Cause of death was therefore considered as unknown, although it c

Cause of death was therefore considered as unknown, although it cannot be excluded that the animal died due to RVFV infection. Statistical comparison of the detected RVFV RNA levels between goats inoculated with Vero E6-produced virus (n = 12) and goats inoculated with C6/36 cells-produced virus (n = 16) indicated that the developed viremia was higher with faster onset in animals infected

with insect cell-derived virus (P = 0.002) ( Fig. 4A). When the dose 107 PFU/animal of virus of either origin was evaluated separately, the insect-derived virus caused faster onset of the viremia, with the significantly higher RNA levels at 1 dpi (P < 0.001) selleck products ( Fig. 4B). Increase in rectal temperature can be used as one of the parameters in challenge studies in sheep to evaluate efficacy of the vaccine A1210477 candidates, but is unfortunately not applicable for goats. All RVFV inoculated lambs experienced minimum one or two days of increased rectal temperatures, with no significant differences between individual inoculation

approaches (Fig. 5). On the other hand, out of all 28 RVFV inoculated goats only 11 random animals developed increased rectal temperatures for one day. Although antibody development was not the main focus of the study, due to limited knowledge on RVFV infection in goats, the animals were kept for 28–30 dpi, and serum collected during the animal inoculation experiments was analyzed by plaque reduction neutralization assay. Development of neutralizing antibodies against RVFV in goats is summarized in Fig. 6. Significant difference in antibody titers, related to inoculation Resveratrol dose, was observed at 14 dpi. Animals infected with 107 PFU of either Vero E6 or C6/36 cell-produced virus developed at least four-fold higher antibody titers than goats infected with

105 PFU, however a continuous gradual increase in antibody titers until the end of the experiment was observed in serum of animals inoculated with the lower dose. Very interestingly, goats infected with high dose of mosquito cell-produced virus experienced a drop in neutralizing titers by 28 dpi, while goats infected with the Vero E6 cell-produced RVFV maintained their antibody levels at 21 dpi also at 28 dpi. A difference in the onset of antibody response was observed between goats and sheep. While serum samples collected at 4 dpi were all negative, first neutralizing antibodies were detected at 5 dpi in 92.5% of goats, and on day 6 post infection all goats seroconverted. In comparison, only 85% of sheep seroconverted at 6 dpi, with all serum samples collected at 7 dpi being positive for neutralizing antibodies. The antibody titers at 7 dpi for both, goats and sheep were about the same, in range of 20–40, for all the animals.

mirabilis 1 76% (3/170) and E cloacae 0 6% (1/170) from UTI only

mirabilis 1.76% (3/170) and E. cloacae 0.6% (1/170) from UTI only. Gram-positive pathogens were mainly S. pneumoniae

10% (17/170) from both LRTIs and UTIs samples followed by E. faecalis 4.11% (7/170), S. aureus 3.52% (6/170) and coagulase-negative staphylococci 1.76% (3/170) from UTIs only. Elores eradicated all gram-positive and gram-negative organisms except 4 pathogens, one A. baumannii recovered from LRTIs and 3 E. coli recovered from UTIs. Contrary to this, ceftriaxone failed to eradicate 16 pathogens, 2 of A. baumannii (recovered from LRTIs), 7 of E. coli (recovered from UTI), 2 each of E. faecalis and S. pneumoniae obtained from UTIs and one each of K. pneumoniae, K. oxytoca (recovered from I-BET-762 nmr Z VAD FMK LRTI) and P. mirabilis (recovered from UTIs). In UTIs, the bacterial eradications rates

were 95% (57/60) and 80.64% (50/62) for Elores and ceftriaxone, respectively and bacteriological failure rates were 5% (3/60) and 19.37% (12/62), for Elores and ceftriaxone, respectively. Similarly for LRTIs, the bacterial eradication rates were 97.05% (33/34) and 71.42% for Elores and ceftriaxone, respectively, and bacteriological failure rates were 2.94% (1/34) and 28.57% (4/14) for Elores and ceftriaxone, respectively. In UTIS, the clinical cure rates were 83.33% (85/102) and 34.31% (35/102) for Elores and ceftriaxone, respectively. Similarly for LRTI, the clinical cure rates were 91.30% (42/46) and 31.91% (15/47) for Elores and ceftriaxone, respectively, suggesting that Elores is superior than ceftriaxone. In UTIs, 6.86% (7/102) and 8.8% (9/102) patients were failed to respond to Elores and ceftriaxone, respectively. In LRTI, 100% (91.3% cured and 8.69% improved) and 4.89% (7/47) patients of failed to respond to Elores (Table 2). Approximately, 20.59% (21/102) and 15.22% (7/46) for Elores in the

