The Value of Recreational Physical Activity in Aotearoa New Zealand: A Scoping Review of Evidence and Implications for Social Value Measurement.

Internationally, there is rising interest in measuring the value of sport and physical activity to society. A critical step in valuing the sector is first establishing the relationship between engagement in sport and physical activity and the societal outcomes that ensue. This paper summarises the findings of a literature review carried out as part of a larger study on the Social Return on Investment (SROI) of recreational physical activity in Aotearoa New Zealand. The review aimed to synthesise existing evidence on the relationship between recreational physical activity and wellbeing outcomes for all New Zealanders, including tangata whenua (Maori, who are Aotearoa New Zealand's Indigenous population). The methodology took the format of a scoping review and included a series of searches for academic and grey literature, including literature concerning Maori that might have been overlooked in a traditional academic search. The findings are grouped into five outcome areas: physical health; subjective wellbeing; individual development; personal behaviour; and social and community development. The review found some compelling evidence which shows examples of the links between sport and physical activity and outcomes in each of these areas for specific population sub-groups. In particular, for Maori, the findings demonstrate a strong impact on social and community development through building social capital and enhancing cultural identity. However, in all outcome areas, there is mixed quality evidence, a small amount of evidence on which to base definitive conclusions, and limited evidence relating to the monetary value of outcomes. The review concludes that there is a need for further research to strengthen the evidence base for social impact measurement, particularly around the impact of sport and physical activity for indigenous populations.

Assessment of Humoral and Long-Term Cell-Mediated Immune Responses to Recombinant Canarypox-Vectored Equine Influenza Virus Vaccination in Horses Using Conventional and Accelerated Regimens Respectively.

During Australia's first and only outbreak of equine influenza (EI), which was restricted to two northeastern states, horses were strategically vaccinated with a recombinant canarypox-vectored vaccine (rCP-EIV; ProteqFlu™, Merial P/L). The vaccine encoded for haemagglutinin (HA) belonging to two equine influenza viruses (EIVs), including an American and Eurasian lineage subtype that predated the EIV responsible for the outbreak (A/equine/Sydney/07). Racehorses in Victoria (a southern state that remained free of EI) were vaccinated prophylactically. Although the vaccine encoded for (HA) belonged to two EIVs of distinct strains of the field virus, clinical protection was reported in vaccinated horses. Our aim is to assess the extent of humoral immunity in one group of vaccinated horses and interferon-gamma ((EIV)-IFN-γ)) production in the peripheral blood mononuclear cells (PBMCs) of a second population of vaccinated horses. Twelve racehorses at work were monitored for haemagglutination inhibition antibodies to three antigenically distinct equine influenza viruses (EIVs) The EIV antigens included two H3N8 subtypes: A/equine/Sydney/07) A/equine/Newmarket/95 (a European lineage strain) and an H7N7 subtype (A/equine/Prague1956). Cell-mediated immune responses of: seven racehorses following an accelerated vaccination schedule, two horses vaccinated using a conventional regimen, and six unvaccinated horses were evaluated by determining (EIV)-IFN-γ levels. Antibody responses following vaccination with ProteqFlu™ were cross-reactive in nature, with responses to both H3N8 EIV strains. Although (EIV)IFN-γ was clearly detected following the in vitro re-stimulation of PBMC, there was no significant difference between the different groups of horses. Results of this study support reports of clinical protection of Australian horses following vaccination with Proteq-Flu™ with objective evidence of humoral cross-reactivity to the outbreak viral strain A/equine/Sydney/07.

Use of stored equine colostrum for the treatment of foals perceived to be at risk for failure of transfer of passive immunity.

