Health benefits of supplementing nursery pig diets with microalgae or fish oil

Weaning stress can negatively impact a pig’s performance; dietary supplementation with omega-3 polyunsaturated fatty acids (n-3 PUFA) reduces inflammatory stress and promotes nursery pig’s health and growth. Fish oil (FO) is a major source of n-3 PUFA; however, microalgae (AL) may provide an alternative source of n-3 PUFA. The aim of this study was to assess the health benefits of supplementing a plant protein-based nursery diet with 3.12% AL or 1.25% FO providing equal total n-3 PUFA compared to a control (CON) diet. Seventy-two pigs were fed experimental diets for three weeks (phases 1 and 2), followed by a common standard diet for three weeks (phase 3). Following phase 2, 8 pigs per treatment underwent a lipopolysaccharide (LPS) immune stress challenge to assess the acute-phase response and 8 pigs per treatment were vaccinated with novel antigens to assess acquired immunity. No significant differences in piglets’ growth were observed, despite decreased feed intake in FO piglets compared to AL piglets in phase 3. AL supplementation tended to reduce, and FO supplementation significantly reduced the LPS-induced fever response. The AL pigs had significantly reduced cortisol responses, increased cytokine concentrations, and increased chromogranin A concentrations compared to FO and CON pigs following LPS challenge. Results suggest that AL or FO supplementation in nursery diets differentially modulate the acute-phase response, possibly due to different n-3 PUFA profiles between the two ingredients

Absence of RstA results in delayed initiation of DNA replication in Escherichia coli.

RstB/RstA is an uncharacterized Escherichia coli two-component system, the regulatory effects of which on the E. coli cell cycle remain unclear. We found that the doubling time and average number of replication origins per cell in an ΔrstB mutant were the same as the wild-type, and the average number of replication origins in an ΔrstA mutant was 18.2% lower than in wild-type cells. The doubling times were 34 min, 35 min, and 40 min for the wild-type, ΔrstB, and ΔrstA strains, respectively. Ectopic expression of RstA from plasmid pACYC-rstA partly reversed the ΔrstA mutant phenotypes. The amount of initiator protein DnaA per cell was reduced by 40% in the ΔrstA mutant compared with the wild-type, but the concentration of DnaA did not change as the total amount of cellular protein was also reduced in these cells. Deletion or overproduction of RstA does not change the temperature sensitivity of dnaA46, dnaB252 and dnaC2. The expression of hupA was decreased by 0.53-fold in ΔrstA. RstA interacted with Topoisomerase I weakly in vivo and increased its activity of relaxing the negative supercoiled plasmid. Our data suggest that deletion of RstA leads to delayed initiation of DNA replication, and RstA may affect initiation of replication by controlling expression of dnaA or hupA. Furthermore, the delayed initiation may by caused by the decreased activity of topoisomerase I in RstA mutant

Comparative efficacy of antibiotic growth promoter and benzoic acid on growth performance, nutrient utilization and indices of gut health in nursery pigs fed corn-wheat-soybean meal diet

Benzoic acid (BA) supplement was evaluated as an alternative to antimicrobial growth promoter (AGP). Ninety-six piglets (21-d-old at weaning) were placed in pens (four piglets pen−1) based on body weight (BW) and allocated (n = 8) to either control corn–soybean meal diet or control + in-feed antibiotic (AGP, 220 mg chlortetracycline hydrochloride and 31.2 mg tiamulin kg−1) or control + 0.5% BA. Feed intake and BW were measured weekly. Fecal scores for incidence of diarrhea and fecal samples for apparent total tract digestibility (ATTD) of components were taken in week 2. One pig per pen was euthanized on day 14 for jejunal histomorphology and digesta for pH and short-chain fatty acids concentration. In weeks 1–6, pigs fed AGP and BA had better (P  0.05) with control pigs. In conclusion, BA supported piglet growth performance to the same extent as AGP.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Novel protective effects of pulsed electromagnetic field ischemia/reperfusion injury rats

Synopsis Extracorporeal pulsed electromagnetic field (PEMF) has shown the ability to regenerate tissue by promoting cell proliferation. In the present study, we investigated for the first time whether PEMF treatment could improve the myocardial ischaemia/reperfusion (I/R) injury and uncovered its underlying mechanisms. In our study, we demonstrated for the first time that extracorporeal PEMF has a novel effect on myocardial I/R injury. The number and function of circulating endothelial progenitor cells (EPCs) were increased in PEMF treating rats. The in vivo results showed that per-treatment of PEMF could significantly improve the cardiac function in I/R injury group. In addition, PEMF treatment also reduced the apoptosis of myocardial cells by up-regulating the expression of anti-apoptosis protein B-cell lymphoma 2 (Bcl-2) and down-regulating the expression of pro-apoptosis protein (Bax). In vitro, the results showed that PEMF treatment could significantly reduce the apoptosis and reactive oxygen species (ROS) levels in primary neonatal rat cardiac ventricular myocytes (NRCMs) induced by hypoxia/reoxygenation (H/R). In particular, PEMF increased the phosphorylation of protein kinase B (Akt) and endothelial nitric oxide synthase (eNOS), which might be closely related to attenuated cell apoptosis by increasing the releasing of nitric oxide (NO). Therefore, our data indicated that PEMF could be a potential candidate for I/R injury

Ectopically-expressed RstA partially reverses the Δ<i>rstA</i> mutant phenotype.

<p>Cultures were grown to OD₄₅₀ = 0.15 in ABTGcasa medium at 37°C to express RstA from the pACYC-<i>rstA</i> plasmid. Cells were treated and fixed as described in Fig 2. The chromosome number per cell was measured by flow cytometry.</p

Topoisomerase I relaxes negative supercoiled plasmid DNA in present RstA.

<p>Lane 1, 0.4 μg pUC19 plasmid with no added protein. Lane 2, 0.4 μg pUC19 plasmid with BSA protein. And the other lanes contain the same concentrations of plasmid as lane 2, but different amounts of purified protein. Lanes 3–8 contain decreasing amounts of purified RstA protein (from 500 ng to 0 μg) and one unit Topoisomerase I. Lane 9, 500 ng purified RstA protein without Topoisomerase I. 6×loading buffer was added to stop the reaction and analyzed by 0.8% agrose gel electrophoresis.</p

RstA interacts the promoter region of <i>hupA</i>.

<p>Cells were grown exponentially at 37°C in ABTGcasa medium and collected 1 ml at OD₄₅₀ = 0.1, 0.2, 0.3, 0.4, 0.5, respectively. The sampled at the time points indicated and fixed in methylbenzene. Activity of the LacZ was measured as the β-galactosidase activity in the cells by Miller method. The values shown at top of the bars are the average of three individual experiments, and the standard errors are shown. The difference between data is analyzed by single factor analysis of variance. The ‘*’ showes significant differences between the wild type and Δ<i>rstA</i> cells, p-value<0.001.</p

Primers used.

<p>Primers used.</p