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Maternal high-fat diet in mice alters immune regulation and lung function in the offspring
- Purevsuren Losol, Lindert P. Mercken, Helena L. Fisk, Philip C. Calder, John W. Holloway, Christopher Torrens
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- Journal:
- British Journal of Nutrition / Volume 126 / Issue 6 / 28 September 2021
- Published online by Cambridge University Press:
- 27 November 2020, pp. 844-852
- Print publication:
- 28 September 2021
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PUFA modulate immune function and have been associated with the risk of childhood atopy and asthma. We investigated the effect of maternal fat intake in mice on PUFA status, elongase and desaturase gene expression, inflammatory markers and lung function in the offspring. C57BL/6J mice (n 32) were fed either standard chow (C, 20·4 % energy as fat) or a high-fat diet (HFD, 39·9 % energy as fat) for 4 weeks prior to conception and during gestation and lactation. At 21 d of age, offspring were weaned onto either the HFD or C, generating four experimental groups: C/C, C/HF, HF/C and HF/HF. Plasma and liver fatty acid composition were measured by GC and gene expression by quantitative PCR. Lung resistance to methacholine was assessed. Arachidonic acid concentrations in offspring plasma and liver phospholipids were increased by HFD; this effect was greater in the post-natal HFD group. DHA concentration in offspring liver phospholipids was increased in response to HFD and was higher in the post-natal HFD group. Post-natal HFD increased hepatic fatty acid desaturase (FADS) 2 and elongation of very long-chain fatty acid 5 expression in male offspring, whereas maternal HFD elevated expression of FADS1 and FADS2 in female offspring compared with males. Post-natal HFD increased expression of IL-6 and C-C motif chemokine ligand 2 (CCL2) in perivascular adipose tissue. The HFD lowered lung resistance to methacholine. Excessive maternal fat intake during development modifies hepatic PUFA status in offspring through regulation of gene expression of enzymes that are involved in PUFA biosynthesis and modifies the development of the offspring lungs leading to respiratory dysfunction.
Millennial-scale increase in winter precipitation in the southern Rocky Mountains during the Common Era
- Meredith C. Parish, W. John Calder, Bryan N. Shuman
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- Journal:
- Quaternary Research / Volume 94 / March 2020
- Published online by Cambridge University Press:
- 14 February 2020, pp. 1-13
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We employed the modern analog technique to quantitatively reconstruct temperature and precipitation over the past 2500 yr based on fossil pollen records from six high-elevation lakes in northern Colorado. Reconstructed annual temperatures for the study area did not deviate significantly from modern over the past 2500 yr despite hemispheric expressions of Medieval Climate Anomaly warmth and Little Ice Age cooling. Annual precipitation, however, shifted from lower than modern rates from 2500 to 1000 cal yr BP to higher than modern rates after 1000 cal yr BP, a greater than 100 mm increase in precipitation. Winter precipitation accounts for the majority of the change in annual precipitation, while summer precipitation rates did not change significantly over the past 2500 yr. The large change in winter precipitation rates from the first to second millennium of the Common Era is inferred from a shift in fossil pollen assemblages dominated by subalpine conifers, which have southern sites as modern analogs, to assemblages representing open subalpine vegetation with abundant Artemisia spp. (sagebrush), which have more northern modern analogs. The change helps to explain regional increases in lake levels and shifts in some isotopic and tree-ring data sets, highlighting the risk of large reductions in snowpack and water supplies in the Intermountain West.
Contributors
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- By Agoston T. Agoston, Syed Z. Ali, Mahul B. Amin, Daniel A. Arber, Pedram Argani, Sylvia L. Asa, Rebecca N. Baergen, Zubair W. Baloch, Andrew M. Bellizzi, Kurt Benirschke, Allen Burke, Kenneth B. Calder, Karen L. Chang, Rebecca D. Chernock, Wang Cheung, Thomas V. Colby, Byron P. Croker, Ronald A. DeLellis, Edward F. DiCarlo, Ralph C. Eagle, Hormoz Ehya, Brett M. Elicker, Tarik M. Elsheikh, Robert E. Fechner, Linda D. Ferrell, Melina B. Flanagan, Douglas B. Flieder, Christopher S. Foster, Lillian Gaber, Karuna Garg, Kim R. Geisinger, Ryan M. Gill, Eric F. Glassy, David J. Glembocki, Zachary D. Goodman, Robert O. Greer, David J. Grignon, Gerardo E. Guiter, Kymberly A. Gyure, Ian S. Hagemann, Michael R. Henry, Jason L. Hornick, Ralph H. Hruban, Phyllis C. Huettner, Peter A. Humphrey, Olga B. Ioffe, Edward C. Klatt, Michael J. Klein, Ernest E. Lack, James N. Lampros, Lester J. Layfield, Robin D. LeGallo, Kevin O. Leslie, James S. Lewis, Virginia A. LiVolsi, Alberto M. Marchevsky, Anne Marie McNicol, Mitra Mehrad, Elizabeth Montgomery, Cesar A. Moran, Christopher A. Moskaluk, George J. Netto, G. Petur Nielsen, Robert D. Odze, Arthur S. Patchefsky, James W. Patterson, Elizabeth N. Pavlisko, John D. Pfeifer, Celeste N. Powers, Richard A. Prayson, Anja C. Roden, Victor L. Roggli, Andrew E. Rosenberg, Sherif Said, Margie A. Scott, Raja R. Seethala, Carlie S. Sigel, Jan F. Silverman, Bruce R. Smoller, Edward B. Stelow, Nora C. J. Sun, Mark W. Teague, Satish K. Tickoo, Thomas M. Ulbright, Paul E. Wakely, Jun Wang, Lawrence M. Weiss, Mark R. Wick, Howard H. Wu, Rhonda K. Yantiss, Charles Zaloudek, Yaxia Zhang, Xiaohui Sheila Zhao
