Total phenol content in terms of catechol equivalent (the standard curve equation: Y = 0.002x + 0.034,

r2 = 0.998) of the samples 1, 2 and 3 were 143, 266 and 384.5 mg/g dry wt. while total flavonoid content in terms of quercetin equivalent (the standard curve equation: Y = 0.002x + 0.207, r2 = 0.934) were 81.5, 160.2 and 226.5 mg/g Venetoclax nmr dry wt. respectively. In case of antioxidant activity, ethanolic extract of the samples showed effective scavengers of DPPH and ABTS radical and this activity was comparable to that of ascorbic acid. The respective percentage inhibition of DPPH was 82.0, 74.7, 80.3 and 88.2% for sample 1, p53 inhibitor 2, 3 and ascorbic acid. On the other hand it was 77.12, 71.2, 75.8 and 83% in case of ABTS. The nutrient content of the samples 1, 2 and 3 were 333.7, 302.9 and 325.5cal/100 mg respectively. The order

of phenolic content, antioxidant activity and nutritive value of the samples were sample 1 > sample 3 > sample 2. The extracts showed antimicrobial activity against Bacillus subtilis and Staphylococcus aureus and the respective zones of inhibition of the samples 1, 2 and 3 were 12, 10 and 11 mm against B. Subtilis and it was 6, 4 and 6 mm against S. aureus. No inhibitory effect against Proteus vulgaris, Escherichia coli and Pseudomonas auroginosa was noted. The MIC of the ethanolic extracts

against B. subtilis and S. aureus were observed as 1.25 mg/ml. Different cultures of the target pathogens responded differently to standard antibiotic streptomycin producing zones of inhibition 7–24 mm. The phenolic and nutrient content, antioxidant and antimicrobial activity of the samples vary with respect to the growing localities of the plants. The results are in support of Singh & Sharma 27 in case of Terminalia chebula. This indicates the effect of growing localities on the secondary metabolite and nutrient content Astemizole of plants. Primary products such as carbohydrates, lipids, proteins, etc are common to all plants and are involved in primary metabolic processes 28 and 29 while secondary metabolites content of the plant may vary with respect to their growing conditions. In fact recognition of important climatic factor(s) in relation to secondary metabolite production is required for understanding the biology of secondary metabolites of the plant and to increase yield in artificial growth medium. 30 There is well established positive relationships between the intensity of solar radiation and the quantity of phenolics produced by plants which can be seen at the intra-individual level by comparing plant part(s) exposed to different amounts of light.

, 2008). Together, these observations strongly suggest that ATP is localized in secretory acidic vesicles in cultured Müller cells. Moreover, together with the observation that Evans blue blockade of quinacrine staining was reversible, our results also suggest that cultured avian Müller cells store ATP in acidic vesicles through the functioning of VNUT or a related vesicular anion transporter sensitive

to Evans blue. One interesting point to be further explored is whether cultured Müller cells express this or some other similar transporter. One major role of Müller glial cells is to regulate the composition of the retinal extracellular fluid. Neuronal activity results in increases in extracellular K+ in the inner and outer plexiform layers and these variations http://www.selleckchem.com/products/BIBW2992.html lead to an influx of K+ into Müller see more cells by a spatial-buffering mechanism, also known as “K+ siphoning”, that depolarizes glial cells (Newman and Reichenbach, 1996). Moreover, Müller cells express voltage-dependent calcium channels (Newman, 1985) that were characterized as L-type of calcium channels in the

human retina (Puro et al., 1996). Accordingly, high concentrations of extracellular K+ can induce an increase in intracellular calcium levels (Keirstead and Miller, 1995 and Wakakura and Yamamoto, 1994). In the present work, we show that incubation of chick Müller glial cells with a 50 mM solution of KCl induced

both a decrease in quinacrine staining of cell vesicles and a significant accumulation of ATP in the culture medium, suggesting that under depolarization, cultured Müller glia cells release ATP through the exocytosis of nucleotide-filled vesicles. Although ATP release from glial cells can occur by many different pathways, such as GBA3 connexin hemichannels (Stout et al., 2002), purinergic P2X7 receptor (Anderson et al., 2004) and ATP transporter proteins (Abraham et al., 1993), the release of ATP by exocytosis was demonstrated in astrocytes (Bal-Price et al., 2002, Coco et al., 2003 and Pangršič et al., 2007) and Schwann cells (Liu et al., 2005). Müller glial cells express several glutamate receptors, including NMDA, AMPA/KA and metabotropic glutamate receptors (Keirstead and Miller, 1997, Lamas et al., 2005, López et al., 1994, López et al., 1997, López-Colomé and Romo-de-Vivar, 1991, Uchihori and Puro, 1993 and Wakakura and Yamamoto, 1994). As for KCl-mediated depolarization, incubations with glutamate induced a decrease in quinacrine staining as well as an increase in extracellular ATP content in retinal Müller cells in culture (Fig. 4 and Fig. 5).

