IMPACT OF FUNCTIONAL FOODS ON GUT HEALTH OF POST-WEANING PIGLETS

Post-weaning is the most crucial period in pig management. Associated with weaning are marked changes to the histology and biochemistry of the gut which cause decreased digestive and absorptive capacity and contribute to post-weaning diarrhoea. In last years, the interest in developing management and feeding strategies to stimulate gut development and health in newly-weaned pigs was increasing. In order to increase general health in post-weaning piglets and be alternative to in-feeding antibiotic, three trials were created in this thesis to determine the utilizations of some functional foods which have been widely used to improve growth performance while minimizing the use of antibiotics and rather expensive feed ingredients in weaned piglets. We utilized essential oils (Thymol and Cinnamaldehyde, EO) and/or enzymes (Xylanase and \u3b2-glucanase, XB) in the first 2 trials. The first trial mainly focused on the effects of those additives on general parameters such as performance and digestibility of weaned piglets. To investigate the possible protective effects of EO and/or XB on health status in weaned piglets, we created a model of challenge using Escherichia coli in the second trial. After first two investigations, we intended to enlarge the categories of functional foods and determine the effects on regulation of systemic inflammatory reaction and, in addition, we supposed that initial body weight might also influence the regulation. Therefore, the third trial was desined to determine the effects of dietary cocktail (bovine colostrums, cranberry extract, encapsulated essential oil, yeast-derived products, the probiotic Pediococcus acidilactici MA18/5M, vitamins A, D, E and B complex, seleno-methionine) and body weight on inflammatory cytokines and time responses under Lipopolysaccharides challenge in early weaned piglets. In the first trial, a total of 192 weaned piglets (Stambo HBI Dalland 40, 24 d) with an average initial body weight of 8.10 kg were allocated according to body weight into 4 experimental treatments (12 replicates per treatment with 4 piglets per replicate). Each group was fed the basal diet alone or supplemented with either essential oils or enzymes, or their combination. There was no effect of essential oils and/or enzymes supplementation on the growth performance of piglets. However, the combination of essential oils and enzymes decreased feed conversion ratio during the last week. Although the fecal digestibilities of all the piglets were increased from d 21 to 35 (P < 0.001), no effect of essential oils or enzymes or the combination on the fecal digestibility was observed. All the additives significantly decreased counts of Coliforms at 42 days of the trial (P < 0.001). Dietary enzymes improved gut morphology by decreasing crypt depth, increasing villus:crypt ratio and reducing the number of macrophages (P < 0.001). Supplementation of essential oils and the combination with enzymes also improved gut morphology by decreasing crypt depth (P = 0.065; P < 0.001), and decreasing the number of lymphatic follicles (P = 0.002; P < 0.001) and macrophages (P < 0.001). No effect of additives on mRNA expression of inflammatory cytokines was observed in ileal mucosa. Results showed that diet supplementation with EO and/or XB had positive effects on intestinal bacterial counts and gut morphology, although there was no significant diet effect on grow performance or digestibility. In the second trial, 192 weaned piglets (Stambo HBI Dalland 40, 8.64 kg) were allocated according to body weight into eight experimental treatments (6 replicates per treatment with 4 piglets per replicate). The treatments were in a factorial arrangement: 1) dietary treatments [a weaned piglet control diet (CTR), CTR + 0.05 g/kg essential oils (EO), CTR + 0.1 g/kg enzymes (XB), and CTR + 0.05 g/kg EO + 0.1 g/kg XB] and 2) with or without an E. coli challenge. On d 8, half of piglets in each dietary group were challenged with E. coli. E. coli challenge significantly impaired growth performance, induced severe diarrhea, increased populations of E. coli, Clostridia and Coliforms, depressed antioxidant activities, damaged gut morphology and promoted TLR-4 and TNF-\u3b1 mRNA expression in ileal mucosa (P < 0.05). In the E. coli challenge group, dietary enzymes or combinated with essential oils improved feed efficiency compared with control treatment during the last week (P = 0.025; P = 0.020). The Coliforms populations in the cecum of challenged piglets fed combination of essential oils and enzymes were lower than control treatment (P < 0.001). In the E. coli challenge group, supplemented essential oils and/or enzymes improved gut morphology by increasing villus height and villus:crypt ratio and decreasing crypt depth (P < 0.001). The positive effects on intestinal bacterial counts and gut morphology suggests that supplementation of EO and/or XB might improve the protective capacity against pathogenic bacteria when piglets were submitted to a bacterial challenge. In the third study, a total of 256 Yorkshire 7 Landrace weaned piglets (20 \ub1 1 d) were allocated into eight experimental treatments (8 replicates per treatment with 4 piglets per replicate). The treatments were in a factorial arrangement: 1) dietary treatments: a basal weaning diet added [spray-dried plasma protein (PP) (CTR), PP + antibiotic (ATB), PP + dietary cocktail (DC), or bovine colostrum + the dietary cocktail (BC+DC)] and 2) low weight (LW) or high weight (HW). At 37 d of age, 2 piglets in each pen were injected with LPS. Stimulations of LPS and PMA in PBMCs of piglets significantly induced TNF-\u3b1, IL-8 and IL-10 (P 0.05). Piglets had low weight tended to increase the concentration of IL-8 (P = 0.106) and IL-10 (P = 0.098) in the PBMCs stimulated by LPS 0.5\ub5g/ml LPS and the concentration of IL-10 (P = 0.097) in PMA stimulated PMBC compared with high weight animals. Infection with LPS increased (P 0.05). At 4 h after challenge, low weight piglets had partially greater serum concentrations of TNF-\u3b1 (P = 0.046), IL-6 (P = 0.158), IL-8 (P = 0.179) and IL-10 (P = 0.185) than high weight animals. Dietary cocktail or combined with bovine colostrum may replace plasma protein and antibiotics and weight difference may influence the production of inflammatory cytokines after infected by LPS. In conclusion, we observed that supplementation of functional foods as essential oils and enzymes might strengthen protective capacity of weaned piglets against pathogenic bacteria by decreasing negative intestinal bacterial counts and improving gut morphology. Dietary cocktail or combined with bovine colostrums, at the amount used in this work, may replace plasma protein and antibiotics. Besides, weight difference may influence the production of inflammatory cytokines after infected by LPS

