Journal articles: 'Endocrine changes'

1

Bayraktar, Miyase, and David H. Van Thiel. "Endocrine Changes in Liver Disease." Endocrinologist 5, no. 6 (November 1995): 403–15. http://dx.doi.org/10.1097/00019616-199511000-00004.

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KLEIN, NANCY A., and MICHAEL R. SOULES. "Endocrine Changes of the Perimenopause." Clinical Obstetrics and Gynecology 41, no. 4 (December 1998): 912–20. http://dx.doi.org/10.1097/00003081-199812000-00017.

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3

Van den Berghe, G. "Endocrine changes in criticallyill patients." Growth Hormone & IGF Research 9 (April 1999): 77–81. http://dx.doi.org/10.1016/s1096-6374(99)80015-x.

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4

Davidson, Michael, Leo Bastiaens, Bonnie M. Davis, Mahendra B. Shah, and Kenneth L. Davis. "Endocrine Changes in Alzheimer’s Disease." Neurologic Clinics 6, no. 1 (February 1988): 149–57. http://dx.doi.org/10.1016/s0733-8619(18)30889-2.

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Davidson, Michael, Leo Bastiaens, Bonnie M. Davis, Mahendra B. Shah, and Kenneth L. Davis. "Endocrine Changes in Alzheimer’s Disease." Endocrinology and Metabolism Clinics of North America 17, no. 1 (March 1988): 149–57. http://dx.doi.org/10.1016/s0889-8529(18)30438-9.

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Ferlazzo, Adriana, Pietro Medica, Cristina Cravana, and Esterina Fazio. "Endocrine changes after experimental showjumping." Comparative Exercise Physiology 6, no. 02 (May 2009): 59. http://dx.doi.org/10.1017/s1755254009990110.

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7

Felicetta, James V., and James R. Sowers. "Endocrine Changes with Critical Illness." Critical Care Clinics 3, no. 4 (October 1987): 855–69. http://dx.doi.org/10.1016/s0749-0704(18)30523-2.

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8

Nylen, Eric S., and Beat Muller. "Endocrine Changes in Critical Illness." Journal of Intensive Care Medicine 19, no. 2 (March 2004): 67–82. http://dx.doi.org/10.1177/0885066603259551.

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9

Hammar, Mats L., Göran E. Berg, Lasse Larsson, Hans-Göran Tiselius, and Eberhard Varenhorst. "Endocrine Changes and Urinary Citrate Excretion." Scandinavian Journal of Urology and Nephrology 21, no. 1 (January 1987): 51–53. http://dx.doi.org/10.3109/00365598709180291.

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10

Khardori, Romesh, and Danielle Castillo. "Endocrine and Metabolic Changes During Sepsis." Medical Clinics of North America 96, no. 6 (November 2012): 1095–105. http://dx.doi.org/10.1016/j.mcna.2012.09.005.

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11

Urbanski, H. "PERIMENOPAUSAL ENDOCRINE CHANGES IN RHESUS MACAQUES." Maturitas 63 (May 2009): S85. http://dx.doi.org/10.1016/s0378-5122(09)70334-2.

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12

Semple, C. G. "Hormonal changes in non-endocrine disease." BMJ 293, no. 6554 (October 25, 1986): 1049–52. http://dx.doi.org/10.1136/bmj.293.6554.1049.

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13

Haroutounian, Simon. "Postoperative opioids, endocrine changes, and immunosuppression." PAIN Reports 3, no. 2 (2018): e640. http://dx.doi.org/10.1097/pr9.0000000000000640.

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14

Solomon, Samuel. "Developmental changes in fetal endocrine systems." Steroids 51, no. 1-2 (January 1988): 1–61. http://dx.doi.org/10.1016/0039-128x(88)90184-5.

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15

Imura, Hiroo, and Jun-ichi Fukata. "Endocrine–paracine interaction in communication between the immune and endocrine systems. Activation of the hypothalamic-pituitary-adrenal axis in inflammation." European Journal of Endocrinology 130, no. 1 (January 1994): 32–37. http://dx.doi.org/10.1530/eje.0.1300032.