OBJECTIVE-To assess the use of stored equine colostrum for the treatment of foals perceived to be at risk for failure of transfer of passive immunity (FTPI). DESIGN-Cohort study. ANIMALS-232 Thoroughbred foals and 191 Thoroughbred mares (41 mares gave birth to 1 foal on 2 occasions). PROCEDURES-Postpartum, presuckle colostrum samples were collected from mares; samples with a colostral refractive index (cRI) > or = 23% were frozen (-20 degrees C [-4 degrees F]) and stored for > or = 7 days but < 2 years. Foals of dams that produced colostrum with a cRI value < 20% were treated with > or = 300 mL of stored colostrum that was thawed and administered via nasogastric tube on 1 to 4 occasions within 6 hours after parturition. Serum samples were obtained from colostrum-treated and nontreated foals 24 hours after treatment or suckling, respectively, for determination of serum IgG (sIgG) concentration. RESULTS-8 foals and their respective dams were excluded from the analyses. For the remaining 30 treated and 194 nontreated foals, mean +/- SD sIgG concentration was 1,597 +/- 574 mg/dL. Thirteen (5.8%) foals had sIgG concentrations < 800 mg/dL, of which 1 (0.4%) had an sIgG concentration < 400 mg/dL. Nine of these foals had suckled mares producing colostrum with a cRI value > or = 20%, and 2 foals had been treated with stored colostrum. CONCLUSIONS AND CLINICAL RELEVANCE-Treatment with stored colostrum appeared to be effective for prevention of FTPI in at-risk foals. However, foals were still at risk for FTPI despite suckling of or treatment with colostrum with adequate cRI values.

Characterisation of K+ currents in the C8-B4 microglial cell line and their regulation by microglia activating stimuli.

Microglia are the intrinsic immune cells of the brain. As such, they are crucially involved in neuro-protection as well as neuro-degeneration. Their activation leads to the induction of cytokine and chemokine release, the production of reactive oxygen species and nitric oxide and an increased outward potassium conductance. In this study, we focus our interest on potassium currents and channels in the C8-B4 murine microglial cell line and compare them with those of primary cultured microglia from neo-natal mice. Using the whole cell patch-clamp technique, we have recorded prominent inward and outward rectifying voltage-dependent potassium currents but no calcium-activated potassium currents. Using pharmacological, biophysical and molecular approaches, we demonstrate that Kv1.3 and Kir2.1 channels underlie outward and inward rectifying potassium currents, respectively. In contrast to primary cultured microglia, we observe that an outward rectifying potassium current is already present in unstimulated C8-B4 cells. However, as seen in primary microglia, this current increases after treatment with LPS, IFN-gamma, TGF-beta and GM-CSF and is suppressed by treatment with protein kinase inhibitors. Our study indicates that the C8-B4 cell line shows similar though not identical potassium channel properties compared to primary cultured microglia. We demonstrate that despite some differences, they are a useful tool to study potassium currents in microglial activation mechanisms by means of electrophysiological methods without the need for preparation of cells as primary culture.

Urinary clinical pathologic findings and glomerular filtration rate in the horse.

Urinary specific gravity (USG) measurements are underused by equine ambulatory veterinarians. Urinary dipstick and USG findings can assist in the diagnosis and prognosis of many disease processes in the horse. Simple methods for measurement of the glomerular filtration rate and urinary biochemical markers can improve equine urinary diagnostic abilities in critical care patients. Fractional excretion of electrolytes and minerals assists in fluid care and in management of nutrition of horses.

Effects of dietary flaxseed oil supplementation on equine plasma fatty acid concentrations and whole blood platelet aggregation.

An 18-week feeding trial was performed to investigate the effects of an omega-3 (n-3) fatty acid-enriched ration on plasma fatty acid concentrations and platelet aggregation in healthy horses. Flaxseed oil served as the source of the n-3 fatty acid alpha-linolenic acid (ALA). Twelve horses were fed dietary maintenance requirements using a complete pelleted ration (80%) and timothy grass hay (20%) for a 2-week acclimation period before being randomly assigned either to a treatment (group 1) or control (group 2) group. Group 2 horses (n = 6) were fed the diet described in the acclimation period, whereas group I horses (n = 6) were fed a 10% flaxseed oil-enriched complete pellet (80%) and grass hay (20%). Biological samples and physical measurements were collected at one point during the acclimation period (week 0) and every 4 weeks thereafter (weeks 4, 8, 12, and 16). Body weight, CBC (including platelet count), plasma fibrinogen. electrolyte (Na, K, and Cl) concentrations, and biochemical profile enzyme activities (aspartate aminotransferase, alkaline phosphatase, gamma-glutamyltransferase, and creatine kinase) did not change markedly with diet. Platelet aggregation was not altered by the supplementation of flaxseed oil in these healthy horses, although increases in plasma cis-polyunsaturated 18-carbon fatty acids C18:3; n-3 (ALA) and C18:2; n-6 (linoleic acid), biologically active C20:5; n-3 (eicosapentaenoic acid [EPA]), and malondialdehyde (MDA) were evident. There were no marked decreases in C20:4; n-6 (arachidonic acid [AA]) or increases in C22:6; n-3 (docosahexaenoic acid [DHA]), signifying that flaxseed oil may have had a high percentage of omega-6 (n-6) fatty acids as well as n-3 fatty acids, and this relatively high n-6: n-3 fatty acid ratio may have affected the biochemical effect of n-3 fatty acids. In healthy horses supplemented with flaxseed oil, platelet aggregation was not altered, which may have been due to the limited biologic effect in healthy subjects or the inability of flaxseed oil to induce the necessary biochemical effect of replacing n-6 fatty acids with n-3 types.

