Packaged hospital food appears safe and feasible to reuse.

AIM: To determine the safety, operational feasibility and environmental impact of collecting unopened non-perishable packaged hospital food items for reuse. METHODS: This pilot study tested packaged foods from an Australian hospital for bacterial species, and compared this to acceptable safe limits. A waste management strategy was trialled (n = 10 days) where non-perishable packaged foods returning to the hospital kitchen were collected off trays, and the time taken to do this and the number and weight of packaged foods collected was measured. Data were extrapolated to estimate the greenhouse gasses produced if they were disposed of in a landfill. RESULTS: Microbiological testing (n = 66 samples) found bacteria (total colony forming units and five common species) on packaging appeared to be within acceptable limits. It took an average of 5.1 ± 10.1 sec/tray to remove packaged food items from trays returning to the kitchen, and an average of 1768 ± 19 packaged food items were per collected per day, equating to 6613 ± 78 kg/year of waste which would produce 19 tonnes/year of greenhouse gasses in landfill. CONCLUSIONS: A substantial volume of food items can be collected from trays without significantly disrupting current processes. Collecting and reusing or donating non-perishable packaged food items that are served but not used within hospitals is a potential strategy to divert food waste from landfill. This pilot study provides initial data addressing infection control and feasibility concerns. While food packages in this hospital appear safe, further research with larger samples and testing additional microbial species is recommended.

Ca2+ Signaling and Its Potential Targeting in Pancreatic Ductal Carcinoma.

Pancreatic cancer (PC) is a major cause of cancer-associated mortality in Western countries (and estimated to be the second cause of cancer deaths by 2030). The main form of PC is pancreatic adenocarcinoma, which is the fourth most common cause of cancer-related death, and this situation has remained virtually unchanged for several decades. Pancreatic ductal adenocarcinoma (PDAC) is inherently linked to the unique physiology and microenvironment of the exocrine pancreas, such as pH, mechanical stress, and hypoxia. Of them, calcium (Ca2+) signals, being pivotal molecular devices in sensing and integrating signals from the microenvironment, are emerging to be particularly relevant in cancer. Mutations or aberrant expression of key proteins that control Ca2+ levels can cause deregulation of Ca2+-dependent effectors that control signaling pathways determining the cells' behavior in a way that promotes pathophysiological cancer hallmarks, such as enhanced proliferation, survival and invasion. So far, it is essentially unknown how the cancer-associated Ca2+ signaling is regulated within the characteristic landscape of PDAC. This work provides a complete overview of the Ca2+ signaling and its main players in PDAC. Special consideration is given to the Ca2+ signaling as a potential target in PDAC treatment and its role in drug resistance.

Sterols as a biomarker in tracing niger and sesame seeds oils adulterated with palm oil.

Food adulteration is a serious social problem all over the world. The oil obtained from the niger and sesame is known for its quality and has a high market value in Ethiopia. The cost of the oil obtained from these oilseed crops is high unlike other plant oils, thus prone to be mixed with other cheap oils to increase profits. The study aimed to quantify the sterol profile of niger seed and sesame oils thereby trace adulteration of these oils with palm oil. Gas Chromatography coupled to Mass Spectrometry was used to analyze the sterol fractions of oils. A blend of palm oil, at a level of 10%, with niger seed and sesame oil was prepared. In all the studied oils; sitosterol (467.2-2778.96 mg/kg), campesterol (295.9-869.85 mg/kg) and stigmasterol (125.6-920 mg/kg) were the dominant sterols identified. Lupeol, Lanosterol, and Olean-12-en-3-one were only identified in a significant proportion for niger seed oil. Moreover, cholestroltrimethyl silyl ether (19.9 mg/kg) and 24-Nor-22,23- methylenecholest-5-en-3ß-ol trimethylsilyl (TMS) ethers (139.14 mg/kg) were only identified in palm oil and used to trace adulteration. An attempt made to trace these compounds by mixing palm oil at a level of 10% with niger seed and sesame oils was successfully detected its presence. Hence, as the physicochemical properties of oils can be arranged to cover adulteration, marker identification provides a reliable identity of the specific oil.

Defining a new model of interdisciplinary cancer cachexia care in regional Victoria, Australia.

PURPOSE: Cachexia is a wasting condition affecting approximately 50% of cancer patients, associated with decreased quality of life and survival. Barwon Health's Cachexia and Nutrition Support Service provides person-centred interdisciplinary care to assist the management of cachexia symptoms. This study describes a novel and effective service model established in a regional cachexia clinic and the patient population it serves. METHODS: A descriptive, retrospective longitudinal study was conducted of records from patients attending Barwon Health between 2008 and 2013 (n = 175), alongside the description of service refinement over this time. Patients with ≥ 2 attendance dates were assessed for anthropometric measures, follow-up intervals, and muscle function outcomes to describe patient trajectory during clinic involvement. RESULTS: This is the first detailed description of a successful interdisciplinary clinic specific to cancer cachexia management, where patients are seen outside established 8- to 12-week structured programs which prevail in other cachexia clinics. Seventy-five patients (43%) attended one appointment only, with almost half of these (n = 33) first attending within 60 days of death. Of the 99 patients with two or more appointments, 49% displayed positive outcomes with > 2-kg weight gain between two consecutive appointments, and > 50% improved functional strength between two consecutive appointments. CONCLUSIONS: The majority of patients attending clinic multiple times maintained or increased weight and functional status during their involvement with the service. However, successes of care provision were muted by high attrition, primarily due to delayed referral and expected high mortality within the study cohort. Planned future analyses with greater patient numbers and cancer stratification will establish cachectic populations most likely to benefit from this novel mode of interdisciplinary care. The Cachexia and Nutrition Support Service provides an effective and efficient service model for the provision of specialist cachexia care to community-dwelling patients in regional Australia.

Muscle Antioxidant Enzymes Activity and Gene Expression Are Altered by Diet-Induced Increase in Muscle Essential Fatty Acid (α-linolenic acid) Concentration in Sheep Used as a Model.

This study investigated the effect of dietary manipulations on muscle fatty acid composition, the activities and relative mRNA expressions of antioxidant enzymes and the relationship between muscle enzyme activity or mRNA expression and alpha linolenic acid (ALA) concentration in sheep. Eighty-four lambs blocked on liveweight were randomly allocated to four dietary treatments, lucerne pasture (Lucerne), annual ryegrass pasture (Ryegrass), feedlot pellets (Feedlot) or annual ryegrass plus feedlot pellets (RyeFeedlot). After six weeks of feeding, lambs were slaughtered and within 30 min post-mortem, samples collected from the longissimus lumborum (LL) muscle for RNA isolation and measurement of antioxidant enzyme activities. At 24 h post-mortem, LL samples were collected for determination of fatty acid concentrations. Feedlot treatment decreased ALA, eicosapentaenoic (EPA), docosapentaenoic (DPA) and docosahexaenoic (DHA) concentrations compared with other treatments and increased linoleic acid (LA) and arachidonic acid (AA) compared with Lucerne and Ryegrass (p < 0.001). The activity of Glutathione peroxidase (GPX1, p < 0.001) and Superoxide dismutase (SOD2, p < 0.001) enzymes in the muscle increased with Lucerne compared to other treatments. Lucerne increased muscle gpx1 mRNA expression by 1.74-fold (p = 0.01) and 1.68-fold (p = 0.05) compared with Feedlot and other diets, respectively. The GPX1 (r² = 0.319, p = 0.002) and SOD2 (r² = 0.244, p = 0.009) enzyme activities were positively related to ALA. There was a positive linear relationship between muscle gpx1 (r² = 0.102, p = 0.017) or sod2 (r² = 0.049, p = 0.09) mRNA expressions and ALA concentration. This study demonstrates that diet can affect concentrations of ALA and other fatty acids as well as change activities and gene expression of antioxidant enzymes in muscle. Increased antioxidant activity may, in turn, have beneficial effects on the performance, health and wellbeing of animals and humans.

Postprandial long-chain n-3 polyunsaturated fatty acid response to krill oil and fish oil consumption in healthy women: a randomised controlled, single-dose, crossover study.

