Books: 'Acid and bile tolerance'

1

G, Paumgartner, Stiehl A, and Gerok W. 1926-, eds. Trends in bile acid research. Dordrecht: Kluwer Academic Publishers, 1989.

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2

Keppler, D., A. Stiehl, U. Beuers, and M. Trauner, eds. Bile Acid Biology and Therapeutic Actions. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-1-4020-9644-0.

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3

Paumgartner, G., D. Keppler, U. Leuschner, and A. Stiehl, eds. Bile Acid Biology and its Therapeutic Implications. Dordrecht: Springer Netherlands, 2005. http://dx.doi.org/10.1007/1-4020-2913-6.

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4

G, Paumgartner, and Falk Symposium (141 : 2004 Jun : Stockholm, Sweden), eds. Bile acid biology and its therapeutic implications: Proceedings of the Falk Symposium 141 (XVIII International Bile Acid Meeting) held in Stockholm, Sweden, June 18-19 2004. Dordrecht: Springer, 2005.

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5

Howell, Peter. The effect of urinary bile acid excretion on renal stone formation. Salford: University of Salford, 1994.

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6

Hossain, Mohammad Anwar, Sergi Munné-Bosch, David J. Burritt, Pedro Diaz-Vivancos, Masayuki Fujita, and Argelia Lorence, eds. Ascorbic Acid in Plant Growth, Development and Stress Tolerance. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-74057-7.

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7

Hanna, Michael N. Molecular mechanisms involved in the acid tolerance response of Streptococcus mutans. Ottawa: National Library of Canada, 2001.

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8

G, Paumgartner, Stiehl A. 1941-, Gerok W. 1926-, and International Bile Acid Meeting (14th : 1996 : Freiburg, Germany), eds. Bile acids in hepatobiliary diseases: Basic research and clinical application : proceedings of the Falk Symposium no. 93, XIV International Bile Acid Meeting, held in Freiburg, Germany, October 22-24, 1996. Dordrecht: Kluwer Academic Publishers, 1997.

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9

1931-, Hofmann Alan F., Paumgartner G, and Stiehl A. (Adolf) 1941-, eds. Bile acids in gastroenterology: Basic and clinical advances : Falk Symposium 80 : proceedings of the 80th Falk Symposium (XIII International Bile Acid Meeting), held in San Diego, California, USA, September 30-October 2, 1994. Dordrecht: Kluwer Academic Publishers, 1995.

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10

Bile Acid Meeting (15th 1998 Titisee, Germany). Bile acids and cholestasis: XV International Bile Acid Meeting : proceedings of the Falk Symposium 108 (part I of the Gastrointestinal Week Titisee 1998) held in Titisee, Germany, October 12-13, 1998. Dordrecht: Kluwer Academic, 1999.

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11

Clark, Sanford J. An assessment of acid tolerance in the leeches Nephelopsis obscura and Haemopis grandis. Sudbury, Ont: Laurentian University, Department of Biology, 1993.

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12

Falk, Symposium (84th 1995 Berlin Germany). Bile acids, cholestasis, gallstones: Advances in basic and clinical bile acid research : proceedings of the Falk Symposium no. 84, held in Berlin, Germany, June 9-10, 1995. Dordrecht: Kluwer Academic Publishers, 1996.

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13

Falk, Symposium (108th 1998 Titisee Germany). Bile acids and cholestasis: (XV International Bile Acid Meeting) : proceedings of the Falk Symposium 108 (Part 1 of the Gastrointestinal Week Titisee 1998) held in Titisee, Germany, October 12-13, 1998. Dordrecht: Kluwer Academic Publishers, 1999.

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14

G, Paumgartner, Stiehl A. 1941-, Gerok W. 1926-, and Bile Acid Meeting (8th : 1984 : Bern, Switzerland), eds. Enterohepatic circulation of bile acids and sterol metabolism: Proceedings of the 42nd Falk Symposium, held during the VIIIth International Bile Acid Meeting, Berne, August 31-Sept. 2, 1984. Lancaster: MTP Press, 1985.

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15

Welin, Björn. Molecular analysis of cold acclimation in Arabidopsis thaliana and engineering of biosynthetic pathways leading to enhanced osmo tolerance. Uppsala: Dept. of Molecular Genetics, Uppsala Genetic Center, Swedish University of Agricultural Sciences, 1994.

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16

Reid, Neil Burton. Tolerance of Carex scoparia to acid-generating/metal contaminated coppermine tailings, and its dependance on substrate moisture. Sudbury, Ont: Laurentian University, Department of Biology, 2000.

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17

NGO Conference on Acid Rain (1986 Stockholm). The limits to nature's tolerance: Report from the NGO conference on acid rain, Lida, Stockholm, Sweden, September 6-7, 1986. Go teborg: Swedish NGO Secretariat on Acid Rain, 1987.

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18

Falk, Symposium (86th 1995 Basel Switzerland). Bile acids and immunology: Proceedings of the 86th Falk Symposium (part I of the Basel Liver Week), held in Basel, Switzerland, October 17-18, 1995. Dordrecht: Kluwer Academic Publishers, 1996.

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19

Torrance, Shona Margaret. The effect of varying levels of acute hypoxia on neonatal acid-base homeostasis, hemodynamic parameters, myocardial metabolism and tolerance to global ischemia. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1992.

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20

1949-, Hinze Willie L., ed. Bile acid/salt surfactant systems. Stamford, Connecticut: JAI Press, 2000.

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21

(Editor), G. Paumgartner, A. Stiehl (Editor), W. Gerok (Editor), D. Keppler (Editor), and U. Leuschner (Editor), eds. Bile Acids and Cholestasis - XV International Bile Acid Meeting. Springer, 1999.

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22

L, Barbara, and International Bile Acid Meeting (8th : 1984 : Bologna, Italy), eds. Recent advances in bile acid research. New York: Raven Press, 1985.

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23

Bile Acid Biology and Therapeutic Actions. Springer, 2009.

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24

Barbara. Recent Adv in Bile Acid Rsch. Lippincott Williams & Wilkins,US, 1985.

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25

(Editor), T. C. Northfield, P. Zentler-Munro (Editor), and R. Jazwari (Editor), eds. Bile Acids in Health and Disease: Update on Cholesterol Gallstones and Bile Acid Diarrhoea. Springer, 1988.

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26

Riadh, Jazrawi, Northfield Tim, and Zentler-Munro Patrick, eds. Bile acids in health and disease: Update on cholesterol gallstones and bile acid diarrhoea. Dordrecht: Kluwer Academic, 1988.

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27

Northfield, T. C. Bile Acids in Health and Disease: Update on Cholesterol Gallstones and Bile Acid Diarrhoea. Springer, 2011.

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28

Northfield, T. C., P. Zentler-Munro, and R. Jazwari. Bile Acids in Health and Disease: Update on Cholesterol Gallstones and Bile Acid Diarrhoea. Springer, 2012.

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29

Hinze, Willie L. Bile Acid/Salt Surfactant Systems (Organized Assemblies in Chemical Analysis , Vol 1). Jai Pr, 1996.

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30

G.P. van Berge Henegouwen (Editor), D. Keppler (Editor), U. Leuschner (Editor), G. Paumgartner (Editor), and A. Stiehl (Editor), eds. Biology of Bile Acids in Health and Disease - XVI International Bile Acid Meeting (Falk Symposium, Volume 120). Springer, 2001.

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31

Lackovic, Kresimir P. Involvement of an amino acid transporter in the acid tolerance of streptococcus mutans. 2003, 2003.

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32

Fujita, Masayuki, Sergi Munné-Bosch, Argelia Lorence, Mohammad Anwar Hossain, David J. Burritt, and Pedro Diaz-Vivancos. Ascorbic Acid in Plant Growth, Development and Stress Tolerance. Springer, 2018.

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33

Fujita, Masayuki, Sergi Munné-Bosch, Argelia Lorence, Mohammad Anwar Hossain, David J. Burritt, and Pedro Diaz-Vivancos. Ascorbic Acid in Plant Growth, Development and Stress Tolerance. Springer, 2018.

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34

(Editor), G. Paumgartner, D. Keppler (Editor), U. Leuschner (Editor), and A. Stiehl (Editor), eds. Bile Acid Biology and its Therapeutic Implications: Proceedings of the Falk Symposium 141 (XVIII Internationale Bile Acid Meeting) held in Stockholm, Sweden, June 18 - 19, 2004 (Falk Symposium). Springer, 2005.

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35

Workshops in Bile Acid Research: Serum Bile Acids in Health and Disease and The Pathophysiology of the Enterohepatic Circulation. Springer, 2011.

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36

Dowling, R. H., L. Barbara, A. F. Hofmann, and E. Roda. Workshops in Bile Acid Research: Serum Bile Acids in Health and Disease and the Pathophysiology of the Enterohepatic Circulation. Springer London, Limited, 2012.

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37

Dowling, R. H., L. Barbara, A. F. Hofmann, and E. Roda. Workshops in Bile Acid Research: Serum Bile Acids in Health and Disease and the Pathophysiology of the Enterohepatic Circulation. Springer Netherlands, 2011.

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38

Tanino, Karen K. Absciscic acid induction of environmental stress tolerance in plant cells. 1989.

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39

Lees, J. H. Genetic variation and acid tolerance in the Nemouridae (Insecta: Plecoptera). 1987.

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40

Casteels, M. Differences in the Peroxisomal B-oxidation of Fatty Acids and Bile Acid Intermediates. Leuven University Press, 1990.

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41

Schepers, L. Peroxisomal B-oxidation of the Carboxyl Side Chains of Prostaglandins and Bile Acid Intermediates. Leuven University Press, 1990.

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42

Lee, Stephen P. Molecular biology of abscisic acid induced freezing tolerance in bromegrass cell suspension cultures. 1992.

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43

Daudon, Michel, and Paul Jungers. Uric acid stones. Edited by Mark E. De Broe. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0202_update_001.

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Uric acid (UA) stones are typically red-orange and often appear as sand/ gravel though they may be large. They are totally radiolucent. They account for about 10% of all kidney stones in most countries, and up to 20% in some populations. It is twice as frequent in males, prevalence increases with age, and it is two to three times higher in patients with type 2 diabetes or with features of the metabolic syndrome. Factors that induce the formation of UA stones are a low urine volume, hyperuricosuria, and, more importantly, a permanently low urine pH (< 5). Indeed, below its pKa of 5.35 at 37°C, UA is in non-dissociated form, whose solubility is at best 100 mg/L, whereas urinary UA excretion normally exceeds 600 mg/day and may exceed 1g/day.Because UA solubility increases up to approximately 500 mg/L at urine pH > 6, urine alkalinization, with a target pH of 6.5–7, is the cornerstone of medical treatment. This most often allows dissolution of existing stones and prevention of recurrent stone formation so that urological intervention is infrequently needed. The preferred agent for alkalinization is potassium citrate (30–60 mEq/day in divided doses), because potassium urate is twice more soluble than sodium urate. However, in patients with poor gastric tolerance to potassium citrate or contraindication to potassium supplements, sodium bicarbonate is an acceptable alternative. Limitation of animal proteins, purine-rich foods (including beer), alcoholic drinks and acidified beverages (sodas) are useful measures, together with large fluid intake (> 2–2.5 L/day). Allopurinol may be indicated in cases of symptomatic hyperuricaemia. Regular observance of alkalinisation, with periodic controls of urine pH by the patient, is needed to prevent the rapid formation of UA stones. Patients affected by UANL, especially if overweight, should be evaluated for type 2 diabetes or glucose intolerance and managed accordingly.

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44

Murray, Eric K. Role of diet in low temperature tolerance and fatty acid composition of the alewife, Alosa pseudoharengus: A thesis in biology. 2000.

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45

Blaser, Annika Reintam, and Adam M. Deane. Normal physiology of the gastrointestinal system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0172.

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The gastrointestinal (GI) system is responsible for digestion and absorption, but also has important endocrine, immune and barrier functions. Additionally, the GI system plays a major role in fluid, electrolyte and acid-base balance. The GI system is regulated by complex myogenic, neural and humoral mechanisms, and, in health, these are affected by the presence of luminal nutrient, thereby modulating function of the GI system. Accordingly, GI function varies depending on whether a person is fasted or in the postprandial state. Adequate fasting and postprandial perfusion, motility and exocrine secretion are required for ‘normal’ functioning. The protective mechanisms of the GI system consist of physical (intact gut mucosa), non-immune (gastric acid, intestinal mucin, bile and peristalsis) and immune (gut-associated lymphoid tissue, GALT) elements. Disruption of GI protection is a putative mechanism underlying the development of multiple-organ dysfunction syndrome. Maintenance of GI function is increasingly recognised as an important factor underlying survival in critical illness.

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46

Verrips, Aad. Cerebrotendinous Xanthomatosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0040.

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Cerebrotendinous xanthomatosis (CTX) is a rare autosomal recessive disease due to a defect in bile acid metabolism. Worldwide, more than 300 patients have been described. Mutations in the CYP27A1 gene result in sterol 27-hydroxylase deficiency leading to the accumulation of cholestanol in multiple body tissues. Premature cataracts, chronic diarrhea, tendon xanthomas, and neurological deterioration are the predominant clinical features. There are several disease stages, from being nearly asymptomatic in the early childhood years to severe disability in later stages of life. Adult CTX patients are often misdiagnosed initially, especially when tendon xanthomasa are absent. CTX should be considered in all patients with premature cataracts and in patients with neurological features such as spasticity, early-onset dementia, ataxia, or Parkinsonism.

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47

Mochel, Fanny. Spastic Paraplegia Type 5. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0041.

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Spastic paraplegia type 5 (SPG5) is an autosomal recessive hereditary spastic paraplegia due to mutations in CYP7B1, which encodes oxysterol 7α‎-hydroxylase. Oxysterol 7α‎-hydroxylase is involved in the synthesis of bile acids from cholesterol. CYP7B1 mutations are responsible for rare forms of liver failure in infancy as well as lower motor neuron degeneration in adults with no obvious genotype-phenotype correlation. SPG5 is mostly characterized by spastic paraplegia with prominent posterior column sensory impairment that can lead to sensory ataxia and bladder dysfunction. SPG5 can easily be diagnosed thanks to the significant elevation of two plasma oxysterols: 27- and 25-hydroxycholesterol. Accordingly, plasma oxysterols are biomarkers that should be included in the screening of any spastic paraplegia of unknown etiology. Furthermore, the dramatic therapeutic response of a child with liver failure due to CYP7B1 mutations using chenodeoxycholic acid opens promising therapeutic perspectives for SPG5 patients, possibly as in cerebrotendinous xanthomatosis.

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48

Deegan, Patrick. Porphyria. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0179.

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This chapter discusses six diseases caused by inborn errors of metabolism affecting the biosynthesis of haem. Haem is a tetracyclic metal-binding compound involved in oxygen transport (in haemoglobin and myoglobin) and redox reactions (e.g. in the cytochrome P450 system). Each of these conditions is caused by a single gene defect in one of the enzymes involved in the biosynthesis of haem. Inheritance is usually autosomal dominant with incomplete penetrance. The enzyme defect results in disease, not as a result of deficiency of the reaction product, but as a result of accumulation of precursors. Early, soluble precursors, 5-aminolaevulinic acid, and porphobilinogen (not porphyrins as such) are neurotoxic and, when present in great excess, as occurs when flux through the haem synthetic pathway is increased in response to particular medications or hormones, lead to acute neurovisceral crises. Later cyclical precursors (porphyrins) in the pathway are also water soluble and excreted in urine, but are susceptible to activation by electromagnetic radiation in the visible spectrum and are converted to free-radical metabolites that cause pain, inflammation, and tissue damage in the skin. The final haem precursors (also porphyrins) are hydrophobic and excreted in the bile and faeces and are also activated by light to toxic metabolites.

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49

Ruskin, David N. Metabolic Therapy and Pain. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0022.

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Chronic pain is associated strongly with poor quality of life. Drug treatments for pain can be problematic; with the understanding that chronic pain syndromes often involve derangement of homeostasis, there is an increased interest in applying nonpharmacological metabolic therapies. This chapter surveys clinical and animal research into the effects of fasting, calorie restriction, ketogenic diet, and polyunsaturated fatty acid supplementation on pain. These dietary treatments can significantly ameliorate pain in inflammatory and neuropathic disorders. The choice among these treatments might depend on the specific pain syndrome and the tolerance of the patient for particular dietary modifications. Several possible mechanisms are discussed, some of which might be in common among these treatments, and some treatments might engage multiple mechanisms. Multiple mechanisms acting together could be ideal for restoring the disordered metabolism underlying some pain syndromes.

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50

Servais, Aude. Nephropathic Cystinosis in Adults. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0060.

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Cystinosis is an autosomal recessive lysosomal storage disorder caused by a defect in the carrier-mediated system that normally transports cystine out of lysosomes. As a consequence, tissues accumulate variable amounts of the disulphide amino acid cystine. Three overlapping clinical phenotypes are recognized, varying in severity and age of onset. The most severe, the infantile nephropathic form (MIM 219800), appears in the first year of life. The late-onset form (MIM 219900) is also nephropathic, while ocular, non-nephropathic cystinosis manifests largely with corneal crystal deposition (MIM 219750). Infantile cystinosis is the most common form. Affected children develop renal proximal tubulopathy at 6 to 12 months of age. In the absence of treatment, renal failure occurs, with progression to end-stage renal disease (ESRD). Cystine crystal deposition in the cornea leads to photophobia and continuous widespread cystine accumulation eventually leads to rickets, retinal, endocrinological (hypothyroidism and impaired glucose tolerance), hepatic, gastrointestinal, muscular, and neurological abnormalities.

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Books on the topic 'Acid and bile tolerance'

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