- Edited by Mark R. Wick, University of Virginia, Virginia A. LiVolsi, University of Pennsylvania School of Medicine, John D. Pfeifer, Washington University School of Medicine, St Louis, Edward B. Stelow, University of Virginia, Paul E. Wakely, Jr
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- Book:
- Silverberg's Principles and Practice of Surgical Pathology and Cytopathology
- Published online:
- 13 March 2015
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- 26 March 2015, pp vii-x
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- By Venkataraman Anantharaman, Philip D. Anderson, Christopher W. Baugh, J. Stephen Bohan, Kirsten Boyd, Matthias Brachmann, Peter R. Brown, Shelley Calder, David Callaway, Peter Cameron, Jody Crane, Meaghan Cussen, Christina Dempsey, Jonathan A. Edlow, Thomas Fleischmann, Robert L. Freitas, John D. Halamka, Manuel Hernandez, Cherri Hobgood, Jock Hoffman, Steven Horng, Kirk B. Jensen, Jennifer R. Johnson, Stephanie Kayden, Tasnim Khan, Daniel G. Kirkpatrick, James Lennon, Mary Leupold, Thom Mayer, J. Lawrence Mottley, Scott B. Murray, Deirdre Mylod, Larry A. Nathanson, Michael P. Pietrzak, Elke Platz, Nadeem Qureshi, Matthew M. Rice, Andrew Schenkel, Chet Schrader, Puneet Seth, Richard B. Siegrist, David Smith, Robert E. Suter, Carrie Tibbles, Sebastian N. Walker, Lee A. Wallis, Julie Welch, Leana S. Wen
- Edited by Stephanie Kayden, Philip D. Anderson, Robert Freitas, Elke Platz
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- Book:
- Emergency Department Leadership and Management
- Published online:
- 05 December 2014
- Print publication:
- 27 November 2014, pp ix-xii
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Differential immunomodulation with long-chain n-3 PUFA in health and chronic disease
- John W. C. Sijben, Philip C. Calder
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- Journal:
- Proceedings of the Nutrition Society / Volume 66 / Issue 2 / May 2007
- Published online by Cambridge University Press:
- 30 April 2007, pp. 237-259
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The balance of intake of n-6 and n-3 PUFA, and consequently their relative incorporation into immune cells, is important in determining the development and severity of immune and inflammatory responses. Some disorders characterised by exaggerated inflammation and excessive formation of inflammatory markers have become among the most important causes of death and disability in man in modern societies. The recognition that long-chain n-3 PUFA have the potential to inhibit (excessive) inflammatory responses has led to a large number of clinical investigations with these fatty acids in inflammatory conditions as well as in healthy subjects. The present review explores the presence of dose-related effects of long-chain n-3 PUFA supplementation on immune markers and differences between healthy subjects and those with inflammatory conditions, because of the important implications for the transfer of information gained from studies with healthy subjects to patient populations, e.g. for establishing dose levels for specific applications. The effects of long-chain n-3 PUFA supplementation on ex vivo lymphocyte proliferation and cytokine production by lymphocytes and monocytes in healthy subjects have been studied in twenty-seven, twenty-five and forty-six treatment cohorts respectively, at intake levels ranging from 0·2 g EPA+DHA/d to 7·0 g EPA+DHA/d. Most studies, particularly those with the highest quality study design, have found no effects on these immune markers. Significant effects on lymphocyte proliferation are decreased responses in seven of eight cohorts, particularly in older subjects. The direction of the significant changes in cytokine production by lymphocytes is inconsistent and only found at supplementation levels ≥2·0 g EPA+DHA/d. Significant changes in inflammatory cytokine production by monocytes are decreases in their production in all instances. Overall, these studies fail to reveal strong dose–response effects of EPA+DHA on the outcomes measured and suggest that healthy subjects are relatively insensitive to immunomodulation with long-chain n-3 PUFA, even at intake levels that substantially raise their concentrations in phospholipids of immune cells. In patients with inflammatory conditions cytokine concentrations or production are influenced by EPA+DHA supplementation in a relatively large number of studies. Some of these studies suggest that local effects at the site of inflammation might be more pronounced than systemic effects and disease-related markers are more sensitive to the immunomodulatory effects, indicating that the presence of inflamed tissue or ‘sensitised’ immune cells in inflammatory disorders might increase sensitivity to the immunomodulatory effects of long-chain n-3 PUFA. In a substantial number of these studies clinical benefits related to the inflammatory state of the condition have been observed in the absence of significant effects on immune markers of inflammation. This finding suggests that condition-specific clinical end points might be more sensitive markers of modulation by EPA+DHA than cytokines. In general, the direction of immunomodulation in healthy subjects (if any) and in inflammatory conditions is the same, which indicates that studies in healthy subjects are a useful tool to describe the general principles of immunomodulation by n-3 PUFA. However, the extent of the effect might be very different in inflammatory conditions, indicating that studies in healthy subjects are not particularly suitable for establishing dose levels for specific applications in inflammatory conditions. The reviewed studies provide no indications that the immunomodulatory effects of long-chain n-3 PUFA impair immune function or infectious disease resistance. In contrast, in some conditions the immunomodulatory effects of EPA+DHA might improve immune function.