Books: 'Paracrine'

1

Krey, Lewis C., Bela J. Gulyas, and John A. McCracken, eds. Autocrine and Paracrine Mechanisms in Reproductive Endocrinology. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5751-3.

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2

Reproductive Endocrinology Study Section Workshop on Autocrine and Paracrine Mechanisms in Reproductive Endocrinology (1988 Shrewsbury, Mass.). Autocrine and paracrine mechanisms in reproductive endocrinology. Plenum Press, 1989.

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3

Marshall, Joanne Louise. Paracrine regulation of renal function in the rat. University of Birmingham, 1998.

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4

Nikula, Hannu. Endocrine and paracrine modulation of gonadotropin action in the rat testis. Turun Yliopisto, 1990.

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5

R, Bellvé Anthony, and Vogel Henry J. 1920-, eds. Molecular mechanisms in cellular growth and differentiation. Academic Press, 1991.

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6

J, Dietze Guenther, ed. A symposium, autocrine and paracrine signaling between contracting myocardium and coronary endothelium during ischemia: Effect of insulin resistance. Excerpta Medica, 1997.

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7

Susan, Heyner, and Wiley Lynn M, eds. Early embryo development and paracrine relationships: Proceedings of a UCLA Symposia Colloquium, held at Taos, New Mexico, February 3-8, 1989. Wiley-Liss, 1990.

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8

1942-, Sowers James R., ed. Endocrinology of the vasculature. Humana Press, 1996.

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9

Walter, Helen Jane. The spatio-temporal modulation of the insulin-like growth factor[s] axis in the lesioned central nervous system: Implications for endocrine, paracrine and autocrine activities. University of Birmingham, 1996.

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10

Lise, Cédard, and Firth Anthony, eds. Placental signals: Autocrine and paracine control of pregnancy. University of Rochester Press, 1992.

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11

F, Piva, and International Symposium on "Cell to Cell Communication in Endocrinology" (1987 : Florence, Italy), eds. Cell to cell communication in endocrinology. Raven Press, 1988.

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12

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

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13

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

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14

Paracrine control. Saunders, 1986.

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15

Krey, L. Autocrine and Paracrine Mechanisms in Reproductive Endocrinology. Springer London, Limited, 2012.

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16

Krey, L. Autocrine and Paracrine Mechanisms in Reproductive Endocrinology. Springer London, Limited, 2013.

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17

Autocrine and Paracrine Mechanisms in Reproductive Endocrinology (Reproductive Biology). Springer, 1990.

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18

Bael, A. Van. Paracrine Growth Factors Control: The Development of Lactotrophs and Somatotrophs. Leuven University Press, 1996.

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19

Erben, Reinhold G., and L. Darryl Quarles, eds. Endocrine and Paracrine Role of FGF23 and Klotho in Health and Disease. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-805-9.

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20

Tilemans, D. Paracrine Control of the Development of Anterior Pituitary Cells in the Rat. Leuven University Press, 1992.

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21

Carmeliet, P. Production, Release and Paracrine Action of Acetylcholine in the Anterior Pituitary of the Rat. Leuven University Press, 1989.

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22

Heyner, Susan, and Lynn M. Wiley. Early Embryo Development and Paracrine Relationships (UCLA Symposia on Molecular and Cellular Biology, New Series). John Wiley & Sons Inc, 1990.

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23

Guraya, Sardul S. Comparative Cellular and Molecular Biology of Testis in Vertebrates: Trends in Endocrine, Paracrine and Autocrine Regulation of Structure and Functions. Science Publishers, 2001.

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24

Sowers, J. R. Endocrinology of the Vasculature. Humana Press, 2012.

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25

Goldberg, Erwin, Barry Zirkin, Vassilios Papadopoulos, and Polina V. Lishko, eds. Endocrine and Paracrine Regulation of Spermatogenesis - A Collection of Up to Date Research Contributions on Testis Formation and Function. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-859-2.

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26

Hoeben, Eva. Local Control of Sertoli Cell Function: Paracrine Factors Produced by Peritubular Myoid Cells and Cytokines (Acta Biomedica Lovaniensia , No 161). Coronet Books Inc, 1998.

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27

Mclver, Bryan, Peter J. Tebben, and Pankaj Shah. Endocrinology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0200.

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Numerous chemical messages control various functions at the levels of cells, organs, and organ systems. Such messages may be autocrine (the chemical message directly affects the cell producing it), paracrine (the message has local effects), or endocrine (the message has distant sites of action). Typically, endocrine effects are caused by hormones that are produced by specialized organs, although several important endocrine functions are performed by nonglandular tissues, most prominently the liver and the kidney. Disorders of the hypothalamus, ovaries, testes, and pituitary, thyroid, and adrenal glands are reviewed.

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28

Menasché, Philippe. Stem Cell Therapy Post-AMI. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0010.

