheet receipt of the samples, MDCK 33016PF cells were inoculated (details see further below) with sample material. The cultures were harvested after 3 days of incubation, and the cell-free supernatants were aliquoted and stored at ≤−60 °C until further use. MDCK 33016PF suspension cells from Novartis working cell bank were cultivated in 500 ml disposable spinner

flasks (Corning) in CDM medium, a chemically defined growth medium used for cell propagation (MDCK 33016 CDM, Lonza) and passaged at 3–4-day intervals. During those 3–4 days the cells grew from an initial seeding density of 1 × 105 cells/ml to densities between 1.0 and 1.5 × 106 cells/ml. For infections 4.5 ml

cells were seeded in 50 ml filter tubes (TPP, Transadingen, Switzerland) at a cell density of 0.8–1.2 × 106 cells/ml. Cells in CDM medium were diluted at a 30/70% ratio into MDCK 33016 PFM medium (“protein-free Levetiracetam medium”, Gibco Invitrogen) supplemented with 0.5% of a penicillin/streptomycin solution (Sigma) and 900 IU/ml trypsin. To obtain a total culture volume of 5 ml, the added viral inoculum was diluted in 0.5 ml infection medium and was pre-diluted by several log10 steps, starting with a total dilution of at least 1:100. Inoculated cultures were then incubated at 33 °C for 3 days in a 5% CO2 atmosphere in a ISF-1-W shaker incubator (Kuhner, Birsfelden, Switzerland). For virus harvests the cells were separated by centrifugation (800–1000 × g for 10 min) and the supernatant was recovered. Unless used freshly, e.g. for haemagglutination tests and subsequent passaging, aliquots of the supernatant were frozen at ≤−60 °C. Haemagglutination (HA) testing was done with harvested material to define the starting material for the next passage. HA testing was performed in U-bottom microwell plates (Greiner Bio-One) using 100 μl of a serial log2 dilution in PBS (pH 7.0) of the test samples and 100 μl chicken or guinea pig red blood cells (0.5% in PBS pH 7.0).

In that study, it was demonstrated that neutralizing antibodies a

In that study, it was demonstrated that neutralizing antibodies are not required for survival following lethal VEEV challenge. In this same Selleck FRAX597 report, Paessler et al evaluated the contribution of T cells subsets in the brain in

protecting mice against lethal VEEV challenge and found αβ T cells are required for protection against a lethal VEEV challenge but that γδ T cells are not. This finding was supported by adoptive transfer studies where CD3+ T cells derived from vaccinated wild-type mice were able to restore protective immunity in αβ TCR deficient mice following a lethal VEEV challenge [41]. The findings from these studies are supported by other reports demonstrating T cell immunity as a key component to protection against VEEV infection [42] and [43]. Based on these reports, it is conceivable that T cell responses may be the predominant protective response following vaccination with the fV3526 formulations and that neutralizing antibodies play a secondary role in protection of the host. Dissecting the specific immune responses induced by the fV3526 formulations which are required for protection were beyond of scope of this study but should be investigated upon

down-selection of a fV3526 formulation. In the Capmatinib in vivo present study, all fV3526 formulations induced an immune response that solidly protected mice against a SC challenge with VEEV TrD. While not statistically different from vaccination with fV3526 formulations, vaccination with C84 did not induce a protective immune response

in all mice as has been previously reported [37]. While this result was unexpected, so were the the findings in similar studies where C84 also failed to solidly protect mice from SC challenge [19] and [44]. One possible explanation for this discrepancy may be a loss of C84 potency. C84 was manufactured nearly 29 years ago and the loss of potency may be due to the prolonged storage. Stability and potency studies were conducted on C84 for several years following manufacture but this testing ended in the late 1990s, and no current potency data on the inactivated vaccine are available. Differences in the protective immune responses induced by the fV3526 formulations were more apparent when mice were challenged by the aerosol route but those differences failed to reach statistical significance. Survival rates in mice vaccinated with the fV3526 formulations following aerosol challenge were also similar to those for C84, however, similar to SC challenge, C84 again failed to induce a protective response in all mice providing additional support to a loss of C84 vaccine potency. In contrast to mice vaccinated with live V3526, mice vaccinated with fV3526 formulations displayed mild clinical signs of disease following aerosol challenge.