NLRP3-Inflammasome Activating DAMPs Stimulate an Inflammatory Response in Glia in the Absence of Priming Which Contributes to Brain Inflammation after Injury.

Inflammation in the absence of infection (sterile inflammation) contributes to acute injury and chronic disease. Cerebral ischemia is a devastating condition in which the primary injury is caused by reduced blood supply and is therefore sterile. The cytokine interleukin-1ß (IL-1ß) is a key contributor to ischemic brain injury and central inflammatory responses. The release of IL-1ß is regulated by the protease caspase-1, and its activating complex, the inflammasome. Of the known inflammasomes the best characterized, and one that is perceived to sense sterile injury is formed by a pattern recognition receptor called NOD-like receptor pyrin domain containing three (NLRP3). A key feature of NLRP3-inflammasome dependent responses in vitro in macrophages is the requirement of an initial priming stimulus by a pathogen (PAMP), or damage associated molecular pattern (DAMP) respectively. We sought to determine the inflammatory responses of NLRP3-activating DAMPs on brain derived mixed glial cells in the absence of an initial priming stimulus in vitro. In cultured mouse mixed glia the DAMPs ATP, monosodium urate, and calcium pyrophosphate dehydrate crystals had no effect on the expression of IL-1α or IL-1ß and induced release only when the cells were primed with a PAMP. In the absence of priming, these DAMPs did however induce inflammation via the production of IL-6 and CXCL1, and the release of the lysosomal protease cathepsin B. Furthermore, the acute phase protein serum amyloid A (SAA) acted as a priming stimulus on glial cells resulting in levels of IL-1 expression comparable to those induced by the PAMP lipopolysaccharide. In vivo, after cerebral ischemia, IL-1 production contributed to increased IL-6 and CXCL1 since these cytokines were profoundly reduced in the ischemic hemispheres from IL-1α/ß double KO mice, although injury-induced cytokine responses were not abolished. Thus, DAMPs augment brain inflammation by directly stimulating production of glial derived inflammatory mediators. This is markedly enhanced by DAMP-induced IL-1-release-dependent responses that require a sterile endogenous priming stimulus such as SAA.

Clinicopathologic evidence of myocardial injury in horses with acute abdominal disease.

OBJECTIVE: To determine whether there is evidence of myocardial injury in horses with acute abdominal disease. DESIGN: Prospective case series. ANIMALS: 18 healthy horses and 69 horses with acute abdominal disease. PROCEDURES: 18 healthy horses had been admitted to the hospital for investigation and were assigned to group 1. Horses examined for acute abdominal disease were assigned to 3 groups: strangulating obstruction, nonstrangulating obstruction, or inflammatory disease (groups 2, 3, and 4, respectively). Heart rate, Hct, and blood lactate and cardiac troponin I (cTnI) concentrations were measured at initial examination. Myocardial function was assessed by echocardiographic measurement of fractional shortening and left ventricular ejection time (LVET). Heart rhythm was evaluated via ECG. RESULTS: The proportion of horses with high (> 0.03 ng/mL) cTnI concentration was significantly greater among horses with strangulating (9/25 [36%]) or inflammatory (9/19 [47%]) lesions, compared with healthy horses (0/18). The proportion of horses with high cTnI concentration was significantly greater among nonsurvivors (12/24 [50%]) than among survivors (10/45 [22%]). Serum cTnI concentration was positively correlated with Hct, heart rate, and blood lactate concentration and negatively correlated with LVET. CONCLUSIONS AND CLINICAL RELEVANCE: Evidence of myocardial injury was observed in horses with acute abdominal disease, and this injury was associated with severity of illness. Recognition of myocardial injury could improve treatment of acute abdominal disease in horses.