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Imura H, Fukata J. Endocrine–paracrine interaction in communication between the immune and endocrine systems. Activation of the hypothalamic-pituitary-adrenal axis in inflammation. Eur J Endocrinol 1994;130:32–7. ISSN 0804–4643 There are bidirectional communications between the immune and endocrine systems. Cytokines produced in inflammatory foci cause changes in the endocrine system, including activation of the hypothalamic-pituitary-adrenal (HPA) axis. Hormones produced in the endocrine system, especially glucocorticoids, affect the immune system to modulate its function. This is an important endocrine system for the defence mechanism. In addition, bacterial lipopolysaccharide produces cytokines in the brain and endocrine organs which are considered to act through the paracrine mechanism to regulate the HPA axis. Endocrine–paracrine interaction is important for the defence mechanism of the organism. Hiroo Imura, Kyoto University School of Medicine, Yoshida Honmachi Sakyo-ku, Kyoto 606-01, Japan

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16

El‐Sakka, Ahmed I., Howayda M. Hassoba, Hisham M. Sayed, and Khalid A. Tayeb. "ORIGINAL RESEARCH—ENDOCRINE: Pattern of Endocrinal Changes in Patients with Sexual Dysfunction." Journal of Sexual Medicine 2, no. 4 (July 2005): 551–58. http://dx.doi.org/10.1111/j.1743-6109.2005.00082.x.

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17

Winger, Jean Merhige, and Thomas Hornick. "AGE-ASSOCIATED CHANGES IN THE ENDOCRINE SYSTEM." Nursing Clinics of North America 31, no. 4 (December 1996): 827–44. http://dx.doi.org/10.1016/s0029-6465(22)00191-8.

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18

Dolecek, Rajko. "Endocrine changes after burn trauma - A review." Keio Journal of Medicine 38, no. 3 (1989): 262–76. http://dx.doi.org/10.2302/kjm.38.262.

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19

Wellby, M. L., J. A. Kennedy, P. B. Barreau, and W. E. Roediger. "Endocrine and cytokine changes during elective surgery." Journal of Clinical Pathology 47, no. 11 (November 1, 1994): 1049–51. http://dx.doi.org/10.1136/jcp.47.11.1049.

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20

Salmon, Peter, Robert Evans, and Diana E. Humphrey. "Anxiety and endocrine changes in surgical patients." British Journal of Clinical Psychology 25, no. 2 (May 1986): 135–41. http://dx.doi.org/10.1111/j.2044-8260.1986.tb00682.x.

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21

Wu, Deqing, Yaping Xu, Yue Zeng, and Xingpeng Wang. "Endocrine Pancreatic Function Changes After Acute Pancreatitis." Pancreas 40, no. 7 (October 2011): 1006–11. http://dx.doi.org/10.1097/mpa.0b013e31821fde3f.

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22

Rose, Susan R., and Bethany A. Auble. "Endocrine changes after pediatric traumatic brain injury." Pituitary 15, no. 3 (November 5, 2011): 267–75. http://dx.doi.org/10.1007/s11102-011-0360-x.

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23

Milewicz, Andrzej, and Marek Demissie. "Metabolic and endocrine changes in climacteric women." International Congress Series 1229 (February 2002): 3–7. http://dx.doi.org/10.1016/s0531-5131(01)00478-2.

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24

Gunn, I. R., and R. B. Payne. "Points: Calcium changes in non-endocrine disease." BMJ 293, no. 6559 (November 29, 1986): 1441. http://dx.doi.org/10.1136/bmj.293.6559.1441-c.

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25

Yamauchi, Hitoshi, Eiji Kobayashi, Takeshi Yoshida, Hirokazu Kiyozaki, Yasuo Hozumi, Ritu Kohiyama, Yoshihisa Suminaga, Ikunosuke Sakurabayashi, Akio Fujimura, and Michio Miyata. "CHANGES IN IMMUNE-ENDOCRINE RESPONSE AFTER SURGERY." Cytokine 10, no. 7 (July 1998): 549–54. http://dx.doi.org/10.1006/cyto.1997.0322.

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26

Ranasinghe, Aaron M., and Robert S. Bonser. "Endocrine changes in brain death and transplantation." Best Practice & Research Clinical Endocrinology & Metabolism 25, no. 5 (October 2011): 799–812. http://dx.doi.org/10.1016/j.beem.2011.03.003.

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27

Banks, W. A., and J. E. Morley. "Endocrine and metabolic changes in human aging." AGE 23, no. 2 (April 2000): 103–15. http://dx.doi.org/10.1007/s11357-000-0011-z.

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28

Dunger, DB, and JA Edge. "Diabetes and the endocrine changes of puberty." Practical Diabetes International 12, no. 2 (March 1995): 63–66. http://dx.doi.org/10.1002/pdi.1960120205.

