FMDV is a single-stranded, positive-sense RNA virus (Genus Aphthovirus, family Picornaviridae). The viral genome is about 8.3 kb long, enclosed within a protein capsid. The capsid is composed of 60 copies each of four different structural proteins (VP1-4); VP1-3 are surface exposed while Regorafenib clinical trial VP4 is entirely internal. Crystallographic studies have identified the structure of the FMDV capsid [1] and [2]

and immunological epitopes have been mostly found on surface-oriented interconnecting loops between structural elements. Studies employing monoclonal antibodies (mAb) have identified antigenic sites by sequencing mAb neutralisation resistant (mar) mutants [3], [4], [5], [6], [7], [8] and [9]. Of the five antigenic sites reported so far for the most extensively studied serotype O, site-1 (G-H loop) is

linear and trypsin-sensitive whereas the others are conformational and trypsin-resistant. Equivalent check details neutralising antigenic sites (except site 3) have also been identified for serotype A, with critical residues present in equivalent positions [3], [4], [5], [6] and [9]. Serotype A viruses are present on all continents where FMD is reported, and is antigenically diverse [10] often exhibiting poor cross-protection [11]. In the Middle East (ME), a new variant, A-Iran-05, was identified in samples collected from Iran in 2003 and subsequently spread to neighbouring countries [10] and North Africa [12]. This genotype replaced the A-Iran-96 and A-Iran-99 genotypes that were previously circulating in the region; did not cross-react with A/Iran/96 vaccine antisera and shared

a closer antigenic relationship with the older A22/Iraq vaccine strain (v/s) [10]. However, many samples isolated after 2006 did not even match with A22/Iraq v/s and so a new v/s, A/TUR/2006 was introduced. From sequence data, Jamal and colleagues indicated candidate amino acid (aa) substitutions in the capsid that might have contributed to these antigenic changes Fossariinae [13]. More recently, there is evidence that viruses from the region now exhibit lower cross-reactivity with the A/TUR/2006 antisera. The aim of this study was to investigate the molecular basis of the antigenic variation in these viruses using capsid sequences and their corresponding antigenic relationship (r1) values. Fifty-seven serotype A viruses from the ME submitted to the Food and Agriculture Organisation’s World Reference Laboratory for FMD (WRLFMD) at the Pirbright Institute were used in this study (Supplementary table). Two are the v/s A22/IRQ/24/64 (A22/Iraq) and A/TUR/2006 that were originally isolated in Iraq and Turkey, in 1964 and 2006 respectively; the 55 other viruses were isolated over a fifteen year period (1996–2011).

Between 2010 and 2030, there will be 69% increase in number of adults with diabetes in developing countries and 20% increase in developed countries.3 Various Selleckchem BI-2536 drugs presently available to reduce diabetes associated hyperglycaemia are associated with several side-effects. Hence, in the recent years, there is growing interest in herbal medicine all over the world, as they have little or no side effects. Ethnopharmacological survey indicates that more than 1200 plants are used in traditional medicine for antihyperglycaemic activity.4 India is well known for its herbal wealth. Many medicinal plants belonging to Leguminosae (11 sp.), Lamiaceae (8

sp.), Liliaceae (8 sp.), Cucurbitaceae (7 sp.), Asteraceae (6 sp.), Moraceae (6 sp.), Rosaceae (6 sp.), Euphorbiaceae (5 sp.) and Araliaceae (5 sp.) have been studied for treatment of DM.5 Therefore the search for effective and safer antihyperglycemic agents has become an area of current research all over the world.6 The drug Kali or Shyah-Musali, of Ayurvedic system of medicine is derived from the bitter mucilaginous rhizomes of Curculigo orchioides Gaertn. (Family-Hypoxidaceae). It is one of the important Rasayana drugs of Ayurvedic Materia Medica for vigour and vitality and also reputed for its various medicinal properties. 7 It has tonic, aphrodisiac, demulcent, diuretic properties and used in asthma, impotency, jaundice, skin, urinary and venereal diseases. 8 It is used in many Ayurvedic and Unani compound

formulations as an important ingredient.