The only axioscapular muscle to record high mean levels of activity in the current study was rhomboid major. This result was expected since scapula downward rotation accompanies adduction and rhomboid major generates scapular torque in a downward rotation direction and into retraction (Oatis 2009). The level of activity recorded in rhomboid major in the current study supports previous research, which reported similar levels during manual muscle testing with a manoeuvre involving adduction (Smith

et al 2004). Activity in serratus anterior, the only other axioscapular muscle to be activated above minimal levels in this study, may be present to prevent rhomboid major from retracting the scapula during isometric adduction or to hold the scapula against the thoracic wall. The pattern of increasing muscle activation with increased load was the same across all angles for all the Alpelisib active muscles in the current study. Muscles recruited at low loads during isometric adduction are the same muscles recruited at higher loads but at a higher percentage of their maximum voluntary contraction. Additional muscles are not activated to cope with the additional load. This seems to contradict the ‘law of minimal muscle action’, proposed by MacConaill and Basmajian (1977), which states that ‘the muscles with least synergistic activity will be recruited first and then as load increases

other muscles

are recruited’. Similar motor patterns at low and high load with systematic increases in activity in all active shoulder muscles Selleckchem Dorsomorphin have been demonstrated previously in normal participants during isometric shoulder rotation exercises (Dark et al 2007), isotonic scaption exercises up to 90° (Alpert et al 2000) and shoulder flexion exercises. This study adds to the evidence that normal shoulder motor patterns tuclazepam do not vary with load. Ethics: Participants were fully informed of the study protocol and signed a consent form prior to participation. The study was approved by The University of Sydney Human Research Ethics Committee. Our thanks to Mr Daniel Tardo for his assistance with participant recruitment and data collection in this study. “
“Walking aids are provided to patients as part of routine rehabilitation following surgery for hip fracture to compensate for pain, reduced strength and balance, and postoperative restrictions on weight-bearing. The ultimate goal of rehabilitation is to reduce the level of assistance required with ambulation and to return to pre-morbid levels of function. However, progression in individual patients varies dramatically depending on the rate of improvement of strength, balance, confidence, and pain (Bohannon 1997). As a result, it would be appropriate for many of the walking aids to be changed over the first six months, although the time of change would vary.

Following challenge, subjects were issued semi-structured ALK tumor diary cards to record symptoms in an attempt to monitor activation of innate immune system or inflammatory pathways. This elicited symptoms relating to the gastrointestinal and upper respiratory tracts, while allowing free text entry for other symptoms. Subjects graded symptoms as mild, moderate or severe, which were allocated a score of 1, 2 or 3, respectively. To analyze symptoms in association with each challenge, the sum of the symptom severity scores of all symptoms recorded

by all subjects on each day in the first 28 days after challenge were summed, to give an aggregate symptom score. The score therefore encapsulates both the frequency and severity of symptoms on any given day for the whole group. Peripheral blood mononuclear selleck kinase inhibitor cells were separated from heparinised blood by Ficoll discontinuous gradient centrifugation and frozen at −80 °C prior to measurement of frequency of IFNγ-secreting cells and secretion of IFNγ into culture supernatant in response to stimulation with the following antigens: PPD (SSI, Copenhagen) 5 μg/mL, Ag85 peptide pool (LUMC, Leiden) 5 μg/mL or MPB70 (Lionex, Germany) 5 μg/mL; and medium alone or PHA 2 μg/mL, all in AIMV medium

