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Books on the topic 'Peptide effects'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

International Agency for Research on Cancer and World Health Organization, eds. Ingested nitrate and nitrite, and cyanobacterial peptide toxins. Lyon, France: International Agency for Research on Cancer, 2010.

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2

Mooney, Mark H. Glucagon-like peptide-1 and gastric inhibitory polypeptide: Effects of N-terminal glycation on hormone degradation, insulin secretion and antihyperglycaemic activity. [S.l: The Author], 2000.

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3

International Symposium on Nonmammalian Peptides (1st 1985 Rome, Italy). First International Symposium on Nonmammalian Peptides: Held in Rome, Italy, May 11-15, 1985 at Accademia Nazionale dei Lincei, honorary president Vittorio Erspamer. Polifarma, Roma: Universitá degli Studi di Roma, 1985.

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4

International Symposium on VIP and Related Peptides (5th 1991 Shizuoka, Japan). Vasoactive intestinal peptide and related peptides: Proceedings of the Fifth International Symposium on VIP and Related Peptides, Shizuoka, Japan, November 12-15, 1991. Edited by Yanaihara Noboru. Tokyo: Biomedical Research Foundation, 1992.

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5

Chinese Peptide Symposium (4th 1996 Chengdu, China). Peptides: Biology and chemistry : proceedings of the 1996 Chinese Peptide Symposium, July 21-25, 1996, Chengdu, China. Dordrecht: Kluwer Academic, 1998.

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6

Khavinson, V. Kh. Peptides and ageing. Prague: Society of Integrated Sciences, 2002.

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7

Harding, Louise M. The effects of locusta peptides on mammalian calcium channels. Oxford: Oxford Brookes University, 1997.

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8

Hubert, Vaudry, and Laburthe Marc, eds. VIP, PACAP, and related peptides: From gene to therapy. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2006.

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9

Adam, Rijnberk, Wimersma Greidanus, Tj. B. van., and Rijksuniversiteit te Utrecht. Vakgroep Geneeskunde van het Kleine Huisdier., eds. Comparative pathophysiology of regulatory peptides. Basel: Karger, 1987.

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10

NATO Advanced Research Workshop on the Role of Melatonin and Pineal Peptides in Neuroimmunomodulation (1990 Erice, Italy). Role of melatonin and pineal peptides in neuroimmunomodulation. New York: Plenum Press, 1991.

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11

Fiziologicheskoe znachenie peptidov mozga dli͡a︡ dei͡a︡telʹnosti pishchevaritelʹnoĭ sistemy. Leningrad: Izd-vo "Nauka," Leningradskoe otd-nie, 1986.

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12

Jenssen, Havard. Antimicrobial activity of lactoferrin and lactoferrin derived peptides. Hauppauge, NY: Nova Science, 2009.

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13

Sandhu, Harmanjit Singh. The effect of GLP-1, glucagon-like peptide 1, on insulin sensitivity in diabetic dogs. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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14

Hettiarachchy, Navam S. Food proteins and peptides: Chemistry, functionality, interactions, and commercialization. Boca Raton, FL: Taylor & Francis, 2012.

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15

Nonsteroidal gonadal factors: Physiological roles and possibilities in contraceptive development, January 6-8, 1988, Omni International Hotel, Norfolk, Virginia, USA. Norfolk, Va: Jones Institute Press, 1988.

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16

Bubbles, drops, and particles in non-Newtonian fluids. Boca Raton, Fla: CRC Press, 1993.

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17

Winter Neuropeptide Conference (5th 1984 Breckenridge, Colo.). Fifth annual Winter Neuropeptide Conference: Breckenridge, Colorado, january 18-211, 1984. Fayetteville, N.Y: ANKHO International, 1985.

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18

Winter Neuropeptide Conference (6th 1985 Breckenridge, Colo.). Sixth annual Winter Neuropeptide Conference : Breckenridge, Colorado, January 23-26, 1985. Fayetteville, N.Y: ANKHO International, 1985.

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19

American Society of Hypertension. Meeting. First Annual Meeting of the American Society of Hypertension, May 29-30, 1986 ; First World Congress on Biologically Active Atrial Peptides, May 31-June 1, 1986: Program and abstracts, Waldorf-Astoria Hotel, New York, New York. Thorofare, N.J: The Society, 1986.

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20

Clinch, David. Peptic ulcer and its drug causation: The role of non-steroidal anti-inflammatory drugs. London: Croom Helm, 1986.

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21

Peptide Hormones: Effects and Mechanisms of Action (Peptide Hormones). CRC, 1988.

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22

(Editor), P. Michael Conn, ed. Peptide Hormones: Effects and Mechanisms of Action (Peptide Hormones). Reader's Digest Young Families, 1988.