A range of characteristics of the route to work were chosen becau

A range of characteristics of the route to work were chosen because they represented constructs that were believed to be important determinants of behaviour (Panter and Jones, 2010 and Pikora et al., 2003). Participants reported their level of agreement with seven statements describing the route environment using a five-point Likert scale

at both t1 and t2 and the change in agreement for each item (t2 − t1) was computed. Dates of birth and of questionnaire completion, gender, highest educational qualification, housing tenure, household composition, access to cars and bicycles, possession of a driving licence, limiting long term illness, height and weight were assessed by questionnaire. see more Age and season of data collection were calculated using the date of questionnaire completion and season was defined as either early summer (May–June), mid-summer (July–August) or autumn (September–October). Participants also

reported their home and work postcodes, workplace car parking provision at both time points, and the occurrence of any life events (such as changes in household composition or work responsibilities) in the last year at t2. Responses were used to derive three binary variables indicating a change in workplace parking, Selleck Autophagy Compound Library a change in home or work location and the occurrence of any (other) life events. We used t-tests to compare average perceptions between t1 and t2; a weighted kappa score (Sim and Wright, 2005) and percentage agreement (Chinn and Burney, Edoxaban 1987) to assess the within-participant agreement between t1 and

t2 perception scores; and one-way analysis of variance (ANOVA) to assess the association between changes in perceptions and their baseline values. In all descriptive analyses we investigated differences by gender. Separate linear regression models were used to assess the independent associations between changes in each of the route perceptions and changes in time spent walking, cycling and the proportion of car-only trips, initially minimally adjusted for age, gender, season and baseline travel behaviour. Given the uncertainty about the magnitude of environmental change required for behaviour change, participants were assigned to one of three groups: those who reported a less supportive condition at t2, those who reported a more supportive condition at t2; and those who reported no change. At this stage we also tested for interactions between environmental perceptions and gender. Although adjustment for baseline values of the outcome in analyses of change is subject to some debate (Fitzmaurice, 2001), our results were consistent in terms of effect size and statistical significance with and without adjustment. All variables associated at p < 0.

La cardioversion électrique expose à un surcroît d’événements thr

La cardioversion électrique expose à un surcroît d’événements thromboemboliques chez les patients atteints de fibrillation atriale. Ce risque est réduit par l’anticoagulation. L’indication d’anticoagulation dans la période qui entoure la cardioversion (3 semaines avant et 4 semaines après) repose sur des études prospectives observationnelles de faible effectif, et sur des études rétrospectives [12], [13] and [14]. Qu’en est-il

des NACO ? Peut-on actuellement effectuer une cardioversion sous dabigatran, rivaroxaban ou apixaban ? Faut-il faire une échographie transœsophagienne systématiquement ? Dans l’étude RE-LY, évaluant la non-infériorité selleck products du dabigatran par rapport à la warfarine, 1983 cardioversions ont été effectuées chez 1270 patients. Environ 80 % de ces cardioversions étaient électriques. Lors d’une analyse post-hoc [15], aucune différence statistiquement significative n’a été observée entre les trois bras de l’étude (dabigatran 150 mg, dabigatran 110 mg, warfarine). Dans l’étude ROCKET-AF, étudiant

la non-infériorité du rivaroxaban vs Selleckchem GDC-941 warfarine, dont la population complète était de 14 264 patients, seuls 143 patients ont subi une cardioversion électrique (181 cardioversions par choc électrique externe) et 142 ont subi une cardioversion médicamenteuse (194 cardioversions médicamenteuses). Aucune différence statistiquement significative n’a été mise en évidence entre les patients sous rivaroxaban et ceux sous warfarine, dans les suites de ces cardioversions. Une étude prospective est en cours avec le rivaroxaban [16]. Dans l’étude ARISTOTLE, étudiant la non-infériorité de l’apixaban vs warfarine, incluant 18 201 patients,