BACKGROUND AND OBJECTIVES: Krill oil (KO) and fish oil (FO) are good sources of health-benefiting long chain n- 3 polyunsaturated fatty acids (LC n-3 PUFA), EPA and DHA. There are conflicting outcomes on the bioavailability of LC n-3 PUFA from KO compared with FO. This study investigated the postprandial incorporation of LC n- 3 PUFA into plasma lipids following consumption of 5 capsules of KO or FO in comparison with olive oil (OO) control in healthy women. METHODS AND STUDY DESIGN: 10 women (aged 18-45 years) consumed a high-fat (15 g) breakfast, supplemented with 5 g of KO, FO, or OO in a random order with a minimum seven-day washout period between the supplementations. The LC n-3 PUFA content in KO was 907 mg compared with 1441 mg in FO. Blood samples were collected in the fasting state and for the next 5 hours after test meal consumption on an hourly basis. RESULTS: Significant increases in plasma EPA concentrations were observed starting at 2 h after KO and FO consumption (p<0.05). There were no significant changes in either DHA or DPA between the three groups. The increases in plasma EPA concentrations were similar between the KO and FO groups (p>0.05). CONCLUSIONS: The lower dose (31%) of EPA from KO led to a similar plasma EPA concentration as in the FO group, suggesting that EPA from KO may be more efficiently incorporated into plasma. This may be related to the high content of phospholipids and free fatty acids in KO.

Experimental and Human Evidence for Lipocalin-2 (Neutrophil Gelatinase-Associated Lipocalin [NGAL]) in the Development of Cardiac Hypertrophy and heart failure.

BACKGROUND: Cardiac hypertrophy increases the risk of developing heart failure and cardiovascular death. The neutrophil inflammatory protein, lipocalin-2 (LCN2/NGAL), is elevated in certain forms of cardiac hypertrophy and acute heart failure. However, a specific role for LCN2 in predisposition and etiology of hypertrophy and the relevant genetic determinants are unclear. Here, we defined the role of LCN2 in concentric cardiac hypertrophy in terms of pathophysiology, inflammatory expression networks, and genomic determinants. METHODS AND RESULTS: We used 3 experimental models: a polygenic model of cardiac hypertrophy and heart failure, a model of intrauterine growth restriction and Lcn2-knockout mouse; cultured cardiomyocytes; and 2 human cohorts: 114 type 2 diabetes mellitus patients and 2064 healthy subjects of the YFS (Young Finns Study). In hypertrophic heart rats, cardiac and circulating Lcn2 was significantly overexpressed before, during, and after development of cardiac hypertrophy and heart failure. Lcn2 expression was increased in hypertrophic hearts in a model of intrauterine growth restriction, whereas Lcn2-knockout mice had smaller hearts. In cultured cardiomyocytes, Lcn2 activated molecular hypertrophic pathways and increased cell size, but reduced proliferation and cell numbers. Increased LCN2 was associated with cardiac hypertrophy and diastolic dysfunction in diabetes mellitus. In the YFS, LCN2 expression was associated with body mass index and cardiac mass and with levels of inflammatory markers. The single-nucleotide polymorphism, rs13297295, located near LCN2 defined a significant cis-eQTL for LCN2 expression. CONCLUSIONS: Direct effects of LCN2 on cardiomyocyte size and number and the consistent associations in experimental and human analyses reveal a central role for LCN2 in the ontogeny of cardiac hypertrophy and heart failure.

Comparisons of the Postprandial Inflammatory and Endotoxaemic Responses to Mixed Meals in Young and Older Individuals: A Randomised Trial.

Postprandial inflammation and endotoxaemia are determinants of cardiovascular and metabolic disease risk which are amplified by high fat meals. We aimed to examine the determinants of postprandial inflammation and endotoxaemia in older and younger adults following a high fat mixed meal. In a randomised cross-over trial, healthy participants aged 20-25 and 60-75 years (n = 15/group) consumed a high-fat breakfast and a low-fat breakfast. Plasma taken at baseline and post-meal for 5 h was analysed for circulating endotoxin, cytokines (monocyte chemotactic protein-1 (MCP-1), interleukin (IL)-1ß, IL-6, and tumour necrosis factor-alpha (TNF-α)), lipopolysaccharide binding protein (LBP), and inflammatory gene expression in peripheral blood mononuclear cells (PBMC). Older subjects had lower baseline PBMC expression of Glutathione peroxidase 1 (GPX-1) but greater insulin-like growth factor-binding protein 3 (IGFBP3) and circulating MCP-1 compared to younger subjects. After either meal, there were no age differences in plasma, chylomicron endotoxin, or plasma LBP concentrations, nor in inflammatory cytokine gene and protein expression (MCP-1, IL-1ß, and TNF-α). Unlike younger participants, the older group had decreased superoxide dismutase (SOD)-2 expression after the meals. After a high-fat meal, older adults have no increased inflammatory or endotoxin response, but an altered oxidative stress gene response compared with younger adults. Healthy older adults, without apparent metabolic dysfunction, have a comparable postprandial inflammatory and endotoxaemia response to younger adults.