(Invitrogen, UK) containing penicillin–streptomycin. Briefly, 1.5 × 105 cells/well were stimulated for 7 days in 96-well plates at 37 °C and 5% CO2 in a humidified incubator with antigens or controls, and concentration of supernatant IFNγ measured by ELISA kit (U-CyTech, Netherlands) expressed in pg/mL using a standard on each plate (NIBSC control Human IFNγ rDNA derived, 88/606, NIBSC, UK) and SoftMax software. For ELISPOT, 1 × 106 cells/well (for PHA 3.6 × 105 cells/well) were first stimulated for 18 h in 48-well plates at 37 °C and 5% CO2 in a humidified incubator with antigens or controls, and transferred to PVDF-backed 96-well plates Sitaxentan (MAHA S45, Millipore, UK) coated with 5 μg/ml anti-human IFNγ mAb 1-D1K (Mabtech, 3420-3-1000) for a further 18 h incubation. Responder cells were detected by sequential incubation with 5 μg/ml anti-human IFNγ mAb biotinylated (Mabtech, 3420-6-250), strepdavidin–alkaline

phosphatase (Mabtech, 3310-10), and BCIP/NBT (Sigma, B5655), and spots counted on an automated reader (ViruSpot Elispot reader, AID UK). Values are reported as number of spot forming cells above background number in unstimulated wells, or pg/mL IFNγ in supernatant after subtraction of level in unstimulated wells. Subjects returned to the study site at predefined times (Table 1) to have blood drawn. Whole blood was drawn directly into PAXgene Blood RNA System tubes (PreAnalytiX, BD, UK) and RNA extracted according to manufacturer’s instructions before freezing at −80 °C. Following QC analysis, samples were selected for amplification and hybridization into Illumina HumanWG-6_V2 arrays from days 0, 2, 4 and 7 after each challenge (see Table 1).

Several

authors have suggested that low adherence to home exercises after discharge is one of the main reasons for the poor long-term effectiveness of exercise in people with osteoarthritis (Marks et al 2005, Pisters et al 2007, Roddy et al 2005). In order to continue exercise after the cessation of an exercise program, it has been suggested that exercises should be task-oriented and include strategies to change behaviour and encourage self-regulation skills buy AZD2281 (Veenhof et al 2005). Home exercises that simulate the conditions of daily tasks should enhance adherence to home exercises after discharge and lead to a more physically active lifestyle. Veenhof and colleagues recently developed and evaluated an exercise program based on these principles called the ‘behavioural graded activity’ program (Veenhof et al 2006). This program consists of a period of facility-based intervention followed by booster sessions. It uses principles of operant conditioning (Fordyce et al 1973, Lindstrom et al 1992) and self-regulation (Leventhal et al 1987) and includes booster sessions to improve and maintain adherence (Noland 1989). The program is directed at enhancing exercise adherence and gradually increasing the amount of physical activity in a time-contingent way so that activities are gradually increased by Z-VAD-FMK cell line preset quotas regardless of impairments, eg, increasing walking time by 2 minutes

per day despite the amount of pain. The ultimate goal is integration of these

activities into daily living, so that patients develop a more physically active lifestyle. Earlier research has shown that both behavioural graded activity and physiotherapy intervention according the Dutch guideline (Vogels et al 2001) result in benefits in terms of pain and physical function measured by WOMAC (Veenhof et al 2006). Long-term benefits in terms Bay 11-7085 of walking and physical function measured by MACTAR-questionnaire were also found. However, it remains unclear if behavioural graded activity succeeds in increasing adherence and physical activity. Therefore, the research questions for the present study were: 1. Does behavioural graded activity result in better exercise adherence than usual care in people with osteoarthritis of hip and/or knee? An analysis of secondary outcomes of a behavioural graded activity trial was performed (Veenhof et al 2006). This trial was a single-blind cluster-randomised trial comparing a behavioural graded activity with usual care according to the Dutch physiotherapy guideline in patients with osteoarthritis of hip and/or knee. To avoid contamination between the interventions, cluster randomisation was performed at the level of centres, ie, physiotherapy practices. The centres were randomly allocated to deliver one of the two interventions by means of a computer-generated random sequence.

Absorbance of the solution was then measured at 562 nm in which the reaction mixture without sample served as the control. The chelating activity of the sample was evaluated using EDTA with concentration 100 μg/ml as the standard. The percentage of inhibition of Ferrozine-Fe2+ complex formation was calculated as in DPPH assay. An aliquot of 100 μg/ml of the sample solution was mixed with 1 ml of reagent solution (0.6 M sulfuric acid, 28 mM sodium phosphate and 4 mM ammonium molybdate) and