Administration of a novel plant extract product via drinking water to post-weaning piglets : effects on performance and gut health

The present study evaluated the effects of a novel plant extract (PE) product (GrazixTM) on the performance and gut health of weaned piglets challenged with Escherichia coli. The PE was a standardised mixture of green tea leaves (Camellia sinensis) and pomegranate fruit (Punica granatum) obtained by using the LiveXtractTM process. A total of 144 piglets were weaned at 24 days and allocated to 8 for a 35-day experiment with a 2 7 2 7 2 factorial design comparing different treatments (water without product (CT) or 8 \u3bcl/kg per day PE in drinking water (PE)), feeding regimens (ad libitum (AD) or restricted (RE)) and oral E. coli challenges on day 9 (sham ( 12 ) or infected ( +)). There were six pens per group with three piglets per pen. On day 35, 24 of the RE feeding piglets were slaughtered. It was found that PE supplementation increased the average daily gain (ADG) from day 28 to day 35 ( P =0.03) and increased the gain to feed ratio (G : F) from day 7 to day 14 ( P = 0.02). RE feeding led to lower feed intake in piglets during the 1st week ( P<0.01), 2nd week ( P = 0.06), 3rd week ( P = 0.05), and throughout the course of the overall study period ( P = 0.05). E. coli challenge decreased the ADG and G : F ratio from day 7 to day 14 ( P = 0.08 and <0.01, respectively) and increased the faecal score (higher values indicate more severe diarrhoea) on days 14, 21, 28 and 35 ( P<0.01). PE supplementation decreased the faecal score in the challenged piglets during the 1st week post-challenge ( P<0.01). E. coli challenge increased the faecal E. coli level on day 14 ( P = 0.03) and increased the Enterobacteriaceae level on day 35 ( P<0.01). Reduced faecal E. coli was observed on days 14 and 35 ( P = 0.05 and 0.02, respectively), and reduced Enterobacteriaceae ( P<0.01) was found on day 35 in the PE animals. RE feeding increased the faecal Lactobacillus, Enterobacteriaceae and E. coli levels on day 35 ( P = 0.02, <0.01 and <0.01, respectively). These results suggest that PE supplementation may improve the gut health status of post-weaning piglets and counteract some of the negative effects that occur when piglets are challenged with E. coli

Filtering and Tracking with Trinion-Valued Adaptive Algorithms

A new model for three-dimensional processes based on the trinion algebra is introduced for the first time. Compared with the pure quaternion model, the trinion model is more compact and computationally more efficient, while having similar or comparable performance in terms of adaptive linear filtering. Moreover, the trinion model can effectively represent the general relationship of state evolution in Kalman filtering, where the pure quaternion model fails. Simulations on real-world wind recordings and synthetic data sets are provided to demonstrate the potentials of this new modeling method