9 In Unani system it is used for treating diabetes. 10 The screening for the biological activities of this plant showed hypoglycaemic and anticancer selleck chemicals activity in the alcoholic extract of rhizome. 11 Although, acclaimed traditionally as antidiabetic, there are very few reports available on scientific studies regarding the effect of C. orchioides Gaertn. rhizome on blood glucose level. Hence, the present study has been undertaken to carry out phytochemical analysis and to not establish the antihyperglycaemic effect of aqueous slurry of C. orchioides Gaertn. rhizome on streptozotocin (STZ) induced diabetic rats. The rhizomes of C. orchioides Gaertn. were collected from Badlapur (Maharashtra, India). The herbarium of C. orchioides Gaertn. plant was prepared and authenticated from Blatter Herbarium, St. Xavier’s College, Mumbai. The rhizomes collected were washed under running tap water and were blotted dry. The rhizomes were then cut into small pieces and kept for drying in oven at temperature 40 ± 2 °C for five days. The dried rhizomes were ground into powder and passed through sieve No. 100 and used for further experimental purpose. The Aqueous Slurry of C. orchioides Gaertn. rhizome powder (ASCO) was prepared in water and used for the dosing purpose (1000 mg powder/kg body weight). Preliminary phytochemical analysis of C. orchioides Gaertn. rhizome using various solvents namely water, methanol, ethanol, benzene and petroleum ether was carried out.

Conversations between HCPs, adolescents, and OTX015 molecular weight parents about this decision could propagate already existing parental misconceptions about adolescent risk and STI vaccines [12], [83] and [84]. HCP communication about STI vaccination may also be shaped by their perceptions of parental concerns about STI vaccination. For example, HCPs in Malaysia and the United States report that parental cultural and/or religious beliefs serve as a barrier to STI vaccination [23] and [29]. While

this has been substantiated by studies demonstrating that adolescents of religious-based political party members or born-again Christians are less likely to initiate HPV vaccination [58] and [85], it has also resulted in hesitancy among some HCPs to recommend HPV vaccine for adolescents in certain cultural and/or religious communities [17]. However, this association may not be uniformly present among all religious/cultural groups. School nurses in the United Kingdom, for example, reported low HPV vaccine uptake in smaller Christian, Church of Wales, and ultra-Orthodox Jewish schools, but good uptake in other schools with a high proportion of Catholic and Muslim students [17]. Many HCPs also believe that the sexual stigma associated with STI vaccination is an important barrier

to vaccine uptake among parents of adolescents [29] and [31]. However, studies of individual Luminespib order and/or parental attitudes suggest STI vaccine uptake may be more from related to other non-STI-specific

factors such as newness of the vaccine, including efficacy and safety concerns, and need for more vaccine information [9], [32], [83], [85], [86], [87], [88], [89] and [90]. In the United States, the HPV vaccine is one of the most commonly refused vaccine [91]. A recent study found that perceived issues around safety are a major reason for parents deciding not to vaccinate their adolescent against HPV, perhaps more so than lack of HCP recommendation [92]. This indicates that accurate and effective HCP communication about such issues in order to reduce common misconceptions is crucial and should be incorporated within the HCP recommendation. Indeed, HCPs who anticipate parental vaccine safety questions are more likely to recommend HPV vaccination [79], and data suggest that HCPs can positively impact vaccination decisions of parents with vaccine safety concerns [93]. Thus, HCP communication may be most effective when tailored to the actual decision-making considerations of adolescents and their parents [34]. Systems-based factors may hinder or facilitate HCP communication with adolescents about STI vaccination. Many studies indicate that time constraints affect HCP communication related to adolescent vaccines, including those targeting STIs [17], [29] and [60].

Dans les « Standards Options Recommandations » de 2003 [2], 20 à 50 % des 9007 patients analysés

(sur 36 études) étaient douloureux au moment du diagnostic de cancer et la prévalence de la douleur augmentait au cours de l’évolution de la maladie avec 55 à 95 % de patients douloureux. Dans l’étude de Breivik et al., regroupant 5084 patients cancéreux adultes contactés entre 2006 et 2007 dans onze pays européens (dont 642 France) et en Israël, la prévalence globale de la douleur était de 84 % et de 75 % en France [3]. Parmi ces patients, 56 % avaient une douleur modérée à sévère et pour 573 patients Erastin tirés au sort, 41 % recevaient un traitement opioïde fort, 69 % mentionnaient un retentissement de la douleur sur la qualité de vie et 50 % avaient selleck chemicals llc le sentiment que la qualité de vie n’était pas une priorité pour les professionnels de santé. La prévalence de la douleur était particulièrement élevée (plus de 85 %) pour les patients qui avaient un cancer du pancréas, des os, du cerveau, de la tête et du cou et les patients porteurs de lymphome. Une enquête nationale, réalisée en