incubated in a water bath at 95 °C for 90 min. The absorbance of the mixture was measured at 695 nm. The result was compared with that of 100 μg/ml of α tocopherol standard, treated similarly. The sample of concentration 100 μg/ml in 99.5% ethanol Selleck GSK1120212 was mixed with 4.1 ml of 2.51% linoleic acid in 99.5% ethanol, 8 ml of 0.05 M phosphate buffer at pH 7 and 3.9 ml of distilled water and kept under dark conditions at 40 °C. To 0.1 ml of this solution, 9.7 ml Forskolin cell line of 75% ethanol and 0.1 ml of 30% ammonium thiocyanate was added. After 3 min, 0.1 ml of 2 M ferrous chloride in 3.5% hydrochloric acid was added to the reaction mixture and the absorbance was measured at 500 nm every 24 h until one day after absorbance of the control reached maximum. α tocopherol with concentration 100 μg/ml was used as the standard. The reaction mixture

containing 2 ml of 20% trichloroacetic acid, 2 ml of 0.67% 2-thiobarbituric acid and 1 ml of sample solution (100 μg/ml), as prepared in FTC method, was placed in a boiling water bath and, after cooling, was centrifuged at 3000 rpm for 20 min. Absorbance of the supernatant was measured at 552 nm. α tocopherol with concentration 100 μg/ml was used as the standard. Antioxidant activity was based on the absorbance on the final day of FTC method. The HEP G2 cells were maintained in RPMI-1640 medium (Roswell Park Memorial Institute medium) supplemented with 10% FBS (Fetal bovine serum), penicillin (100 U/ml), and streptomycin (100 μg/ml) in a humidified atmosphere others of 50 μg/ml CO2 at 37 °C. Cells (1 × 105/well) were plated in 100 μl of RPMI-1640 medium/well in 96-well plates. After 48 h

incubation the cells reached the confluence. Then the cells were incubated in the presence of various concentrations of the samples in 0.1% DMSO for 48 h at 37 °C. After removal of the sample solution and washing with phosphate-buffered saline (pH 7.4), 20 μl/well (5 mg/ml) of 0.5% 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl–tetrazolium bromide (MTT) solution was added. After 4 h incubation, 0.04 M of isopropanol was added. Viable cells were determined by the absorbance at 570 nm with a microplate reader (Bio-Rad, Richmond, CA), using wells containing cells without sample as controls. Measurements were performed in triplicates, and the concentration required for 50% inhibition of viability (IC50) was determined graphically.

Polatajko, PhD, OT(C) Editor-in-Chief Canadian Journal of Occupational Therapy Derick T. Wade, MD Editor-in-Chief Clinical Rehabilitation Suzanne McDermott, PhD, and Margaret A.

Turk, MK-2206 nmr MD Co-Editors-in-Chief Disability and Health Journal Stefano Negrini, MD Editor-in-Chief European Journal of Physical and Rehabilitation Medicine Steven Vogel, DO(Hon) Editor-in-Chief The International Journal of Osteopathic Medicine Črt Marinček, MD, PhD Editor-in-Chief International Journal of Rehabilitation Research M. Solomonow, PhD, MD(hon) Editor-in-Chief Journal of Electromyography & Kinesiology Paolo Bonato, PhD Editor-in-Chief Journal of NeuroEngineering and Rehabilitation Edelle [Edee] Field-Fote, PT, PhD Editor-in-Chief Journal of Neurologic Physical Therapy Guy G. Simoneau, PhD, PT Editor-in-Chief Journal of Orthopaedic & Sports Physical Therapy (JOSPT) Mark Elkins, PhD, MHSc, BA, BPhty Editor-in-Chief Journal of Physiotherapy

Stacieann C. Yuhasz, PhD Editor-in-Chief Journal of Rehabilitation Research and Development Bengt H. Sjölund, MD, DMSc Editor-in-Chief Talazoparib cell line Journal of Rehabilitation Medicine Carl G. Mattacola, PhD, ATC Editor-in-Chief Journal of Sport Rehabilitation Ann Moore, PhD and Gwendolen Jull, PhD Co-Editors-in-Chief Manual Therapy Randolph J. Nudo, PhD Editor-in-Chief Neurorehabilitation & Neural Repair Kathleen Matuska, PhD, OTR/L Editor-in-Chief Occupational Therapy Journal of Research: Occupation, Participation, and Health Ann F Van Sant, PT, PhD Editor-in-Chief Pediatric Physical Therapy Greg Carter, MD Consulting Editor Physical Medicine and Rehabilitation Clinics of North America Rebecca L. Craik, PT, PhD Editor-in-Chief Physical Therapy Dina Brooks, PhD Scientific Editor Physiotherapy Canada Stuart

