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      The Need to Consider Pregnancy As a Biological Variable to Reduce Preventable Suffering Related to Pregnancy

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          Abstract

          Maternal morbidity and mortality constitute a national health crisis, and pain is a significant component of maternal morbidity. One important way to reduce maternal morbidity is to reduce the pain associated with pregnancy. Unfortunately, our understanding of how to reduce pain in women is hampered because, historically, mostly male subjects have been used in the study of pain. However, more recently, females increasingly have been included in pain research studies, and astounding differences in how males and females process pain have been uncovered. Moreover, pain in nonpregnant women differs in many ways from pain experienced by pregnant women. We argue here that to better address maternal morbidity, we must better address the pain associated with pregnancy. Furthermore, just as it is important to include both men and women in pain research to better understand pain in both sexes, conducting pain research in pregnant women is essential to finding ways to reduce pain in pregnant women.

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          Most cited references48

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          Different immune cells mediate mechanical pain hypersensitivity in male and female mice.

          A large and rapidly increasing body of evidence indicates that microglia-to-neuron signaling is essential for chronic pain hypersensitivity. Using multiple approaches, we found that microglia are not required for mechanical pain hypersensitivity in female mice; female mice achieved similar levels of pain hypersensitivity using adaptive immune cells, likely T lymphocytes. This sexual dimorphism suggests that male mice cannot be used as proxies for females in pain research.
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            A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man.

            A peripheral mononeuropathy was produced in adult rats by placing loosely constrictive ligatures around the common sciatic nerve. The postoperative behavior of these rats indicated that hyperalgesia, allodynia and, possibly, spontaneous pain (or dysesthesia) were produced. Hyperalgesic responses to noxious radiant heat were evident on the second postoperative day and lasted for over 2 months. Hyperalgesic responses to chemogenic pain were also present. The presence of allodynia was inferred from the nocifensive responses evoked by standing on an innocuous, chilled metal floor or by innocuous mechanical stimulation, and by the rats' persistence in holding the hind paw in a guarded position. The presence of spontaneous pain was suggested by a suppression of appetite and by the frequent occurrence of apparently spontaneous nocifensive responses. The affected hind paw was abnormally warm or cool in about one-third of the rats. About one-half of the rats developed grossly overgrown claws on the affected side. Experiments with this animal model may advance our understanding of the neural mechanisms of neuropathic pain disorders in humans.
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              Th1/Th2/Th17 and regulatory T-cell paradigm in pregnancy.

              T-helper (Th) cells play a central role in modulating immune responses. The Th1/Th2 paradigm has now developed into the new Th1/Th2/Th17 paradigm. In addition to effector cells, Th cells are regulated by regulatory T (Treg) cells. Their capacity to produce cytokines is suppressed by immunoregulatory cytokines such as transforming growth factor (TGF)-beta and interleukin (IL)-10 or by cell-to-cell interaction. Here, we will review the immunological environment in normal pregnancy and complicated pregnancy, such as implantation failure, abortion, preterm labor, and preeclampsia from the viewpoint of the new Th1/Th2/Th17 and Treg paradigms.
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                Author and article information

                Journal
                J Womens Health (Larchmt)
                J Womens Health (Larchmt)
                jwh
                Journal of Women's Health
                Mary Ann Liebert, Inc., publishers (140 Huguenot Street, 3rd FloorNew Rochelle, NY 10801USA )
                1540-9996
                1931-843X
                February 2021
                02 February 2021
                02 February 2021
                : 30
                : 2
                : 260-264
                Affiliations
                [ 1 ]Office of Research on Women's Health, Office of the Director, National Institutes of Health, Bethesda, Maryland, USA.
                [ 2 ]Office of FOA Development and Referral, Division of Extramural Research Activities, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.
                Author notes
                [*]Address correspondence to: David A. Thomas, PhD, Office of Research on Women's Health, Office of the Director, National Institutes of Health, 6707 Democracy Boulevard (Democracy II), Suite 400, Bethesda, MD 20892-5484, USA david.thomas@ 123456nih.gov
                Article
                10.1089/jwh.2020.8870
                10.1089/jwh.2020.8870
                8020516
                33216677
                fe3776ba-9bb1-4ac2-be49-f07f6aa22e71
                © David A. Thomas et al. 2021; Published by Mary Ann Liebert, Inc.

                This Open Access article is distributed under the terms of the Creative Commons Attribution Noncommercial License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and the source are cited.

                History
                Page count
                References: 52, Pages: 5
                Categories
                Special Issue Articles

                pain,pregnancy,analgesia,maternal morbidity
                pain, pregnancy, analgesia, maternal morbidity

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