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29

P, Nivedha. "The Impact of Environmental Endocrine Disruptors on Mammalian Endocrine Systems and Hormonal Changes." Technoarete Transactions on Recent Research in Applied Microbiology and Biotechnology 1, no. 1 (March 3, 2022): 16–20. http://dx.doi.org/10.36647/ttrramb/01.01.a004.

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This study discusses the impact of the EDCS or environmental endocrine disruptors in the mammalian endocrine system and also in the hormonal changes. As the EDCs have a role to mimic the pathway and the activity of hormones then the detection method is the first and foremost important concern in this scenario. This study also reflects some detection assays of environmental endocrine disruptors by which their impact can be effectively understood. As EDCs alter the hormonal function then it can be said that beta lactamase activity is the main theme for detecting endocrine disruptors. Endocrine disrupting chemicals can be chosen in the human samples by using the biosensor protein. The final nitrocefin concentration effectively detects the activity of EDCs. The study also discusses some key aspects of changes of hormonal function by EDCs in gene and protein level. The gene and protein level study are beneficial in this scenario for understanding the mode of action of each and every type of environmental endocrine disruptors. The graph has been presented in this scenario for understanding the expression level of proteins. Keyword : Environmental endocrine disruptors, EDCs, biosensor protein, beta lactamase activity

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30

Fowden, A. L., and A. J. Forhead. "Endocrine mechanisms of intrauterine programming." Reproduction 127, no. 5 (May 2004): 515–26. http://dx.doi.org/10.1530/rep.1.00033.

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Epidemiological findings and experimental studies in animals have shown that individual tissues and whole organ systems can be programmedin uteroduring critical periods of development with adverse consequences for their function in later life. Detailed morphometric analyses of the data have shown that certain patterns of intrauterine growth, particularly growth retardation, can be related to specific postnatal outcomes. Since hormones regulate fetal growth and the development of individual fetal tissues, they have a central role in intrauterine programming. Hormones such as insulin, insulin-like growth factors, thyroxine and the glucocorticoids act as nutritional and maturational signals and adapt fetal development to prevailing intrauterine conditions, thereby maximizing the chances of survival bothin uteroand at birth. However, these adaptations may have long-term sequelae. Of the hormones known to control fetal development, it is the glucocorticoids that are most likely to cause tissue programmingin utero. They are growth inhibitory and affect the development of all the tissues and organ systems most at risk of postnatal pathophysiology when fetal growth is impaired. Their concentrationsin uteroare also elevated by all the nutritional and other challenges known to have programming effects. Glucocorticoids act at cellular and molecular levels to alter cell function by changing the expression of receptors, enzymes, ion channels and transporters. They also alter various growth factors, cytoarchitectural proteins, binding proteins and components of the intracellular signalling pathways. Glucocorticoids act, directly, on genes and, indirectly, through changes in the bioavailability of other hormones. These glucocorticoid-induced endocrine changes may be transient or persist into postnatal life with consequences for tissue growth and development both before and after birth. In the long term, prenatal glucocorticoid exposure can permanently reset endocrine systems, such as the somatotrophic and hypothalamic–pituitary–adrenal axes, which, in turn, may contribute to the pathogenesis of adult disease. Endocrine changes may, therefore, be both the cause and the consequence of intrauterine programming.

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31

Freeman, Hugh J. "Pancreatic endocrine and exocrine changes in celiac disease." World Journal of Gastroenterology 13, no. 47 (2007): 6344. http://dx.doi.org/10.3748/wjg.v13.i47.6344.

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32

Apter, D. "049 Menstrual cycle and endocrine changes during puberty." European Journal of Obstetrics & Gynecology and Reproductive Biology 273 (June 2022): e19. http://dx.doi.org/10.1016/j.ejogrb.2022.02.078.

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33

Ichijo, Sadatoshi, Kiyoo Koseki, Yoshinari Sakagami, and Yasuo Shiraiwa. "CYTOLOGICAL CHANGES BY ENDOCRINE THERAPIES OF PROSTATIC CARCINOMA." Japanese Journal of Urology 81, no. 5 (1990): 701–6. http://dx.doi.org/10.5980/jpnjurol1989.81.701.

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34

Güven, M., F. Bayram, K. Ünlühizarci, and F. Kelestimur. "Endocrine changes in patients with acute organophosphate poisoning." Human & Experimental Toxicology 18, no. 10 (October 1999): 598–601. http://dx.doi.org/10.1191/096032799678839419.

