Four experiments were conducted to evaluate guar meal as a source of prebiotic galactomannans for laying hens. In the 1st experiment, late phase laying hens were fed diets with 0, 5, 10% guar meal (GM) for 56 days or 15% GM for 28 days then switched to the 0% GM diet for the final 28 days. In the 2nd experiment, young pullets were fed guar germ (GG) or GM at 0, 2.5 or 5% for 20 weeks. In the 1st and 2nd experiments, egg production and feed consumption were not affected by feeding up to 5% guar by-products whereas feed efficiency was decreased by guar feeding. Feeding of GG or GM did not affect egg weight or shell quality, but decreased the egg yolk color and Haugh units. Guar increased absolute and relative liver weight, but did not affect the weights of the pancreas, spleen, or the incidence of fatty liver or liver hemorrhage. Feeding 10% GM depressed feed consumption and increased body weight loss. Feeding 15% GM severely depressed egg production followed by a recovery of production after returning to 0% GM feeding. In the 3rd and 4th experiments, late phase laying hens were induced to molt by feed withdrawal (FW) or feeding 15 or 20% GM with or without β-mannanase (Hemicell??). All hens except those fed 15% GM with enzyme obtained a complete cessation of lay in 10 days. Compared to FW birds, hens fed GM had lower body weight reduction and mortality, while hens fed 20% GM with enzyme had higher post-molt egg production. Salmonella enteritidis (SE) present in 6 organs (crop, liver, spleen, ovary, oviduct and cecum), and SE in cecal contents were significantly reduced by 20% GM feeding with and without enzyme. The results showed that GG or GM can be safely fed to laying hens up to 5% without adverse effects on performance. An alternative molting method employing 20% GM with or without β-mannanase is preferable to FW because GM feeding results in a complete molt and decreases mortality, as well as enhances the resistance to SE of molted hens.

No description available.

The enrichment of egg with folate is a viable option for supplying the general population of a food product rich in natural folates. However, attempts to increase the concentration of folate in egg beyond the achieved level of enrichment had been unsuccessful because egg folate reached a maximum plateau when folic acid (FA) was increased in the diet. Thus, experiments were conducted to determine the factors regulating the deposition of dietary FA into the eggs. In the first study, the effect of feeding equimolar intake of FA and 5-methyltetrahydrofolate (5-methylTHF), the biologically active form of folate; on egg folate concentrations, indices of folate status, and activities of folate-dependent enzymes was evaluated. Folic acid and 5-methylTHF demonstrated equivalent effects in enhancing the egg folate concentrations and improving the indices of folate status in the laying hen. The activities of folate-dependent enzymes were similar between the two forms of folate except for hepatic dihydrofolate reductase (DHFR) activity which increased in FA-fed birds compared to 5-methylTHF-fed birds. However, this demonstrated the ability of the laying hen to metabolically convert FA into its biologically active forms. Therefore, the influence of intestinal FA absorption in the regulation of FA deposition in the egg was subsequently evaluated. Using the in vitro everted intestinal sac technique, FA was absorbed in all regions of the intestine. Absorption was maximum at acidic pH 6.0, and increased in the duodenum and jejunum compared to the ileum and cecum. The rate of FA absorption in the jejunum diminished at higher FA concentrations. Therefore, further study was conducted to determine the regulation of FA absorption when levels of FA in the laying hen diet are increased. Supplementation of increased FA levels resulted to a down-regulation of FA absorption in the duodenum, but not in the jejunum of the laying hen. This down-regulation was not associated to a decreased mRNA gene expression of the duodenal folate transporters. Overall, decreased intestinal rate of FA absorption possibly associated to a post-transcriptional or translational regulation of specific folate transporters in the intestine of the laying hen may contribute to the saturation in the egg folate concentration.

We investigated the effects of dietary folic acid and age, on immunological parameters in laying hens challenged with LPS. 48 Shaver White hens at different ages were fed 2 wheat-soybean based diets with 0 or 4 mg supplemental FA per kg of diet for 8 wk. 6 hens from each dietary treatment were injected with 8 mg/kg body weight of LPS or saline and observed for 4 h. A few diet X challenge interaction were observed in young hens, whereas FA and LPS independently influenced a number of parameters. In older hens, there were very few diet X challenge interactions as well as effects of FA, whereas LPS affected several parameters. In conclusion, dietary FA influenced some immune responses in younger hens, but no such effects were observed in older hens. FA may modulate immune responses in laying hens under acute LPS challenge which could be tissue and age dependent.