Partial Wave Analysis of J/ψ→γ(K+K−π+π−)J/\psi \to \gamma (K^+K^-\pi^+\pi^-)

BES data on $J/\psi \to \gamma (K^+K^-\pi^+\pi^-)$ are presented. The $K^*\bar K^*$ contribution peaks strongly near threshold. It is fitted with a broad $0^{-+}$ resonance with mass $M = 1800 \pm 100$ MeV, width $\Gamma = 500 \pm 200$ MeV. A broad $2^{++}$ resonance peaking at 2020 MeV is also required with width $\sim 500$ MeV. There is further evidence for a $2^{-+}$ component peaking at 2.55 GeV. The non-$K^*\bar K^*$ contribution is close to phase space; it peaks at 2.6 GeV and is very different from $K^{*}\bar{K^{*}}$.Comment: 15 pages, 6 figures, 1 table, Submitted to PL

Investigation on viscosity and non-isothermal crystallization behavior of P-bearing steelmaking slags with varying TiO2 content

The viscous flow and crystallization behavior of CaO-SiO2-MgO-Al2O3-FetO-P2O5-TiO2 steelmaking slags have been investigated over a wide range of temperatures under Ar (High purity, >99.999 pct) atmosphere, and the relationship between viscosity and structure was determined. The results indicated that the viscosity of the slags slightly decreased with increasing TiO2 content. The constructed nonisothermal continuous cooling transformation (CCT) diagrams revealed that the addition of TiO2 lowered the crystallization temperature. This can mainly be ascribed to that addition of TiO2 promotes the formation of [TiO6]-octahedra units and, consequently, the formation of MgFe2O4-Mg2TiO4 solid solution. Moreover, the decreasing viscosity has a significant effect on enhancing the diffusion of ion units, such as Ca2+ and [TiO4]-tetrahedra, from bulk melts to the crystal–melt interface. The crystallization of CaTiO3 and CaSiTiO5 was consequently accelerated, which can improve the phosphorus content in P-enriched phase (n2CaO·SiO2-3CaO·P2O5). Finally, the nonisothermal crystallization kinetics was characterized and the activation energy for the primary crystal growth was derived such that the activation energy increases from −265.93 to −185.41 KJ·mol−1 with the addition of TiO2 content, suggesting that TiO2 lowered the tendency for the slags to crystallize

ELM mitigation by supersonic molecular beam injection: KSTAR and HL-2A experiments and theory

We report recent experimental results from HL-2A and KSTAR on ELM mitigation by supersonic molecular beam injection (SMBI). Cold particle deposition within the pedestal by SMBI is verified in both machines. The signatures of ELM mitigation by SMBI are an ELM frequency increase and ELM amplitude decrease. These persist for an SMBI influence time τI. Here, τI is the time for the SMBI influenced pedestal profile to refill. An increase in fELMSMBI/fELM0 and a decrease in the energy loss per ELM ΔWELM were achieved in both machines. Physical insight was gleaned from studies of density and vΦ (toroidal rotation velocity) evolution, particle flux and turbulence spectra, divertor heat load. The characteristic gradients of the pedestal density soften and a change in vΦ was observed during a τI time. The spectra of the edge particle flux Γ ∼ 〈ṽrñe〉 and density fluctuation with and without SMBI were measured in HL-2A and in KSTAR, respectively. A clear phenomenon observed is the decrease in divertor heat load during the τI time in HL-2A. Similar results are the profiles of saturation current density Jsat with and without SMBI in KSTAR. We note that τI/τp (particle confinement time) is close to ∼1, although there is a large difference in individual τI between the two machines. This suggests that τI is strongly related to particle-transport events. Experiments and analysis of a simple phenomenological model support the important conclusion that ELM mitigation by SMBI results from an increase in higher frequency fluctuations and transport events in the pedestal. © 2014 IAEA, Vienna

Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980�2015: a systematic analysis for the Global Burden of Disease Study 2015