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23

Peptide Hormones: Effects and Mechanisms of Action (Peptide Hormones). Reader's Digest Young Families, 1988.

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24

Andrés, Negro-Vilar, and Conn P. Michael, eds. Peptide hormones: Effects and mechanisms of action. Boca Raton, Fla: CRC Press, 1988.

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25

1955-, Quirion Remi, Björklund Anders 1945-, and Hökfelt Tomas, eds. Peptide receptors. Amsterdam: Elsevier, 2000.

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26

(Editor), Xiao-Jie Xu, Yun-Hua Ye (Editor), and James P. Tam (Editor), eds. Peptides: Biology and Chemistry (Chinese Peptide Symposia). Springer, 1998.

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27

(Editor), R. Quirion, A. Björklund (Editor), and T. Hökfelt (Editor), eds. Peptide Receptors, Part I (Handbook of Chemical Neuroanatomy). Elsevier Science, 2000.

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28

Tracy, Derek K., and Fiona Gaughran. Treatment with medication: Side effects, adherence, and risk. Edited by Alec Buchanan and Lisa Wootton. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198738664.003.0009.

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Antipsychotic medications revolutionized the care of psychosis, but they have brought with them significant side effects and issues around adherence; these latter factors, and informed co-working with patients, are primary drivers for specific medication choices. The data remain limited for polypharmacy and above-maximum dose prescribing, though there may be individuals for whom this is considered. Long-acting injectables (LAIs or ‘depots’) have a good evidence base, and are probably underutilized, though clozapine remains our drug of choice in refractory illness. Forensic-population data show that medications significantly reduce recidivism, including of violent crime. Whilst side effect data are disheartening for both patient and clinician, there are rational management strategies for them all. Novel future therapies being evaluated include acetylcholinergic and glutamatergic enhancers, anti-inflammatory drugs, and the neural peptide oxytocin, to improve negative and cognitive functioning; neuromodulation through rTMS and tDCS are also showing early promise.

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29

Rocca, Antonio Stevereves. Direct and indirect effects of fatty acids on secretion of the antidiabetic hormone, glucagon-like peptide-1. 2000.

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30

Raeburn, D. Airways Smooth Muscle: Peptide Receptors, Ion Channels, and Signal Transduction (Agents and Actions Supplements). Birkhauser, 1995.

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31

Fawcett, Erin Eileen. The skeletal effects of a growth hormone-derived peptide (AOD9604) in the aged rat model of postmenopausal osteoporosis. 2004.

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32

Bird, Mark F., and David G. Lambert. Deorphanization of ORL-1/LC132 by reverse pharmacology in two landmark studies. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0026.

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Deorphanization of ORL-1/LC132 in 1995 by reverse pharmacology in two simultaneously published landmark studies added a new member to the opioid family of G-protein coupled receptors. Meunier and Reinscheid used cells expressing recombinant ORL-1 (human) or LC132 (rat) and the presumed intracellular inhibition of cyclic AMP formation to ‘fish’ for endogenous peptide ligands in rat whole-brain and pig hypothalamic extracts. Both studies reported the isolation of a 17-amino-acid peptide, which was named nociceptin and orphanin FQ by the two authors, respectively. The behaviour of the isolated peptide was a complete surprise, as a general hyperalgesia was observed when the peptide was administered at supraspinal sites. We now know that this peptide has, in fact, anti-opioid action, particularly in the medulla. The endogenous peptide exerts a multitude of effects both in the nervous system and, unlike classical opioids, has efficacy in neuropathic pain.

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33

Truncated glucagon-like peptide-1: Mechanism of action and effects on hormone synthesis and secretion in isolated rat pandreatic islets. Ottawa: National Library of Canada, 1993.

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34

Donini, Andrew. The physiological effects and mode of action of crustacean cardioactive peptide and tyramine on visceral muscle of the locust, Locusta migratoria. 2003.

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35

K, Klimov P., Barashkova G. M, Zami͡a︡tnin A. A, Institut ėvoli͡u︡t͡s︡ionnoĭ fiziologii i biokhimii im. I.M. Sechenova., Nauchnyĭ t͡s︡entr biologicheskikh issledovaniĭ (Akademii͡a︡ nauk SSSR), and Peptides-90 (1990 : Gorʹkiĭ, R.S.F.S.R.), eds. Fiziologicheskoe i klinicheskoe znachenie reguli͡a︡tornykh peptidov: 27-29 noi͡a︡bri͡a︡ 1990 g., Gorʹkiĭ : tezisy dokladov. Pushchino: Nauch. t͡s︡entr biologicheskikh issl. AN SSSR v Pushchine, 1990.