The enrichment of egg with folate is a viable option for supplying the general population of a food product rich in natural folates. However, attempts to increase the concentration of folate in egg beyond the achieved level of enrichment had been unsuccessful because egg folate reached a maximum plateau when folic acid (FA) was increased in the diet. Thus, experiments were conducted to determine the factors regulating the deposition of dietary FA into the eggs. In the first study, the effect of feeding equimolar intake of FA and 5-methyltetrahydrofolate (5-methylTHF), the biologically active form of folate; on egg folate concentrations, indices of folate status, and activities of folate-dependent enzymes was evaluated. Folic acid and 5-methylTHF demonstrated equivalent effects in enhancing the egg folate concentrations and improving the indices of folate status in the laying hen. The activities of folate-dependent enzymes were similar between the two forms of folate except for hepatic dihydrofolate reductase (DHFR) activity which increased in FA-fed birds compared to 5-methylTHF-fed birds. However, this demonstrated the ability of the laying hen to metabolically convert FA into its biologically active forms. Therefore, the influence of intestinal FA absorption in the regulation of FA deposition in the egg was subsequently evaluated. Using the in vitro everted intestinal sac technique, FA was absorbed in all regions of the intestine. Absorption was maximum at acidic pH 6.0, and increased in the duodenum and jejunum compared to the ileum and cecum. The rate of FA absorption in the jejunum diminished at higher FA concentrations. Therefore, further study was conducted to determine the regulation of FA absorption when levels of FA in the laying hen diet are increased. Supplementation of increased FA levels resulted to a down-regulation of FA absorption in the duodenum, but not in the jejunum of the laying hen. This down-regulation was not associated to a decreased mRNA gene expression of the duodenal folate transporters. Overall, decreased intestinal rate of FA absorption possibly associated to a post-transcriptional or translational regulation of specific folate transporters in the intestine of the laying hen may contribute to the saturation in the egg folate concentration.

We investigated the effects of dietary folic acid and age, on immunological parameters in laying hens challenged with LPS. 48 Shaver White hens at different ages were fed 2 wheat-soybean based diets with 0 or 4 mg supplemental FA per kg of diet for 8 wk. 6 hens from each dietary treatment were injected with 8 mg/kg body weight of LPS or saline and observed for 4 h. A few diet X challenge interaction were observed in young hens, whereas FA and LPS independently influenced a number of parameters. In older hens, there were very few diet X challenge interactions as well as effects of FA, whereas LPS affected several parameters. In conclusion, dietary FA influenced some immune responses in younger hens, but no such effects were observed in older hens. FA may modulate immune responses in laying hens under acute LPS challenge which could be tissue and age dependent.

The principal objective of this investigation was to evaluate the effects of mycotoxin contaminated diets (deoxynivalenol (DON)), aflatoxin B1 (AFB1), and fumonisin (FUM)), with or without the use of a commercially available deactivating compound (DC), in young pullets and replacement laying hens on performance, reproductive, serological, and histopathological parameters. In trial 1, experimental treatments consisted of control, low toxin (1 µg DON/g + 1 µg AFB1/g), and high toxin (2 µg DON/g + 2 µg AFB1/g) diets. Pullets fed the high toxin diet had reduced (P<0.05) body weights compared to control and low toxin diets at d 14, 35, 49, 56, and 63. At d 21 and 28, there was a significant interaction observed between mycotoxin and DC inclusion in body weights. Following necropsies (d 35 and 65), relative liver weights and histopathological liver tissue damage were increased (P<0.05) in pullets fed high toxin diets when compared to control and low toxin diets. Relative kidney weights were increased (P<0.05) due to high toxin diet at d 65. Expected negative effects of toxin administration on titer development were not observed. The only interaction observed between mycotoxin administration and DC inclusion in trial 1 was on body weights. In trial 2, experimental treatments consisted of control, DON (9 µg/g) challenge, AFB1 (2 µg/g) + FUM (54 µg/g) challenge, and a mixed challenge (6 µg DON/g, 1 µg AFB1/g, and 27 µg FUM/g). All mycotoxin diets fed to hens negatively influenced (P<0.05) feed efficiency for the trial period spanning weeks 6 through 10 when compared to control diets. Egg production was not affected (P>0.05) by all mycotoxin diets weeks 6 through 10. Relative weights of the liver and kidney were increased (P<0.05) by AFB1+FUM challenge weeks 4 and 9 compared to control diet. The data reported in this study demonstrate that dietary DON and / or AFB1+FUM influence some performance, reproductive, histopathological, and egg quality traits, but by and large, replacement layer pullets seem to be relatively resistant to the mycotoxins evaluated in this trial at the described levels of administration.

Das Ziel kontinuierlicher Messungen über zwei Jahre war die Bewertung der Stickstoffdepositionen und Ammoniakimmissionen einer Bodenhaltung (Voliere) mit Auslauf für 20.000 Hennen auf das Umfeld. Untersucht wurden weiterhin die Staub- und Geruchskonzentrationen in Stall- und Abluft. Die untersuchte Bodenhaltung emittiert im Jahr 41 g Ammoniak je Tierplatz. Die Vergleiche 14-tägiger Messdatenreihen zeigen, dass Emissionsmessungen an Tierhaltungen in möglichst langen Zeitfenstern und mindestens viermal jährlich durchzuführen sind. Die Immissionswerte für Ammoniak sind 40 m vom Stall am höchsten und erreichen nach ca. 350 m wieder das Hintergrundniveau am Standort. Unter Abzug der nicht dem Stall zuzurechnenden Hintergrundkonzentrationen verursacht der Stall im Nahbereich (40 m) eine Stickstoffdeposition von 18 kg/ha. Ab 230 m Distanz werden nur noch ca. 3 kg/ha deponiert. Die mittlere Tageskonzentration der Staubgehalte im Abluftstrom wurde in Abhängigkeit vom Außenklima zwischen 1,2 und 9,0 mg/m³ ermittelt. Der Anteil von PM-10 und PM-2.5 am Gesamtstaub betrug 80 bzw. 30 %. Für Gesamtstaub wurde ein Emissionsfaktor von 145,4 g/Tpl. zur Berechnung der Jahresemissionen ermittelt. Die in den Außenklimabereichen ermittelten Geruchsstoffkonzentrationen (Geruchsschwelle) im Abluftstrom liegen zwischen 25 und 115 GE/m³. Die mittleren Referenzwerte der Außenluft liegen bei 19 GE.

The aim of this work was to investigate the effects of feather availability and imprinting to loose feathers in the litter on the incidence of feather pecking behaviour (FP), condition of the integument and fear reactions in two genotypes of laying hens. Hens that were deprived from loose feathers in the litter (feathers were collected 4 times/week) exhibited a significantly less rate of feather pecking, less number of severe FP and showed a better feather score in the laying period compared to the control groups (no feather treatment) in both Lohmann Tradition (LT) & Lohmann Silver (LS) genotypes. Addition of brown feathers to the floor in LT hens (feathers were added once/week) was associated with a reduction in feather pecking rate, the severe form of this behaviour and improved plumage and skin conditions. Contrary, the addition of white feathers to the floor in LS was associated with the highest rate of feather pecking, the highest severe form of this behaviour as well as the worst feather and skin conditions in the laying period compared to other groups of the same genotype. The LT birds in all feather treatments had a better feather cover than the LS birds. Hens that were imprinted to loose feathers in the litter in the rearing period exhibited a higher rate of FP, higher number of severe FP and showed the worst feather and skin conditions when feathers were collected from the floor during the laying period. Also, these hens reacted more fearful during the tonic immobility test. It is concluded that loose feathers may play a role in the development of feather pecking behaviour in laying hens. Large differences between genotypes were found in respect to the availability of loose feathers, feather pecking and plumage and integument condition. Imprinting of chicks to loose feathers from the floor may affect the incidence of feather pecking later on. Ziel dieser Arbeit war es, die Einflüsse des Federangebotes und der Prägung auf lose Federn in der Einstreu auf die Häufigkeit des Auftretens von Federpicken (FP), den Zustand des Integuments und die Furchtreaktionen an zwei Legehennengenotypen zu untersuchen. Hühnern beider untersuchter Genotypen (Lohmann Tradition (LT) und Lohmann Silber (LS)), denen die losen Federn 4 mal/ Woche aus der Einstreu abgesammelt wurden, zeigten eine geringere Federpickrate, eine geringere Anzahl der schweren Form des FP und eine bessere Gefiederbeschaffenheit in der Legeperiode verglichen mit der Kontrollgruppe (keine Federbehandlung). Das Hinzufügen brauner Federn zur Einstreu bewirkte bei LT Hennen eine Reduktion der FP-Rate, der schweren Form des Federpickens und verbesserte die Gefieder- und Hautbeschaffenheit. Dagegen führte das Hinzufügen weißer Federn in die Einstreu während der Legeperiode bei LS Hennen zur höchsten Federpickrate und Anzahl der schweren Form des Federpickens sowie zur schlechtesten Gefieder- und Hautbeschaffenheit im Vergleich zu anderen Gruppen des gleichen Genotyps. Hühner der LT Linie wiesen in allen Federbehandlungen eine bessere Befiederung als die LS Hühner auf. Hennen, die während der Aufzuchtsperiode auf lose Federn in der Einstreu geprägt wurden, zeigten nach Absammeln der Federn während der Legeperiode eine erhöhte FP-Rate mit einer erhöhten Anzahl der schweren Form des FP und die schlechteste Gefieder- und Hautbeschaffenheit. Außerdem reagierten diese Hühner ängstlicher während des Tests auf tonische Immobilität. Es kann geschlussfolgert werden, dass lose Federn in der Einstreu eine Rolle bei der Entwicklung des Federpickverhaltens von Legehennen spielen und dass Federpicken als Futtersuchverhalten interpretiert werden kann. Grosse Unterschiede zwischen den Genotypen bestanden hinsichtlich der Verfügbarkeit von losen Federn in der Einstreu, des Federpickens sowie der Gefieder- und Integumentbeschaffenheit. Eine Prägung der Junghennen auf lose Federn in der Einstreu könnte das Auftreten von Federpicken zu einem späteren Zeitpunkt beeinflussen.

