Consequences of timing of organic enrichment provision on pig performance, health and stress resilience after weaning and regrouping

Publication history: Accepted - 20 August 2022; Published online - 29 September 2022Most pigs in slatted systems are provided with enrichment meeting only minimum legal requirements. We aimed to explore the effects of a novel enrichment treatment consisting of daily provided fodder beet and jute bags for pigs in slatted systems, and investigate the timing of enrichment provision on performance, health and stress resilience. We used 280 weaners allocated into standard (S, meeting only legal requirements consisting of a plastic toy and softwood) or enriched (E) treatment (n = 14 groups/treatment). At regrouping during the grower to finisher transition, pigs were either kept in the same treatment (EE, SS) or switched from enriched to standard (ES) and vice versa (SE); each treatment was replicated on five groups. Pigs were weighted at the start and end of weaner, and finisher stage, and feed intake was recorded. Occurrence of scouring, respiratory problems, locomotor disorders, tail, ear, and body lesions were recorded twice a week. Ten males per treatment were sampled for saliva on days 1, 2 and 4, either postweaning or after the housing switch. Saliva samples were analysed for cortisol, alpha-amylase, haptoglobin (Hp), and adenosine deaminase. Additionally, these pigs were sampled for hair at the start and end of weaner, and end of finisher stage to analyse for hair cortisol and cortisone. We found that E weaners consumed less feed (P = 0.04), had better FCR (feed conversion ratio, P = 0.03) and less ear lesions for two weeks postweaning (P = 0.04), and tended to have lower occurrence of scouring (P = 0.07) and higher salivary cortisol concentrations (P = 0.09) than S weaners. Effects of enrichment treatment during weaner stage on performance were carried through to finisher stage, with EE and ES pigs having better FCR (P = 0.0009) and higher BW (P = 0.0001) compared to SS and SE pigs. E treatment during finisher stage decreased feed intake (P = 0.04) and tended to decrease Hp levels (P = 0.07). There was a significant interaction between enrichment treatments during weaner and finisher stages on finisher body lesions: EE finishers had less lesions than SS, ES, and SE finishers (P = 0.04). There were no other significant differences caused either by enrichment treatment during weaner/finisher stage or their interaction. We conclude that the novel enrichment applied at weaner stage had positive effects on ear lesions and performance, which were carried through to finisher stage. Body lesions were affected by its application during both stages, with finishers receiving the enrichment treatment throughout (EE) having reduced body lesions than the rest of the finishers.This research was part of the EU-China HealthyLivestock project. The authors wish to acknowledge that HealthyLivestock is funded by the European Union H2020 research and innovation programme under grant agreement number 773436. The European Commission’s support for the production of this publication does not constitute an endorsement of the contents, which reflect the views only of the authors, and the Commission cannot be held responsible for any use which may be made of the information contained therein

The frequency of transforming growth factor-TGF-B gene polymorphisms in a normal southern Iranian population

Several single nucleotide polymorphisms (SNPs) of the transforming growth factor-β1 gene (TGFB1) have been reported. Determination of TGFB1 SNPs allele frequencies in different ethnic groups is useful for both population genetic analyses and association studies with immunological diseases. In this study, five SNPs of TGFB1 were determined in 325 individuals from a normal southern Iranian population using polymerase chain reaction-restriction fragment length polymorphism method. This population was in Hardy-Weinberg equilibrium for these SNPs. Of the 12 constructed haplotypes, GTCGC and GCTGC were the most frequent in the normal southern Iranian population. Comparison of genotype and allele frequencies of TGFB SNPs between Iranian and other populations (meta-analysis) showed significant differences, and in this case the southern Iranian population seems genetically similar to Caucasoid populations. However, neighbour-joining tree using Nei's genetic distances based on TGF-β1 allele frequencies showed that southern Iranians are genetically far from people from the USA, Germany, UK, Denmark and the Czech Republic. In conclusion, this is the first report of the distribution of TGFB1 SNPs in an Iranian population and the results of this investigation may provide useful information for both population genetic and disease studies. © 2008 The Authors

Facilitators and barriers to behavior change in overweight and obesity management using the COM-B model

IntroductionIncreasing overweight and obesity rates represent one of the global public health challenges. COM-B is a theoretical model used to identify areas to target to achieve behavior change. It identifies three factors that are needed for any behavior to occur: capability, opportunity, and motivation. We aimed to assess the potential facilitators and barriers to behavior change in weight management using the COM-B.MethodsThe study included 139 people with overweight and obesity (mean age 48.81 ± 14.49 years; 64.5% female; body mass index 32.64 ± 6.51 kg/m2; waist-to-height ratio 0.62 ± 0.10) from primary care settings. All participants completed the Brief Measure of Behavior Change (COM-B), the General Self-Efficacy Scale (GSE), the Rosenberg Self-esteem Scale (RSE), and the Overall Evaluation of Health (OEH). Multiple linear regression was performed to analyse the data.ResultsThe associations between sociodemographic and clinical variables and COM-B domains attenuated or were no longer significant when psychological resources were added to the regression models. Self-efficacy was identified as a stronger facilitator of health behavior change (p < 0.001) when compared to self-esteem (p < 0.05). No associations between automatic motivation and psychological resources were identified, however. Automatic motivation was found to be associated with higher age, being in a relationship, and better health.DiscussionBehavioral interventions for weight management should specifically target different components of COM-B. Self-efficacy and self-esteem may play a significant role in individual capabilities, opportunities, and reflective motivation and should be included in tailored public health interventions. Health programs targeting younger and single people, and people with chronic conditions may help to promote sustainable behavior change

Parental Smoking Modifies the Relation between Genetic Variation in Tumor Necrosis Factor-α (TNF) and Childhood Asthma

BACKGROUND: Polymorphisms in the proinflammatory cytokine genes tumor necrosis factor-α (TNF) and lymphotoxin-α (LTA, also called TNF-β) have been associated with asthma and atopy in some studies. Parental smoking is a consistent risk factor for childhood asthma. Secondhand smoke and ozone both stimulate TNF production. OBJECTIVES: Our goal was to investigate whether genetic variation in TNF and LTA is associated with asthma and atopy and whether the association is modified by parental smoking in a Mexican population with high ozone exposure. METHODS: We genotyped six tagging single nucleotide polymorphisms (SNPs) in TNF and LTA, including functional variants, in 596 nuclear families consisting of asthmatics 4–17 years of age and their parents in Mexico City. Atopy was determined by skin prick tests. RESULTS: The A allele of the TNF-308 SNP was associated with increased risk of asthma [relative risk (RR) = 1.54; 95% confidence interval (CI), 1.04–2.28], especially among children of non-smoking parents (RR = 2.06; 95% CI, 1.19–3.55; p for interaction = 0.09). Similarly, the A allele of the TNF-238 SNP was associated with increased asthma risk among children of nonsmoking parents (RR = 2.21; 95% CI, 1.14–4.30; p for interaction = 0.01). LTA SNPs were not associated with asthma. Haplotype analyses reflected the single SNP findings in magnitude and direction. TNF and LTA SNPs were not associated with the degree of atopy. CONCLUSIONS: Our results suggest that genetic variation in TNF may contribute to childhood asthma and that associations may be modified by parental smoking

Expression analysis of asthma candidate genes during human and murine lung development

<p>Abstract</p> <p>Background</p> <p>Little is known about the role of most asthma susceptibility genes during human lung development. Genetic determinants for normal lung development are not only important early in life, but also for later lung function.</p> <p>Objective</p> <p>To investigate the role of expression patterns of well-defined asthma susceptibility genes during human and murine lung development. We hypothesized that genes influencing normal airways development would be over-represented by genes associated with asthma.</p> <p>Methods</p> <p>Asthma genes were first identified via comprehensive search of the current literature. Next, we analyzed their expression patterns in the developing human lung during the pseudoglandular (gestational age, 7-16 weeks) and canalicular (17-26 weeks) stages of development, and in the complete developing lung time series of 3 mouse strains: A/J, SW, C57BL6.</p> <p>Results</p> <p>In total, 96 genes with association to asthma in at least two human populations were identified in the literature. Overall, there was no significant over-representation of the asthma genes among genes differentially expressed during lung development, although trends were seen in the human (Odds ratio, OR 1.22, confidence interval, CI 0.90-1.62) and C57BL6 mouse (OR 1.41, CI 0.92-2.11) data. However, differential expression of some asthma genes was consistent in both developing human and murine lung, e.g. <it>NOD1, EDN1, CCL5, RORA </it>and <it>HLA-G</it>. Among the asthma genes identified in genome wide association studies, <it>ROBO1</it>, <it>RORA, HLA-DQB1, IL2RB </it>and <it>PDE10A </it>were differentially expressed during human lung development.</p> <p>Conclusions</p> <p>Our data provide insight about the role of asthma susceptibility genes during lung development and suggest common mechanisms underlying lung morphogenesis and pathogenesis of respiratory diseases.</p

Controversy surrounding the increased expression of TGFβ1 in asthma

Asthma is a waxing and waning disease that leads to structural changes in the airways, such as subepithelial fibrosis, increased mass of airway smooth muscle and epithelial metaplasia. Such a remodeling of the airways futher amplifies asthma symptoms, but its etiology is unknown. Transforming growth factor β1 is a pleiotropic cytokine involved in many fibrotic, oncologic and immunologic diseases and is believed to play an essential role in airway remodeling that occurs in asthmatic patients. Since it is secreted in an inactive form, the overall activity of this cytokine is not exclusively determined by its level of expression, but also by extensive and complex post-translational mechanisms, which are all importanin modulating the magnitude of the TGFβ1 response. Even if TGFβ1 upregulation in asthma is considered as a dogma by certain investigators in the field, the overall picture of the published litterature is not that clear and the cellular origin of this cytokine in the airways of asthmatics is still a contemporaneous debate. On the other hand, it is becoming clear that TGFβ1 signaling is increased in the lungs of asthmatics, which testifies the increased activity of this cytokine in asthma pathogenesis. The current work is an impartial and exhaustive compilation of the reported papers regarding the expression of TGFβ1 in human asthmatics. For the sake of comparison, several studies performed in animal models of the disease are also included. Inconsistencies observed in human studies are discussed and conclusions as well as trends from the current state of the litterature on the matter are proposed. Finally, the different points of regulation that can affect the amplitude of the TGFβ1 response are briefly revised and the possibility that TGFβ1 is disregulated at another level in asthma, rather than simply in its expression, is highlighted