UTIs and LRTIs, respectively compared to 36.27% (37/102) and 31.91% (15/47) of the patients for ceftriaxone in the UTIs and LRTIs, respectively were experienced at least one adverse reactions (Tables 3 and 4). Treatment of patients with LRTIs and UTIs represents a significant most therapeutic challenge since these patients often have multiple underlying risk factors. The prime objective of this study was to compare clinical and bacteriological efficacy of Elores compared with ceftriaxone. Most of infections are caused by gram-negative bacteria. 58.8% (100/170) in UTI and 22.35% (38/170) in LRTI. Overall, clinical cure rate was high in the group of patients treated with Elores in comparison to ceftriaxone. The enhanced susceptibility of Elores (ceftriaxone plus EDTA plus sulbactam) against gram-positive and gram-negative organisms are likely to be associated with synergistic activity of ceftriaxone plus sulbactam plus disodium edetate.

Pair feeding of control mice, instead of ad libitum access to an

Pair feeding of control mice, instead of ad libitum access to an isocaloric control diet, would have further strengthened our design by controlling for potential effects of amount of rations consumed. We predicted that undernourished mice would be more susceptible to rotavirus replication and have more severe disease, however this was clearly not the case. As previously observed by Offor et al. in malnourished suckling mice check details [36], we found accelerated rotavirus shedding in undernourished mice, however both undernourished and nourished animals were able to clear rotavirus effectively. These later results stand in contrast to findings

by Guerrant and co-workers that report more severe disease and exacerbation of malnutrition when undernourished mice are infected with Cryptosporidium [37], Giardia, [38] and enteroaggregative E. coli [39]. Of note, by choosing to challenge adult mice, our models were better designed to examine rotavirus infection and shedding rather than frank diarrhea—a response limited to EDIM infection of young mice. Additional host factors that might account for Crizotinib nmr the divergence of our findings from other published mouse models of malnutrition and gut infection include mouse strain and the method by which undernutrition is induced, e.g., caloric restriction vs. multideficient diets vs. timed separations of pups

from dams. To our knowledge, the “vicious cycle” of diarrhea and undernutrition has not yet been definitively recapitulated in rodent models of viral diarrhea. In addition, the findings of our mouse study parallel results of a large case–control study of diarrhea hospitalizations in Bangladesh, which found that children admitted with rotavirus-positive diarrhea had better too nutritional status than children admitted for parasitic or bacteria-associated diarrheal illnesses [40]. Another recent mouse study also

found that underweight mice had one less day of diarrhea as compared to their normal-weight and overweight counterparts [41]. The current animal data, together with previously published clinical findings, suggest that undernutrition may indeed be an important risk factor for initial or even repeat rotavirus infections, but that mild-to-moderate malnutrition is not a significant contributor to the severity of rotavirus infections. When nourished and undernourished mice were vaccinated with RRV, we found no group differences in viral clearance following EDIM challenge; however, we did detect group differences in serum and stool antibody responses. Lower levels of total stool IgA in RBD vaccinated mice compared to CD mice might be explained by a deficiency of mucosal IgA production or transport secondary to a delay in maturation of the secretory IgA system due to protein malnutrition, as reported by Green and Heyworth [42]. Our finding of increased serum IgA and IgG in RBD-fed mice is also supported by the work of Neumann et al.

, 1983) It will be of particular interest to see whether

, 1983). It will be of particular interest to see whether PI3K inhibitor prolonged prazosin use can restore PFC gray matter in patients with PTSD. Prazosin

may also be helpful in reducing substance abuse, which is common in those with PTSD. Preliminary trials suggest that prazosin can reduce craving and use of alcohol (Simpson et al., 2009), including stress-induced craving of alcohol (Fox et al., 2012a), in subjects without PTSD. Based on these initial trials, prazosin RCTs for alcohol use disorders with and without comorbid PTSD are underway in civilians, military Veterans and active duty military service members. Finally, there is anecdotal evidence that prazosin may enhance the effectiveness and utility of exposure therapy. Therapists have speculated that Veterans with PTSD who would have been “dropouts” during the early anxiety-increasing stages of exposure therapy may have been able to complete their course of therapy successfully because they were taking prazosin; the prazosin appeared to allow them to tolerate (or not develop) the intensely dysphoric hyperarousal