Background Improving survival and extending the longevity of life for all populations requires timely, robust evidence on local mortality levels and trends. The Global Burden of Disease 2015 Study (GBD 2015) provides a comprehensive assessment of all-cause and cause-specific mortality for 249 causes in 195 countries and territories from 1980 to 2015. These results informed an in-depth investigation of observed and expected mortality patterns based on sociodemographic measures. Methods We estimated all-cause mortality by age, sex, geography, and year using an improved analytical approach originally developed for GBD 2013 and GBD 2010. Improvements included refinements to the estimation of child and adult mortality and corresponding uncertainty, parameter selection for under-5 mortality synthesis by spatiotemporal Gaussian process regression, and sibling history data processing. We also expanded the database of vital registration, survey, and census data to 14�294 geography�year datapoints. For GBD 2015, eight causes, including Ebola virus disease, were added to the previous GBD cause list for mortality. We used six modelling approaches to assess cause-specific mortality, with the Cause of Death Ensemble Model (CODEm) generating estimates for most causes. We used a series of novel analyses to systematically quantify the drivers of trends in mortality across geographies. First, we assessed observed and expected levels and trends of cause-specific mortality as they relate to the Socio-demographic Index (SDI), a summary indicator derived from measures of income per capita, educational attainment, and fertility. Second, we examined factors affecting total mortality patterns through a series of counterfactual scenarios, testing the magnitude by which population growth, population age structures, and epidemiological changes contributed to shifts in mortality. Finally, we attributed changes in life expectancy to changes in cause of death. We documented each step of the GBD 2015 estimation processes, as well as data sources, in accordance with Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER). Findings Globally, life expectancy from birth increased from 61·7 years (95 uncertainty interval 61·4�61·9) in 1980 to 71·8 years (71·5�72·2) in 2015. Several countries in sub-Saharan Africa had very large gains in life expectancy from 2005 to 2015, rebounding from an era of exceedingly high loss of life due to HIV/AIDS. At the same time, many geographies saw life expectancy stagnate or decline, particularly for men and in countries with rising mortality from war or interpersonal violence. From 2005 to 2015, male life expectancy in Syria dropped by 11·3 years (3·7�17·4), to 62·6 years (56·5�70·2). Total deaths increased by 4·1 (2·6�5·6) from 2005 to 2015, rising to 55·8 million (54·9 million to 56·6 million) in 2015, but age-standardised death rates fell by 17·0 (15·8�18·1) during this time, underscoring changes in population growth and shifts in global age structures. The result was similar for non-communicable diseases (NCDs), with total deaths from these causes increasing by 14·1 (12·6�16·0) to 39·8 million (39·2 million to 40·5 million) in 2015, whereas age-standardised rates decreased by 13·1 (11·9�14·3). Globally, this mortality pattern emerged for several NCDs, including several types of cancer, ischaemic heart disease, cirrhosis, and Alzheimer's disease and other dementias. By contrast, both total deaths and age-standardised death rates due to communicable, maternal, neonatal, and nutritional conditions significantly declined from 2005 to 2015, gains largely attributable to decreases in mortality rates due to HIV/AIDS (42·1, 39·1�44·6), malaria (43·1, 34·7�51·8), neonatal preterm birth complications (29·8, 24·8�34·9), and maternal disorders (29·1, 19·3�37·1). Progress was slower for several causes, such as lower respiratory infections and nutritional deficiencies, whereas deaths increased for others, including dengue and drug use disorders. Age-standardised death rates due to injuries significantly declined from 2005 to 2015, yet interpersonal violence and war claimed increasingly more lives in some regions, particularly in the Middle East. In 2015, rotaviral enteritis (rotavirus) was the leading cause of under-5 deaths due to diarrhoea (146�000 deaths, 118�000�183�000) and pneumococcal pneumonia was the leading cause of under-5 deaths due to lower respiratory infections (393�000 deaths, 228�000�532�000), although pathogen-specific mortality varied by region. Globally, the effects of population growth, ageing, and changes in age-standardised death rates substantially differed by cause. Our analyses on the expected associations between cause-specific mortality and SDI show the regular shifts in cause of death composition and population age structure with rising SDI. Country patterns of premature mortality (measured as years of life lost YLLs) and how they differ from the level expected on the basis of SDI alone revealed distinct but highly heterogeneous patterns by region and country or territory. Ischaemic heart disease, stroke, and diabetes were among the leading causes of YLLs in most regions, but in many cases, intraregional results sharply diverged for ratios of observed and expected YLLs based on SDI. Communicable, maternal, neonatal, and nutritional diseases caused the most YLLs throughout sub-Saharan Africa, with observed YLLs far exceeding expected YLLs for countries in which malaria or HIV/AIDS remained the leading causes of early death. Interpretation At the global scale, age-specific mortality has steadily improved over the past 35 years; this pattern of general progress continued in the past decade. Progress has been faster in most countries than expected on the basis of development measured by the SDI. Against this background of progress, some countries have seen falls in life expectancy, and age-standardised death rates for some causes are increasing. Despite progress in reducing age-standardised death rates, population growth and ageing mean that the number of deaths from most non-communicable causes are increasing in most countries, putting increased demands on health systems. Funding Bill & Melinda Gates Foundation. © 2016 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY licens

