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Добірка наукової літератури з теми "Reticuloendothelial system; Poultry Physiology"

Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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Статті в журналах з теми "Reticuloendothelial system; Poultry Physiology"

1

LEWIS, S. M. "The Reticuloendothelial System: A Comprehensive Treatise (7A Physiology)." Biochemical Society Transactions 13, no. 5 (October 1, 1985): 975. http://dx.doi.org/10.1042/bst0130975.

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2

Kerr, Michael. "The Reticuloendothelial System: A Comprehensive Treatise Volume 78A Physiology." Biochemical Education 13, no. 4 (October 1985): 188. http://dx.doi.org/10.1016/0307-4412(85)90094-9.

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3

Kurahashi, Kiyoyasu, Teiji Sawa, Maria Ota, Osamu Kajikawa, Keelung Hong, Thomas R. Martin, and Jeanine P. Wiener-Kronish. "Depletion of phagocytes in the reticuloendothelial system causes increased inflammation and mortality in rabbits withPseudomonas aeruginosapneumonia." American Journal of Physiology-Lung Cellular and Molecular Physiology 296, no. 2 (February 2009): L198—L209. http://dx.doi.org/10.1152/ajplung.90472.2008.

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Phagocytes of the reticuloendothelial system are important in clearing systemic infection; however, the role of the reticuloendothelial system in the response to localized infection is not well-documented. The major goals of this study were to investigate the roles of phagocytes in the reticuloendothelial system in terms of bacterial clearance and inflammatory modulation in sepsis caused by Pseudomonas pneumonia. Macrophages in liver and spleen were depleted by administering liposome encapsulated dichloromethylene diphosphonate (clodronate) intravenously 36 h before the instillation of Pseudomonas aeruginosa into the lungs of anesthetized rabbits. Blood samples were analyzed for bacteria and cytokine concentrations. Lung injury was assessed by the bidirectional flux of albumin and by wet-to-dry weight ratios. Blood pressure and cardiac outputs decreased more rapidly and bacteremia occurred earlier in the clodronate-treated rabbits compared with the nondepleted rabbits. Plasma TNF-α (1.08 ± 0.54 vs. 0.08 ± 0.02 ng/ml) and IL-8 (6.8 ± 1.5 vs. 0.0 ± 0.0 ng/ml) were higher in the depleted rabbits. The concentration of IL-10 in liver of the macrophage-depleted rabbits was significantly lower than in normal rabbits at 5 h. Treatment of macrophage-depleted rabbits with intravenous IL-10 reduced plasma proinflammatory cytokine concentrations and reduced the decline in blood pressure and cardiac output. These results show that macrophages in the reticuloendothelial system have critical roles in controlling systemic bacteremia and reducing systemic inflammation, thereby limiting the systemic effects of a severe pulmonary bacterial infection.
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4

DuBose, D. A., C. B. Matthew, J. A. Balcius, D. H. Morehouse, and I. V. Sils. "Hyperthermic effects on reticuloendothelial system particulate uptake." Journal of Thermal Biology 25, no. 5 (October 2000): 387–90. http://dx.doi.org/10.1016/s0306-4565(99)00111-4.

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5

Allen, T. M., L. Murray, Carl R. Alving, and James Moe. "Effects on the murine mononuclear phagocyte system of chronic administration of liposomes containing cytotoxic drug or lipid A compared with empty liposomes." Canadian Journal of Physiology and Pharmacology 65, no. 2 (February 1, 1987): 185–90. http://dx.doi.org/10.1139/y87-035.