and reexperiencing symptoms that often occur early in the course of exposure therapy prior to therapeutic reductions. These positive effects of prazosin may involve its ability selleck inhibitor to strengthen PFC and weaken amygdala, thus facilitating the process of extinction and enhancing the therapeutic response. There have only been two published studies of the effects of guanfacine in adults with PTSD. These experiments examined the effects of 8 weeks of guanfacine in subjects with long-established PTSD, and found no effect of

treatment (Neylan et al., 2006 and Davis et al., 2008). The negative effects in this cohort may be due to a loss of substrate for drug actions, e.g. due to spine loss with chronic illness. Guanfacine has Edoxaban been shown to ameliorate stress-induced substance abuse in adults (Fox et al., 2012b and Fox and Sinha, 2014), and thus may be helpful in patients for whom the PTSD is more recently initiated. Supported by pre-clinical and clinical studies that demonstrate dysregulated CNS noradrenergic functioning and PFC under-functioning, adrenergic medications are increasingly being used in the treatment of trauma in children. Centrally acting α2-agonists including guanfacine, guanfacine extended release (GXR), and clonidine appear effective in diminishing the intensity of trauma-induced hyperarousal symptoms, including impaired concentration, poor impulse control, hypervigilance, nightmares and insomnia, and exaggerated startle response in children and adolescents. Although there are no controlled trials of these agents in pediatric PTSD, case reports and open trials suggest that clonidine may reduce flashbacks and traumatic repetitive play in children and that guanfacine may reduce trauma-induced nightmares (Harmon and Riggs, 1996 and Horrigan, 1996).

54(m, 4H), 7 41(m, 4H), 7 29(m, 2H), 6 96(t, J = 18 2 Hz, 1H), 6

13C NMR (CDCl3, 400 MHz): 165.2, 164.1, 160.1, 159.2, 157.2, 134.2, 133.2, 130.2, CX-5461 concentration 128.4, 127.1, 125.1, 123.3, 117.7, 116.5, 115.7, 114.9, 113.2, 113.2, 106.5, 104.9, 104.2, 102.3. Wt: 401.33 for C22H12F4NO, LCMS: 402(M+1); 1H NMR (CDCl3, 400 MHz): δ 7.56(d, J = 6.4 Hz, 1H), 7.47(d, J = 6.4 Hz, 1H), 7.41(m, 7H), 6.98(t, J = 18.2 Hz, 1H), 6.8(t,

J = 20.4 Hz, 1H). 13C NMR (CDCl3, 400 MHz): 167.9, 165.2, 158.7, 157.2, 156.7, 132.1, 131.5, 129.5, 128.2, 127.2, 123.9, 122.7, 116.8, 114.3, 113.7, 113.1, 112.6, 111.2, 104.5, 104.2, 103.2, 101.2. Yield: 88% as white solid. M. pt: 148.1–149.4 °C. Mol. Wt: 347.35 for C22H15F2NO, LCMS: 348.1(M+1); 1H NMR (CDCl3, 400 MHz): δ 7.6(d, J = 6.4 Hz, 2H), 7.34(m, 4H), 7.12(d, J = 8 Hz, 2H), 7.07(d, J = 12 Hz, 2H), 6.93(t, J = 18 Hz, 1H), 6.81(t, J = 16 Hz, 1H), 2.37(s, 3H). 13C NMR (CDCl3, 400 MHz): 168.5, 166.9, 164.7, 159.2, 158.2, 156.7, 136.5, 129.9, Sorafenib research buy 129.5, 129.2, 128.5, 125.2, 124.4, 115.4, 113.2, 112.5, 105.9,

104.8, 102.3, 21.3. Yield: 78% as white solid. M. pt: 130.2–131.1 °C. Mol. Wt: 363.35 for C23H15F2NO2, LCMS: 364.0(M+1); 1H NMR (CDCl3, 400 MHz): δ 7.62(d, J = 8 Hz, 2H), 7.37(m, 4H), 7.07(d, J = 16 Hz, 2H), 6.85(m, 4H), 3.83(s, 3H). 13C NMR (CDCl3, 400 MHz): 165.6, 163.2, 161.82, 159.17, 132.53, 132.24, 130.85, 128.9, 126.9,