MicroRNAs in a hypertrophic heart: from foetal life to adulthood.

The heart is the first organ to form and undergoes adaptive remodelling with age. Ventricular hypertrophy is one such adaptation, which allows the heart to cope with an increase in cardiac demand. This adaptation is necessary as part of natural growth from foetal life to adulthood. It may also occur in response to resistance in blood flow due to various insults on the heart and vessels that accumulate with age. The heart can only compensate to this increase in workload to a certain extent without losing its functional architecture, ultimately resulting in heart failure. Many genes have been implicated in cardiac hypertrophy, however none have been shown conclusively to be responsible for pathological cardiac hypertrophy. MicroRNAs offer an alternative mechanism for cellular regulation by altering gene expression. Since 1993 when the function of a non-coding DNA sequence was first discovered in the model organism Caenorhabditis elegans, many microRNAs have been implicated in having a central role in numerous physiological and pathological cellular processes. The level of control these antisense oligonucleotides offer can often be exploited to manipulate the expression of target genes. Moreover, altered levels of microRNAs can serve as diagnostic biomarkers, with the prospect of diagnosing a disease process as early as during foetal life. Therefore, it is vital to ascertain and investigate the function of microRNAs that are involved in heart development and subsequent ventricular remodelling. Here we present an overview of the complicated network of microRNAs and their target genes that have previously been implicated in cardiogenesis and hypertrophy. It is interesting to note that microRNAs in both of these growth processes can be of possible remedial value to counter a similar disease pathophysiology.

Oxidized fish oil in rat pregnancy causes high newborn mortality and increases maternal insulin resistance.

Fish oil is commonly taken by pregnant women, and supplements sold at retail are often oxidized. Using a rat model, we aimed to assess the effects of supplementation with oxidized fish oil during pregnancy in mothers and offspring, focusing on newborn viability and maternal insulin sensitivity. Female rats were allocated to a control or high-fat diet and then mated. These rats were subsequently randomized to receive a daily gavage treatment of 1 ml of unoxidized fish oil, a highly oxidized fish oil, or control (water) throughout pregnancy. At birth, the gavage treatment was stopped, but the same maternal diets were fed ad libitum throughout lactation. Supplementation with oxidized fish oil during pregnancy had a marked adverse effect on newborn survival at day 2, leading to much greater odds of mortality than in the control (odds ratio 8.26) and unoxidized fish oil (odds ratio 13.70) groups. In addition, maternal intake of oxidized fish oil during pregnancy led to increased insulin resistance at the time of weaning (3 wks after exposure) compared with control dams (HOMA-IR 2.64 vs. 1.42; P = 0.044). These data show that the consumption of oxidized fish oil is harmful in rat pregnancy, with deleterious effects in both mothers and offspring.

Depression is a risk factor for incident coronary heart disease in women: An 18-year longitudinal study.

BACKGROUND: According to a recent position paper by the American Heart Association, it remains unclear whether depression is a risk factor for incident Coronary Heart Disease (CHD). We assessed whether a depressive disorder independently predicts 18-year incident CHD in women. METHOD: A prospective longitudinal study of 860 women enrolled in the Geelong Osteoporosis Study (1993-2011) was conducted. Participants were derived from an age-stratified, representative sample of women (20-94 years) randomly selected from electoral rolls in South-Eastern Australia. The exposure was a diagnosis of a depressive disorder using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Outcomes data were collected from hospital medical records: (1) PRIMARY OUTCOME: a composite measure of cardiac death, non-fatal Myocardial Infarction or coronary intervention. (2) Secondary outcome: any cardiac event (un/stable angina, cardiac event not otherwise defined) occurring over the study period. RESULTS: Seven participants were excluded based on CHD history. Eighty-three participants (9.6%) recorded ≥1 cardiac event over the study period; 47 had a diagnosis that met criteria for inclusion in the primary analysis. Baseline depression predicted 18-year incidence, adjusting for (1) anxiety (adj. OR:2.39; 95% CIs:1.19-4.82), plus (2) typical risk factors (adj. OR:3.22; 95% CIs:1.45-6.93), plus (3) atypical risk factors (adj. OR:3.28; 95% CIs:1.36-7.90). This relationship held when including all cardiac events. No relationship was observed between depression and recurrent cardiac events. CONCLUSION: The results of this study support the contention that depression is an independent risk factor for CHD incidence in women. Moreover, the strength of association between depression and CHD incidence was of a greater magnitude than any typical and atypical risk factor.