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In experiments designed to examine the adverse effects of chronic liposome administration in vivo on the mononuclear phagocyte system (reticuloendothelial system), the presence of drug entrapped in the liposomes may increase the level of reticuloendothelial impairment. We have compared the effects on the mononuclear phagocyte system in mice of chronic administration of empty liposomes with the effects of liposomes containing the anti-leishmanial drug meglumine antimoniate. We have also examined the effect on the mononuclear phagocyte system of continued injections of liposomes containing lipid A, a component of bacterial lipopolysaccharide, which is responsible for macrophage activation. Ten intravenous injections of multilamellar liposomes composed of dipalmitoylphosphatidylcholine and cholesterol (1:0.75 M ratio) were given to ICR mice over a 25-day period. Two individual groups of mice received endotoxin-free liposomes in which meglumine antimoniate was either present or absent. One addition group received liposomes containing lipid A derived from Escherichia coli lipopolysaccharide. A control group received sterile saline injections. In each group, a depression of the phagocytic index, as measured by reduction of uptake of particulate carbon, was observed among some of the individual animals 24 h after the first injection. In many mice a marked splenomegaly was observed. A depressed phagocytic index and splenomegaly were most marked for mice receiving lipid A liposomes. However, there was a large individual variability among mice receiving these preparations and some mice in each group had normal spleen size and a nearly normal phagocytic index. Tissue distribution of liposomes containing [14C]dipalmitoylphosphatidylcholine as a phospholipid marker was examined in all groups in mice 24 h after the last injection. Mice receiving liposomes with entrapped meglumine antimoniate showed decreased liver and increased spleen uptake of radiolabel as compared with controls. This has previously been suggested to be an indication of reticuloendothelial blockade. Mice receiving liposomes without meglumine antimoniate had tissue distributions of liposomes similar to control mice, and mice receiving liposomes containing lipid A had greatly decreased spleen uptake and increased liver uptake of liposomes as compared with control mice and mice receiving endotoxin-free liposomes (an indication of reticuloendothelial stimulation), suggesting that liposomes are being treated differently from particulate carbon in the presence of lipid A.
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6

Jones, Michael A., Paul Wigley, Kerrie L. Page, Scott D. Hulme, and Paul A. Barrow. "Salmonella enterica Serovar Gallinarum Requires the Salmonella Pathogenicity Island 2 Type III Secretion System but Not the Salmonella Pathogenicity Island 1 Type III Secretion System for Virulence in Chickens." Infection and Immunity 69, no. 9 (September 1, 2001): 5471–76. http://dx.doi.org/10.1128/iai.69.9.5471-5476.2001.

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ABSTRACT Salmonella enterica serovar Gallinarum is a host-specific serotype that causes the severe systemic disease fowl typhoid in domestic poultry and a narrow range of other avian species but rarely causes disease in mammalian hosts. Specificity of the disease is primarily at the level of the reticuloendothelial system, but few virulence factors have been described other than the requirement for an 85-kb virulence plasmid. In this work, by making functional mutations in the type III secretion systems (TTSS) encoded by Salmonella pathogenicity island 1 (SPI-1) and SPI-2, we investigated the role of these pathogenicity islands in interactions between Salmonella serovar Gallinarum and avian cells in vitro and the role of these pathogenicity islands in virulence in chickens. The SPI-1 mutant showed decreased invasiveness into avian cells in vitro but was unaffected in its ability to persist within chicken macrophages. In contrast the SPI-2 mutant was fully invasive in nonphagocytic cells but failed to persist in macrophages. In chicken infections the SPI-2 mutant was attenuated while the SPI-1 mutant showed full virulence. In oral infections the SPI-2 mutant was not observed in the spleen or liver, and following intravenous inoculation it was cleared rapidly from these sites. SPI-2 function is required by Salmonella serovar Gallinarum for virulence, primarily through promoting survival within macrophages allowing multiplication within the reticuloendothelial system, but this does not preclude the involvement of SPI-2 in uptake from the gut to the spleen and liver. SPI-1 appears to have little effect on virulence and survival of Salmonella serovar Gallinarum in the host.
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7

Renaud, G., J. Marais, and R. Infante. "Role of the reticuloendothelial system in the catabolism of low density lipoprotein in the rat." Archives Internationales de Physiologie et de Biochimie 95, no. 4 (January 1987): 355–59. http://dx.doi.org/10.3109/13813458709113147.