126.96, 126.47, 115.2, 113.2, 112.01, 104.88, 52.3. Yield: 79% as white solid. M. pt: 145.4–146.41 °C. Mol. Wt: 389.43 for C25H21F2NO, LCMS: 390.0(M+1); 1H NMR (CDCl3, 400 MHz): δ 7.62(d, J = 8 Hz, 2H), 7.33(m, 6H), 7.12(d, J = 8 Hz, 2H), 6.91(m, 4H), 1.57(s, 9H). 13C NMR (CDCl3, 400 MHz): 164.5, 163.2, 161.5, 159.2, 157.2, 155.5, 136.2, 129.8, 129.5, 128.2, 125.3, 123.8, 114.2, 114.0, 113.8, 112.3, 105.2, 103.2, 102.5, 34.5, 31.2. Yield: 86% as white solid. M. pt: 195.9–196.8 °C. Mol. Wt: 409.42 for C27H17F2NO, LCMS: 410.0(M+1); 1H NMR (DMSO-d6, 400 MHz): δ 7.72(m, 4H), 7.59(m, 3H), 7.48(m, 5H), 7.37(m, 2H), 7.28(d, J = 8 Hz, 2H), 7.21(t, J = 20 Hz, 1H). 13C NMR (CDCl3, 400 MHz): 166.6, 163.2, 161.82, 159.6, 156.2, 142.5, 139.2, 132.9, 129.8, 129.2, 128.5, 127.3, 126.5, 124.5, 114.0, 113.2, 112.5, 105.2, 104.2, 102.5. Yield: 80% as white solid. TCL M.

Only 7% of the patients displayed assay resistance to all 7 agent

Only 7% of the patients displayed assay resistance to all 7 agents, while 5% were sensitive to all 7 agents. Thus, 93% of the patients were nonresistant (sensitive or IS) to at least 1 agent. Specifically, 35% were IS to at least 1 agent, and 58% were sensitive to at

least 1 agent. Of note, 18% of these tumors were resistant to carboplatin but, of those, 59% of them were nonresistant (sensitive or IS) to at least 1 other agent in the chemoresponse assay. The standard of care for first-line treatment of patients with advanced-stage EOC consists of aggressive cytoreductive surgery followed by platinum/taxane-based chemotherapy14; however, in this treatment approach, approximately 20-30% of patients will have platinum-resistant disease.15 If identified early, platinum-resistant EOC patients may benefit from alternate and/or

additional therapeutic Gefitinib ic50 options in first-line therapy. At mTOR inhibitor the time of recurrence, clinicians will classify patients as being platinum sensitive (EOC relapsing >6 months after the end of first-line chemotherapy) or platinum resistant (EOC relapsing within 6 months after the end of first-line chemotherapy).16 and 17 This platinum status classification is the primary covariate used in determining future prognosis and subsequent treatment strategies. However, as with most clinical covariates, its accuracy is not absolute; additional measures of platinum responsiveness may be beneficial in further personalizing treatment strategies. Using the current standard clinical approach, identification of platinum-resistant disease is delayed until after the patient has already experienced Thiamine-diphosphate kinase the costs and toxicities associated with first-line therapy. Earlier identification of effective first-line treatment may improve the disease course in EOC patients, potentially allowing them to demonstrate response,

avoid recurrence for a longer time, and delay the onset of decline in overall health, thereby allowing more therapies to be given that may further extend OS. Unfortunately, molecular characterization of EOC has not yet been able to substitute for the clinically observed platinum status classification. The current study evaluates the potential utility of a chemoresponse assay in identifying platinum resistance in advanced-stage EOC patients undergoing standard first-line treatment. Determining platinum status earlier in the treatment of advanced-stage EOC may prevent this high-risk group of patients from being exposed to multiple cycles of ineffective therapy and allow for more effective alternate therapeutic options earlier in the disease, with the ultimate goal of improving patient outcomes.