ADP ribosylation factor M. Weinstein, MD Editor-in-Chief PM&R Elaine L. Miller, PhD, RN Editor-in-Chief Rehabilitation Nursing Elliot J. Roth, MD Editor-in-Chief Topics in Stroke Rehabilitation Dilşad Sindel, MD Editor-in-Chief Turkish Journal of Physical Medicine and Rehabilitation “
“Patellar tendinopathy (jumper’s knee) is a clinical diagnosis of pain and dysfunction in the patellar tendon. It most commonly affects jumping athletes from adolescence through to the fourth decade of life. This condition affects health and quality of life by limiting sports and activity participation for recreational athletes and can be career-ending for professional athletes. Once symptoms are aggravated, activities of daily living are affected, including stairs, squats, stand to sit, and prolonged sitting. Patellar tendinopathy clinically presents as localised pain at the proximal tendon attachment to bone with high-level tendon loading, such as jumping and changing direction. Tendon pain at the superior patellar attachment (quadriceps tendinopathy) and at the tibial attachment occurs less frequently, but the diagnosis and management are similar to jumper’s knee.

Pour le rivaroxaban, il faut attendre 24 heures avant de commencer l’anticoagulation par voie parentérale. Cette situation qui peut paraître simple présente quelques particularités. En effet, pour le dabigatran et l’apixaban, le relais apparaît logique, on arrête les AVK, et dès que l’INR est inférieur à 2, on débute le dabigatran ou l’apixaban (tableau IV). Par contre, pour le rivaroxaban, le traitement doit être instauré une fois que l’INR est inférieur ou égal à 3, ce qui peut paraître contre-intuitif. Cette différence de seuil d’introduction de traitement est liée à une prudence accrue concernant le rivaroxaban, du fait de l’augmentation des événements thromboemboliques observée à la fin de

l’étude dite ROCKET-AF, dans le bras rivaroxaban, lorsque les patients arrêtaient le traitement à l’insu et reprenaient des AVK en non PD173074 solubility dmso insu. En effet, les investigateurs ont observé une recrudescence des événements thromboemboliques à l’arrêt

du rivaroxaban, en fin de protocole [21]. L’analyse post-hoc des données de cette étude a démontré une augmentation transitoire du risque d’emboles artériels systémiques lors de la période de transition vers un traitement ouvert à la fin de l’étude (principalement un AVK), pour les patients sous rivaroxaban, soulignant l’importance d’une couverture anticoagulante adéquate lors de Panobinostat ces transitions. Pour chacun des NACO étudiés dans cet article, un temps de co-administration est nécessaire avant l’arrêt du NACO et la poursuite these de l’AVK seul (tableau V). Pour le dabigatran, le temps de co-administration

est fondé sur la fonction rénale. Si la clairance de la créatinine est supérieure à 50 mL/min, il est de trois jours. Si la clairance de la créatinine est entre 30 et 50 mL/min, il est de deux jours. Pour le rivaroxaban, ainsi que l’apixaban, un temps de co-administration minimal de deux jours est nécessaire avant de commencer à doser l’INR. Après deux jours de co-administration, dès que l’INR est supérieur ou égal à 2, on peut arrêter le rivaroxaban ou l’apixaban. L’INR est modifié par la prise de NACO, comme le laisse supposer leur mécanisme d’action. Le dosage de l’INR lors de la co-administration doit donc être effectué lorsque le NACO est à sa concentration minimale, c’est-à-dire avant la prise suivante. Des recommandations ont été éditées par la société européenne de cardiologie, en 2012, sur l’utilisation des NACO dans la fibrillation atriale non valvulaire [11]. D’après les auteurs de ces recommandations, les grandes études randomisées [3], [4] and [5] ayant démontré la non-infériorité des NACO comparés aux AVK, avec une meilleure sécurité d’emploi en diminuant de façon statistiquement significative le risque d’hémorragie intracrânienne, les NACO sont recommandés en première intention dans la fibrillation atriale non valvulaire, chez les patients à risque.