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• Experimental studies suggest that bone marrow-derived stem cells can improve function of infarcted myocardium• This benefit seems to involve paracrine signalling and limitation of left ventricular remodelling rather than true regeneration of cardiomyocytes from donor cells• These experimental findings have been translated in the clinical setting into significant, although moderate, improvements in cardiac function and LV remodelling but the extent to which these benefits impact on event-free long term survival remains to be determined• Optimisation of this therapeutic strategy will require a more comprehensive characterisation of cell functionality and an improvement in the methods used in cell transfer, engraftment, survival and integration.

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29

Yang, Zhihong, and Xiu-Fen Ming. Adventitia and perivascular adipose tissue—the integral unit in vascular disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0020.

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Obesity and obesity-associated metabolic disorders are highly associated with cardiovascular disease. Abnormal ectopic deposition and accumulation of adipose tissue in organs, including perivascular space (perivascular adipose tissue, PVAT) in obesity are emerging to contribute to vascular disease development through pathological paracrine and/or endocrine secretion of cytokines, namely adipokines, which are vasoactive factors including vascular relaxing and contracting factors, smooth muscle growth promoting and inhibiting factors, and pro- and anti-inflammatory factors. In obesity, production of these factors from PVAT is altered and in imbalance which favours vascular contraction, pathological remodelling, and inflammation. In cross-talk with the endothelium, the functional changes of adventitia and PVAT are detrimental and importantly contribute to the acceleration of vascular atherosclerosis and complications associated with obesity and metabolic disorders

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30

Bhattacharya, Jahar. Cell Signaling in Vascular Inflammation. Humana, 2010.

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31

Bhattacharya, Jahar. Cell Signaling in Vascular Inflammation. Humana Press Inc.,U.S., 2005.

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32

Placental Signals Autocrine and Paracine Control of Pregnancy (Trophoblast Research). University of Rochester Press, 1993.

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33

van Hinsbergh, Victor W. M. Physiology of blood vessels. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0002.

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This chapter covers two major fields of the blood circulation: ‘distribution’ and ‘exchange’. After a short survey of the types of vessels, which form the circulation system together with the heart, the chapter describes how hydrostatic pressure derived from the heartbeat and vascular resistance determine the volume of blood that is locally delivered per time unit. The vascular resistance depends on the length of the vessel, blood viscosity, and, in particular, on the diameter of the vessel, as formulated in the Poiseuille-Hagen equation. Blood flow can be determined in vivo by different imaging modalities. A summary is provided of how smooth muscle cell contraction is regulated at the cellular level, and how neuronal, humoral, and paracrine factors affect smooth muscle contraction and thereby blood pressure and blood volume distribution among tissues. Subsequently the exchange of solutes and macromolecules over the capillary endothelium and the contribution of its surface layer, the glycocalyx, are discussed. After a description of the Starling equation for capillary exchange, new insights are summarized(in the so-called glycocalyx cleft model) that led to a new view on exchange along the capillary and on the contribution of oncotic pressure. Finally mechanisms are indicated in brief that play a role in keeping the blood volume constant, as a constant volume is a prerequisite for adequate functioning of the circulatory system.

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34

Dussaule, Jean-Claude, Martin Flamant, and Christos Chatziantoniou. Function of the normal glomerulus. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0044_update_001.

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Glomerular filtration, the first step leading to the formation of primitive urine, is a passive phenomenon. The composition of this primitive urine is the consequence of the ultrafiltration of plasma depending on renal blood flow, on hydrostatic pressure of glomerular capillary, and on glomerular coefficient of ultrafiltration. Glomerular filtration rate (GFR) can be precisely measured by the calculation of the clearance of freely filtrated exogenous substances that are neither metabolized nor reabsorbed nor secreted by tubules: its mean value is 125 mL/min/1.73 m² in men and 110 mL/min/1.73 m² in women, which represents 20% of renal blood flow. In clinical practice, estimates of GFR are obtained by the measurement of creatininaemia followed by the application of various equations (MDRD or CKD-EPI) and more recently by the measurement of plasmatic C-cystatin. Under physiological conditions, GFR is a stable parameter that is regulated by the intrinsic vascular and tubular autoregulation, by the balance between paracrine and endocrine agents acting as vasoconstrictors and vasodilators, and by the effects of renal sympathetic nerves. The mechanisms controlling GFR regulation are complex. This is due to the variety of vasoactive agents and their targets, and multiple interactions between them. Nevertheless, the relative stability of GFR during important variations of systemic haemodynamics and volaemia is due to three major operating mechanisms: autoregulation of the afferent arteriolar resistance, local synthesis and action of angiotensin II, and the sensitivity of renal resistance vessels to respond to NO release.

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35

Niehoff, Debra. Language of Life: How Cells Communicate in Health and Disease. National Academies Press, 2005.

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36

Niehoff, Debra. Language of Life: How Cells Communicate in Health and Disease. National Academies Press, 2005.

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37

Niehoff, Debra. Language of Life: How Cells Communicate in Health and Disease. National Academies Press, 2005.

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38

Biochemical messengers: Hormones, neurotransmitters, and growth factors. Chapman & Hall, 1991.

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39

Hardie, D. G. Biochemical Messengers. Springer, 2012.

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40

Panzica, Giancarlo, Roberto C. Melcangi, and Italy) International Meeting on Steroids and the Nervous System (2nd : 2003 : Turin. Steroids and the Nervous System (Annals of the New York Academy of Sciences, V. 1007). New York Academy of Sciences, 2003.

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41

Steroids and the Nervous System (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2004.

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42

Whitworth, Caroline, and Stewart Fleming. Malignant hypertension. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.

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Malignant hypertension (MH) is recognized clinically by elevated blood pressure together with retinal haemorrhages or exudates with or without papilloedema (grades III or IV hypertensive retinopathy); and may constitute a hypertensive emergency or crisis when complicated by evidence of end-organ damage including microangiopathic haemolysis, encephalopathy, left ventricular failure, and renal failure. Though reversible, it remains a significant cause of end-stage renal failure, and of cardiovascular and cerebrovascular morbidity and mortality in developing countries.MH can complicate pre-existing hypertension arising from diverse aetiologies, but most commonly develops from essential hypertension. The absolute level of blood pressure appears not to be critical to the development of MH, but the rate of rise of blood pressure may well be relevant in the pathogenesis. The pathogenesis of this transformation remains unclear.The pathological hallmark of MH is the presence of fibrinoid necrosis (medial vascular smooth muscle cell necrosis and fibrin deposition within the intima) involving the resistance arterioles in many organs. Fibrinoid necrosis is not specific to MH and this appearance is seen in other conditions causing a thrombotic microangiopathy such as haemolytic uraemic syndrome, scleroderma renal crisis, antiphospholipid syndrome, and acute vascular rejection post transplant. MH can both cause a thrombotic microangiopathy (TMA) but can also complicate underlying conditions associated with TMA.The pathophysiological factors that interact to generate and sustain this condition remain poorly understood. Risk factors include Afro-Caribbean race, smoking history, younger age of onset of hypertension, previous pregnancy, and untreated hypertension associated with non-compliance or cessation of antihypertensive therapy.Evidence from clinical studies and animal models point to a central role for the intrarenal renin–angiotensin system (RAS) in MH; there is good evidence for renal vasoconstriction and activation of the renal paracrine RAS potentiating MH once established; however, there may also be a role in the predisposition of MH suggested by presence of increased risk conferred by an ACE gene polymorphism in humans and polymorphisms for both ACE and AT1 receptor in an animal model of spontaneous MH. Other vasoactive mediators such as the endothelin and the inflammatory response may be important contributing to and increasing endothelial damage. There have been no randomized controlled trials to define the best treatment approach, but progressive lowering of pressures over days is considered safest unless made more urgent by critical clinical state. It seems logical to introduce ACE inhibition cautiously and early, but in view of the risk of rapid pressure lowering some recommend delay.

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43

Cónsole-Avegliano, Gloria Miriam. Glándula hipofisaria: morfología normal y patológica. Editorial de la Universidad Nacional de La Plata (EDULP), 2017. http://dx.doi.org/10.35537/10915/61267.

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La obra Glándula hipofisaria: morfología normal y patológica integra y actualiza las investigaciones morfológicas normales y patológicas del eje hipotálamo-hipofisario desarrolladas en el Laboratorio de Investigaciones Neuroendocrinas de la Cátedra B de Citología, Histología y Embriología de la Facultad de Ciencias Médicas de la Universidad Nacional de La Plata (período 1990-2016). Los estudios morfológicos de la glándula pituitaria aportan una revisión de la embriología molecular, la histología óptica y ultraestructural de las diferentes poblaciones hipofisarias, las interacciones paracrinas adenohipofisarias y la fisiología del eje hipotálamo-hipofisario. En los diferentes capítulos se presentan los estudios colaborativos con equipos de investigación dirigidos por reconocidos especialistas en el campo de la Neuroendocrinología que aportaron aspectos bioquímicos, fisiológicos y de terapia génica neuroendocrina. Se abordan diversos diseños experimentales: envejecimiento, malnutrición, obesidad por denervación hipotalámica, fotoperíodos, antiandrógenos no esteroides, sialilación de la hormona folículo-estimulante, retardo del crecimiento intrauterino, isoformas de prolactina y numerosos ensayos de terapia génica con el factor neurotrófico insulino símil tipo I (IGF-I) aplicados al eje timo-pituitario, a los prolactinomas experimentales y a los procesos de neurodegeneración, utilizando adenovectores de última generación. Además, se aporta una caracterización morfológico-funcional de los adenomas hipofisarios y una actualización de las estrategias terapéuticas, haciendo énfasis en los promisorios ensayos con terapia génica experimental.

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Books on the topic 'Paracrine'

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