2010, sous l’égide de l’INCa (Institut national du cancer) en collaboration avec l’Institut BVA, a été menée auprès de 1507 patients atteints de cancer traités en ambulatoire. L’objectif principal était de préciser l’état des lieux concernant les modalités de prise en charge de la douleur du cancer en France [4]. Ce document s’inscrit

dans la mise en œuvre du Plan cancer 2009–2013, à savoir « renforcer la qualité des prises en charge pour tous les malades atteints de cancer », et plus précisément la mesure 19.1 du plan cancer : « généraliser l’accès aux mesures transversales lancées par le Plan cancer précédent, améliorant la qualité de toute prise en charge en cancérologie ». Cette enquête visait à décrire la douleur des patients en phase de traitement of curatif, en situation de cancer avancé et également à distance des traitements (en phase de surveillance ou de rémission), à individualiser la douleur neuropathique, les crises douloureuses et leurs prises en charge. Sur les 1507 patients interrogés, 28 % étaient en phase de traitement curatif, 53 % en situation de cancer avancé, 18 % en phase de surveillance ou de rémission avec, pour la majorité d’entre eux, un recul de plus d’un an par rapport à la fin de la chimiothérapie. La prévalence déclarée de la douleur dans cette enquête est identique à celle des données de la littérature, la douleur étant présente chez 53 % des patients interrogés. Une douleur chronique (présente depuis plus de trois mois) est rapportée par 30 % des patients douloureux en situation de cancer avancé, mais aussi par 25 % des patients douloureux à distance de tout traitement ou bien en rémission.

Excision of the kanamycin

resistance FRT cassette was confirmed by PCR and sequencing to be correct. Southern blot using the FRT scar site region as a probe was also used to confirm that the final mutants were as intended. LPS serotype was confirmed by agglutination with anti-04 serotype antiserum using anti-09 antiserum as a negative control SAR405838 order (Remel Europe Ltd./Oxoid Ltd., Basingstoke UK). For complementation of SL1344 atp, lacking the entire atp operon, PCR was used to amplify the entire atp operon from SL1344 fused to a chloramphenicol resistance cassette, from pACYC184. This was inserted into the malXY pseudogene region on the Salmonella chromosome using ODM with selection on chloramphenicol. Insertion of the atp operon into malXY was confirmed by PCR and sequencing Veliparib mouse of the mutated malXY junction and by Southern blotting using atpG as the probe. In addition to the complemented strain, SL1344 atp (malXY atp operon+), a complementation control strain was also generated, SL1344 atp

(malXY CmR). For this control strain a chloramphenicol resistance cassette was inserted into the malXY pseudogene region of SL1344 atp to ensure the insertion into the pseudogene had no phenotypic effects. Cultures in 5 ml of LB broth were incubated overnight with shaking (180 rpm) at 37 °C. Cultures were diluted 1:100,000 into 100 ml of pre-warmed LB broth, and incubated with shaking at 37 °C. Growth was measured by viable count on LB agar plates. Exponential generation times were calculated from growth rates between 4 and 6 h. To assess the ability to utilise succinate as a sole carbon source wild type and the many various atp mutants were grown in M9 minimal medium supplemented

with 0.4% (w/v) of sodium succinate. Growth was assessed by OD595 after 24 and 48 h. Inocula were prepared from overnight cultures grown statically in LB broth at 37 °C. Cultures were centrifuged and bacteria were re-suspended in phosphate buffered saline (pH 7.4) to the required concentration. Seven to nine week-old female BALB/c mice (Harlan, Oxon, UK) were inoculated with 200 μl of bacteria suspension via intravenous injection, or they were lightly anaesthetised with halothane and inoculated by oral gavage. Doses of bacteria given were confirmed by viable counts in LB agar. Gene knock-out mice lacking gp91phox or IFNγR1 on a C57/BL6j background where originally purchased from Jackson Laboratory (Bar Marbour, ME) and maintained as homozygous matings at the Wellcome Trust Sanger Institute. C57/BL6j age- and sex-matched control mice were purchased from Harlan (Oxon, UK). At pre-determined time points postinfection animals were killed, spleens and livers removed and homogenised in 5 ml of sterile water in a Stomacher® 80 Lab System (Seward). Bacterial numbers were enumerated via serial dilutions and plating in LB agar. When required, blood was collected via cardiac puncture under terminal anaesthesia.