Choi and LeDoux (2003) had rodents learn to perform an instrumental shuttling response in the presence of a CS to avoid an imminent electric shock. A specific subset of ‘non-learners’ were unable to perform this avoidance response because of high levels of conditioned fear responses (i.e., freezing). However, selleck compound after lesions to the CE, these animals were capable of adopting the avoidance strategy, indicating that excessive fear expression can impair the capacity to perform

actions that promote safety and reduce fear. This implies that higher levels of trait anxiety or acute exposure to stress may impair the capacity to acquire or retain avoidance strategies when confronted with threat. Of the limited studies that have directly assessed the effects of stress or stress hormones on avoidance learning, most have examined passive (i.e., inhibitory) avoidance learning. In contrast to active avoidance processes that requires the use of an instrumental response to prevent or terminate an aversive outcome, passive avoidance requires the suppression

of an innate behavior in order to successfully avoid an aversive outcome. A common way to test passive avoidance is to measure the latency with which an animal crosses from a naturally preferred selleck chemicals llc darkened chamber that has been paired with shock to a less preferred bright chamber that the animal has learned to associate with safety. Passive avoidance involves the amygdala as well as the hippocampus due to the contextual nature of the task (Ogren and Stiedl, 2010). As with other forms of aversive learning, passive avoidance is dependent on stress hormones to facilitate learning and consolidation.

For example, blocking noradrenaline systemically or within the LA or B after avoidance training disrupts its consolidation as measured by weaker subsequent retention (Ferry et al., 1999, Gallagher et al., 1977, Liang et al., 1986 and Quirarte et al., 1997). In contrast, enhancing noradrenaline after avoidance training enhances its retention (McGaugh et al., 2002 and McIntyre many et al., 2002). Furthermore, infusion of glucocorticoid agonists into the LA directly after training on a fear avoidance and escape task enhances subsequent retention, while GR antagonists infused prior to training impaired retention. Notably, infusions at either time point into the CE had no effect on memory retrieval (Roozendaal and McGaugh, 1997). The effect of acute stress on passive avoidance was recently tested in rodents. Before training, animals were classified into high, medium and low anxiety based on the elevated plus-maze test; subsequently, half of the mice in each group then underwent an acute stress manipulation. Stress altered avoidance performance in the high anxiety group only.

5A) as did mice lacking IFNγR1 ( Fig. 5B). These data indicate a significant role for NADPH oxidase and IFNγ in controlling bacterial proliferation following infection with SL1344 atp. Similarly, both immune components were

needed for control of SL3261 replication ( Fig. 5). SL1344 atp was assessed for its ability to protect against subsequent oral re-challenge ( Fig. 6). Again, the wild type challenge grew rapidly, as expected, in unimmunised mice whereas mice immunised with SL1344 atp had significantly reduced bacterial counts in spleens on days 3, 4 and 7 and in livers on days 4 and 7 postinfection AZD8055 concentration ( Fig. 6). Similar levels of protection were observed between SL1344 atp and SL3261-immunised mice ( Fig. 6). Therefore, SL1344 atp is protective

against subsequent oral challenge and this protection is as effective as immunisation with SL3261. SL1344 atp was further assessed for protection following oral immunisation, given that this would SP600125 research buy be the preferred route of immunisation with a live attenuated vaccine. The wild type infection grew as expected in unimmunised mice whereas those immunised with SL1344 atp had significantly lower bacterial counts in spleens and livers after being re-challenged intravenously ( Fig. 7A and B). Little net bacterial growth was observed in challenged SL1344 atp immunised mice, with similar levels of bacteria seen over 14 days. Following oral re-challenge, SL1344 atp immunised mice showed reduced bacterial counts on days 3 and 7 postinfection relative to unimmunised mice ( Fig. 7C and D). Furthermore, bacterial numbers following SL1344 atp oral immunisation were comparable to those seen in SL3261-immunised mice PDK4 regardless of the re-challenge route. The SL1344 atp mutant is therefore protective following oral administration and is as effective as SL3261 as a vaccine. Pooled sera from mice immunised intravenously and orally were assayed for antibodies specific for S. Typhimurium. Mice intravenously immunised with SL1344 atp had significantly higher levels of total antibody against S. Typhimurium than unimmunised mice

( Fig. 8A). Levels of total antibody in mice intravenously immunised with SL1344 atp were comparable to those elicited in SL3261-immunised mice. Total antibody levels following oral immunisation were lower than those seen in intravenously immunised animals, however SL1344 atp immunised mice showed higher levels of total antibody compared to unimmunised mice although this did reach statistical significance. Compared with SL3261-immunised mice the antibody levels were lower in SL1344 atp immunised mice although this was not statistically significant. The humoral immune response was further characterised with the determination of IgG subclass levels elicited following immunisation with SL1344 atp ( Fig. 8B and C).