Epithelial ovarian cancer is the most lethal gynecologic malignancy, with a 5-year survival rate of less than 40%. This is due in part to a lack of early detection markers and lack of specific symptoms during early disease. The laying hen is the only accessible animal model which develops epithelial ovarian cancer spontaneously, with features closely resembling the human disease. It has been estimated that approximately 30% of all cancers can be prevented with diet, exercise, and maintenance of an optimal weight, and the chronic low-grade inflammation that accompanies obesity is implicated as a causal factor in the development of cancer. Flaxseed, a rich plant source of anti-inflammatory omega-3 fatty acids and lignans which act as phytoestrogens and antioxidants, exhibits chemosuppressive effects against the development and progression of ovarian cancer. We have shown that a diet of 10% flaxseed reduces the incidence and severity of ovarian cancer when fed to laying hens over 4 years, due in part to the ability of flaxseed to suppress the production of proinflammatory PGE2 in the ovary by decreasing expression of COX enzymes. To investigate other potential specific mechanisms by which flaxseed acts to suppress ovarian cancer, we examined expression and activity of pathways known to be involved in the etiology and progression of human epithelial ovarian cancer in ovarian cancer in the laying hen, and determined whether flaxseed affected these pathways during cancer development. We investigated the effect of flaxseed and its individual components upon oxidative stress in the normal ovary and in ovarian cancer by analyzing expression of target genes of the NRF2 transcription factor. The NRF2 pathway is a "master switch" that regulates expression of ROS-responsive detoxification genes. Results revealed that expression of four genes was significantly downregulated in then ovaries of hens on the defatted flaxmeal (DFM) and whole flaxseed (WF) diets compared to hens on diets that are high in pro-inflammatory omega-6 fatty acids, suggesting that flaxseed decreases oxidative stress in the ovary. Conversely, one target gene was upregulated in ovarian cancer compared to normal ovaries, and this observation was not affected by flaxseed. Additionally, nuclear accumulation Nrf2 protein was not observed in tumor cells, suggesting that flaxseed does not exert chemosuppressive effects by modulating NRF2 signaling in ovarian cancer. To further investigate pathways potentially regulated by flaxseed, we performed a microarray with 44k features and found that a set of genes involved in branching morphogenesis was upregulated in ovarian cancer and significantly decreased by flaxseed, including E-cadherin and miR-200, suggesting that flaxseed impedes the activity of an aberrantly activated developmental program that controls gland formation during ovarian cancer progression. Lack of nuclear accumulation of ZEB1 protein in tumor cells suggests that this decrease in expression is likely not due to EMT. Finally, due to its known roles in controlling developmental programs such as EMT as well as regulating cell growth and proliferation, we performed a set of experiments to examine activity of the TGF-beta pathway. PCR array analysis revealed that SMAD target genes, ligands, receptors, and co-regulatory proteins were upregulated in ovarian tumors from hens on both diet groups, suggesting TGF-beta signaling is enhanced in ovarian cancer. However, expression of SMAD6 and SMAD7 was upregulated in tumors from hens on the flaxseed diet but not control diet, with SMAD7 protein being expressed in both epithelial tumor cells and intratumoral stromal cells. Additionally, immunohistochemical staining for pSMAD2/3 was decreased in epithelial tumor cells and absent from intratumoral stromal cells in tumors from hens on the flaxseed diet compared to tumors from hens on the control diet, and these data together suggest that flaxseed may inhibit pro-oncogenic TGF-beta signaling in ovarian cancer. Finally, flaxseed prevents the downregulation of expression of p15 and the upregulation of CCNA and CCNE in ovarian tumors, suggesting that flaxseed may slow cell cycle progression. Data from these studies provides preliminary evidence that flaxseed exerts pleiotropic effects upon gene expression to negatively regulate pathways driving the progression of ovarian cancer, including aberrant TGF-beta signaling and glandular development. These studies provide groundwork for in vitro studies to test the specific effects of flaxseed upon proteins involved in TGF-beta signaling and upon the expansion of tumor epithelia.