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In critical illness, several drugs and various stressful conditions modify the functions of neurotransmitters which consequently affect the secretion of pituitary hormones. Although the role of neurotransmitters in the regulation of endocrine system is well known, cholinergic actions have been less investigated. In animals, cholinesterase inhibitors were shown to modify the pituitary-thyroid and pituitary-adrenal axes, and to affect prolactin levels. The aim of the present study was to determine the effect of the organophosphate compounds on endocrine system, particularly pituitary hormones. This prospective study was performed in Medical Intensive Care Unit of Erciyes University Medical School Hospital. Twenty-two consecutive patients (ten males and 12 females aged 28+8 years) with organophosphate poisoning were included in the study. ACTH (P50.002), cortisol (P50.0005) and PRL (P50.005) levels were significantly higher during poisoning than after resolution of poisoning. FSH levels were significantly lower during poisoning (P50.05). Sick euthyroid syndrome was determined in seven patients (31.8%). Two of them had low fT3 (with normal fT4 and TSH), two had low fT4 (with normal fT3 and TSH) and three had low TSH (with normal fT3 and fT4) levels. Serum levels of these hormones returned to normal values after resolution of poisoning. The present study demonstrated that organophosphate compounds affected PRL, ACTH and cortisol levels, but did not change LH levels. Organophosphate compounds may result in sick euthyroid syndrome. These conditions may be related to the effects of acetylcholine and direct effect of organophosphate compounds.

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35

Buckler, Helen. "The menopause transition: endocrine changes and clinical symptoms." British Menopause Society Journal 11, no. 2 (June 1, 2005): 61–65. http://dx.doi.org/10.1258/136218005775544525.

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Several biological changes take place during the menopause transition. The number of oocytes declines progressively from before birth but reaches a critically low level by the time of the menopause. The regular pattern of the menstrual cycle becomes disrupted and the frequency of normal ovulatory cycles declines. Rising gonadotrophin levels, particularly of follicle stimulating hormones (FSH), and declining estrogen levels are thought to characterize the menopausal transition. It now appears that declining levels of inhibin may play an important role in maintaining estrogen levels until just before the menopause, while causing increased levels of gonadotrophins. Wide variations in hormonal profiles between and within individuals occur. The clinical responses to this endocrine instability include vasomotor symptoms, psychological symptoms, sexual dysfunction and irregular menstrual bleeding. Estradiol deficiency induces a rapid phase of increased bone turnover in the early postmenopausal period, which can contribute to osteoporosis later in life. Similarly, changes in lipid profiles, particularly high-density lipoprotein (HDL) and triglycerides, can also occur.

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36

Neville, Margaret C., and Jane Morton. "Physiology and Endocrine Changes Underlying Human Lactogenesis II." Journal of Nutrition 131, no. 11 (November 1, 2001): 3005S—3008S. http://dx.doi.org/10.1093/jn/131.11.3005s.

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37

Aba, M. A., P. W. Bravo, M. Forsberg, and H. Kindahl. "Endocrine changes during early pregnancy in the alpaca." Animal Reproduction Science 47, no. 4 (July 1997): 273–79. http://dx.doi.org/10.1016/s0378-4320(97)00028-6.

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38

Støving, R. K., J. Hangaard, M. Hansen-Nord, and C. Hagen. "A review of endocrine changes in anorexia nervosa." Journal of Psychiatric Research 33, no. 2 (March 1999): 139–52. http://dx.doi.org/10.1016/s0022-3956(98)00049-1.

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39

Drewes, Jörg E., Jocelyn Hemming, Sarah Ladenburger, Jamie Schauer, and William Sonzogni. "ENDOCRINE DISRUPTING ACTIVITY CHANGES IN WATER RECLAMATION SYSTEMS." Proceedings of the Water Environment Federation 2005, no. 13 (January 1, 2005): 3196–212. http://dx.doi.org/10.2175/193864705783865172.

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40

Cameron, Oliver G., Myung A. Lee, George C. Curtis, and Daisy S. McCann. "Endocrine and physiological changes during “spontaneous” panic attacks." Psychoneuroendocrinology 12, no. 5 (January 1987): 321–31. http://dx.doi.org/10.1016/0306-4530(87)90061-8.

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41

Fudvoye, Julie, David Lopez-Rodriguez, Delphine Franssen, and Anne-Simone Parent. "Endocrine disrupters and possible contribution to pubertal changes." Best Practice & Research Clinical Endocrinology & Metabolism 33, no. 3 (June 2019): 101300. http://dx.doi.org/10.1016/j.beem.2019.101300.