This truncated TSOL16A cDNA (herein referred to as TSOL16 with respect to the cDNA and encoded protein) was cloned directionally into the EcoRI and XhoI sites of pGEX-1TEX and transformed into E. coli JM109 strain by electroporation. Use of the pGEX plasmid allowed

expression and purification of TSOL16 as a fusion with glutathione S-transferase (GST) [15]. The truncated TSOL16 cDNA was excised from pGEX-1 by digestion with EcoRI and XhoI, HKI-272 order and cloned into EcoRI/SalI-digested pMAL-C2. The pMAL-C2 plasmid allowed expression and purification of TSOL16 as a fusion with maltose binding protein (MBP) [16]. The plasmid construct was transformed into E. coli JM109. The TSOL45-1A protein was cloned into the pGEX and pMAL-C2 plasmids, and expressed in E. coli as a fusion protein with GST and MBP as described in [4]. The TSOL45-1A fusion proteins lacked 16 N-terminal amino acids that encoded a predicted secretory signal. The TSOL45-1B

cDNA was originally cloned from T. solium oncosphere mRNA as described in [7]. TSOL45-1B lacked exon II of the TSOL45-1 gene. PCR amplification was used to produce a cDNA construct that encoded a protein also lacking the 16 N-terminal amino acids of the secretory signal. The following PCR primers were used to amplify TSOL45-1B for cloning into pGEX and pMAL as described above: 5′CCG GAA TTC GGA AAC CAC AAG GCA ACA TC3′; 5′CCG CTC GAG GGA AAT GGG CAT TGA CCG3′. E. coli SAR405838 molecular weight cultures expressing TSOL16, TSOL45-1A and TSOL45-1B were prepared and recombinant fusion proteins were purified as detailed in [14]. Freeze-dried aliquots of antigens were prepared by the addition of Quil A adjuvant (1 mg per dose) and a much sixfold (w/w) amount of maltose as a stabilizing agent for transport to Lima, Peru, where

the vaccine trial was conducted. Aliquots of GST and MBP, for use as negative controls, were also prepared for the vaccine trial. The antigens were reconstituted in sterile de-ionized water immediately prior to vaccination of pigs. The purified GST and MBP fusions of TSOL16, TSOL45-1A and TSOL45-1B were tested in a pig vaccine trial against challenge infection with T. solium. The study was reviewed and approved by the Animal Ethics Committee of the School of Veterinary Medicine, Universidad de San Marcos, Lima, Peru. Twenty 8-week old piglets were obtained from a cysticercosis free farm located in Huaral, Lima. Animals were divided into four groups of 5 pigs each. All animals were vaccinated against Classical Swine Fever prior to the start of the trial. Each pig received 200 μg of antigen and 1 mg Quil A (Brenntag Biosector, Denmark) per immunization in a 1 ml dose. Immunizations were given intramuscularly in the right hind-quarter via a 0.9 mm × 38 mm needle and 1 ml syringe (Becton Dickinson, U.K.). Piglets received their first immunization with recombinant antigen prepared as a GST fusion.

1A) (P < 0.0001), and greater with the 97 day interval than the 57 day interval (P = 0.0006). The antibody response induced by protein–protein (P–P) vaccination was markedly variable with three mice mounting high responses comparable to those receiving A–P immunization, and three very weakly responding mice ( Fig. 1A and B). There was no significant difference Crenolanib between median antibody responses following protein–protein, adenovirus–MVA and adenovirus–protein regimes after a 57 day dose interval (P = 0.37 by Kruskal–Wallis test), but there was a clear increase in the variance of the

response after two shot protein regimes compared to viral-vector containing regimes. In contrast with the antibody results, greater

percentages of IFNγ+ CD8+ T cells were detected by ICS 14 days after A–M immunization than A–P, and the 57 day dose interval was superior (P < 0.0001 for both comparisons) ( Fig. 1A and B). Clear boosting of CD8+ T cell responses by MVA was evident at both dose intervals. As expected, given the lack of the CD8+ T cell epitope in the MSP119 protein sequence in BALB/c mice [5], CD8+ T cell responses were not detectable following P–P vaccination. Additional experiments in C57BL/6 mice (in which a CD8+ T cell epitope is present in the MSP119 protein [5]) confirmed that, in contrast to the A–M regime, P–P Talazoparib vaccination did not induce a CD8+ T cell response detectable by IFNγ splenic ELISPOT or peripheral blood ICS, and that CD8+ T cell responses were unaltered by A–P immunization as compared to adenovirus priming alone ( Fig. 1C and D). CD8+ T cell responses after A–P immunization of either mouse strain thus presumably represent the contracting or effector memory CD8+ T cell response induced Tryptophan synthase by the adenovirus. We subsequently compared the immunogenicity of three-component sequential adenovirus–MVA–protein (A–M–P) and adenovirus–protein–MVA (A–P–M) regimes to two-component regimes (Fig. 2 and Fig. 3). The kinetics of the responses induced by these regimes were markedly different. We found that addition of