Global, regional, national, and selected subnational levels of stillbirths, neonatal, infant, and under-5 mortality, 1980�2015: a systematic analysis for the Global Burden of Disease Study 2015

Background Established in 2000, Millennium Development Goal 4 (MDG4) catalysed extraordinary political, financial, and social commitments to reduce under-5 mortality by two-thirds between 1990 and 2015. At the country level, the pace of progress in improving child survival has varied markedly, highlighting a crucial need to further examine potential drivers of accelerated or slowed decreases in child mortality. The Global Burden of Disease 2015 Study (GBD 2015) provides an analytical framework to comprehensively assess these trends for under-5 mortality, age-specific and cause-specific mortality among children under 5 years, and stillbirths by geography over time. Methods Drawing from analytical approaches developed and refined in previous iterations of the GBD study, we generated updated estimates of child mortality by age group (neonatal, post-neonatal, ages 1�4 years, and under 5) for 195 countries and territories and selected subnational geographies, from 1980�2015. We also estimated numbers and rates of stillbirths for these geographies and years. Gaussian process regression with data source adjustments for sampling and non-sampling bias was applied to synthesise input data for under-5 mortality for each geography. Age-specific mortality estimates were generated through a two-stage age�sex splitting process, and stillbirth estimates were produced with a mixed-effects model, which accounted for variable stillbirth definitions and data source-specific biases. For GBD 2015, we did a series of novel analyses to systematically quantify the drivers of trends in child mortality across geographies. First, we assessed observed and expected levels and annualised rates of decrease for under-5 mortality and stillbirths as they related to the Soci-demographic Index (SDI). Second, we examined the ratio of recorded and expected levels of child mortality, on the basis of SDI, across geographies, as well as differences in recorded and expected annualised rates of change for under-5 mortality. Third, we analysed levels and cause compositions of under-5 mortality, across time and geographies, as they related to rising SDI. Finally, we decomposed the changes in under-5 mortality to changes in SDI at the global level, as well as changes in leading causes of under-5 deaths for countries and territories. We documented each step of the GBD 2015 child mortality estimation process, as well as data sources, in accordance with the Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER). Findings Globally, 5·8 million (95 uncertainty interval UI 5·7�6·0) children younger than 5 years died in 2015, representing a 52·0% (95% UI 50·7�53·3) decrease in the number of under-5 deaths since 1990. Neonatal deaths and stillbirths fell at a slower pace since 1990, decreasing by 42·4% (41·3�43·6) to 2·6 million (2·6�2·7) neonatal deaths and 47·0% (35·1�57·0) to 2·1 million (1·8-2·5) stillbirths in 2015. Between 1990 and 2015, global under-5 mortality decreased at an annualised rate of decrease of 3·0% (2·6�3·3), falling short of the 4·4% annualised rate of decrease required to achieve MDG4. During this time, 58 countries met or exceeded the pace of progress required to meet MDG4. Between 2000, the year MDG4 was formally enacted, and 2015, 28 additional countries that did not achieve the 4·4% rate of decrease from 1990 met the MDG4 pace of decrease. However, absolute levels of under-5 mortality remained high in many countries, with 11 countries still recording rates exceeding 100 per 1000 livebirths in 2015. Marked decreases in under-5 deaths due to a number of communicable diseases, including lower respiratory infections, diarrhoeal diseases, measles, and malaria, accounted for much of the progress in lowering overall under-5 mortality in low-income countries. Compared with gains achieved for infectious diseases and nutritional deficiencies, the persisting toll of neonatal conditions and congenital anomalies on child survival became evident, especially in low-income and low-middle-income countries. We found sizeable heterogeneities in comparing observed and expected rates of under-5 mortality, as well as differences in observed and expected rates of change for under-5 mortality. At the global level, we recorded a divergence in observed and expected levels of under-5 mortality starting in 2000, with the observed trend falling much faster than what was expected based on SDI through 2015. Between 2000 and 2015, the world recorded 10·3 million fewer under-5 deaths than expected on the basis of improving SDI alone. Interpretation Gains in child survival have been large, widespread, and in many places in the world, faster than what was anticipated based on improving levels of development. Yet some countries, particularly in sub-Saharan Africa, still had high rates of under-5 mortality in 2015. Unless these countries are able to accelerate reductions in child deaths at an extraordinary pace, their achievement of proposed SDG targets is unlikely. Improving the evidence base on drivers that might hasten the pace of progress for child survival, ranging from cost-effective intervention packages to innovative financing mechanisms, is vital to charting the pathways for ultimately ending preventable child deaths by 2030. Funding Bill & Melinda Gates Foundation. © 2016 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY license