Relevant bibliographies by topics / Cataboliti / Books
To see the other types of publications on this topic, follow the link: Cataboliti.

Books on the topic 'Cataboliti'

Author: Grafiati
Published: 1 April 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 books for your research on the topic 'Cataboliti.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse books on a wide variety of disciplines and organise your bibliography correctly.

1

Suzuki, Koichi, and Judith S. Bond, eds. Intracellular Protein Catabolism. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0335-0.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Revhaug, Arthur, ed. Acute Catabolic State. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-48801-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

1950-, Revhaug A., ed. Acute catabolic state. Berlin: Springer, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Rojas, A. E. Carvajal de. Carbon catabolism in streptomyces venezuelae. Manchester: UMIST, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

McVitty, Rosalind Shirley. In vitro studies of folate catabolism. [S.l: The Author], 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Beck, Susan Anne. Catabolic factors in tumour-induced cachexia. Birmingham: Aston University. Department of Pharmaceutical Sciences, 1989.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Floderus, Eugenie. Aminopeptidases and arginine catabolism in oral streptococci. [Stockholm: Karolinska Institute, Dept. of Oral Microbiology], 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Floderus, Eugenie. Aminopeptidases and arginine catabolism in oral straptococci. Stockholm: Kongl. Carolinska Medico Chirurgiska Institutet, 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

International Symposium on Intracellular Protein Catabolism (6th 1986 Büchenberg (Magdeburg, Germany)). Intracellular protein catabolism: Abstracts of the 6th symposium. Edited by Aurich H, Kirschke Heidrun, Wiederanders Bernd, Proteolysis Group in Halle, and Biochemische Gesellschaft der Deutschen Demokratischen Republik. Halle, Saale: Martin-Luther-Universität Halle-Wittenberg, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Engel, Norbert G. Chlorophyll catabolism in algae and higher plants: A chemical approach. Freiburg (Schweiz): Department of Chemistry, Universität Freiburg (Schwiez), 2001.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
11

A, Khairallah Edward, Bond Judith S, and Bird John W. C, eds. Intracellular protein catabolism: Proceedings of the Fifth International Symposium on Intracellular Protein Catabolism, held May 29-June 2, 1984, at the Airlie Conference Center, Airlie, Virginia. New York: A.R. Liss, 1985.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
12

Koosha, Homa. Investigations into the expression of catabolic Gene derived from Pseudomonas and Azotobacter. Uxbridge: Brunel University, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
13

Joshi, Harshad. Investigation of the catabolic plasmid involvement in naphthalene-degrading strains of Pseudomonas spp.. Wolverhampton: University of Wolverhampton, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
14

Al-Bader, Dhia A. Investigating the role of the oxidative pentose phosphate pathway as the major route of carbohydrate catabolism in the cyanobacterium Synechocystis sp. PCC 6803. [s.l.]: typescript, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
15

1924-, Suzuki Koichi, Bond Judith S, and International Symposium on Intracellular Protein Catabolism (10th : 1994 : Tokyo, Japan), eds. Intracellular protein catabolism. New York: Plenum Press, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
16

Koichi Suzuki Judith S. Bond. Intracellular Protein Catabolism. Springer US, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
17

Suzuki, Koichi, and Judith S. Bond. Intracellular Protein Catabolism. Springer London, Limited, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
18

Revhaug, Arthur. Acute Catabolic State. Springer Berlin / Heidelberg, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
19

Acute Catabolic State. Springer, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
20

Revhaug, Arthur. Acute Catabolic State. Springer London, Limited, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
21

Turk, Vito. Intracellular Protein Catabolism II. Springer London, Limited, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
22

KHAIRALLAH, EA. Khairallah Intracellular Protein Catabolism. John Wiley & Sons Inc, 1985.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
23

Turk, Vito. Intracellular Protein Catabolism II. Springer, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
24

Dutz, H., A. Graffi, and R. Baumann. 3rd Symposium Intracellular Protein Catabolism. de Gruyter GmbH, Walter, 2022.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
25

Catabolic Diseases ; Nutritional Aspects and Diet Implications. Adhyayan Publishers & Distributors, 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
26

Mottram, Linda-Jayne, and Gavin G. Lavery. The metabolic and nutritional response to critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0202.

Full text
Abstract:
The metabolic response to critical illness is complex and affects every body system. The first phase of this response is characterized by increased hypothalamic pituitary activity and resistance (decreased response) to effector hormones in many target tissues. Cytokines released in the early stages of such illness may be important as they appear to stimulate the hypothalamic pituitary axis directly as part of this ‘stress response’. This phase is considered ‘adaptive’ (helpful), increasing the availability of glucose, free fatty acids, and amino acids as substrates for vital organs. However, in prolonged illness, the neuroendocrine response is very different with damped hypothalamic responses, leading to a state in which catabolism predominates, leading to what might be termed the critical illness wasting syndrome. The gastrointestinal (GI) failure often associated with prolonged critical illness appears to be due, at least in part, to an altered neuroendocrine environment. The poor nutritional state associated with GI failure exacerbates the catabolic response, prolonging illness and the period of intensive care management required by the patient. The result is increased mortality and, in survivors, a more prolonged recovery/rehabilitation process.
APA, Harvard, Vancouver, ISO, and other styles
27

Egreteau, Pierre-Yves, and Jean-Michel Boles. Assessing nutritional status in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0204.

Full text
Abstract:
Decreased nutrient intake, increased body requirements, and/or altered nutrient utilization are frequently combined in critically-ill patients. The initial nutritional status and the extent of the disease-related catabolism are the main risk factors for nutrition- related complications. Many complications are related to protein energy malnutrition, which is frequent in the ICU setting. Assessing nutritional status pursues several different goals. Nutritional assessment is required for patients presenting with clinical evidence of malnutrition, with chronic diseases, with acute conditions accompanied by a high catabolic rate, and elderly patients. Recording the patient’s history, nutrient intake, and physical examination, and subjective global assessment allows classification of nutritional status. All the traditional markers of malnutrition, anthropometric measurements and plasma proteins, lose their specificity in the sick adult as each may be affected by a number of non-nutritional factors. Muscle function evaluated by hand-grip strength in cooperative patients and serum albumin provide an objective risk assessment. Several nutritional indices have been validated in specific groups of patients to identify patients at risk of nutritionally-mediated complications and, therefore, the need for nutritional support. A strong suspicion remains the best way of uncovering potentially harmful nutritional deficiencies.
APA, Harvard, Vancouver, ISO, and other styles
28

Leyn, P. De. Patterns and Site of Adenosine Triphosphate Catabolism in Lung Tissue. Leuven University Press, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
29

Perkins, Edward Joseph. The molecular biology of the halogenated aromatic catabolic plasmid pJP4. 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
30

Revhaug, A. Acute Catabolic State (Update in Intensive Care and Emergency Medicine). Springer-Verlag, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
31

Intracellular protein catabolism: Proceedings of the Fifth International Symposium on Intracellular Protein Catabolism, held May 29-June 2, 1984, at the ... in clinical and biological research). A.R. Liss, 1985.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
32

Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0032.

Full text
Abstract:
Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
APA, Harvard, Vancouver, ISO, and other styles
33

Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_001.

Full text
Abstract:
Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
APA, Harvard, Vancouver, ISO, and other styles
34

Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_002.

Full text
Abstract:
Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
APA, Harvard, Vancouver, ISO, and other styles
35

The catabolism of glucagon-like peptidea 2: A novel intestinal growth factor. Ottawa: National Library of Canada, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
36

Kraus, Jennifer. Nutrient exchange in the Rhizobium-legume symbiosis: Glutamate catabolism by Rhizobium meliloti. 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
37

Blaser, Annika Reintam, and Adam M. Deane. Normal physiology of nutrition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0201.

Full text
Abstract:
Energy is derived from three major categories of macronutrient—carbohydrate, lipid, and protein. While energy requirements to maintain stable weight can be estimated, it is uncertain if meeting these energy requirements improves outcomes in the critically ill. In health, excess energy is stored via non-oxidative metabolism and during periods of inadequate energy delivery catabolism of storage products occurs. Both storing and using the stores cost energy, each may require up to quarter of energy contained in stored nutrient. Excess carbohydrate stored as glycogen is easily available, albeit in a limited amount. Storage of lipid is the largest energy repository, but requires complex metabolism and is limited by low oxidative capacity. Protein catabolism normally contributes less than 5% of energy requirements, but during periods of inadequate energy delivery or increased catabolism there is a marked increase in endogenous protein breakdown.
APA, Harvard, Vancouver, ISO, and other styles
38

Sheehan, Patrick J. Starvation effects on the physiology and morphology of catabolic Pseudomonas putida isolates. 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
39

Christianson, Alan. Catabolism Reset Diet : : Repair Your Liver, Stop Storing Fat, and Lose Weight Naturally. Independently Published, 2022.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
40

Guo, Chao. Concentration of genes involved in aromatic catabolism in fuel oil contaminated and noncontaminated soils. 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
41

Metabolism, Structure and Function of Plant Tetrapyrroles: Introduction, Microbial and Eukaryotic Chlorophyll Synthesis and Catabolism. Elsevier, 2019. http://dx.doi.org/10.1016/s0065-2296(19)x0002-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
42

Grimm, Bernhard. Metabolism, Structure and Function of Plant Tetrapyrroles: Introduction, Microbial and Eukaryotic Chlorophyll Synthesis and Catabolism. Elsevier Science & Technology Books, 2019.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
43

Krunic, Nancy. Prostaglandin transport and catabolism in the choroid plexus during perinatal and postnatal development in sheep. 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
44

Turner, C. Catabolic Starvation : The Microbiota Diet: The Real Reason You Can't Lose Weight & How to Fix It. Independently Published, 2019.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
45

Energy expenditure and protein catabolism in ventilated trauma patients: The effect of head injury and neuromuscular blockade. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
46

Rabier, Daniel. Amino Acids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0083.

Full text
Abstract:
Amino acids present in the different biological fluids belong to two groups: the protein group, with the 21 classical amino acids constituting the backbone of the protein, and the nonprotein group, appearing in different metabolic pathways as intermediate metabolites. It is important to know and to be able to recognize the latter, as they are the markers of many inherited metabolic diseases. Three kinds of pathways must be considered: the catabolic pathways, the synthesis pathways, and the transport pathways. A disorder on a catabolic pathway induces an increase of all metabolites upstream and so an increase of the starting amino acid in all fluids. Any disorder on the synthetic pathway of a particular amino acid will induce a decrease of this amino acid in all fluids. When a transporter is located on a plasma membrane, its deficiency will result in normal or low concentration in plasma concomitant to a high excretion in urine.
APA, Harvard, Vancouver, ISO, and other styles
47

Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Refeeding syndrome. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0011.

Full text
Abstract:
Guidelines for the prevention of refeeding syndrome 82Refeeding syndrome is a term used to describe the various metabolic complications that can arise as a result of instituting nutritional support (enteral or parenteral) in malnourished patients.• Such patients are catabolic and their major sources of energy are fat and muscle; total body stores of nitrogen, phosphate, magnesium, and potassium are depleted....
APA, Harvard, Vancouver, ISO, and other styles
48

Tremblay, Mark Stephen. The effects of training status, exercise mode, and exercise duration on endogenous anabolic and catabolic steroid hormones in males. 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
49

Rabier, Daniel. Hyperammonemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0078.

Full text
Abstract:
Ammonia, an end-product of protein and amino acid catabolism toxic to the brain, must be removed quickly from the circulation. Its removal is achieved in two steps: glutamine synthesis and urea synthesis. Hyperammonemia results from either an excess of production or defective elimination. There are two main etiologies of hyperammonemia: inherited or acquired. Inherited causes are mainly related to defective elimination while acquired ones result either from excess production or deficient detoxification. Good laboratory diagnostic tools are necessary to make the right diagnosis.
APA, Harvard, Vancouver, ISO, and other styles
50

Raman, Vidya T. Perioperative Management of Diabetes Mellitus Type 1 and 2. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0046.

Full text
Abstract:
Diabetes management offers unique challenges in children and adolescents versus adults especially in the perioperative environment. The obvious challenges of monitoring dietary intake plus possible communication barriers with increased risk of diabetic ketoacidosis and hypoglycemia. Adding the catabolic stressors from surgery also add challenges to the perioperative physician managing the patient’s glycemic control. It is important to work with endocrinology in order to manage their diabetes. Lengthier procedures also complicate glycemic control. It involves sometimes close monitoring of not only glucose but electrolytes and blood and urine ketones.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Cataboliti' for other source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography