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Books on the topic 'Sterol metabolism'

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Published: 21 June 2022

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1

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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2

Ntambi, Ph.D., James M., ed. Stearoyl-CoA Desaturase Genes in Lipid Metabolism. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7969-7.

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3

Symposium on Lipoprotein and Cholesterol Metabolism in Steroidogenic Tissues (1984 Laval University). Lipoprotein and cholesterol metabolism in steroidogenic tissues. Philadelphia: Georg F. Stickley Co., 1985.

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4

Steroid-protein interactions II. Berlin: Springer-Verlag, 1986.

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5

Cologne Workshop on Dope Analysis (10th 1992). 10th Cologne Workshop on Dope Analysis, 7th to 12th June 1992: Proceedings. Edited by Donike M. Köln: Sport und Buch Strauss, Edition Sport, 1993.

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6

S, Bhatt Tarlochan, ed. Cyclopenta(a)phenanthrenes: Polycyclic aromatic compounds structurally related to steroids. Cambridge [Cambridgeshire]: Cambridge University Press, 1987.

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7

Maximum muscle and minimum fat: The secret science behind physical transformation. Berkeley, Calif: North Atlantic Books, 2008.

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8

Freedman, Jeri. Steroids: High-risk performance drugs. New York: Rosen Pub. Group, 2009.

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9

International, Meeting on Steroids and the Nervous System (2nd 2003 Turin Italy). Steroids and the nervous system. New York: New York Academy of Sciences, 2003.

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10

International Meeting on Steroids and the Nervous System (2nd 2003 Turin, Italy). Steroids and the nervous system. New York: New York Academy of Sciences, 2003.

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11

Advanced Course on Steroid Enzymes and Cancer (9th 2008 Erice, Italy). Steroid enzymes and cancer. Malden, MA: Wiley-Blackwell, 2009.

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12

Pertschuk, Louis P. Immunocytochemistry for steroid receptors. Boca Raton: CRC Press, 1990.

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13

(Editor), G. Paumgartner, A. Stiehl (Editor), and W. Gerok (Editor), eds. Enterohepatic Circulation of Bile Acids and Sterol Metabolism (Falk Symposium). Springer, 1985.

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14

1938-, Patterson Glenn W., Nes W. David, and American Oil Chemists' Society, eds. Physiology and biochemistry of sterols. Champaign, Ill: American Oil Chemists' Society, 1991.

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15

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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16

Henry, Danielsson, and Sjövall Jan, eds. Sterols and bile acids. Amsterdam: Elsevier, 1985.

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17

J, Parish Edward, and Nes W. David, eds. Biochemistry and function of sterols. Boca Raton: CRC Press, 1997.

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18

Ph.D. James M. Ntambi. Stearoyl-CoA Desaturase Genes in Lipid Metabolism. Springer, 2013.

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19

James M. Ntambi Ph.D. Stearoyl-CoA Desaturase Genes in Lipid Metabolism. Springer, 2013.

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20

Nicholson, Grainne, and George M. Hall. Neuroendocrine physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0008.

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This chapter describes the hormonal, metabolic, and inflammatory response to surgery—commonly known as the surgical stress response. The changes in protein, carbohydrate, and fat metabolism to provide fuel for oxidation are outlined as well as changes in salt and water metabolism. Psychological sequelae of fatigue and malaise are also common in patients undergoing surgery. Attenuating the metabolic and endocrine changes associated with surgery may reduce postoperative morbidity and expedite recovery; the choice of anaesthetic drugs and techniques (regional vs general anaesthesia) and the increasing use of laparoscopic surgery have all been used to try to achieve this objective. The most common metabolic disease which anaesthetists have to manage is diabetes mellitus (DM) and its pathophysiology and medical management, as well as that of the related metabolic syndrome are discussed. Adrenal tumours are rare but usually require surgical excision. Phaeochromocytomas present unique anaesthetic challenges, but pre-, intra-, and postoperatively in terms of fluid management and blood pressure control. Conn’s syndrome (primary hyperaldosteronism) can also result in hypertension and electrolyte disturbances. Cushing’s disease (glucocorticoid excess) presents with the clinical effects of steroid excess and many patients have concomitant DM. Finally, perioperative steroid supplementation for patients already taking steroids and undergoing surgery is discussed.

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21

1947-, Strauss Jerome F., and Menon K. M. J, eds. Lipoprotein and cholesterol metabolism in steroidogenic tissues. Philadelphia: G. F. STickley, 1985.

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22

Prout, Jeremy, Tanya Jones, and Daniel Martin. Endocrinology, metabolism, and body temperature. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199609956.003.0005.

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This chapter summarizes endocrine physiology that is of particular relevance to anaesthesia. Disorders of the adrenal cortex and medulla, pituitary and thyroid are described with perioperative management considerations highlighted. Current guidelines in perioperative steroid replacement are included. Diabetes is a particularly common problem encountered in clinical practice. Diabetic complications, pre-assessment and perioperative management aims are included. The surgical stress response is summarized with details of the neuroendocrine changes and their modification with anaesthetic technique. Consequences of perioperative hypothermia and use of therapeutic hypothermia are detailed.

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23

Blanshard, Hannah. Endocrine and metabolic disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198719410.003.0008.

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This chapter describes the anaesthetic management of the patient with endocrine and metabolic disease. Topics covered include diabetes mellitus, thyroid and parathyroid disease, acromegaly, adrenocortical disease, steroid therapy, Cushing’s and Conn’s syndromes, apudoma (including phaeochromocytoma), and abnormalities of sodium and potassium. For each topic, preoperative investigation and optimization, treatment, and anaesthetic management are described. The perioperative management of the diabetic patient is discussed in detail, including insulin and oral hypoglycaemic therapy. Perioperative steroid management is described.

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24

Blanshard, Hannah. Endocrine and metabolic disease. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198719410.003.0008_update_001.

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This chapter describes the anaesthetic management of the patient with endocrine and metabolic disease. Topics covered include diabetes mellitus, thyroid and parathyroid disease, acromegaly, adrenocortical disease, steroid therapy, Cushing’s and Conn’s syndromes, apudoma (including phaeochromocytoma), and abnormalities of sodium and potassium. For each topic, preoperative investigation and optimization, treatment, and anaesthetic management are described. The perioperative management of the diabetic patient is discussed in detail, including insulin and oral hypoglycaemic therapy. Perioperative steroid management is described.

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25

David, Nes W., Parish Edward J, Trzaskos James M, American Chemical Society. Division of Agricultural and Food Chemistry., and American Chemical Society Meeting, eds. Regulation of isopentenoid metabolism. Washington, DC: American Chemical Society, 1992.

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26

Cok, Steven Jon. Cholestrol transport and metabolism by mitochondria of steroidogenic cells. 1993.

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27

1967-, Xie Wen, ed. Nuclear receptors in drug metabolism. Hoboken, NJ: John Wiley & Sons, 2008.

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28

L, Castagnetta, Università di Messina. Institute of Oncology and Research on Cancer., New York Academy of Sciences., and International Symposium on Steroid Formation, Degradation, and Action in Peripheral Normal and Neoplastic Tissues (1st : 1989 : Taormina, Italy), eds. Steroid formation, degradation, and action in peripheral tissues. New York, N.Y: New York Academy of Sciences, 1990.

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29

(Editor), W. David Nes, Edward J. Parish (Editor), and James M. Trzaskos (Editor), eds. Regulation of Isopentenoid Metabolism (Acs Symposium Series). An American Chemical Society Publication, 1998.

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30

1930-, Sluyser M., ed. Interaction of steroid hormone receptors with DNA. Chichester, England: Ellis Horwood, 1985.

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31

Elder, Grahame J. Metabolic bone disease after renal transplantation. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0288.

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Patients who undergo kidney transplantation have laboratory, bone, and soft tissue abnormalities that characterize chronic kidney disease mineral and bone disorder (CKD-MBD). After successful transplantation, abnormal values of parathyroid hormone, fibroblast growth factor 23, calcium, phosphate, vitamin D sterols, and sex hormones generally improve, but abnormalities often persist. Cardiovascular risk remains high and is influenced by prevalent vascular calcification, and fracture risk increases due to a combination of abnormal bone ‘quality’, compounded by immunosuppressive drugs and reductions in bone mineral density. Patients with well managed CKD-MBD before transplantation generally have a smoother post-transplant course, and it is useful to assess patients soon after transplantation for risk factors relevant to the general population and to patients with CKD. Targeted laboratory assessment, bone densitometry, and X-ray of the spine are useful for guiding therapy to minimize post-transplant effects of CKD-MBD. To reduce fracture risk, general measures include glucocorticoid dose minimization, attaining adequate 25(OH)D levels, and maintaining calcium and phosphate values in the normal range. Calcitriol or its analogues and antiresorptive agents such as bisphosphonates may protect bone from glucocorticoid effects and ongoing hyperparathyroidism, but the efficacy of these therapies to reduce fractures is unproven. Alternate therapies with fewer data include denosumab, strontium ranelate, teriparatide, oestrogen or testosterone hormone replacement therapy, tibolone, selective oestrogen receptor modulators, and cinacalcet. Parathyroidectomy may be necessary, but is generally avoided within the first post-transplant year. A schema is presented in this chapter that aims to minimize harm when allocating therapy.

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32

Patisaul, Heather B., and Scott M. Belcher. Receptor and Enzyme Mechanisms as Targets for Endocrine Disruptors. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199935734.003.0005.

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In this chapter, the current understanding of the mechanisms of endocrine disruption on the brain and nervous system are presented. Because the overwhelming majority of mechanistic studies on EDCs have focused on the actions mediated by nuclear hormone receptors, this mechanisms is described in detail. The chapter also discusses the classic transcriptional mechanisms of steroid action and the impact of EDCs on rapid signaling (non-genomic) mechanisms. It presents an overview of the enzymes and pathways involved in the biosynthesis of steroid hormones, which are critical to proper functioning of the HPA and HPG axis, and the neuroactive steroids synthesized and active in the mammalian brain. The potential for EDCs to alter metabolic enzymes, with a focus on possible targets in the metabolic blood-brain barrier, is presented as a potential, though largely unexplored, mode of EDC action in the brain.

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33

Gordan, Gilbert S., and Luciano Martini. Steroid Modulation of Neuroendocrine Function Sterols, Steroids and Bone Metabolism: Proceedings of the XI Meeting of the International Study Group for ... 2, 1983 (International congress series). Excerpta Medica, 1985.

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34

Khavandi, Kaivan, Halima Amer, Sarah Withers, and Behdad Afzali. Pleiotropic effects of vitamin D. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0127.

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Vitamin D is a fat-soluble steroid pro-hormone integral to physiological health, fulfilling a central role in skeletal mineralization, bone metabolism, and immune biology. Although vitamin D is synthesized photochemically in the skin and some is absorbed from dietary sources, vitamin D insufficiency and deficiency are very common. Epidemiological studies have demonstrated a strong association between vitamin D and kidney and heart disease, and some supplementation studies have suggested that repletion may prevent and/or ameliorate cardiorenal injury. This chapter focuses on vitamin D biology and discusses the many associations of vitamin D perturbation with diseases of humans.

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35

The effects of sex steroids and related menstrual cycle hormones on muscle metabolism. 1985.

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36

The effects of sex steroids and related menstrual cycle hormones on muscle metabolism. 1988.

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37

Martin, Wehling, ed. Genomic and non-genomic effects of aldosterone. Boca Raton: CRC Press, 1995.

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38

Klaus, Ruckpaul, and Rein Horst, eds. Molecular mechanisms of adrenal steroidogenesis and aspects of regulation and application. London: Taylor & Francis, 1990.

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39

Robin, Fears, and Sabine John R, eds. Cholesterol 7 [alpha]-hydroxylase (7 [alphamonooxygenase). Boca Raton, Fla: CRC Press, 1986.

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40

(Editor), Naftolin F., ed. The New Biology of Steroid Hormones (Serono Symposia Publications from Raven Press). Lippincott Williams & Wilkins, 1991.

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41

B, Hochberg Richard, Naftolin Frederick, and Serono Foundation Symposium (1990 : Budapest, Hungary), eds. The New biology of steroid hormones. New York: Raven Press, 1991.

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42

Fotherby, K., and S. B. Bal. Steroid Converting Enzymes and Diseases. De Gruyter, Inc., 2019.

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43

Erminio, Costa, and Paul Steven M, eds. Neurosteroids and brain function. New York: Thieme Medical Publishers, 1991.

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44

Paul, Steven, and E. Costa. Neurosteroids and Brain Function (FIDIA Research Foundation Symposium Series). Thieme Publishing Group, 1992.

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45

Coombs, Maurice M., and Tarlochan S. Bhatt. Cyclopenta[a]-phenanthrenes (Cambridge Monographs on Cancer Research). Cambridge University Press, 1987.

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46

(Editor), A. R. Genazzani, and F. Petraglia (Editor), eds. The Brain: Source and Target for Sex Steroid Hormones, 1st Tuscania Conference on Reproductive Medicine. Informa Healthcare, 1996.

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47

McEwen, Bruce S., and Natalie L. Rasgon. The Brain and Body on Stress. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0002.

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Neuroscientists have treated the brain in isolation from the rest of the body, while endocrinology and general medicine have viewed the body largely without regard to the influence of systemic physiology and pathophysiology on higher brain centers outside of the hypothalamus and pituitary gland. But now there is greater recognition of brain–body interactions affecting the limbic and cognitive systems of brain and altering systemic physiology; these are conceptualized as allostasis and allostatic load and overload. These concepts look at both the interactions of brain and body to stressors and health-promoting and health-damaging behaviors, and they help integrate behavior and mood with systemic functions. These interactions involve genetic predispositions and epigenetic alterations mediated by circulating steroid and metabolic hormones. Comorbidity and multi-morbidity of disorders will be illustrated by the relationship of systemic and brain insulin resistance to the psychopathology of depression and to the increased risk for dementia.

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48

Rees, Lesley. Growth and development. Edited by Norbert Lameire and Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0291.

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Enabling achievement of full height potential in a child with chronic kidney disease (CKD) is one of the major and most challenging goals for the paediatric nephrologist. Short stature is associated with psychological maladjustment and with increased morbidity and mortality. The causes of poor growth are multifactorial and include poor nutrition, and metabolic, haematological, and endocrine disturbances. The most vulnerable times are the periods of most rapid growth, that is, infancy and puberty. Growth during infancy is principally dependent on nutrition so many infants need supplemental enteral feeding. Growth delay correlates with severity of CKD, with those on dialysis faring the worst such that by CKD stage 5, approximately 25% of patients are below the normal range for height. Height achieved post transplant is dependent on graft function and is better in younger children and those who have the best height attainment pre transplant. The use of steroid-free immunosuppressive regimens is encouraging. The prognosis for final height is improving.

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49

Robert, Morfin, ed. DHEA and the brain. London: Taylor & Francis, 2002.

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50

Hofmekler, Ori. Maximum Muscle, Minimum Fat: The Secret Science Behind Physical Transformation. North Atlantic Books, 2008.

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