protein to adenovirus–MVA (A–M–P) was able to boost antibody but not CD8+ T cell responses (again as would be predicted due to lack of the T cell epitope in this protein) (Fig. 2A), while addition of MVA to adenovirus–protein (A–P–M) boosted CD8+ T cell responses but not antibody titer (Fig. 2B). Total IgG responses to A–M–P and A–P–M were significantly higher than those to A–M (P < 0.05 by ANOVA with Bonferroni post-test), with no significant differences between the responses to A–M–P, A–P–M and A–P (P > 0.05, Fig. 3A). There were no statistically significant differences in CD8+ T cell responses between A–M–P, A–P–M and A–M regimes (P > 0.05 by ANOVA with Bonferroni post-test, Fig. 3B). In general, any two- or three-component regime including AdCh63 and MVA induced maximal CD8+ T cell responses as measured in the blood.

This burden is also similar to earlier studies on rotavirus burden in hospitalized AGE cases [5] and [6]. We found G1 and G2 as the most common G types, P[4] and P[8] as the most common P types and G1P[8] and G2P[4] as common GP types. Some rotavirus samples could not be typed for selleck G and/or P type. The most common G/P/GP types found in this study are similar to other Indian studies (including IRSN) conducted in children hospitalized with RVGE [2], [3], [4],

[5] and [6]. Our results show that G12 comprised 6.4% of rotavirus strains: a finding in concordance with IRSN [4] and [6]. G12 strain was first detected in India in 2001 and over the decade has been increasingly reported in recent Indian studies [4], [6], [17] and [18]. More than 75% of the children enrolled in the study were in the age group of less than 2 years. This reflects the age profile of diarrhea burden in India, where majority of the diarrhea episodes in children under 5 years of age are reported to occur in children of age less than 3 years [19] and [20]. In our study, mean age of RV positive

subjects was lower compared to RV negative subjects and majority of RVGE (85%) cases occurred in children ≤24 months of age. The difference between rotavirus and non-rotavirus groups was significant w.r.t. age distribution – result similar to previous observations of the epidemiologic profile of rotavirus infection in India [4] and [5]. In IRSN, it was observed that the mean age of RV positive children was significantly lower than RV negative children. In addition to younger Cabozantinib mouse age of RVGE subjects, our results also indicate that RV positive subjects experience severe and multiple AGE symptoms. We found that more than half of the RVGE cases were severe by Vesikari scale (77.2%) while a few were severe by Clark scale (3.9%). Similar distribution was seen in non-RVGE cases. Higher proportion of severe cases in our study may be due to late referral of the subjects to OPDs after disease

onset. A 10 district survey in India by UNICEF titled “Management Practices of Childhood Diarrhea in India” has reported that in India in rural as well as urban areas, there is delay of at least 1 day between onset of diarrhea and time of seeking medical care outside home. The report also mentions that parents Dipeptidyl peptidase took the child outside home for managing diarrhea when child had too many stools, appeared very weak, did not eat anything, and diarrhea continued for too long [20]. It is likely therefore that majority of parents take their child to health care setting when diarrhea becomes severe. We used Clark and Vesikari scale for categorizing acute gastroenteritis into different severity levels. This categorization is dependent on multiple factors like study methodology such as where, how and when data is collected, active or passive method surveillance and frequency, timing, method of assessment in active studies.