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8

D’Anna, María Cecilia, and Marta Elena Roque. "Physiological focus on the erythropoietin–hepcidin–ferroportin axis." Canadian Journal of Physiology and Pharmacology 91, no. 5 (May 2013): 338–45. http://dx.doi.org/10.1139/cjpp-2012-0214.

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To analyze the interconnection between erythropoiesis and iron metabolism, one of the issues raised in this study was to know iron bioavailability under physiopathological conditions. Our aim was to understand the functional axis response composed of erythropoietin (Epo)—hepcidin—ferroportin (FPN), when 2 dysfunctional states coexist, using an animal model of iron overload followed by hypoxia. FPN and prohepcidin were assessed by immunohistochemistry using rabbit anti-mouse FPN polyclonal and prohepcidin monoclonal antibodies. Goat-labeled polymer − horseradish peroxidase anti-rabbit EnVision + System (DAB) was used as the secondary antibody. Epo levels were measured by ELISA. Tissue iron was studied by Prussian blue iron staining. Erythropoietic response was assessed using conventional hematological tests. Iron overload increased prohepcidin that remained high in hypoxia, coexisting with high levels of Epo in hypoxia, with or without iron overload. In hypoxia, FPN was clearly evident in reticuloendothelial macrophages, more than in hypoxia with iron overload. Interestingly, duodenal FPN was clearly identified on the basolateral membrane in hypoxia, with or without iron overload. Our data indicate that 2 signals could induce the cell-specific response as follows: (i) iron signal, induced prohepcidin, which reduced reticuloendothelial FPN and reduced iron availability; and (ii) hypoxia signal, stimulated Epo, which affected iron absorption by stabilizing duodenal FPN and allowed iron supply to erythropoiesis independently of store size.
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9

Edelson, Paul J. "The Reticuloendothelial System: A Comprehensive Treatise. Volume 7B, Physiology. Sherwood M. Reichard , James P. Filkins , Herman Friedman." Quarterly Review of Biology 60, no. 4 (December 1985): 558. http://dx.doi.org/10.1086/414707.

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10

Ahmad, Rafiq, Yu-Hsiang Yu, Felix Shih-Hsiang Hsiao, Chin-Hui Su, Hsiu-Chou Liu, Isabel Tobin, Guolong Zhang, and Yeong-Hsiang Cheng. "Influence of Heat Stress on Poultry Growth Performance, Intestinal Inflammation, and Immune Function and Potential Mitigation by Probiotics." Animals 12, no. 17 (September 5, 2022): 2297. http://dx.doi.org/10.3390/ani12172297.

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Анотація:
Heat stress has emerged as a serious threat to the global poultry industry due to climate change. Heat stress can negatively impact the growth, gut health, immune function, and production and reproductive performances of poultry. Different strategies have been explored to mitigate heat stress in poultry; however, only a few have shown potential. Probiotics are gaining the attention of poultry nutritionists, as they are capable of improving the physiology, gut health, and immune system of poultry under heat stress. Therefore, application of probiotics along with proper management are considered to potentially help negate some of the negative impacts of heat stress on poultry. This review presents scientific insight into the impact of heat stress on poultry health and growth performance as well as the application of probiotics as a promising approach to alleviate the negative effects of heat stress in poultry.
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Більше джерел

Книги з теми "Reticuloendothelial system; Poultry Physiology"

1

Friedman, Herman. The Reticuloendothelial System: A Comprehensive Treatise Volume 9 Hypersensitivity. Boston, MA: Springer US, 1986.

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2

Reichard, Sherwood M. Reticuloendothelial System: A Comprehensive Treatise Volume 7B Physiology. Springer London, Limited, 2012.

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3

Reichard, Sherwood M. The Reticuloendothelial System: A Comprehensive Treatise Volume 7B Physiology. Springer, 1986.

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4

Reichard, Sherwood M. The Reticuloendothelial System: A Comprehensive Treatise, Part B : Physiology. Springer, 1985.