Tripartite motif-containing 55 identified as functional candidate for spontaneous cardiac hypertrophy in the rat locus cardiac mass 22.

BACKGROUND: Left ventricular (LV) hypertrophy is a risk factor for cardiovascular death, but the genetic factors determining LV size and predisposition to hypertrophy are not well understood. We have previously linked the quantitative trait locus cardiac mass 22 (Cm22) on chromosome 2 with cardiac hypertrophy independent of blood pressure in the spontaneously hypertensive rat. From an original cross of spontaneously hypertensive rat with F344 rats, we derived a normotensive polygenic model of spontaneous cardiac hypertrophy, the hypertrophic heart rat (HHR) and its control strain, the normal heart rat (NHR). METHODS AND RESULTS: To identify the genes and molecular mechanisms underlying spontaneous LV hypertrophy we sequenced the HHR genome with special focus on quantitative trait locus Cm22. For correlative analyses of function, we measured global RNA transcripts in LV of neonatal HHR and NHR and 198 neonatal rats of an HHR × NHR F2 crossbred population. Only one gene within locus Cm22 was differentially expressed in the parental generation: tripartite motif-containing 55 (Trim55), with mRNA downregulation in HHR (P < 0.05) and reduced protein expression. Trim55 mRNA levels were negatively correlated with LV mass in the F2 cross (r = -0.16, P = 0.025). In exon nine of Trim55 in HHR, we found one missense mutation that functionally alters protein structure. This mutation was strongly associated with Trim55 mRNA expression in F2 rats (F = 10.35, P < 0.0001). Similarly, in humans, we found reduced Trim55 expression in hearts of subjects with idiopathic dilated cardiomyopathy. CONCLUSION: Our study suggests that the Trim55 gene, located in Cm22, is a novel candidate gene for polygenic LV hypertrophy independent of blood pressure.

The addition of depression to the Framingham Risk Equation model for predicting coronary heart disease risk in women.

BACKGROUND: Depression is widely considered to be an independent and robust predictor of Coronary Heart Disease (CHD), however is seldom considered in the context of formal risk assessment. We assessed whether the addition of depression to the Framingham Risk Equation (FRE) improved accuracy for predicting 10-year CHD in a sample of women. DESIGN: A prospective, longitudinal design comprising an age-stratified, population-based sample of Australian women collected between 1993 and 2011 (n=862). METHODS: Clinical depressive disorder was assessed using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders (SCID-I/NP), using retrospective age-of-onset data. A composite measure of CHD included non-fatal myocardial infarction, unstable angina coronary intervention or cardiac death. Cox proportional-hazards regression models were conducted and overall accuracy assessed using area under receiver operating characteristic (ROC) curve analysis. RESULTS: ROC curve analyses revealed that the addition of baseline depression status to the FRE model improved its overall accuracy (AUC:0.77, Specificity:0.70, Sensitivity:0.75) when compared to the original FRE model (AUC:0.75, Specificity:0.73, Sensitivity:0.67). However, when calibrated against the original model, the predicted number of events generated by the augmented version marginally over-estimated the true number observed. CONCLUSIONS: The addition of a depression variable to the FRE equation improves the overall accuracy of the model for predicting 10-year CHD events in women, however may over-estimate the number of events that actually occur. This model now requires validation in larger samples as it could form a new CHD risk equation for women.

Telomere dynamics during aging in polygenic left ventricular hypertrophy.