540 ont subi une cardioversion (743 cardioversions). Durant la période de suivi de 30 jours, aucun événement thromboembolique n’a été observé, et le taux de décès n’a pas différé entre les patients recevant de l’apixaban et ceux recevant de la warfarine [17]. Au vu de ces essais cliniques, en accord Tolmetin avec les recommandations actuelles de la société européenne de cardiologie [11], l’auteur de cette mise au point déconseille la cardioversion électrique sous rivaroxaban et apixaban dans l’attente d’essais randomisés. La réalisation d’une échographie transœsophagienne systématique chez les patients sous NACO est une alternative logique, mais non validée dans des essais de phase III. Le dabigatran est le NACO le mieux étudié à ce jour dans ce contexte, et une cardioversion chez un patient observant avec 3 semaines pré- et 4 semaines post-cardioversion est une prise en charge tout à fait acceptable. En ce qui concerne l’apixaban, le rivaroxaban et l’edoxaban, il n’y a pas eu de majoration du taux d’infarctus du myocarde dans les études ARISTOTLE, ROCKET-AF et ENGAGE-AF.

For the MMR group, the children (71 girls; 76 boys) were aged 1–4

For the MMR group, the children (71 girls; 76 boys) were aged 1–4 years (mean = 2.71; SD = 0.75;

median = 3). For the dTaP/IPV group, the children (50 girls; 58 boys) were aged 1–4 years (mean = 2.72; SD = 0.76; median = 3). Self-reported uptake of primary immunisation was high. For children in the MMR group, 132 (89.8%) had received the first MMR, three (2%) had received the separate measles, mumps and rubella components, and nine (6.1%) were not immunised against these diseases; 138 (93.9%) had completed vaccinations against diphtheria, tetanus, pertussis, polio and Hib before 1 year of age; three (2%) were not immunised and for four children (2.7%) the parents indicated that this was unknown (information was not provided for the remaining children). For children in the dTaP/IPV group, 98 http://www.selleckchem.com/products/MK-1775.html (90.7%) had received the first see more MMR, one had received the separate components,

seven (6.5%) were not immunised and for one child the parent indicated that this was unknown; 105 (97.2%) had completed vaccinations against diphtheria, tetanus, pertussis, polio and Hib, one child was not immunised against these diseases and one parent indicated this was unknown (one parent did not provide uptake information). Parents in the two groups differed only in terms of sex, χ2(1, n[MMR] = 147, n[dTaP/IPV] = 108) = 5.543, exact p = 0.024 and number of children, U = 6621.500, n[MMR] = 147, Thymidine kinase n[dTaP/IPV] = 108, p = 0.012; with more fathers in the dTaP/IPV group and those in the MMR group having more children. No differences were found on other parent or child characteristics (p > 0.05). The items measuring each TPB component should correlate with each other and exhibit high internal consistency [12]. Thus, it was necessary to determine whether the items designed to measure each component (Table 1) fulfilled these requirements. Firstly, because parents were asked to complete an identical set of questions about either MMR or dTaP/IPV, the following check was conducted

for each TPB component in turn to determine whether the two datasets had a similar structure and could be combined in order to conduct reliability analysis [22]: (1) Combining the two datasets (MMR and dTaP/IPV), the raw scores for items in the TPB component were subjected to principal components analysis (PCA) with a forced single-factor solution; Table 3 shows that for each TPB component, the correlation between the two sets of loadings was high (close to 1) and the constant was not significantly different from zero. This indicated that even though the absolute values in the dTaP/IPV and MMR groups might differ, the interrelationship between items was similar. Thus, reliability statistics could be examined within the combined dataset.

The IgA-GMT did not increase significantly in group 3H (from 61 p

The IgA-GMT did not increase significantly in group 3H (from 61 post dose 2 to 83 post dose 3), while the GMT did not increase in group 3L. The RV-IgA seroconversion rate in group Rotarix™ was 58% (95%CI (42%, 73%)). The IgA-GMT among seropositive children did not differ between groups (Table 2). For children receiving 3 doses of vaccine (groups 3L and 3H), serum samples were collected 1 month after dose 2 and 1 month after dose 3 to determine whether

