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Books on the topic 'PALATABILITE'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Damiran, Daalkhaijav. Palatability of Mongolian rangeland plants. Eastern Oregon Agricultural Research Center/Union Station, 2005.

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2

O'Connor, Cheryl E. Palatability of rodent baits to wild house mice. Dept. of Conservation, 2001.

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3

Chicago, Ill ). Focus on Palatability 2000 (2000. Focus on Palatability, 2000: April 5-6, 2000, Chicago, Illinois. Watt Pub. Co., 2000.

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4

Richardson, Randi. The effects of pre-exposure and palatability on food intake. Laurentian University, 2007.

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5

Ill.) Focus on Palatability (2006 Chicago. Focus on Palatability: [proceedings] : April 5-April 6, 2006, Chicago, Illinois. Watt Pub. Co., 2006.

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6

Herlocker, Dennis J. Palatability ratings of range plants in Ceel Dhere and Bulo Burte districts. Central Rangelands Development Project, 1986.

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7

Lamothe, Suzanne S. Palatability of winter browse to the snowshoe hare (Lepus americanus): Animal plant interactions. s.n.], 1991.

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8

Bechard, Juli M. Automimicry and the palatability spectrum. 1996.

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9

Kirkpatrick, Mary E. Quality of Apples for Household Use: Histological, Chemical, and Palatability Studies (Classic Reprint). Forgotten Books, 2018.

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10

Nishimura, Toshihide, and Motonaka Kuroda. Koku in Food Science and Physiology: Recent Research on a Key Concept in Palatability. Springer, 2019.

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11

Cruz-Guerra, Ruben. Relative palatabilities of Great Basin forages and mechanisms elicting selective grazing by cattle. 1994.

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12

A, Morriss G., and New Zealand. Dept. of Conservation., eds. Factors influencing palatability and efficacy of toxic baits in ship rats, Norway rats and house mice. Science & Technical Publishing, Dept. of Conservation, 2008.

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13

Klepper, Joerg, and Baerbel Leiendecker. Glut1 Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0005.

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Glut1 Deficiency (Glut1D, OMIM #606777) is caused by impaired glucose transport into the brain. The resulting cerebral “energy crisis” causes intractable seizures, developmental delay, and a complex movement disorder. The diagnosis is based on clinical features, low CSF glucose and/or mutations in the SLC2A1 gene. Paroxysmal exertion-induced dystonia (PED) and hereditary cryohydrocytosis have been described as allelic variants. Adults are increasingly being recognized through family pedigrees. The condition is effectively treatable by mimicking the metabolic state of fasting. High-fat carbohydrate-restricted ketogenic diets generate ketones that serve as an alternative fuel for the brain. In adults with Glut1D, novel modified ketogenic diets can be used, allowing more carbohydrates and greater palatability and compliance.

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14

Yvonne Loetscher, Andrea R. Hospenthal, M. Kreuzer, and Ruth E. Messikommer. Do antioxidants induce feed selection behavior in laying hens? Preference for, and palatability of, different antioxidant sources. Verlag Eugen Ulmer, 2014. http://dx.doi.org/10.1399/eps.2014.65.

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15

Xie, Ye-Rong. Effects of sire and time on feed on carcass characteristics, lipid composition and palatability of crossbred Wagyu beef. 1994.

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16

Klepper, Joerg. Glut1 Deficiency and the Ketogenic Diets. Edited by Eric H. Kossoff. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0005.

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Abstract:

Glucose is the essential fuel for the brain. Transport into brain is exclusively mediated by the facilitative glucose transporter Glut1. Glut1 deficiency results in a “brain energy crisis,” causing global developmental delay, epilepsy, and complex movement disorders including paroxysmal nonepileptic events. Early-onset absence epilepsy, paroxysmal exertion-induced dystonia, and stomatin-deficient cryohydrocytosis have been recognized as variants. Diagnosis is based on phenotype, isolated low CSF glucose, and mutations in the SLC2A1 gene. The condition is treated effectively by classical ketogenic diets providing ketones as an alternative fuel for the brain. The modified Atkins diet in adolescents and adults improves palatability and compliance at the expense of lower ketosis. Dietary treatment is continued into adolescence to meet the energy demand of the developing brain, raising concerns about long-term adverse effects. Current fields of research include novel compounds such as ketoesters and genetic approaches in Glut1-deficient mice as potential treatment options.

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