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36

Rahimi, Kazem. Chronic heart failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0092.

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The European Society of Cardiology defines heart failure as a clinical syndrome in which patients have the following features: symptoms typical of heart failure (breathlessness, fatigue, ankle swelling); signs typical of heart failure (tachycardia, tachypnoea, pulmonary crackles, pleural effusion, raised jugular venous pressure, peripheral oedema, hepatomegaly); and objective evidence of a structural or functional abnormality of the heart at rest (cardiomegaly, third heat sound, cardiac murmurs, abnormality on the echocardiogram, raised natriuretic peptide concentration). Heart failure results in activation of the sympathetic nervous system and the renin–aldosterone–angiotensin system, and release of a number of hormones such as natriuretic peptides, and cytokines, including tumour necrosis factor amongst others. While neurohormone activation is initially compensatory and helps in the short term to maintain circulatory needs, ultimately it has detrimental effects on the myocardium and compromises its function further. These mechanisms are therefore therapeutic targets to improve symptoms and lessen the risk of death.

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37

Mason, Peggy. Synthesis, Packaging, and Termination of Neurotransmitters. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0012.

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The synthesis, packaging, and termination of action of neurotransmitters are detailed. There are far more varieties of peptide neurotransmitters than there are of low-molecular-weight neurotransmitters. Yet low-molecular-weight neurotransmitters are the ubiquitous workhorses of the nervous system. Acetylcholine, the catecholamines norepinephrine and dopamine, serotonin, glutamate, and GABA are examined in some depth. The vesicular transporters that carry low-molecular-weight neurotransmitters from the cytoplasm into synaptic vesicles are covered. The role of monoamines in affect and mood and the psychotropic effects of monoaminergic drugs are discussed. Principles of catecholamine synthesis are applied to understand phenylketonuria. Uptake of monoamines into neurons is discussed in the context of amphetamine, cocaine, and other drugs of abuse. Stiff-person syndrome, which results from an impairment of GABA synthesis, is introduced. The modes of action for peptide and gaseous neurotransmitters are briefly covered.

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38

Dickenson, Tony. Endogenous opioids in the CNS. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0019.

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This short and concise paper was the first to unequivocally reveal that there were endogenous opioids in the central nervous system (CNS), identify their peptide nature and sequence, and show that they exerted physiological inhibitory effects. The idea that there were natural opioids fitted with concurrent reports of opiate-binding sites, and this led to the description of multiple receptors with their own families of peptide transmitters. No truly novel opioid drugs have emerged since, and attempts to protect and manipulate the enkephalins for pain control have yet to be successful. This does not detract from this key study, which made us think about pain modulation in a different way, and subsequent work has clearly shown how endogenous opioid signalling is critical in CNS function, perhaps most importantly in endogenous pain control, such as that harnessed by placebo analgesia.

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39

Wójcik-Gładysz, Anna. Ghrelin – hormone with many faces. Central regulation and therapy. The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 2020. http://dx.doi.org/10.22358/mono_awg_2020.

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Discovered in 1999, ghrelin, is one of the peptides co-creating the hypothalamicgastrointestinal axis, otherwise known as the brain-gut axis. Ghrelin participates in many physiological processes and spectrum of its activity is still being discovered. This 28 amino acid peptide ‒ a product of the ghrl gene, was found in all vertebrates and is synthesized and secreted mainly from enteroendocrine X/A cells located in the gastric mucosa of the stomach. Expression of the ghrelin receptor has been found in many nuclei of the hypothalamus involved in appetite regulation. Therefore it’s presumed that ghrelin is one of the crucial hormones deciphering the energy status required for the maintenance of organism homeostasis. Ghrelin acts as a signal of starvation or energy insufficiency and its level in plasma is reduced after the meal. Neuropeptide Y (NPY) and agouti-related peptide (AgRP; NPY/AgRP) neurons located in the arcuate nucleus (ARC) area are the main target of ghrelin in the hypothalamus. This subpopulation of neurons is indispensable for inducing orexigenic action of ghrelin. Moreover ghrelin acting as a neurohormone, mainly in the hypothalamus area, plays an important role in the regulation of growth and reproduction processes. Indeed, ghrelin action on reproductive processes has been observed in the systemic effects exerted at both hypothalamus-pituitary and gonadal levels. Similarly the GH-releasing ghrelin action was observed both on the hypothalamus level and directly on the somatotrophic cells in the pituitary and this dose-related GH releasing activity was found in in vitro as well as in in vivo experiments. In recent years, numerous studies revealed that ghrelin potentially takes part in the treatment of diseases associated with serious disturbances in the organism energy balance and/or functioning of the gastrointestinal tract. It was underlined that ghrelin may be a hormone with a broad spectrum of therapeutic effect on obesity and anorexia nervosa, as well as may also have protective effect on neurodegenerative diseases, inflammatory disorders or functional changes in the body caused by cancers. In overall, ghrelin treatment has been tested in over 100 preclinical studies with healthy volunteers as well as patients with various types of cancer, eating disorders such as anorexia nervosa and bulimia nervosa. It was observed that ghrelin has an excellent clinical safety profile and emerging side effects occurred only in 3–10% of patients and did not constitute a sufficient premise to discontinue the therapy. In general, it can be concluded that ghrelin may be sufficiently used as a prescription drug.

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40

Hinder, Lucy M., Kelli A. Sullivan, Stacey A. Sakowski, and Eva L. Feldman. Mechanisms Contributing to the Development and Progression of Diabetic Polyneuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0114.

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Advances in our understanding of diabetes in human patients and experimental models indicate that a number of mechanisms may contribute to sensory nerve damage in diabetic polyneuropathy (DPN). In addition to oxidative stress, hyperglycemia and hyperlipidemia, recent research in pain, advanced glycation endproduct (AGE), and proteomics specify a contributory role for altered neuronal calcium homeostasis in DPN. Technology advances indicate neuronal energy balance and mitochondrial biogenesis, fission, and fusion are additional potential mechanisms. The effects of dysregulation or loss of insulin signaling and the effects of glucagon-like peptide-1 (GLP-1) and its receptor (GLP-1R) are also implicated.

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41

Bioactive Peptides. CRC, 2009.

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42

John, Howl, and Jones Sarah Dr, eds. Bioactive peptides. Boca Raton: CRC Press/Taylor & Francis, 2009.

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43

Atrial natriuretic peptides. New York: Churchill Livingstone, 1989.

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44

1937-, Brenner Barry M., and Stein Jay H. 1937-, eds. Atrial natiuretic peptides. Churchill Livingstone, 1989.

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45

Progress in atrial peptide research. New York: Raven Press, 1989.

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46

1937-, Brenner Barry M., and Laragh John H. 1924-, eds. Advances in atrial peptide research. New York: Raven Press, 1988.

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47

I͡U︡, Budant͡s︡ev A., Sherstnev V. V, Akademii͡a︡ medit͡s︡inskikh nauk SSSR, and Institut biologicheskoĭ fiziki (Akademii͡a︡ nauk SSSR), eds. Fiziologicheski aktivnye peptidy: Sbornik nauchnykh trudov. Pushchino: Nauch. t͡s︡entr biologicheskikh issledovaniĭ, 1988.

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48

Carter, C. Sue, Inbal Ben-Ami Bartal, and Eric C. Porges. The Roots of Compassion. Edited by Emma M. Seppälä, Emiliana Simon-Thomas, Stephanie L. Brown, Monica C. Worline, C. Daryl Cameron, and James R. Doty. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190464684.013.14.

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Compassion for others and social support have survival value and health benefits. Although compassion is sometimes considered uniquely human, critical components of compassion have been described in nonhuman mammals. Studies originally conducted in social mammals and now in humans have implicated neuropeptide hormones, especially oxytocin, in social cognition, a sense of safety, and the capacity of sociality to permit compassionate responses. In contrast, the related peptide vasopressin and its receptor may be necessary for forming selective relationships and for the apparently paradoxical effects of oxytocin, which can include increases in fear and avoidance. Oxytocin and vasopressin may contribute to sex differences in compassion. Furthermore, among the processes through which oxytocin and vasopressin influence behavior and health are complex effects on the autonomic nervous system. Knowledge of the mechanisms underlying the benefits of compassion offers new insights into the healing power of positive social behaviors and social support.

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49

P, Illes, Farsang C, and International Brain Research Organization. Congress, eds. Regulatory roles of opioid peptides. Weinheim, Federal Republic of Germany: VCH, 1988.

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50

Nutt, David J., and Liam J. Nestor. Appetite hormones and addiction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198797746.003.0012.

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Many of the same behavioural and brain disturbances observed in addiction are also seen in obesity and binge-eating disorder. This suggests that there are shared neural substrates between substance addiction and compulsive food consumption. Food intake and appetite are regulated by numerous appetite hormones that exert their effects through brain systems involved in reward sensitivity, stress, impulsivity, and compulsivity. There is now emerging evidence that appetite hormones (e.g. ghrelin, glucagon-like peptide-1, orexin) can modulate addictive behaviours (e.g. craving) and the intake of alcohol and drugs. Therefore, there is an emerging shift into a new field of testing drugs that affect appetite hormones and their receptors in the brain, and their use in regulating the brain mechanisms that lead to relapse in addiction disorders.

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