The measurement of the extracellular L-Glu concentration in the medium was performed according to the methods previously

described (8). Real-Time Quantitative RT-PCR, Western Pictilisib chemical structure blotting, immunocytochemistry were also performed according to the methods previously described (8). The microglia culture was treated with LPS for 24 h in the presence or absence of antidepressants and the concentration of L-Glu in the medium was measured. All sets of the experiments were repeated in triplicate. All procedures described above were in accordance with institutional guidelines. In the previous report, we showed that the expression level of astrocytic L-Glu transporters was decreased Lumacaftor cell line in the astrocyte-microglia-neuron mixed culture in LPS (10 ng/ml, 72 h)-induced inflammation model without cell death (8). We first compared the effects of various groups of antidepressants, i.e., selective serotonin reuptake inhibitors (SSRIs) (paroxetine, fluvoxamine, and sertraline), serotonin–norepinephrine

reuptake inhibitor (SNRI) (milnacipran), and tricyclic antidepressant (TCA) (amitriptyline), on the decrease in the astrocytic L-Glu transporter function in this inflammation model. To quantify L-Glu transport activity, we measured the concentration of L-Glu remaining 30 min after changing the medium to the one containing 100 μM of L-Glu. In each set of experiment, LPS-induced decrease in the L-Glu transport activity was stably reproduced (Fig. 1A–E). Among antidepressants, only paroxetine prevented the LPS-induced decrease in L-Glu transport activity (Fig. 1A). The effect was concentration-dependent and reached significant at 1 μM. The other antidepressants had no effects (Fig. 1B–E). Typical image of the astrocyte-microglia-neuron mixed culture was shown in Fig. 1F. We have clarified that LPS-induced medroxyprogesterone decrease in L-Glu transport activity was caused by the decrease in the expression level of GLAST, a predominant L-Glu transporter in the mixed culture, in both of mRNA and protein levels (8). In this study, LPS-induced decreases in the

expression of GLAST, were reproduced at both of mRNA (28.8 ± 4.7% of the control) and protein (69.5 ± 4.7% of the control) levels (Fig. 1G, H). We then examined the effects of paroxetine on the LPS-induced decrease in the L-Glu transporter expression. Paroxetine significantly prevented the decreases at both of mRNA (28.8 ± 4.7 to 49.6 ± 3.3%; n = 10) and protein (from 69.5 ± 4.7% to 91.0 ± 5.1%; n = 5) levels ( Fig. 1G, H). As is shown in Fig. 1, fluvoxamine and sertraline, the other SSRIs in this study, did not affect the decrease in L-Glu transport activity, suggesting that paroxetine revealed the effects through the mechanisms independent of its inhibitory effect on serotonin selective transporter.

S.) (Ogden et al., 2012). Public health authorities are beginning to look for cost-effective ways to reduce this epidemic. Increased physical activity is a candidate strategy because of its numerous health benefits, including the potential to attenuate cardiovascular disease and diabetes risk ( Kahn et al., 2002, Norman et al., 2006 and Task Force on Community Preventive Services (USTFCPS), 2001).

Research has shown that there is a positive association between proximity to parks/recreational facilities and increased physical activity levels ( Roemmich et al., 2006 and Sallis et al., 2011). Programming INK 128 datasheet and group activities, for example, have been found to be related to increased usage of school facilities and improved levels of moderate-to-vigorous physical activity ( Lafleur et al., 2013). Having convenient, reliable access to Apoptosis Compound Library ic50 open space/recreational areas or programing that encourages physical activity, however, can be challenging, especially for under-resourced communities ( Marie, 2007, Powell et al., 2006 and Spengler et al., 2007). Shared-use agreements (SUAs) where school property (i.e., the grounds, facilities, or both) and programming are shared between schools and

community-based entities represent a strategy to address this public health problem. A shared-use agreement outlines an agreement between two or more parties that details and enumerates each party’s responsibilities in the partnership. Shared-use encompasses a diverse array of agreement types, including joint-use agreements (JUA) and Memoranda of Understanding (MOUs). These contractual documents may be legally binding or non-binding; but whether or not they are legally binding does not diminish their potential benefits. A formal agreement adds value to each partnership by laying out the expectations of the entering parties, reducing the odds that the relationship would dissolve prematurely. School grounds offer clean, protected, and often underutilized space that community members can use for physical activity

(Maddock et al., 2008). Communities that seek to promote physical activity and improve access to recreational space can partner with school districts. Non-profit organizations are also important CYTH4 partners as they often receive outside funding to provide programming (Lafleur et al., 2013). SUAs offer the opportunity for both parties to clarify their intent and roles in the partnership, as well as to identify their individual interests. Even when state laws generally provide schools strong protection against liability for injuries to recreational users of school properties (California Tort Claims Act, 2012), the perceived threat of tort liability remains an important deterrent to schools’ decisions to participate (Spengler et al., 2007 and Zimmerman et al., 2013).