Short telomeres are associated with increased risk of cardiovascular disease. Here we studied cardiomyocyte telomere length at key ages during the ontogeny of cardiac hypertrophy and failure in the hypertrophic heart rat (HHR) and compared these with the normal heart rat (NHR) control strain. Key ages corresponded with the pathophysiological sequence beginning with fewer cardiomyocytes (2 days), leading to left ventricular hypertrophy (LVH) (13 wk) and subsequently progression to heart failure (38 wk). We measured telomere length, tissue activity of telomerase, mRNA levels of telomerase reverse transcriptase (Tert) and telomerase RNA component (Terc), and expression of the telomeric regulator microRNA miR-34a. Cardiac telomere length was longer in the HHR compared with the control strain at 2 days and 38 wk, but shorter at 13 wk. Neonatal HHR had higher cardiac telomerase activity and expression of Tert and miR-34a. Telomerase activity was not different at 13 or 38 wk. Tert mRNA and Terc RNA were overexpressed at 38 wk, while miR-34a was overexpressed at 13 wk but downregulated at 38 wk. Circulating leukocytes were strongly correlated with cardiac telomere length in the HHR only. The longer neonatal telomeres in HHR are likely to reflect fewer fetal and early postnatal cardiomyocyte cell divisions and explain the reduced total cardiomyocyte complement that predisposes to later hypertrophy and failure. Although shorter telomeres were a feature of cardiac hypertrophy at 13 wk, they were not present at the progression to heart failure at 38 wk.

Forms of n-3 (ALA, C18:3n-3 or DHA, C22:6n-3) Fatty Acids Affect Carcass Yield, Blood Lipids, Muscle n-3 Fatty Acids and Liver Gene Expression in Lambs.

The effects of supplementing diets with n-3 alpha-linolenic acid (ALA) and docosahexaenoic acid (DHA) on plasma metabolites, carcass yield, muscle n-3 fatty acids and liver messenger RNA (mRNA) in lambs were investigated. Lambs (n = 120) were stratified to 12 groups based on body weight (35 ± 3.1 kg), and within groups randomly allocated to four dietary treatments: basal diet (BAS), BAS with 10.7 % flaxseed supplement (Flax), BAS with 1.8 % algae supplement (DHA), BAS with Flax and DHA (FlaxDHA). Lambs were fed for 56 days. Blood samples were collected on day 0 and day 56, and plasma analysed for insulin and lipids. Lambs were slaughtered, and carcass traits measured. At 30 min and 24 h, liver and muscle samples, respectively, were collected for determination of mRNA (FADS1, FADS2, CPT1A, ACOX1) and fatty acid composition. Lambs fed Flax had higher plasma triacylglycerol, body weight, body fat and carcass yield compared with the BAS group (P < 0.001). DHA supplementation increased carcass yield and muscle DHA while lowering plasma insulin compared with the BAS diet (P < 0.01). Flax treatment increased (P < 0.001) muscle ALA concentration, while DHA treatment increased (P < 0.001) muscle DHA concentration. Liver mRNA FADS2 was higher and CPT1A lower in the DHA group (P < 0.05). The FlaxDHA diet had additive effects, including higher FADS1 and ACOX1 mRNA than for the Flax or DHA diet. In summary, supplementation with ALA or DHA modulated plasma metabolites, muscle DHA, body fat and liver gene expression differently.

Cholinesterase Research Outreach Project (CROP): measuring cholinesterase activity and pesticide use in an agricultural community.

BACKGROUND: Australian farmers and their workers are exposed to a wide variety of pesticides. Organophosphate (OP) insecticides are a widely used class of pesticide used for animal husbandry practices (Naphthalophos for sheep dipping, jetting and drench), crop production for pest control (Dimethoate) and in public health (Maldison for head lice). Acute poisonings with this class of insecticide are reported among agricultural workers and children around the globe, due to the inhibition of acetylcholinesterase (AChE). Less is known about chronic exposures. Regular monitoring of erythrocyte AChE will enable farmers to identify potential exposure to organophosphate insecticides and take action to reduce exposures and improve their health and safety practices. This study aims to assess and improve the integration of AChE monitoring into routine point of care health clinics, and provide farming and non-farming people with a link between their AChE activity and their household chemical and agrichemical use. METHODS/DESIGN: The research will target individuals who work on mixed farming enterprises and routinely using OPs (n = 50) and non-farmers (n = 30). Baseline data are collected regarding demographic, health conditions and behaviours, Kessler 10 (K10) scores, chemical use and personal protection. Baseline anthropometric measures include height, weight, hip and waist circumference, body fat analysis and, biochemical analysis of fasted total serum cholesterol, triglycerides, low-density cholesterol (LDL), high-density cholesterol (HDL) and blood glucose. Analysis of erythrocyte cholinesterase (EAChE) activity is also conducted using a finger prick test. Testing of EAChE is then repeated in all participants every 3 weeks for a maximum of three times over a period 10 weeks. Participants are provided with full feedback and counselling about their EAChE activity after each reading and a detailed summary provided to all participants at the completion of the study. Data will be analysed using repeated measures within a general linear model. DISCUSSION: This work will provide an evidence base and recommendations for the integration of EAChE monitoring into Australian rural health clinics, leading to research which will further quantify pesticide exposure both on the farm and in the home, highlighting the importance of sustaining and providing a safe work and home environment for farming communities. TRIAL REGISTRATION: ACTRN12613001256763.

What Is the Most Effective Way of Increasing the Bioavailability of Dietary Long Chain Omega-3 Fatty Acids--Daily vs. Weekly Administration of Fish Oil?

The recommendations on the intake of long chain omega-3 polyunsaturated fatty acids (n-3 LC-PUFA) vary from eating oily fish ("once to twice per week") to consuming specified daily amounts of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) ("250-500 mg per day"). It is not known if there is a difference in the uptake/bioavailability between regular daily consumption of supplementsvs. consuming fish once or twice per week. In this study, the bioavailability of a daily dose of n-3 LC-PUFA (Constant treatment), representing supplements, vs. a large weekly dose of n-3 LC-PUFA (Spike treatment), representing consuming once or twice per week, was assessed. Six-week old healthy male Sprague-Dawley rats were fed either a Constant treatment, a Spike treatment or Control treatment (no n-3 LC-PUFA), for six weeks. The whole body, tissues and faeces were analysed for fatty acid content. The results showed that the major metabolic fate of the n-3 LC-PUFA (EPA+docosapentaenoic acid (DPA) + DHA) was towards catabolism (ß-oxidation) accounting for over 70% of total dietary intake, whereas deposition accounted less than 25% of total dietary intake. It was found that significantly more n-3 LC-PUFA were ß-oxidised when originating from the Constant treatment (84% of dose), compared with the Spike treatment (75% of dose). Conversely, it was found that significantly more n-3 LC-PUFA were deposited when originating from the Spike treatment (23% of dose), than from the Constant treatment (15% of dose). These unexpected findings show that a large dose of n-3 LC-PUFA once per week is more effective in increasing whole body n-3 LC-PUFA content in rats compared with a smaller dose delivered daily.

Postexercise muscle cooling enhances gene expression of PGC-1α.

PURPOSE: This study aimed to investigate the influence of localized muscle cooling on postexercise vascular, metabolic, and mitochondrial-related gene expression. METHODS: Nine physically active males performed 30 min of continuous running at 70% of their maximal aerobic velocity, followed by intermittent running to exhaustion at 100% maximal aerobic velocity. After exercise, subjects immersed one leg in a cold water bath (10°C, COLD) to the level of their gluteal fold for 15 min. The contralateral leg remained outside the water bath and served as control (CON). Core body temperature was monitored throughout the experiment, whereas muscle biopsies and muscle temperature (Tm) measurements were obtained from the vastus lateralis before exercise (PRE), immediately postexercise (POST-EX, Tm only), immediately after cooling, and 3 h postexercise (POST-3H). RESULTS: Exercise significantly increased core body temperature (PRE, 37.1°C ± 0.4°C vs POST-EX, 39.3°C ± 0.5°C, P < 0.001) and Tm in both CON (PRE, 33.9°C ± 0.7°C vs POST-EX, 39.1°C ± 0.5°C) and COLD legs (PRE, 34.2°C ± 0.9°C vs POST-EX, 39.4°C ± 0.3°C), respectively (P < 0.001). After cooling, Tm was significantly lower in COLD (28.9°C ± 2.3°C vs 37.0°C ± 0.8°C, P < 0.001) whereas PGC-1α messenger RNA expression was significantly higher in COLD at POST-3H (P = 0.014). Significant time effects were evident for changes in vascular endothelial growth factor (P = 0.038) and neuronal nitric oxide synthase (P = 0.019) expression. However, no significant condition effects between COLD and CON were evident for changes in both vascular endothelial growth factor and neuronal nitric oxide synthase expressions. CONCLUSIONS: These data indicate that an acute postexercise cooling intervention enhances the gene expression of PGC-1α and may therefore provide a valuable strategy to enhance exercise-induced mitochondrial biogenesis.

Elevated hydrogen peroxide and decreased catalase and glutathione peroxidase protection are associated with aging sarcopenia.

BACKGROUND: Sarcopenia is the progressive loss of skeletal muscle that contributes to the decline in physical function during aging. A higher level of oxidative stress has been implicated in aging sarcopenia. The current study aims to determine if the higher level of oxidative stress is a result of increased superoxide (O2‾) production by the NADPH oxidase (NOX) enzyme or decrease in endogenous antioxidant enzyme protection. METHODS: Female Balb/c mice were assigned to 4 age groups; 6, 12, 18 and 24 months. Body weight and animal survival rates were recorded over the course of the study. Skeletal muscle tissues were collected and used to measure NOX subunit mRNA, O2‾ levels and antioxidant enzymes. RESULTS: Key subunit components of NOX expression were elevated in skeletal muscle at 18 months, when sarcopenia was first evident. Increased superoxide dismutase 1 (SOD1) activity suggests an increase in O2‾ dismutation and this was further supported by elevated levels of hydrogen peroxide (H2O2) and decline in catalase and glutathione peroxidase (GPx) antioxidant protection in skeletal muscle at this time. NOX expression was also higher in skeletal muscle at 24 months, however this was coupled with elevated levels of O2‾ and a decline in SOD1 activity, compared to 6 and 12 months but was not associated with further loss of muscle mass. CONCLUSIONS: While the source of ROS in sarcopenic muscle remains unknown, this study provides evidence that the NOX enzyme could be involved in ROS production by regulating superoxide in ageing muscles. This study also suggests that H2O2 is the key ROS in the onset of sarcopenia and that the decline in antioxidant protection by catalase and GPx is indicative of antioxidant dysfunction and may therefore be a major contributing factor in the development or onset of sarcopenia. Furthermore, the changes in ROS and antioxidant activity after sarcopenia was first evident gives some evidence for a compensatory mechanism, in response to insult, in order to maintain muscle integrity.

The effect of physical activity on psychological distress, cortisol and obesity: results of the Farming Fit intervention program.

BACKGROUND: Rural and regional Australians have a higher likelihood of mental illness throughout their lifetime than people living in major cities, although the underlying reasons are not yet well defined. Additionally, rural populations experience more lifestyle associated co-morbidities including obesity, diabetes and cardiovascular disease. Research conducted by the National Centre for Farmer Health between 2004 and 2009 revealed a positive correlation between obesity and psychological distress among the farming community. Chronic stress is known to overstimulate the regulation of the hypothalamic-pituitary-adrenal (HPA) axis and cortisol secretion which are associated with abdominal adiposity. Increasing physical activity may normalise cortisol secretion and thereby positively impact both physical and mental health. This paper assesses the effects of increasing physical activity on obesity, health behaviors and mental health in Victorian farming men and women. METHODS: Farming Fit was a six month quasi-experimental (convenience sample) longitudinal design control-intervention study. Overweight or obese (BMI ≥25 kg/m2) farm men (n = 43) and women (n = 29) were recruited with demographic, health behaviors, anthropometric, blood pressure and biochemistry data collected at baseline and at a six months. Salivary cortisol and depression anxiety stress scale results were collected at baseline, three and six months. The intervention group (n = 37) received a personalized exercise program and regular phone coaching to promote physical activity. RESULTS: The intervention group showed significant reductions in body weight and waist circumference. Results indicated that following the six month exercise program, the intervention group were 2.64 ± 0.65 kg lighter (p < 0.001), had reduced waist circumference by 2.01 ± 0.86 cm (p = 0.02) and BMI by 0.97 ± 0.22 kg/m2 (p < 0.001) relative to the control group. CONCLUSION: Increasing physical activity altered measures of obesity in farm men and women but did not affect mental health measures or cortisol secretion levels. TRIAL REGISTRATION: ACTRN12610000827033.