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42

Khairallah, Ahmed, Abo‐Alela Farag, Dina Johar, and Larry Bernstein. "Endocrine Imbalance Associated With Proteome Changes in Diabetes." Journal of Cellular Biochemistry 118, no. 11 (May 26, 2017): 3569–76. http://dx.doi.org/10.1002/jcb.26071.

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43

Brunton, Paula J., and John A. Russell. "Endocrine induced changes in brain function during pregnancy." Brain Research 1364 (December 2010): 198–215. http://dx.doi.org/10.1016/j.brainres.2010.09.062.

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44

Romero Lluch, Ana, Ignacio Jiménez, Emilio García-García, Raquel Guerrero, and María Asunción Martínez-Brocca. "Endocrine and psychological changes in polysomy 48,XXXY." Endocrinología y Nutrición (English Edition) 59, no. 6 (June 2012): 396–98. http://dx.doi.org/10.1016/j.endoen.2012.07.003.

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45

Araújo, Flávio Henrique Souza de, Raquel Borges de Barros Primo, Mi Ye Marcaida Olimpio, Nathalia Oliveira da Silva, Catherine Alexia Yoshikawa, Lígia Harumi Vilela Bartnick Tanaka, Vinício Guimarães Freitas, Luiz Fernando Benazet de Assunção Pereira, Thais Gimenes Bachega, and Silvia Aparecida Oesterreich. "Changes In Hormonal Response Caused By Different Types Of Physical Exercise." International Journal for Innovation Education and Research 9, no. 4 (April 1, 2021): 215–22. http://dx.doi.org/10.31686/ijier.vol9.iss4.3042.

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The regular practice of physical exercises brings benefits to health, as long as it is done correctly. Therefore, it is essential to know the type of activity practiced and its relationship with the individual's organism, especially regarding the endocrine response. The objective of this study was to investigate the main hormonal axes that act in physical exercises and to understand their different responses according to the type of activity. A literature search was carried out in the Scielo, PubMed, and VHL databases with the combinations "exercise AND hormones", "sports AND endocrine", "endocrine regulation AND exercise", and "endocrine regulation". After analysis, seven studies were selected for the development of this paper. The physical exercises were divided into two modalities - strength and endurance - which vary according to the homeostatic change imposed on the body. The responses were analyzed according to the acting hormonal axis, as follows: hypophysary, by the action of a hormonal cascade; adrenal, catecholamines and cortisol; and pancreatic, represented by insulin and glucagon. This review revealed the modulation of endocrine responses varies whether the activity is one of strength, which relates to anaerobic processes, or endurance, which interacts with the cardiovascular system. Therefore, it is recommended that further studies be conducted on this subject so that the practice of physical exercises suits each individual's uniqueness and may contribute to the prevention and treatment of diseases.

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46

Khamidova, Farida Muinovna. "MORPHOFUNCTIONAL CHANGES IN THE PANCREAS IN EXPERIMENTAL HYPOTHYROIDISM." American Journal of Medical Sciences and Pharmaceutical Research 04, no. 02 (February 1, 2022): 28–32. http://dx.doi.org/10.37547/tajmspr/volume04issue02-07.

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Thyroid pathology is rather frequent among endocrine diseases and according to WHO, covers 7% of the world population. According to specialists' prognoses the tendency of thyroid gland (TSH) diseases number increase will remain in the nearest years due to fast industrial growth and environmental pollution with industrial and radioactive wastes, changes in microelement composition of soil, hereditary predisposition. The morphofunctional state of the thyroid gland depends directly on anthropogenic factors and is a marker of environmental disadvantage in a given region.

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47

Carlson, H. E., M. L. Graber, M. C. Gelato, and J. M. Hershman. "Endocrine Effects of Erythropoietin." International Journal of Artificial Organs 18, no. 6 (June 1995): 309–14. http://dx.doi.org/10.1177/039139889501800603.

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Uremic men may manifest a variety of hormonal abnormalities, including decreased serum concentrations of testosterone and thyroid hormones and increased serum levels of growth hormone and prolactin. Some previous investigations have reported that erythropoietin therapy may reverse these hormonal changes. To investigate this possibility further, we measured serum prolactin, testosterone, LH, FSH, TSH, free thyroxine, triiodothyronine, growth hormone and IGF-I in 21 generally elderly male hemodialysis patients before and during erythropoietin therapy; many of the patients also received an anabolic steroid or metoclopramide treatment. Despite a significant erythropoietic response in a majority of the subjects, no significant changes were seen in any of the hormonal parameters other than a small decrease in serum growth hormone concentrations. Advanced age and chronic illness in our patients may have played a role in limiting the hormonal response reported by others.

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48

Wasyluk, Weronika, Martyna Wasyluk, and Agnieszka Zwolak. "Sepsis as a Pan-Endocrine Illness—Endocrine Disorders in Septic Patients." Journal of Clinical Medicine 10, no. 10 (May 12, 2021): 2075. http://dx.doi.org/10.3390/jcm10102075.

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Sepsis is defined as “life-threatening organ dysfunction caused by a dysregulated host response to infection”. One of the elements of dysregulated host response is an endocrine system disorder. Changes in its functioning in the course of sepsis affect almost all hormonal axes. In sepsis, a function disturbance of the hypothalamic–pituitary–adrenal axis has been described, in the range of which the most important seems to be hypercortisolemia in the acute phase. Imbalance in the hypothalamic–pituitary–thyroid axis is also described. The most typical manifestation is a triiodothyronine concentration decrease and reverse triiodothyronine concentration increase. In the somatotropic axis, a change in the secretion pattern of growth hormone and peripheral resistance to this hormone has been described. In the hypothalamic–pituitary–gonadal axis, the reduction in testosterone concentration in men and the stress-induced “hypothalamic amenorrhea” in women have been described. Catecholamine and β-adrenergic stimulation disorders have also been reported. Disorders in the endocrine system are part of the “dysregulated host response to infection”. They may also affect other components of this dysregulated response, such as metabolism. Hormonal changes occurring in the course of sepsis require further research, not only in order to explore their potential significance in therapy, but also due to their promising prognostic value.

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49

Ulhôa, M. A., E. C. Marqueze, L. G. A. Burgos, and C. R. C. Moreno. "Shift Work and Endocrine Disorders." International Journal of Endocrinology 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/826249.

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The objective of this review was to investigate the impact of shift and night work on metabolic processes and the role of alterations in the sleep-wake cycle and feeding times and environmental changes in the occurrence of metabolic disorders. The literature review was performed by searching three electronic databases for relevant studies published in the last 10 years. The methodological quality of each study was assessed, and best-evidence synthesis was applied to draw conclusions. The literature has shown changes in concentrations of melatonin, cortisol, ghrelin, and leptin among shift workers. Melatonin has been implicated for its role in the synthesis and action of insulin. The action of this hormone also regulates the expression of transporter glucose type 4 or triggers phosphorylation of the insulin receptor. Therefore, a reduction in melatonin can be associated with an increase in insulin resistance and a propensity for the development of diabetes. Moreover, shift work can negatively affect sleep and contribute to sedentarism, unhealthy eating habits, and stress. Recent studies on metabolic processes have increasingly revealed their complexity. Physiological changes induced in workers who invert their activity-rest cycle to fulfill work hours include disruptions in metabolic processes.

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50

Jabbour, Henry N., Rodney W. Kelly, Hamish M. Fraser, and Hilary O. D. Critchley. "Endocrine Regulation of Menstruation." Endocrine Reviews 27, no. 1 (September 13, 2005): 17–46. http://dx.doi.org/10.1210/er.2004-0021.

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In women, endometrial morphology and function undergo characteristic changes every menstrual cycle. These changes are crucial for perpetuation of the species and are orchestrated to prepare the endometrium for implantation of a conceptus. In the absence of pregnancy, the human endometrium is sloughed off at menstruation over a period of a few days. Tissue repair, growth, angiogenesis, differentiation, and receptivity ensue to prepare the endometrium for implantation in the next cycle. Ovarian sex steroids through interaction with different cognate nuclear receptors regulate the expression of a cascade of local factors within the endometrium that act in an autocrine/paracrine and even intracrine manner. Such interactions initiate complex events within the endometrium that are crucial for implantation and, in the absence thereof, normal menstruation. A clearer understanding of regulation of normal endometrial function will provide an insight into causes of menstrual dysfunction such as menorrhagia (heavy menstrual bleeding) and dysmenorrhea (painful periods). The molecular pathways that precipitate these pathologies remain largely undefined. Future research efforts to provide greater insight into these pathways will lead to the development of novel drugs that would target identified aberrations in expression and/or of local uterine factors that are crucial for normal endometrial function.

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Journal articles on the topic 'Endocrine changes'

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