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5

Friedman, Herman. Reticuloendothelial System: A Comprehensive Treatise Volume 5 Cancer. Springer London, Limited, 2012.

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6

Friedman, Herman. The Reticuloendothelial System: A Comprehensive Treatise Volume 5 Cancer. Springer, 2012.

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Частини книг з теми "Reticuloendothelial system; Poultry Physiology"

1

Brain, Joseph D. "Physiology and Pathophysiology of Pulmonary Macrophages." In The Reticuloendothelial System, 315–37. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2353-2_13.

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2

Weiss, Günter. "Iron and the Reticuloendothelial System." In Iron Physiology and Pathophysiology in Humans, 211–31. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60327-485-2_11.

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3

Sembulingam, K., and Prema Sembulingam. "Reticuloendothelial System." In Essentials of Medical Physiology, 130. Jaypee Brothers Medical Publishers (P) Ltd., 2006. http://dx.doi.org/10.5005/jp/books/10283_24.

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4

Sembulingam, K., and Prema Sembulingam. "Reticuloendothelial System and Tissue Macrophage." In Essentials of Medical Physiology, 151. Jaypee Brothers Medical Publishers (P) Ltd., 2012. http://dx.doi.org/10.5005/jp/books/11696_102.

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5

Sembulingam, K., and Prema Sembulingam. "Reticuloendothelial System and Tissue Macrophage." In Essentials of Medical Physiology, 141. Jaypee Brothers Medical Publishers (P) Ltd., 2010. http://dx.doi.org/10.5005/jp/books/11093_24.

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6

Sembulingam, K., and Prema Sembulingam. "Reticuloendothelial System and Tissue Macrophage." In Essentials of Physiology for Dental Students, 101. Jaypee Brothers Medical Publishers (P) Ltd., 2011. http://dx.doi.org/10.5005/jp/books/11397_31.

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7

Sembulingam, K., and Prema Sembulingam. "Reticuloendothelial System, Tissue Macrophage and Spleen." In Essentials of Physiology for Dental Students, 111. Jaypee Brothers Medical Publishers (P) Ltd., 2016. http://dx.doi.org/10.5005/jp/books/12902_22.

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Тези доповідей конференцій з теми "Reticuloendothelial system; Poultry Physiology"

1

Bobeck, Elizabeth. "Bioactive lipids and related nutrients in companion animal and poultry diets for reducing inflammation and improving immunity." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/vqxl3869.

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Beyond meeting nutritional requirements for growth and maintenance, select dietary ingredients can have additional effects, intended or not, on animal physiology and immune function. Diets can be enriched to benefit the animal, and a dual benefit can be achieved in the case of enriching animal products for the downstream human consumer. Many immune-altering nutrients are fat-soluble, including Vitamin E and D. Importantly, dietary lipids themselves can impact immune function; therefore, a focused and intentional selection of specific dietary fats, specifically omega-3 polyunsaturated fatty acids (PUFA), is one method to alter inflammatory cascades in animals consuming the diet. Examples of other related ingredients to which the immune system is responsive include zinc and probiotics. While work in human, livestock, and companion animal models is working to identify therapeutic inclusion rates for these nutrients and ingredients, it should be noted that physiological alterations are seen in both over and under-inclusion and are nutrient-specific. For example, inclusion above currently recommended levels may optimize immune function and reduce inflammation in the case of vitamin D or omega-3 PUFA, while for zinc, additional pharmacological supplementation above requirements may inhibit immune function. Importantly, when a diet is formulated to reduce overall systemic inflammation, it must be considered that important “background” functions of the immune system, including monitoring for and clearing pathogenic microbial populations, may be down-regulated due to a general reduction in immune reactivity. Continued work to understand how diet and nutrition impact immunity, and how to balance inflammation through nutrition, is an area of active research and will inform downstream users how to best use data to impact consumers of that feed in desirable ways.
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