a third dose might improved the seroresponse. The 3rd dose induced seroconversion in 5 and 3 more children in group 3L and 3H, respectively, who had failed to seroconvert after the first 2 doses. The majority of children (14 in group 3L and 16 in group 3H) converted after second dose and did not further convert after the third dose. Three children (7.5%) from each group (3L and 3H) seroconverted after both dose 2 and dose 3. We examined AG-014699 cost the kinetics of rotavirus shedding in vaccinated children (Fig. 2 and Fig. 3). The prevalence of children shedding virus was greater in the group of children who received Rotarix™ (65% after the 1st

dose) vs. any PD98059 cost group that received Rotavin-M1 (44–48% after the 1st dose) (Fig. 2). Furthermore, after the first dose, shedding of Rotarix™ peaked 1 or 2 days earlier than shedding of Rotavin-M1 (Fig. 3). Nonetheless, we observed little difference in the pattern of shedding between the 4 groups received Rotavin-M1. Viral shedding reduced significantly in any group after dose 2 (6–20%) (Fig. 2). Interestingly after dose 3, 30–37% of children shed the virus at day 3 post-vaccination in both 3L and 3H groups. This report documents the first Phase 1 and Phase 2 clinical studies of a new candidate rotavirus vaccine developed in Vietnam, Rotavin-M1. The live oral vaccine, which has been described previously, is derived

from the most common strain of Rotavirus, genotype G1P [8], obtained from a Vietnamese child with diarrhea, attenuated by cell passage (>30×), plaque purification, and prepared in Vero cells for human studies [6]. A Phase 1 trial in 29 adult volunteers demonstrated that the vaccine administered orally in a titer of 106.3 FFU/dose was not associated others with symptoms, adverse events or laboratory changes in blood counts or selected chemistry and little virus shedding, similar to that reported for Rotarix™ [11]. The DSMB reviewed the data and approved the continuation of studies in infants. In the Phase 1–2 adaptive study, the candidate vaccine administered in either a low (106.0 FFU/dose) or high (106.3 FFU/dose) titer on a 2- or 3-dose schedule to infants 6–12 weeks of age did not cause significant or more diarrhea than that associated with the licensed vaccine, Rotarix™, demonstrating that the candidate strain had been successfully attenuated.

Dans les addictions avec substance, le topiramate a montré un int

Dans les addictions avec substance, le topiramate a montré un intérêt principalement dans l’alcoolodépendance. Néanmoins, la fréquence des effets indésirables fait que ce médicament ne peut être utilisé en

première intention, mais après les traitements habituels. Il n’existe que peu d’études dans les autres addictions. La prudence est de mise pour les addictions pour lesquelles il n’existe pas de traitements validés, telles que la dépendance à la cocaïne et la dépendance à la méthamphétamine. Dans les addictions comportementales, le topiramate a montré un intérêt, principalement dans la boulimie et le binge eating disorder. Dans la boulimie, l’American Psychiatric Association (APA) a recommandé que le topiramate ne soit utilisé qu’en cas d’inefficacité des autres traitements en raison de ses effets indésirables fréquents. La tendance du topiramate à induire une selleck compound perte de poids a été relevée comme problématique chez les patients avec un poids normal ou inférieur à la normale (IMC < 20 kg/m2) [69]. Dans le futur, la réalisation d’essais cliniques sur l’utilisation du topiramate en addictologie chez des patients ayant une comorbidité psychiatrique permettrait de mieux refléter la réalité des pratiques

au quotidien, ce dans la mesure où la corrélation entre troubles psychiatriques et troubles liés à une substance est bien établie. les auteurs déclarent ne pas avoir de conflits selleck chemicals llc d’intérêts en relation avec cet article. “
“Le diagnostic et la classification des hypertensions pulmonaires (HTP) ont été au centre des débats de plusieurs symposiums au cours de ces quarante dernières années : Genève 1973, Evian 1998, Venise 2003, Dana Point 2008 et Nice en 2013. La dernière définition de l’HTP tient compte de la pression artérielle pulmonaire moyenne (PAPm) mesurée au moment du cathétérisme cardiaque droit, qui doit être supérieure ou égale à 25 mmHg [1]. Pour le moment, nous ne disposons pas de suffisamment de données pour pouvoir définir une hypertension pulmonaire à l’effort [1]. L’ancienne

Adenosine définition qui parlait d’une PAPm à l’effort ≥ 30 mmHg a été abandonnée en 2008, principalement en raison d’une grande variabilité de l’hémodynamique à l’effort selon l’âge et de l’impossibilité d’imposer un standard unique pour l’épreuve d’effort. L’hypertension artérielle pulmonaire (HTAP) est définie par une PAPm ≥ 25 mmHg, une pression capillaire pulmonaire (PCP) ≤ 15 mmHg (télé-expiratoire) et des résistances vasculaires pulmonaires (RVP) > 3 unités Wood au moment du cathétérisme cardiaque droit [1]. Les RVP sont calculées en tenant compte du débit cardiaque (DC) selon la formule : (PAPm-PCP) / DC. L’examen essentiel pour le diagnostic de l’hypertension pulmonaire est le cathétérisme cardiaque droit.

Diagnostic accuracy studies appeared to show improvement in repor

Diagnostic accuracy studies appeared to show improvement in reporting standards when the STARD guidelines were applied.6 Early evidence also suggests that inclusion of reporting standards during Dasatinib peer review raises manuscript quality.7 The International Committee of Medical Journal Editors now encourages all journals to monitor reporting standards and collect associated reporting guideline checklists in the process.8 Furthermore, the National Library of Medicine also now actively promotes the use of reporting guidelines.9 By January 1, 2015, all of the journals publishing this editorial will have worked through implementation and the mandatory use of guidelines and checklists

will be firmly in place. Because each journal has its unique system for managing submissions, there may be several ways that these reporting requirements will be integrated into the manuscript flow. Some journals will make adherence to reporting criteria and associated checklists mandatory for all submissions. Other journals may require them only when the article is closer to acceptance for publication. In any case, the onus will be on the author not only to ensure the inclusion of the appropriate reporting criteria but also to document evidence of inclusion through the use of the reporting guideline checklists. Authors should consult the Instructions for Authors of participating journals for more information. We hope that simultaneous implementation of this

new reporting requirement will send a strong message to all disability and rehabilitation KU-55933 datasheet researchers of the need to adhere to the highest standards when performing and disseminating research.

Although we expect that there will be growing pains with this process, we hope that within a short period, researchers will begin to use these guidelines during the design phases of their research, thereby improving their methods. The potential Tryptophan synthase benefits to authors are obvious: articles are improved through superior reporting of a study’s design and methods, and the usefulness of the article to readers is enhanced. Reporting guidelines also allow for greater transparency in reporting how studies were conducted and can help, hopefully, during the peer review process to expose misleading or selective reporting. Reporting guidelines are an important tool to assist authors in the structural development of a manuscript, eventually allowing an article to realise its full potential. As this issue went to press, the following Editors agreed to participate in the initiative to mandate reporting guidelines and publish this Position Statement in their respective journals. As a collective group, we encourage others to adopt these guidelines and welcome them to share this editorial with their readerships. Sharon A. Gutman, PhD, OTR Editor-in-Chief American Journal of Occupational Therapy Walter R. Frontera, MD, PhD Editor-in-Chief American Journal of Physical Medicine and Rehabilitation Leighton Chan, MD, MPH, and Allen W.

Their model included a calculation of the opportunity cost of equ

Their model included a calculation of the opportunity cost of equity, based on the health improvements that would be forgone in order to select the most equitable Selleck Regorafenib solutions. Jehu-Appiah et al. demonstrated the usefulness

of a similar modeling approach to quantify the trade-offs between efficiency and equity in health investment priorities in Ghana [16]. One of the simplest approaches to assessing distributional effects is to explicitly estimate costs and impacts for distinct sub-populations. This may include stratifying by age, sex, socio-economic status and/or geographic regions. Coyle et al. provide a general framework for population stratified cost-effectiveness analysis [17] and Sculpher describes the application of the approach in contexts such as the UK’s NICE evaluation process [18]. We used an existing country-level rotavirus impact and cost-effectiveness model [1] that has been updated with newly available data [5]. Estimates here are for vaccinating a single birth cohort, including outcomes

during their first five years of life. National rotavirus mortality estimates were based on recently published figures [19]. Estimates of inpatient and outpatient visits are also from previously published studies [20]. Vaccine efficacy estimates Y-27632 manufacturer were based on region and mortality strata [21], [22] and [23]. Estimates for high mortality countries were based on pooled estimates from recent trials [21] and are described in full detail in Atherly et al. [5]. Efficacy was adjusted for

the expected age at which first and second dose would be received in each country, based on DPT1 and DPT2 coverage from DHS surveys [3] and [24]. This was done by modeling coverage of 1 and 2 doses of vaccine at 0–2, 3–5, 6–8 and 9–11 months. Reported DPT1 and DPT2 coverage among 12–23 month old children was used to estimate the fraction of those that would receive each vaccine at the different age ranges [5]. Vaccination effectiveness was based on the fraction of children at each age with 0, 1, or 2 doses and the expected protection of each, assuming 50% lower efficacy for a single dose in the 2-dose regime. For each age band, the effectiveness was click here applied to the proportion of rotavirus deaths that would occur during that period. Current SAGE recommendations suggest that children over 8 months or 32 weeks not receive a vaccine in order to avoid potential adverse effects. The model used in this study assumes that children receiving their second DPT dose between 8 and 12 months of age would still receive it [25]. Medical treatment costs were estimated for inpatient and outpatient visits, using cost-estimates from WHO-CHOICE for facility charges and extrapolations of medication and diagnostic costs from published studies, as described elsewhere [1] and [3]. Medical costs were in 2010 US Dollars and presented in more detail elsewhere [5]. All costs and DALY estimates were discounted at 3%.

Negative scores on combinations of Criteria 5–7 could have led to

Negative scores on combinations of Criteria 5–7 could have led to bias in an unknown

direction. Where one or more of these three criteria were unknown, no statement was made regarding the presence or direction of potential bias. Finally, because AZD2281 price of clinical and methodological heterogeneity between studies, we did not attempt to statistically summarise data by calculating pooled estimates of reliability. Searching MEDLINE yielded 326 citations of which 26 papers were retrieved in full text. CINAHL (95 citations) and EMBASE (34) yielded no additional relevant articles. Hand searching supplied another 20 potentially relevant studies. Of these 46, 25 studies were excluded (see Appendix 2 on eAddenda for excluded studies). In total, 21 studies fulfilled all inclusion criteria (Figure 1). The included studies are summarised in Table 1. Thirteen studies investigated inter-rater reliability selleck compound of measurement of passive shoulder movements (Awan et al 2002, Chesworth et al 1998, De Winter et al 2004, Hayes et al 2001, Hayes and Petersen 2001, Heemskerk et al 1997, Lin

and Yang 2006, MacDermid et al 1999, Nomden et al 2009, Riddle et al 1987, Terwee et al 2005, Tyler et al 1999, Van Duijn and Jensen 2001), two investigated elbow movements (Patla and Paris 1993, Rothstein et al 1983), four investigated wrist movements (Bovens et al 1990, Horger 1990, LaStayo and Wheeler 1994, Staes et al 2009), one investigated phalangeal joint movements (Glasgow et al 2003), and one investigated thumb movements (De Kraker et al 2009). In all except two studies (Bovens

et al 1990, De Kraker et al 2009), physiotherapists acted as raters. There were no disagreements between reviewers on selection of studies. The methodological quality of included studies is presented in Table 2. One study (MacDermid et al 1999) fulfilled all four criteria Sitaxentan for external validity and four studies satisfied three criteria. Two studies (Glasgow et al 2003, Nomden et al 2009) fulfilled all three criteria for internal validity representing a low risk of bias, while six studies satisfied two criteria. Criteria on internal and external validity could not be scored on 52 (28%) occasions because of insufficient reporting. Twenty (10%) disagreements occurred between reviewers which were all resolved by discussion. The inter-rater reliability for measurement of physiological range of motion is presented in Table 3, accessory range of motion in Table 4 and physiological end-feel in Table 5. Shoulder (n = 13): One study ( MacDermid et al 1999) fulfilled all criteria for external validity and another ( Nomden et al 2009) fulfilled all criteria for internal validity. ICC for measurement of physiological range of motion using vision ranged from 0.26 (95% CI –0.01 to 0.69) for internal rotation ( Hayes et al 2001) to 0.