For example, Kaltoft et al [48] demonstrated that a serum broth

For example, Kaltoft et al. [48] demonstrated that a serum broth (beef infusion supplemented with horse serum and blood) improved the ability of traditional methods to detect multiple serotypes. Similarly, Carvalho et al. [49] found that an enrichment step in Todd Hewitt broth supplemented with yeast extract and rabbit serum increased selleck the proportion of specimens with pneumococcus identified, as well as increasing the detection of multiple serotypes by culture and molecular methods. However, there are some remaining

concerns with broth culture-amplification. The pneumococci may be overgrown by other species, and not all pneumococcal strains or serotypes grow at the same rate in vitro [50], [51] and [52]. Moreover, broth culture enrichment may reduce detection of co-colonization of other species [53], or may not be appropriate for all sample types. In addition, some media components (such as animal serum) may be difficult to access in developing countries. There is insufficient evidence to make a recommendation regarding inclusion of a broth culture-based enrichment

step for the detection of pneumococci. Quantification of pneumococcal load should not be determined using samples that have undergone UMI-77 concentration broth enrichment. Whole-genome amplification methods may overcome limitations of low amounts of DNA. It would be useful to optimize broth culture-amplification (e.g. by including a selective agent), and to test the effects of broth-culture amplification on culture and molecular-based identification and serotyping methods. These recommendations establish the minimum set of criteria to determine the presence of pneumococci, Thalidomide and the dominant pneumococcal serotype, in order to ascertain the prevalence of pneumococcal carriage and the serotypes present in the overall population under study. Given this objective, there are two main issues to consider: how many colonies to

pick, and how to select them. Detecting multiple serotype carriage is important for some epidemiologic questions, but serotyping a few colonies is an insensitive method to detect the true prevalence of multiple serotype carriage [54], [55] and [56]. For colony selection, the truly random approach (e.g. where the STGG medium is diluted and spread on agar plates to obtain single colonies, then all the colonies are numbered and selected using a list of random numbers) may be optimal statistically, but is considered impractical for routine use. Choosing colonies based on morphology is more efficient [54], but leads to a bias towards detecting those that are morphologically distinct such as serotype 3 or nontypeable (NT) pneumococci [57]. Select one colony from the selective plate. If more than one morphology is present, this colony should be from the predominant morphology.

Currently, lentogenic strains are widely used as live NDV vaccine

Currently, lentogenic strains are widely used as live NDV vaccines for poultry throughout the world. NDV has several properties that are useful

in a vaccine vector in non-avian hosts. NDV is attenuated in non-human primates, and likely in other non-avian species, due to a natural host range restriction [22] and [23]. NDV is antigenically distinct from common animal and human pathogens, and thus would not be affected by preexisting immunity in humans and animals. NDV can infect efficiently via the intranasal (IN) route and has been shown to induce humoral and cellular immune responses both at the mucosal and systemic levels Quizartinib price in murine and nonhuman primate models. NDV was used to express protective antigens of simian immunodeficiency virus, respiratory syncytial virus, H5N1 avian influenza virus and human immunodeficiency virus in mice; human parainfluenza virus type 3, severe acute respiratory syndrome associated coronavirus and H5N1 avian influenza virus in monkeys [22], [23], [24], [25], [26], [27] and [28]. However, NDV has not been explored as a viral vector for pathogens of cattle. There are many diseases of cattle for which effective vaccines are not available. Recently we evaluated the replication

and immunogenicity of NDV in calves and showed that NDV was highly attenuated due to host range ATM Kinase Inhibitor cell line restriction and yet induced virus-specific humoral and mucosal antibody responses in this unnatural host [29]. In the present study, we examined the widely used avirulent

NDV vaccine strain LaSota as a topical respiratory vaccine vector to deliver the gD of BHV-1 as a test foreign antigen. Two different recombinant NDVs, one expressing the native gD and the other expressing a chimeric version of the gD, were constructed. These NDV vectored vaccines were evaluated for replication, pathogenicity for birds, immunogenicity and protection against BHV-1 following IN and intratracheal (IT) immunization of calves. Our results indicated that a single IN administration of recombinant NDVs expressing BHV-1 gD resulted in the induction of mucosal and systemic antibody responses against Thiamine-diphosphate kinase BHV-1 and provided partial protection against IN challenge with a virulent BHV-1. The NDV vectored vaccines were safe and attenuated in cattle, suggesting that NDV can be used to elicit antigen specific immune responses against other pathogens of cattle. Further our data indicated that the gD alone may not be sufficient to confer complete protection against BHV-1 challenge. Inclusion of other BHV-1 glycoproteins, namely gC and gB, along with gD may be necessary for generation of complete protection against BHV-1.

Data were collected in 2006 The primary outcome of interest was

Data were collected in 2006. The primary outcome of interest was the number of falls in the six months after the initial mobility assessment. The definition of a fall used was ‘a person unintentionally coming to rest on the ground’ (Jensen et al 2002, Vu et al 2006). Participant medical notes and incident reports were audited Pomalidomide mw at two-monthly intervals by the research physiotherapist for entries relating to falls. The putative predictors assessed were the individual items and total score of the Physical Mobility Scale (Nitz et al 2006).

The Physical Mobility Scale includes nine mobility tasks ranging from bed mobility to ambulation, which are scored on a six-point scale from full dependence (0) to highest independence (5). Item scores are summed to give a total score (0–45) representing overall mobility, with lower scores indicating greater mobility impairment. Physical Mobility Scale assessments were carried out by physiotherapists who were independent of the staff employed by the residential aged care facilities. Physical Mobility Scale assessments were completed at three time Rigosertib price points: baseline, and at two and four months after the baseline assessment. Thus, multiple Physical Mobility Scale assessments and fall data were included for each resident. The association between Physical

Mobility Scale total score and item scores, and risk of falling was assessed using Prentice, Williams, and Peterson conditional risk set survival models for recurrent events (Prentice et al 1981). An advantage of these models over traditional survival models is that they can be applied to data that include multiple observations for each participant, eg, multiple risk factor assessments and multiple outcome events. The recurrent event models used in this analysis were based on data that included up to three Physical Mobility Scale score observations for each resident corresponding to the baseline, two, and four month assessments and additional observations for each fall event that occurred. Total scores were coded into a priori specified

score categories to allow non-linear associations to be explored. Five score categories were selected to ensure an adequate number of observations Unoprostone in each category. Too few observations in categories can lead to predictive models that are unstable and may provide imprecise and inaccurate associations. Each Physical Mobility Scale total score category was entered in a univariable model to establish the risk, reported as a hazard ratio, of sustaining a fall for each Physical Mobility Scale total score category. The ability of the Physical Mobility Scale items and total score categories to discriminate fallers from non-fallers was also explored through Prentice, Williams, and Peterson conditional risk set survival models for recurrent events (Prentice et al 1981).

Zimmermann et al (2011) found an overall agreement of only 3% for

Zimmermann et al (2011) found an overall agreement of only 3% for coding patients’ expressions of concern among 10 different classification systems. The reliability estimates on the use

of the communication coding systems have also been reported as poor (eg, intracoder Epacadostat cost reliability of 0.1, inter-coder reliability of 0.2) (Mead et al 2002, Street and Buller 1987). The use of these unreliable systems may account for conflicting findings for the association of a specific communication construct with satisfaction with care, as for instance the directional contrast in correlation estimates shown for the verbal factor anxiety (r = –0.33) and the nonverbal factor anxious tone of voice (r = 0.32) used by clinicians (Hall et al 1981). Another limitation of this review is that in order to reduce the complexity in reporting the findings we did not investigate how the characteristics of the consultation (eg, gender and context) modify association between communication

Erastin datasheet factors and satisfaction with care. These analyses are currently underway. In conclusion, 38 communication factors were identified as consistently associated with patient ratings of satisfaction with care. The number of potential modifiable communication factors associated with satisfaction with care and the magnitude of their association partially support interventions of communication skills training valuing patient autonomy. These factors could be used by physiotherapists, for instance, to build an interaction with their patients, based on emotional support

(eg, length of consultation, interest, and caring). Further investigations should focus on these factors and their predictive ability on clinical outcomes associated with health care interventions. Communication skills training should include specific communication factors likely to reflect patient satisfaction with care. Footnote: aComprehensive mafosfamide Meta-Analysis version 2.2.04, www.meta-analysis.com eAddenda: Appendix 1 available at jop.physiotherapy.asn.au “
“Contracture is characterised by a loss of range of motion secondary to adaptive shortening of soft tissues spanning joints (Botte et al 1988, Harburn and Potter 1993). It is a common problem for people with acquired brain injury (Fergusson et al 2007, Kwah et al 2012). Contracture is undesirable because of its potentially serious implications for motor recovery, function, care, hygiene, and posture (Fergusson et al 2007). Thus treating and preventing contracture are often important aspects of rehabilitation. While passive stretch has been the mainstay of physiotherapy management for contracture, a recent Cochrane systematic review of passive stretch concluded that regular stretch provided for less than 6 months is not effective in people with neurological conditions (Katalinic et al 2010).